Cardiovascular

Front 1

Vasculitis Definition, Histology, Etiology

Back 1

-inflammation of the blood vessel wall

---arterial wall is composed of: endothelial intima, SM media (endothelial cells on BM), and connective tissue adventitia

-Etiology unknown

Front 2

Clinical Features of Vasculitis

Back 2

-nonspecific symptoms: inflammation = fever, fatigue, weight loss, and myalgias

-symptoms of organ ischemia

---1. inflammation >> endothelial damage >> coagulation cascade >> thrombus

---2. inflammation >> healing & fibrosis >> luminal narrowing

Front 3

Categorization of Vasculitis & Definition of Each

Back 3

-Large Vessel Vasculitis: involves aorta and its major branches

-Medium Vessel Vasculitis: involves muscular arteries that supply organs

-Small Vessel Vasculitis: involves arterioles, capillaries, and venules

Front 4

Types of Large Vessel Vasculitis

Back 4

-Temporal (Giant Cell) Arteritis

-Takayasu Arteritis

Front 5

Temporal Arteritis

Definition/ Involvement? Seen in?

Back 5

-Large Vessel Vasculitis (of temporal artery & its branches)

-Granulomatous vasculitis that classically involves branches of the carotid artery

-most common form of vasculitis in older adults (>50 yrs old); usually affects women

Front 6

Temporal Arteritis Presentation & Associated Vascular Involvement

Back 6

-Headache from temporal artery involvement; unilateral headache

-Visual disturbances from ophthalmic artery involvement/occlusion >> irreversible blindness

-Jaw Claudication (muscles of jaw affected)

-Polymyalgia rheumatica: Flu-like symptoms with joint and muscle pain (if no elevated CK, then it is this, if elevated CK, polymyositis)

---ESR elevated in these patients (>100) - if this isn't elevated, then it isn't a vasculitis >> TIA

Front 7

Temporal Arteritis Biopsy/Diagnosis

Back 7

-reveals inflamed vessel wall with giant cells and intimal fibrosis

---Lesions are segmental; diagnosis requires biopsy of a long segment of vessel and a negative vessel doesn't exclude the disease

-inflammation >> increased ESR

Front 8

Temporal Arteritis Treatment & Complications

Back 8

-Treatment: corticosteroids prior to temporal artery biopsy to avoid vision loss

-High Risk of blindness without treatment; therefore, treat immediately

Front 9

Biopsy of Vessel

Back 9

-broad area of fibrosis in between intima and media (separation should not be there)

-fibrosis >> narrow lumen

-inflammation in blood vessel wall

-giant cells also observed

Front 10

Takyasu Arteritis

Definition? Seen In? Presentation? Treatment

Back 10

-Large Vessel Arteritis (elastic arteries)

-Granulomatous vasculitis (thickening & narrowing) that classically involves the aortic arch & proximal great vessels

-Presents in adults <40-50 yo (classically, young, Asian females) as visual and neurologic symptoms with a weak or absent pulse in the upper extremitiy ('pulseless disease'), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances

-Elevated ESR

-Treatment: corticosteroids

Front 11

Aortic Arch

Back 11

Takayasu arteritis

thickening and narrowing of aortic arch and its branches (proximal great vessels)

Front 12

Difference Between Temporal Arteritis & Takyasu Arteritis

Back 12

-Temporal Arteritis affects individuals > 50 old & distal (branches of carotid artery)

-Takyasu affects Asian females < 50 yo & proximal (aortic arch branch points)

Front 13

Polyarteritis Nodosa

Definition? Seen In?

Back 13

-Medium Vessel Vasculitis - muscular arteries that supply organs

-Necrotizing vasculitis involving multiple organs (renal and visceral) EXCEPT the lung

-Seen In: young adults

Front 14

Polyarteritis Nodosa

Presentation & Pathogenesis/Involvement?

Back 14

-Hypertension: due to renal artery involvement >> renal damage

-Abdominal Pain with melena: mesenteric artery involvement

-Neurologic disturbances

-Skin lesions - cutaneous eruptions

-fever, weight loss, malaise, headache

-Associated with HBsAg (30%)

-pANCA (according to Goljan's)

Front 15

Polyarteritis Nodosa

Lesions/Stages? Pathogenesis of Imaging?

Back 15

-Lesions of varying stages are present

-Early lesions consist of transmural inflammation with fibrinoid necrosis >> eventually heals (end stage) with fibrosis (feels bumpy) >> string of pearls appearance on imaging (long vessel w/ lesions of varying stage of dense fibrosis and inflammation >> weakened wall of vessel >> numerous microaneurysms & vasopasm on arteriogram)

Front 16

Polyarteritis Nodosa

Treatment? Prognosis?

Back 16

-Treatment: corticosteroids of cyclophosphamide

-Fatal if not treated

Front 17

Back 17

Polyarteritis Nodosa

-numerous microaneurysms

Front 18

Biopsy of Vessel

Back 18

Polyarteritis Nodosa

-fibrinoid necrosis w/ highlighter pink!

Front 19

Kawasaki Disease

definition? Seen in?

Back 19

-medium vessel vasculitis (muscular)

-Seen In: Asian children < 4 yo

Front 20

Kawasaki Disease

Presentation?

Back 20

-presents with nonspecific symptoms: fever, conjunctivitis, strawberry tongue (and lips), erythematous rash of palms and soles, enlarged cervical lymph nodes, desquamating rash

-risk of thrombosis >> infarction >> can present with MI

Front 21

Kawasaki Disease

Pathogenesis/Involvement? Complications?

Back 21

-coronary artery involvement common >> risk of thrombosis with MI and aneurysm with rupture

-so could present with a child with an MI!

Front 22

Kawasaki Disease

Treatment? Prognosis?

Back 22

-Treat with aspirin to protect against thrombus (watch out!: this presents similar to a viral illness >> can't give a child w/ a viral illness aspirin or they will get Reye Syndrome) and IVIG

-Disease is self-limited

Front 23

Reye Syndrome

Back 23

-when you give ASA to a child with a viral illness

-results in encephalopathy & massive liver necrosis

Front 24

Buerger Disease

Pathogenesis/Involvement? Seen in? Treatment?

Back 24

-medium-vessel (muscular) segmental, thrombosing vasculitis involving the digits

-Highly associated heavy smoking, males < 40

-Treat with smoking cessation

Front 25

Buerger Disease Presentation

Back 25

-Intermittent claudication >> ulceration, gangrene, superficial nodular phlebitis, and autoamputation of fingers & toes

-Raynaud phenomenon often present (caused by vasospasm)

Front 26

Wegener Granulomatosis

Pathogenesis/Involvement? Seen In?

Back 26

-small-vessel vasculitis (muscular)

=granulomatosis w/ polyangiitis

-necrotizing granulomatous vasculitis involving the nasopharynx, lungs, and kidneys

-middle aged male

Front 27

Wegener Granulomatosis Presentation, Findings, & Biopsy

Back 27

-middle aged male with chronic sinusitis or nasopharyngeal ulceration (perfration of nasal septum >> saddle nose deformity), otitis media, mastoiditis, hemoptysis, cough, dyspnea, with bilateral nodular lung infiltrates on CXR, and hematuria & red cell casts due to rapidly progressive glomerulonephritis

-serum PR3-ANCA/c-ANCA (anti-neutrophil cytoplasmic antibody) levels correlate with disease activity

-Biopsy: large necrotizing granulomas with adjacent necrotizing vasculitis

Front 28

Wegener Granulomatosis Treatment & Prognosis

Back 28

-cyclophosphamide and steroids

-relapse common

Front 29

Vessel Biopsy

Back 29

Wegener Granulomatosis

-large area of necrosis (forms lung nodules)

-wall has giant cells

Front 30

Vessel Biopsy

Back 30

Wegener Granulomatosis

-giant cells with epithelial histiocytes

Front 31

Microscopic Polyangiitis

Pathogenesis/Involvement?

Back 31

-small vessel vasculitis

-necrotizing vasculitis involving multiple organs, especially lung, kidney, and skin

Front 32

Microscopic Polyangiitis

Presentation? How is it different from Wegener Granulomatosis?

Back 32

-hemoptysis due to lung involvement

-hematuria due to pauci-immune glomerulonephritis

-palpable purpura

-MPO-ANCA/p-ANCA levels correlate with disease activity

-Difference: no nasopharyngeal involvement, no granulomas, & p-ANCA instead of c-ANCA

Front 33

Microscopic Polyangiitis

Treatment?

Back 33

-cyclophosphamide & corticosteroids

-relapse common

Front 34

Churg-Strauss Syndrome

Pathogenesis/Involvement

Back 34

-small vessel vasculitis

-necrotizing granulomatous inflammation with eosinophils involving multiple organs, especially lungs and heart

Front 35

Churg-Strauss Syndrome

Presentation? How to distinguish from Microscopic Polyangiitis?

Back 35

-Asthma, sinusitis, palpable purpura, wrist/foot dropp due to peripheral neuropathy, peripheral eosinophilia, increased IgE

-Can also involve heart, GI, kidneys (pauci- immune glomerulonephritis)

-serum MPO-ANCA/ p-ANCA levels correlate with disease activity

-Distinguish from MP: MP has no granulomas, no hx of asthma, no eosinophilia

Front 36

Henoch-Schonlein Purpura

Pathogenesis/Involvement? Seen In?

Back 36

-Small vessel vasculitis

-Vasculitis due to IgA immune complex deposition
-GI and kidney involvement

-most common vasculitis in children

Front 37

Henoch-Schonlein Purpura

Presentation & associated pathogenesis

Back 37

-Palpable purpura on buttocks and legs (bleeding into skin purpura are NOT palpable)

-GI pain and bleeding (melana & multiple lesions of same age)

-Arthrlagias

-Hematuria (IgA nephropathy) - RBC casts

-follow an URI (due to high levels of IgA >> deposits)

Front 38

Henoch-Schonlein Purpura

Treatment and Prognosis

Back 38

-Disease is self-limited, but may recur

-Treat with steroids if severe

Front 39

Infectious vasculitis

Affects what? Seen in? Causes

Back 39

-small vessel vasculitis involving skin vessels

-Seen in children and adults

-Involves all microbial pathogens

-Rickettsia rickettsii & Neisseria meningitidis

Front 40

Infectious vasculitis

Tick associated? Cause? Pathogenesis? Presentation?

Back 40

-RMSF most prevalent in SE then central states

-Caused by dog tick by transferring Rickettsia reckettsii

-Organisms invade endothelial cells >> vasculitits

-Fever in 100% of cases

-Petechiae begins on palms and spreads to trunk

---appear in irst days in 50% of cases, and by 5th day in 80%; no petechiae in 10%

Front 41

Infectious vascultiis

Neisseria meningitidis - Pathogenesis? Treatment?

Back 41

-Disseminated meningococcemia due to Neisseria meningitidis

-Capillary thromboses, usually due to DIC, produce minute hemorrhages into the skin (petechiae) that become confluent ecchymoses as the disease progresses. Hemorrhagic infractions of both adrenal glands commonly occurs producing acute hypocortisolism and death (Waterhouse-Friderichsen syndrome)

-Treat: IV penicillin G

Front 42

Hypertension definition

Back 42

-increased BP in pulmonary or systemic circuit

-Systemic HTN = pressure ≥ 140/90 mmHg (20% of population); can be just systolic ≥140 or diastolic ≥ 90

-Normal BP ≤120/80 mmHg

-usually systolic and diastolic increased together, but can be one or the other

Front 43

Primary Hypertension

% of cases? Risk Factors? Pathogenesis?

Back 43

-etiology unknown - related to increase CO and TPR

-95% (90% in first AID) of cases

-Risk factors: age, race (increased in African Americans, decreased in Asians), obesity, stress, lack of physical activity, high-salt diet

-Pathogenesis: excess salt increased blood volume >> stroke volume >> effects systolic BP excess salt enters muscles, opens Ca channels >> contraction >> increased TPR >>increased diastolic pressure

Front 44

Is Renin high or low in primary HTN?

First-line treatment? Why?

Back 44

-low b/c of the increased BP due to Na retention

-Hydrochlorathizide first line treatment for essential HTN in elderly and blacks because you get rid of salt and water

Front 45

Secondary Hypertension

% of cases? most common cause?

Back 45

-5% (10% in First Aid) of cases

-due to identifiable cause

-Most common cause: renal artery stenosis

----also related to fibromuscular dysplasia

Front 46

Hypertension Risk Factors

[causes]

Hypertension Predisposes you to...?

Back 46

-Risk Factors: age, obesity, diabetes, smoking, genetics, black > white > Asian

-Causes: [sleep apnea, CKD is most common, drug-induced, primary aldosteronism, renovascular disease, chronic steroid therapy/Cushing's, Pheochromocytoma, coarctation of the aorta, thyroid/parathyroid disease

-Predisposes to: atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, aortic dissection, Charcot Bouchard aneurysms (MCA)

Front 47

Back 47

-Hyaline arteriosclerosis, specifically hypertensive nephropathy

Front 48

Renovascular Hypertension

Pathogenesis?

Back 48

-Due to renal artery stenosis

-stenosis >> decreased blood flow to glomerulus >> JGA secretes renin >> angiotensinogen converted to angiotensin I >> angiotensin I converted to angiotensin II by ACE >> angiotensin II raises BP by contracting arteriolar SM increasing TPR and by promoting adrenal release of aldosterone, which increases resporption of Na in the distal convoluted tubule expanding plasma volume >> causes HTN with increased plasma renin and unilateral atropy (due to low blood flow) of the affected kidney

Front 49

Renovascular Hypertension

Causes? Seen In?

Back 49

-Renal artery stenosis caused by

---atherosclerosis (elderly males)

---fibromusclular dyspasia (thickening of wall) (young females)

Front 50

Fibromuscular Dysplasia

Back 50

development defect of the blood vessel wall, resulting in irregular thickening of large- and medium-sized arteries, especially the renal artery

cause of renovascular hyptertension/ secondary hypertension

Front 51

Back 51

Fibromuscular dysplasia

-"string beads" appearance of renale artery in this picture

-important cause of HTN in young patients

Front 52

Benign Hypertension

Back 52

-mild or moderate elevation in BP

-most cases are benign

-clinically silent: vessels and organs slowly damaged over time

Front 53

Malignant Hypetension

Definition? Presentation?

Back 53

-severe elevation in BP ≥180/120 mmHg

-5% of cases

-Can arise from preexisting HTN or de novo

-Presents with acute, ongoing end-organ damage: acute renal failure, headache, mental status changes, and papilledema

-MEDICAL EMERGENCY

-another cause of fibrinoid necrosis of the blood vessel

Front 54

Arteriosclerosis Definition

Back 54

-thickening of blood vessel wall

-hard arteries

Front 55

Atherosclerosis

Definition and Composition

Back 55

-disease of elastic and medium & large arteries

-intimal plaque that obstructs blood flow

---constists of necrotic lipic core (mostly cholesterol) with a fibromusular cap that can undergo dystrophic calicification

Front 56

Back 56

-Atherosclerosis

-Necrotic plaque in intima with cholesterol deposition and fibromusclar cap

Front 57

Atherosclerosis

Involvement? Most common?

Back 57

-Involves large and medium sized arteries

-Most common: abominal aorta > coronary artery > popliteal artery > internal carotid artery

Front 58

Atherosclerosis

Risk Factors/Seen In?

Back 58

-Modifiable: HTN, hypercholesterolemia/hyperlipidemia (LDL increases risk, HDL decreases risk), smoking, diabetes

-Nonmodifiable: age (number & severity increase with age), gender (increased in males and postmenopausal women b/c estrogen is protective), genetics (multifactorial - family history slightly predictive of risk)

Front 59

Atherosclerosis Pathogenesis

Back 59

-Damage to endothelium/endothelial cell dysfunction allows lipids to leak into the intima >> Lipids are oxidized and then consumed by macrophages via scavenger receptors >> foam cells (lipid laden macrophages) >> fatty streaks (begins in teens)

-Inflammation and healing leads to deposition lipid in intima>> thickening of intima with necrotic lipid core >> healing >> deposition of ECM and proliferation/migration of SM (via PDGF and FGF) >> fibromuscular cap >> fibrous cap >> complex atheroma

Front 60

[Why is oxidized LDL so bad?]

Back 60

-activates inflammatory cytokines

-attracts macrophages to vessel walls & up regulates chemotactic factors (IL-1, TNF, IFN-y & IL-6 >> acute phase reactants)

-promotes endothelial and smooth muscle apoptosis

-promotes platelet aggregation and thrombosis

-activates endothelium >> up regulation of LAMs

Front 61

Atherosclerosis Complications/Symptoms

Back 61

-complications of atherosclerosis account for >50% of disease in Western countries

-no symptoms until >70% stenosis >> angina, claudication

1. Stenosis of medium-sized vessels results in impaired blood flow (narrowing) and ischemia >>

---peripheral vascular disease (lower extremity arteries like popliteal)

---Angina (coronary arteries)

---Ischemic bowel disease (mesenteric arteries)

2. Plaque rupture w/ thrombosis >> MI (coronary arteries) or stroke (middle cerebral arteries)

3. Plaque rupture with emobilization >> atherosclerotic emboli, characterized by cholesterol clefts (crystals in embolus)

4. Weakening of vessel wall (intimal thickening >> diffusion barrier >> wall becomes atrophic) >> aneurysm (abdominal aorta)

Front 62

Back 62

Atherosclerotic embolus with cholesterol clefts

Front 63

Hyaline Arteriolosclerosis Pathogenesis

Back 63

-caused by proteins leaking into the vessel wall >> vascular thickening

---proteins seen as pink hyaline on microscopy

Front 64

Hyaline Arteriolosclerosis Etiology/Causes & Complications

Back 64

-Consequence of long-standing benign (essential) hypertension (forces protein into wall) or diabetes (nonenzymatic glycosylation of basement membrane >> vessel leaky)
-Results in reduced vessel caliber with end-organ ischemia
---classically produces glomerular scarring (arteriolonephrosclerosis) that slowly progresses to renal failure

Front 65

Back 65

Hyaline Arteriolosclerosis

wall thickened by hyaline

Front 66

Back 66

arteriolonephrosclerosis

-can see the scarring on the cortex of the kidney

Front 67

Hyperplastic Arteriolosclerosis Pathogenesis

Caused by?

Back 67

-involves thickening of vessel wall by hyperplasia of smooth muscle >> 'onion skin' appearance

Front 68

Back 68

Hyperplastic Arteriolosclerosis

-onion skinning = too many layers of smooth muscle cells

-narrow lumen >> reduced vessel caliber

Front 69

Hyperplastic Arteriolosclerosis Causes & Complications

Back 69

-consequence of malignant hypertension

-Results in reduced vessel caliber with end-organ ischemia

-May lead to fibrinoid necrosis of the vessel wall with hemorrhage

---Classically causes acute renal failure with characteristic 'flea bitten' appearance (pinpoint hemorrhages on surface of kidney due to blowing out of blood vessel)

Front 70

Monckeberg Medial Calcific Sclerosis

What is it? Complications?

Back 70

-Calcification of the media of musclar (medium sized) arteries, esp. radial and ulnar arteries

-Non-obstructive (doesn't alter lumen caliber/ intima not involved)

-Not clinically significant: seen as an incidental findings on xray or mammography ("pipestem" arteries"

Front 71

Back 71

Monckeberg Medial Calcific Sclerosis

-media up against intima like it should be

-media calcifed

Front 72

Back 72

Monckenberg (medial calcific sclerosis)

-showing "pipestem" arteries on xray

-ulnar and radial arteries most common

Front 73

Mammogram

Back 73

Monckeberg Medial Calcification

-calcification running in vascular pattern

Front 74

Aortic aneurysms

What are they? Presentation? Indications of presentation?

Back 74

-localized pathologic dilation of the Aorta

-May present with pain, which may indicate leaking, dissection, or imminent rupture

Front 75

Aortic Dissection

What is it? Where is it & requirements?

Back 75

-Intimal tear with dissection of blood through the media of the aortic wall >> longitudinal intraluminal tear >> false lumen

-Occurs in the proximal 10 cm of the aorta (high stress region) with preexissting weakness of the media

Front 76

Back 76

Aortic Dissection

-blood through intima, through media to wall

Front 77

Aortic Dissection

Causes & their associated pathogenesis

Back 77

-Most common causes is hypertension (older adults)

-also associated with bicuspid aortic valve, and inherited defects of connective tissue (younger adults)

1. Hypertension >> hyaline arteriolosclerosis of the vasa vasorum >> decreased flow flow >> atrophy of media

2. Marfan Syndrome and Ehlers-Danlos >> weakness of connective tissue in media (cystic medial necrosis)

3. also seen in pregnant women due to increase in plasma volume

Front 78

Aortic Dissection Presentation & Complications

Back 78

-Presentation: sharp, tearing chest pain that radiates to the back +/- unequal BP in the arms

-CXR shows mediastinal widening (wide aortic knob)

-Complications: pericardial tamponade due to proximal dissection (most common cause of death), rupture with fatal hemorrhage (into mediastinum), and obstruction of arteries (coronary or renal) branching off the aorta with resultant end-organ ischemia

Front 79

What is this? What kind is it? Where can they be located in general?

Back 79

-aortic dissection involving the ascending and descending aorta = Stanford type A

-The false lumen can be limited to the ascending aorta, propagate from the ascending aorta, or propagate from the descending aorta

Front 80

Thoracic Aortic Aneurysm

What is it? Due to? Seen In? Pathogenesis?

Back 80

-balloon like dilatation of the thoracic aorta

-Due to weakness in the aortic wall

-Seen in Tertiary syphilis: obliterative endarteritis of the vasa vasorum >> luminal narrowing, decreased flow, and atrophy of vessel wall >> 'tree bark appearance 'of aorta (due to scarring and fibrosis from endartaritis)

-Seen in cystic medial degeneration due to hypertension (older patients)

-Seen in Marfan's (younger patients)

Front 81

Thoracic Aorta

Back 81

Thoracic Aortic Aneurysm

-caused classically by tertiary syphilis

-tree bark appearance of aorta

Front 82

Thoracic Aneurysm Complications

Back 82

-Major Complication is dilation of the aortic valve root >> aortic insufficiency

-Compression of mediastinal structures (airway, esophagus)

-Thrombosis due to nonlaminar flow >> can lead to embolism

Front 83

Back 83

Thoracic aortic aneurysm - large aneurysm of ascending aorta with dissection

Front 84

Abdominal Aortic Aneurysm

What and where? Commonality

Back 84

-balloon-like dilatation of the abdominal aorta that arises below the renal arteries & above the aortic bifurcation

-most common site of aortic aneurysm b/c no vaso vasorum

Front 85

Abdominal Aorta

Back 85

Abdominal aortic aneurysm below renal arteries, above bifurcation

-notice ballooning

Front 86

Abdominal Aortic Aneurysm

Causes/Pathogenesis? Seen In?

Back 86

-Primarily due to atherosclerosis

-Classically seen in male smokers > 60 yo (> 50 yo in First Aid) with hypertension

---atherosclerosis increases the diffusion barrier to the media >> atrophy and weakness of the vessel wall

Front 87

Abdominal Aortic Aneurysm Presentation

Back 87

-60 yo male smoker w/ hx of hypertension

-presents with pulsatile abdominal mass that grows with time

Front 88

Abdominal Aortic Aneurysm Complications

Back 88

-Major Complication is rupture, especially when > 5 cm

-compression of local structures (ureter) and thrombosis/embolism (disruption of laminar flow)

Front 89

Back 89

Abdominal aortic aneurysm - suprarenal anuerysm with eccentric mural thrombus

Front 90

Abdominal Aortic Aneurysm Rupture Presentation

Back 90

Triad: hypotension, pulsatile abdominal mass, flank pain (severe left)

Front 91

Syphilitic Heart Disease

What does it cause? Findings? Complications

Back 91

3° syphilis disrupts the vasa vasorum of the aorta (aortic arch has largest vaso vasorum) with consequent atrophy of the vessel wall (edarteritis obliterans) and dilation of the aorta and valve ring.

May see calcification of the aortic root and ascending aortic arch. Leads to “tree bark” appearance of the aorta. Also see head bobbing, water-hammer pulse, pulsating uvula (any thoracic anuerysm >> aortic insufficiency)

Can result in aneurysm of the ascending aorta or aortic arch and aortic insufficiency (AV regurg)

Front 92

Hemangioma

What is it? Affects who? Involvement?

Back 92

-Benign tumor comprised of blood vessels

-Commonly present at birth

-Often regresses during childhood (so don't surgically remove)

-Most often involves skin and liver

Front 93

What is it?

DDx?

Back 93

Hemanigioma

-could be purpura which is a bleed into the skin: hemangioma blanches with pressure, purpura doesn't

Front 94

Strawberry hemangioma

Back 94

Benign capillary hemangioma of infancy. Appears in first few weeks of life (1/200 births); grows rapidly and regresses spontaneously at 5–8 years old.

Front 95

Cherry hemangioma

Back 95

Benign capillary hemangioma of the elderly. Does not regress. Frequency increases with age.

Front 96

Angiomyolipoma

Back 96

-Kidney hamartoma: composed of blood vessels, muscle, and mature adipose tissue

-Associated with tuberous scerlosis

Front 97

Cavernous hemangioma

Back 97

-Most common benign tumor of the liver and spleen

-May rupture if large and produce hemopertineum

Front 98

Angiosarcoma

What is it? Prognosis? Sites? Associations?

Back 98

-Malignant proliferation of endothelial cells

-Common sites: skin (head, neck), breast, liver

---Liver angiocarcinoma associated with polyvinyl chloride (plastics), arsenic, radiation and Thorotrast (thorium dioxide)

-Highly aggressive and difficult to resect due to delay in diagnosis

Front 99

Kaposi Sarcoma

What is it? Associated with?

Back 99

-Low-grade malignant proliferation of endothelial cells, mainly of the skin, but also seen in mouth, GI tract, and respiratory tract

-Associated with HHV-8

Front 100

Kaposi Sarcoma Presentation

Back 100

-Presents with purple patches plaques, and nodues(proliferation of endothelial cells NOT blood vessels so doesn't blanch)

-may also involved visceral organs

Front 101

Kaposi Sarcoma

Seen in & treatment for those populations

Back 101

-Older Eastern European males: tumor reminas localized to skin; treatment involves surgical removal

-AIDS- tumor spreads early; treatment is antiretroviral agents (boost immune system to kill virus)

-Transplant recipients: skin, tumor spreads early; treatment involves decreasing immunosuppression

Front 102

Back 102

Kaposi Sarcoma

Purplish nodules that do NOT blanch (blood isn't in a channel)

Front 103

Pyogenic granuloma

Back 103

Polypoid capillary hemangioma that can ulcerate and bleed. Associated with trauma and

pregnancy.

Front 104

Cystic hygroma

Back 104

Cavernous lymphangioma of the neck. Associated with Turner syndrome.

Front 105

Glomus tumor

Back 105

Benign, painful, red-blue tumor under fingernails. Arises from modified smooth muscle cells of glomus body.

Front 106

Bacillary angiomatosis

Back 106

Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections. Frequently mistaken for Kaposi sarcoma.

-use silver stain

-has satellite lesions at periphery of main lesion

Front 107

Hereditary Telangiectasia

Back 107

-AD

-Dilated vessels on the skin and mucous membranes in the mouth and throughout the GI tract

-Chronic iron deficiency anemia may occur because of bleeding from telangiectasias in the GI tract

Front 108

Von Hippel-Lindau Syndrome

Back 108

-AD

-Cavernous hemangiomas in the cerebellum and retina

-Increased incidence of bilateral pheochromocytoma and bilateral renal cell carcinomas

Front 109

Spider Telangiectasia

Back 109

-Arteriovenous fistula (disappears when the body is compressed)

-Associated with hyperestrinism (cirrhosis - can't metabolize 17ketosteroids or estrogen, normal pregnancy)

Front 110

Lymphangiosarcoma

Back 110

Lymphatic malignancy associated with persistent lymphedema (e.g., post–radical mastectomy).

Front 111

Sturge-Weber Syndrome

Back 111

-nevus flemmeus (birthmark) on the face in the distribution of the opthalmic branch and/or maxillary branch of CN V

-some cases show ipsilateral AV malformation of pia mater vessels overlying the occipital and parietal lobes >> can bleed >> subarachnoid hemorrhage

-some pts can show signs of MR

Front 112

Raynaud phenomenon

affects what? causes what? types?

Back 112

-affects small vessels

- decreased blood flow to skin due to arteriolar vasospasm in response to cold temperature or emotional stress. Most often in fingers and toes. Called Raynaud disease when 1° (idiopathic), Raynaud syndrome when 2° to a disease process like mixed connective tissue disease, SLE, or CREST (limited form of systemic sclerosis) syndrome.

Front 113

Ischemic Heart Disease

General Epidemiology & Cause/Risk Factors

Back 113

-syndromes related to myocarcial ischemia

-IHD is the leading cause of death in the US

-Usually due to atherosclerosis of coronary arteries, which decreases blood flow to the myocardium

-Risk factors similar to those of atherosclerosis: incidence increases with age (biggest risk factor for CAD = age)

Front 114

Stable Angina

What is it? Cause?

Back 114

-chest pain that arises with exertion or emotional stress that resolves with rest

-Due secondarily to atherosclerosis of the coronary arteries with > 70% stenosis >> decreased blood flow can't meet metabolic demands of the myocardium

-Represents reversible injury to myocytes (no necrosis, will see cellular swelling)

Front 115

Stable Angina

Presentation & Treatment

Back 115

-Presents as chest pain -Levine's sign (lasting < 20 min; > 20 min = irreversible injury & cell death) that radiates to the left arm or jaw, diaphoresis, and shortness of breath

-EKG shows ST-segment depression due to subendocardial ischemia

-Relieved by rest or nitroglycerin

Front 116

Unstable Angina

What is it? Cause?

Back 116

-chest pain that occurs at rest; increase in frequency and/or intensity of chest pain (stable >> unstable angina)

-Usually due to rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of the coronary artery

-Represents reversible injury to myocytes (blood still getting through)

Front 117

Unstable Angina

Presentation? Treatment? Complications?

Back 117

-EKG shows ST-segment depression due to subendocarcial ischemia

-Relieved by nitroglycerin

-High risk of progression to MI

Front 118

Back 118

-Thrombosis of coronary artery

-partial occlusion = unstable angina

Front 119

Prinzmetal angina

What is it? Cause? Triggers?

Back 119

-episodic chest pain unrelated to exertion

-Due secondarily to coronary artery vasospasm (completely clamps down >> ischemia)

-Represents reversible injury to myocytes (no necrosis)

-Known triggers: cocaine, tobacco, triptans

-occurs in the morning more

Front 120

Prizmetal angina

Presentation? Treatment?

Back 120

-Non-exertional chest pain

-EKG shows transient ST-segment elevation due to transmural ischemia

-Relieved by nitroglycerin or Ca-channel blockers (or smoking cessation if applicable)

Front 121

Coronary Steal Syndrome

Back 121

Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators (e.g., dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas >> decreased flow and ischemia in the post-stenotic region. Principle behind pharmacologic stress tests.

Front 122

Myocardial infarction

What is it? Cause?

Back 122

-Necrosis of cardiac myocytes (>20 min occlusion)

-Usually due to rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery

-Other causes: coronary artery vasospasm (due to Prizmetal angina or cocaine use), emboli, and vasculitis (Kawasaki disease preferentially affects coronary artery)

Front 123

Myocardium

Back 123

Myocardium w/ complete occulusion of coronary arteries = MI

Front 124

Myocardial Infarction

Presentation

Back 124

-Generally: severe crushing chest pain (last > 20 minutes) that radiates to the left arm or jaw, diaphoresis, and dyspnea (due to decreased CO and pulmonary edema), nausea, vomiting, fatigue

-LAD occlusion: crushing chest pain, that radiates to jaw & left arm

-RCA: bradycardia & atypical chest pain & epigastric pain, simulating GERD

-Symptoms NOT relieved by nitroglycerin

Front 125

Myocardial Infarction

Locations/Commonality & associated complications?

Back 125

-Usually involves the LV; RV & atria generally spared

---Occlusion of LAD >> infarction of anterior wall and anterior septum; most commonly involved artery (45% of cases); complication: complete heart block

---Occlusion of RCA >> infarction of posterior wall, posterior septum, and posterior papillary muscle of the LV, RV; 2nd most commonly involved artery; Complication: rupture of papillary muscle >> insufficiency; AV block

---Occlusion of the left circumflex >> infarction of the lateral wall of the LV

Front 126

Myocardial Infarction

Initial involvement & EKG findings during this time? Progession?

Back 126

-ECG is gold standard for diagnosis of MI in the first 6 hours

-Initial phase of infarction >> subendocardial necrosis (most distal of blocked artery) involving <50% of the myocardial thickness (=subendocardial infarction)

---EKG shows ST-segment depression

-Continued/Severe ischemia >> transmural necrosis involving most of the myocardial wall (transmural infarction)

---EKG shows ST-segment elevation

---pathological Q waves indicate an evolving or old transmural infarct

Front 127

Myocardial Infarction

Lab values & their timelines?

Back 127

-To see if there is irreversible damage to myocytes >> membrane damage >> enzymes in myocytes leak

-Troponin I is the most sensitive and specific marker (gold standard) for MI

---Level rises 2-4 hours after infarction, peaks at 24 hours, and returns to normal by 7-10 days

-CK-MB useful for detecting reinfarction that occurs days after initial MI

---CK-MB rises 4-6 hours after infarction, peaks at 24 hours, and returns to normal after 72 hours

-LDH2 higher than LDH1 usually - see LDH flip in MI to LDH 1 being higher - showes up at 18 hours, peaks at 3 days, lasts for 7 days

Front 128

Myocardial Infarction Treatment

Back 128

-ASA and/or heparin - limits additional thrombosis [effective in decreasing mortality rate - 20% releative risk reduction if ASA + Clopidogrl]

-Supplemental O2 - minimize ischemia

-Nitrates - vasodilate coronary arteries and veins

-B-blocker - slows HR >> decreasing O2 demand and risk for arrhythmia

-ACE inhibitor - decrease LV dilation

-Fibrinolysis or angioplasty - opens blocked vessel [STEMI only]

-ALWAYS check EF after MI b/c that is biggest prognostic factor

Front 129

What occurs after fibrinolysis/angioplasty to treat MI?

Back 129

-Contraction band necrosis: Reperfusion of irreversible-damage cells>> Ca influx >> hypercontraction of myofibrils

-Reperfusion injury: return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes

---cardiac enzymes continue to rise after you unblock the vessel

Front 130

Back 130

-area of dead heart, myocytes w/ no nucleus

-Contraction band necrosis

Front 131

What do you see with reperfusion injury?

Back 131

-Continued rise in cardiac enzymes due to additional myocardial damage/necrosis

Front 132

<4 hrs from MI

Gross changes? Microscopic changes ? Complications?

Back 132

-Gross changes: none

-Microscopic changes: none

-Complications: Cardiogenic shock (massive infarction), CHF (seen as decreased EF), arrhythmia, sudden death

Front 133

4-12 hours from MI

Gross changes? Microscopic changes ? Complications?

Back 133

-Gross changes: dark mottling; pale with tetrazolium stain

-Microscopic: early coagulative necrosis (pyknosis, karyohexis, karyolysis), release of necrotic cell contents into blood; edema hemorrhage, wavy fibers

-Complications: arrhythmia, HF, cardiogenic shock, death

Front 134

12-24 hours from MI

Gross changes? Microscopic changes? Complications?

Back 134

-Gross changes: dark discoloration; pale with tetrazolium stain

-Microscopic changes: coagulative necrosis (pyknosis, karyohexis, karyolysis) >> neutrophil migration begins; repurfusion injury may cause contraction bands due to free radical damage

-Complications: arrhythmia (caused by damage to conducting system), cardiogenic shock, death; less likely to occur > 24 hours

Front 135

1-3 days from MI

Gross changes? Microscopic changes? Complications?

Back 135

-Gross changes: yellow pallor, hyperemia

-Microscopic changes: extensive coagulative necrosis; neutrophils (acute inflammation always follows necrosis)

-Complications: Fibrinous pericarditis (inflammatory exudate) - ONLY SEEN WITH TRANSMURAL INFARCTION; presents as chest pain with friciton rub

Front 136

4-7 days from MI

Gross changes? Microscopic changes? Complications?

Back 136

-Gross change: yellow pallor (hyperemic border)

-Microscopic changes: Macrophages

-Complications:

---Rupture of ventricular wall (due to macrophage mediate structural degradation) >> cardiac tamponade (most occur with LAD thrombosis)

---Rupture of interventricular septum >> L to R shunt (step up O2 in RV)

---Rupture of posterior medial papillary muscle (w/ occlusion of RCA) >> mitral insufficiency (mitral regurgitation murmur - pansystolic w/ S3, S4)

--- LV pseudoaneurysm (mural thrombus “plugs” hole in myocardium>> “time bomb”).

Front 137

1-3 weeks from MI

Gross changes? Microscopic changes? Complications?

Back 137

-Gross changes: Red border (capillaries) emerges as granulation tissue enters from edge of infarct; hyperemic border w/ central yellow- brown softening - maximally yellow at 10 days

-Microscopic changes: Granulation tissue with plump fibroblasts, collagen, and blood vessels (healing)

-Complications: none - may still be susceptible to ruptures seen at 4-7 days;

Front 138

Months from MI

Gross changes? Microscopic changes? Complications?

Back 138

-Gross changes: contracted white scar

-Microscopic changes: Fibrosis

-Complications: aneurysm (scar = weak wall >> true ventricular aneurysm: outward bulging during contraction, dyskinesia), mural thrombus (wall not moving as well near scar), Dressler syndrome, HF, arrhythmias

Front 139

Dressler Syndrome

Cause? Pathogenesis?

Back 139

rare: transmural infarction >> inflammation to pericardium >> exposed antigens >> formation of antibodies to pericardium >> autoimmune fibrinous pericarditis 6-8 weeks after infarction

Front 140

Mural Thrombus

Caused by? Treatment?

Back 140

-almost always from LAD thrombi >> transmural infarction >> injury to endothelium >> platelets stick + muscle not contracting b/c injurred >> stasis >> platelets + venous clot so factors V, VII, and RBCs >> so give aspirin (platelets) and heparin and warfarin for the factors

-with anterior infarct, give aspirin + warfarin + heparain

-

Front 141

What is it? Time of?

Back 141

-subendocardial infarction

-dark discoloration of part of myocardium = 4-24 hours after MI

Front 142

What is it? Timing?

Back 142

-Myocytes w/ no nuclei = coagulative necrosis; w/o neutrophils = 4-24 hours

Front 143

What is it? Timing?

Back 143

-MI w/ neutrophils = day 1-3

Front 144

What is it? Timing?

Back 144

-Fibrinous pericarditis = transmural infarct

-1-3 days post MI

Front 145

Heart - What is it? Timing?

Back 145

-Rupture of ventricular free wall

-Happens when macrophages come in day 4-7

Front 146

What is it? Timing?

Back 146

-Ruptured papillary muscle = occurs with RCA blockage

-4-7 days post MI

Front 147

What is it? Timing?

Back 147

-Myocardial scar

-months after MI

Front 148

What is it? Timing? Complications?

Back 148

-myocardial scar showing dense collagen (type I)

-months after MI

-Complications: causes weak wall >> aneurysm

Front 149

What is it? Timing? Complications?

Back 149

-dilated ventricular aneurysm

-months after MI

-Could form mural thrombosis along scar

-patients die to HF - does NOT rupture

Front 150

Sudden cardiac death

What is it? Timing? Death due to?

Back 150

-unexpected death due to cardiac disease

-occurs without symptoms or <1 hr after symptoms arise

-usually due to fatal ventricular arrhythmia

Front 151

Sudden cardiac death

Causes/Etiology

Back 151

-most common etiology = acute ischemia

-90% of patients have preexisting atherosclerosis; associated with CAD (up to 70% of cases)

-less common causes: mitral valve prolapse, cardiomyopathy, cocaine abuse (vasospasm)

hereditary ion channelopathies (e.g., long QT syndrome).

Front 152

ECG Diagnosis of MI

Anterior Wall - vessel? ECG leads?

Back 152

-LAD

-Q waves in V1-V4

Front 153

ECG Diagnosis of MI

Anteroseptal Wall - vessel? ECG leads?

Back 153

-LAD

-Q waves in V1-V2

Front 154

ECG Diagnosis of MI

Anterolateral wall - vessel? ECG leads?

Back 154

-LAD or LCX

-V4-V6

Front 155

ECG Diagnosis of MI

Lateral wall- vessel? ECG leads?

Back 155

-LCX

- I, avL

Front 156

ECG Diagnosis of MI

Inferior Wall - vessel? ECG leads

Back 156

-RCA

-II, III, aVF

Front 157

MI Complications & timelines

Back 157

-Cardiac arrhythmia—important cause of death before reaching hospital; common in first few days. LV failure and pulmonary edema.
-Cardiogenic shock (large infarct—high risk of mortality).
-Ventricular free wall rupture >> cardiac tamponade; papillary muscle rupture >> severe mitral regurgitation; and interventricular septum rupture >> VSD. Greatest risk 6–14 days postinfarct.

-Ventricular pseudoaneurysm formation---CO, risk of arrhythmia, embolus from mural thrombus; greatest risk approximately 1 week post-MI.
-Postinfarction fibrinous pericarditis—friction rub (1–3 days post-MI).
-Dressler syndrome—autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI).

-Ventricular Aneurysm - 3 wks out, pt has systolic bulge of pericardium >> HF

Front 158

Chronic Ischemic Heart Disease

Back 158

-poor myocardial function due to chronic ischemic damage w/ or w/o infarction

-small subendocardial infarctions >> muscle replaced by fibrous tissue >> low ejection fraction >> progresses to CHF

-2nd most common indication for heart transplant

Front 159

CHF - Symptoms? Signs?

Back 159

Clinical syndrome of cardiac pump dysfunction. Symptoms include dyspnea, orthopnea, and fatigue; signs include rales, JVD, and pitting edema

Front 160

CHF - systolic vs. diastolic dysfunction

Back 160

Systolic dysfunction—low EF, poor contractility, often 2° to ischemic heart disease or DCM.

Diastolic dysfunction—normal EF and contractility, impaired relaxation, decreased compliance.

Front 161

CHF Treatment

Back 161

ACE inhibitors, β-blockers (except in acute decompensated HF), angiotensin II receptor blockers, and spironolactone decrease mortality. Thiazide or loop diuretics are used mainly for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms and mortality in select patients.

Front 162

Left-Side Heart Failure

Causes & Associated Pathogenesis?

Back 162

-ischemia: damage >> can't pump properly

-hypertension: concentric hypertrophy >> can't oxygenate wall >> ischemia

-Dilated cardiomyopathy: 4 chamber dilation >> stretches muscle >> can't contract

-Myocardial infarction: myocardium can't function

-Restricted cardiomyopathy: can't fill heart appropriately >> therefore, can't pump what's not there

Front 163

Left-Sided Heart Failure

Clinical Features & their pathogenesis

Back 163

-due to decreased forward progression and pulmonary congestion

1.Pulmonary congestion >> increased pulmonary venous presure >> pulmonary venous distention & transudation of fluid >>pulmonary edema

---Results in dyspnea, paroxysmal nocturnal dyspnea (pillow orthopnea) (due to increased venous return when lying flat), orthopnea, & crackles (fluid in interstium)

---Small, congested capillaries may burst >> intraalveolar hemorrhage >> hemosiderin-laden macrophages (iron in macs) ('heart-failure' cells) >> rusty sputum

2. Decreased flow to kidneys (decreased forward perfusion) >> activation of RAAS >> fluid retention & exacerbation of CHF

Front 164

Lung biopsy

Back 164

-Hemosiderin-laden macrophages in alveolar air sac seen in left-sided CHF

Front 165

Treatment of Left-Sided Heart Failure

Why this?

Back 165

-ACE inhibitor b/c it decreases preload and afterload at the same time

-ACE inhibitors increase longevity by (1) decreased aldosterone, therefore decreased salt and water reabsorption which decreases preload and (2) by blocking Angiotensin II, will lead to a decrease in vasoconstrictor effect on peripheral resistance arterioles, which will decrease afterload.

-add spironolactone w/ aldosterone escape

Front 166

Right-Sided Heart Failure

Causes? Most common cause?

Back 166

-Most commonly due to left-sided HF

-Other causes: left-to-right shunt, chronic lung disease (cor pulmonale) (hypoxia >> vasoconstriction of hypoxic area which is the whole lung)

Front 167

Right-Sided Heart Failure

Clinical Features

Back 167

Backward failure

-JVD due to increased venous pressure

-increased central venous pressure >> increased resistance to portal flow >> Painful hepatosplenomegaly with 'nutmeg' liver >> cardiac cirrhosis

-Dependent pitting edema due to increased hydrostatic pressure (increased venous presure >> fluid transudation)

Front 168

Liver

Back 168

Nutmeg liver / cardiac cirrhosis

Front 169

Congenital Defects

Arise when & how? Seen in how many live births? & cause what?

Back 169

-Arise during embryogenesis (weeks 3-8)

-Seen in 1% of live births

-Most are sporadic

-Results in shunting between left (systemic) and right (pulmonary) circulations

Front 170

Left-to-right shunting

Features? Causes & their frequency? Pathogenesis/Complications?

Back 170

-can be relatively asymptomatic at birth, but the shunt can eventually reverse >> late cyanosis "blue kids"

-Causes: VSD > ASD > PDA

1. increased flow through pulmonary circulation >> hypertrophy of pulmonary vessels and pulmonary hypertension

2. Increased pulmonary resistance results in reversal of shunt >> late cyanosis (Eisenmenger syndrome) with RVH, polycythemia, and clubbing

Front 171

Eisenmenger Syndrome

Back 171

-Uncorrected left-to-right shunt (VSD,
ASD, PDA) >> increased pulmonary blood flow >> pathologic remodeling of vasculature >> pulmonary arteriolar hypertension.

-RVH occurs to compensate >> shunt becomes right to left.

-Causes late cyanosis, clubbing, and polycythemia

-Age of onset varies

Front 172

Right-to-left shunting

Features? Causes? Common Treatment?

Back 172

Present with cyanosis shortly after birth - "blue babies"

-often diagnosed prenatally, or become evident right after birth.

-causes polycythemia

Causes: 5 Ts

1. Trucus arteriosus

2. Transposition

3. Tricuspid Atresia

4. Tetralogy of Fallow

5. TAPVR

-Treatment: maintenance of PDA and early surgical intervention

Hint 172

5T's

1 - 5 involvement of vessels all beginning with T

Front 173

Ventricular Septal Defect

What is it? Association? [Mild, Moderate, Severe?]

Back 173

-Defect in the septum that divides the R & L ventricles

-Most common heart defect

-Associated with Fetal Alcohol Syndrome

[-mild: Qp/Qs = 1.25-1.5; moderate: Qp/Qs - these 2 are considered restrictive 1.5-2.5; severe: Qp/Qs > 2.5 - nonrestrictive >> can lead to aortic regurgitation]

Front 174

Ventricular Septal Defect

Describe the murmur.

Back 174

-holosystolic, harsh-sounding murmur

-loudest at tricuspid area (left-sternal border)

-accentuated with hand-grip due to increased afterload

Front 175

Ventricular Septal Defect

Complications? Treatment?

Back 175

-Results in left-to-right shunt; may manifest weeks later

-Size of defect determines extent of shunting and age at presentation

---small defects asymptomatic, often self-resolve

---large defects >> Eisenmenger syndrome w/ RVH, polycythemia, clubbing (reversal of shunt due to pulmonary hypertension caused by increased volume in pulmonary volume) [RV heave, loud P2]

-Treatment: surgical closure; small may close spontaneously [moderately restructive and nonrestrictive should be closed immediately and/or Qp/Qs >2 + evidence of LV volume overload] [if pulm HTN present, close if shunt 1.5/1, pulm reactivity when challenged w/ vasodilation, PA pressure <2/3 systemic BP]

Front 176

Atrial Septal Defect

What is it? Types? Most common? Associated with who?

Back 176

-Defect in septum that divides the right and left atria; [1 of the 2 most common defects in adults & more common in females 2:1]

-Most common type is ostium/septum secundum (90% of cases) [60% according to lecture]

-Osteium primum type associated with Down Syndrome and other anomalies [also causes mitral regurge >> pansystolic murmur]

-Also associated with Fetal Alcohol Syndrome

Front 177

Atrial Septal Defect

Results in? Complications?

Back 177

-Results in left-to-right shunt >> loud S1 and a wide fixed split S2 on auscultation (increased blood in right heart delays closure of pulmonary valve)

-Complication: paradoxical emboli (DVT normally goes to lung, but b/c ASD, it could cross to left side >> systemic embolus); can also cause HF/ Eisenmenger Syndrome (b/c volume overloading the right side heart >> RV dilation >> presents with SOB [usually happens around 4th decade])

Front 178

ASD

Presentation heart sound wise & progression

Back 178

-ASD commonly presents with a pulmonary flow murmur (increased flow through the pulmonary valve) and a diastolic rumble (increased flow across tricuspid valve)

-blood flow across the ASD itself doesn't cause a murmur b/c there is not pressure gradient

-Murmur later progress to a louder diastolic murmur of pulmonic regurgitation from dilation of the pulmonary artery

-loud S1, wide fixed split S2

[can also have palpitations due atrial arrhythmias]

Front 179

[How to/ who to treat for ASD]

How is an ASD different from a patent foramen ovale?

Back 179

-indications for treatment: dilated RV pulmonary artery or mean pressure 50% or < than the corresponding aortic pressures even if asymptomatic; close regardless of age

-survival benefit is if the ASD is surgically closed by <25 yo >> reduces risk for RHF, pulmonary HTN, and arrhythmias (pts > 40 yo remain at risk for arrhythmias)

-in ASD, septa are missing rather than unfused

Front 180

Patent Ductus Arteriosis

Caused by? Associated with?

Back 180

-Failure of ductus arteriosus to close

-Associated with congenital rubella or prematurity

Front 181

Patent Ductus Arteriosis

What does it cause/Pathogenesis?

Back 181

-Results in left-to-right shunt between aorta and pulmonary artery >> step up in O2
---During development, ductus arteriosus normally shunts blood form pulmonary artery to aorta, bypassing the lungs >> first breath decreases lung resistance >> closure of PDA
-Baby gets differential cyanosis b/c PDA is distal to subclavian - baby is pink up top and blue/cyanotic on the bottom
[associated lesions: VSD & coarctation of the aorta]

Front 182

Patent Ductus Arteriosis

Clinical Features and why?

Describe the associated murmur.

Back 182

-Asymptomatic at birth with continuous/holosystolic 'machine like' murmur loudest at S2 best heard at left infraclavicular area

>> can lead to Eisenmenger syndrome, RVH and/or LVH >> HF - if PAH severe >> PA dilation and pulmonic valve regurge - also get lower extremity cyanosis (b/c PDA arises after major branches of aortic arch)

Front 183

Patent Ductus Arteriosis

Treatment?

Back 183

-Indomethacin: decreases PGE >> PDA closure

---PGE kEEps PDA open

Front 184

Tetralogy of Fallot

Caused by? What 4 things?

Back 184

Caused by anteriorsuperior displacement of the infundibular septum

Characterized by:

1. Pulmonary infundibular stenosis = stenosis of RV outflow tract (most important determinant of prognosis/cyanosis)

2. RVH

3. Aorta that overrides VSD

4. VSD

Front 185

Tetralogy of Fallot

Leads to what? What determines prognosis?

Back 185

-right-to-left shunt across VSD >> early cyanosis >> step down >> "tet" spells (HR & CO increase >> venous return increase >> increased R to L shunt >> perpeturation of cycle)

-degree of pulmonic stenosis determines extent of shunting and cyanosis

-can cause polycythemia

Front 186

Tetralogy of Fallot

Clinical Features & Treatment

What congenital heart defects would be good to have with Tetralogy of Fallow

Back 186

-most common cause of early childhood cyanosis

-Patients learn to squat in response to cyanotic spell to increase arterial resistance and decrease shunting >> more blood can reach lungs >> improves cyanosis

-'Boot-shaped' heart on xray

-Treatment: surgical correction [long term, can see pulmonary regurge]

Front 187

Back 187

-Tetralogy of Fallot

-boot shaped heart

Front 188

Transposition of the Great Vessels

What is it? Caused by? Associated with?

Back 188

-Characterized by pulmonary artery arising from left ventricle and aorta arising from right ventricle >> separation of systemic and pulmonary circulations

-Caused by failure of the aorticopulmonary septum to spiral

-Associated with maternal diabetes

Front 189

Transposition of the Great Vessels

Presentation? Treatment? Complications?

Back 189

-Presents with early cyanosis: pulmonary & systemic circuits don't mix = do independent circuits - not compatible w/ life unless shunts present to allow mixing of blood (VSD, PDA, patent foramen ovale)
-Treatment:
1. creation of shunt (allowing blood to mix) after birth is required for survival 2. PGE can be used to maintain PDA until surgical repair >> w/o surgical intervention, infants die within months
-Results in RVH and atrophy of left ventricle

Front 190

Total anomalous pulmonary venous return (TAPVR)

Back 190

Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc.); associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.

Front 191

Truncus Arteriosus

What is it? Caused by? What is also seen in this condition?

Back 191

-Characterized by a single large vessel arising from both ventricles

---Truncus fails to divide into the pulmonary trunk and the aorta

-most patients have accompanying VSD

Front 192

Truncus Arteriosus

Presentation?

Back 192

-Presents with early cyanosis: deoxygenated blood from the RV mixes with oxygenated blood from LV before pulmonary and aortic circulations seperate

Front 193

Tricuspid Atresia

What is it? Associated with? Presentation?

Back 193

-Tricuspid valve orifice fails to develop >> hypoplastic RV

-requires ASD and VSD for viability

-Often associated with ASD >> R to L shunt

-Presents with early cyanosis

Front 194

Coarctation of the Aorta

What is it? Generally associated with what?

Back 194

-Narrowing of the aorta

-associated with bicuspid aortic valve and other heart defects

Front 195

Infantile coarctation of the aorta

Associated with what? Where is it? Presentation? Associated with who?

Back 195

-Associated with a PDA

-Coarctation lies distal to aortic arch but proximal to PDA >> R to L shunt due to low pressure caused by block

-Presents as lower extremity cyanosis in infants, often at birth (can present with closure of PDA)(also see different pressures in upper vs. lower extremities)

-Associated with Turner Syndrome

Front 196

Adult coarctation of the aorta

-Where is it? Presentation? Seen in? Associated with?

Back 196

-Coarctation lies distal to aortic arch (distal to ligamentum arteriosum)

-Presents as HTN in upper extremities (blood being shunted into early branches of aorta) and hypotension w/ weak pulses in lower extremities (radiofemoral delay) >> claudication of lower extremities, decreased perfusion to kidneys >> activation of RAAS >> HTN

-can develop Berry aneurysm at jxn of comm. branches to main cerebral arteries (no elastic lamina there)

-Discovered in adulthood

-Collateral circulation develops across intercostal arteries >> engorged arteries >> 'notching' of ribs on xray

-Associated with bicuspid aortic valve

Front 197

Back 197

-Coarctation of the aorta

-notice the narrowing

Front 198

Back 198

-Adult coarctation of the aorta

-notching of ribs due to collateral circulations running across ribs

Front 199

Acute Rheumatic Fever

What is it? Culprit? Seen in who? When? How does it cause this disease?

Back 199

-Systemic complication of pharyngitis due to group A Beta-hemolytic strepotococci

Front 200

Acute Rheumatic Fever

Who is it seen in? When does it present?

Back 200

Affects children 2-3 weeks after an episode of streptococcal pharyngitis

Front 201

Acute Rheumatic Fever

How does the culprit cause systemic disease?

Back 201

Caused by molecular mimicry: bacterial M protein resembles human tissue

Front 202

Acute Rheumatic Fever

Diagnosis based on?

Back 202

Jones Criteria: Evidence of prior group A Beta-hemolytic streptococcal infection (elevated ASO or anti-DNAase B titers) w/ presence of major and minor criteria

Front 203

Jones criteria: minor

Back 203

nonspecific: include fever and elevated ESR

Front 204

Jone criteria: major (describe them)

Back 204

1. Migratory polyarthritis - swelling and pain in a large joint (wrist, knees, ankles) that resolves withing days and migrates to involved another large joint

2. Pancarditis - each layer of the heart will be inflamed

---Endocarditis - Mitral valve more commonly involved than aortic valve (mitral > aortic >> tricuspid). Characterized by small vegetations along lines of closure >> regurgitation

---Myocarditis - w/ Aschoff bodies characterized by foci of chronic inflammation, reactive histiocytes w/ slender wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material; MOST COMMON CAUSE OF DEATH DURING ACUTE PHASE

---Pericarditis - >> friction rub and chest pain

3. Subcutaneous nodules

4. Erythema marginatum - annular, nonpruritic rash with erythematous border, commonly involving trunk & limbs

Hint 204

J - joints

O - <3

N - nodules

E - erythema marginatum

S - Sandringham's? chorea

Front 205

Acute Rheumatic Fever

Prognosis/Progression/Complications

Back 205

-Acute attack often resolves, but may progress to chronic rheumatic heart disease (Acute RF >> mitral regurgitation)

-Repeat exposure to group A Beta-hemolytic streptococci >> relapse of acute phase and increases risk for chronic disease

---Usually mitral valve, can involve aortic valve: leads to thickening of chordae tendinae & cusps, fusion of commisures >> stenosis w/ "fish mouth" or "button hole" appearance of valve (chronic RF =mitral stenosis)

-Complication of damaged valves = future endocarditis

Front 206

Mitral Valve

Back 206

Acute Rheumatic Fever

-Mitral Valve vegetations - endocarditis

Front 207

Back 207

Acute Rheumatic Fever

-Aschoff Body: chronic inflammation with giant cells and fibrinoid materal w/ Anitschkow cells (histiocytes with slender wavy nuclei running down middle)

-showing myocarditis

Front 208

Back 208

Acute Rheumatic Fever

Anitschkow cells - slender wavy nuclei/ catepillar nucleus

Front 209

Back 209

Chronic Rheumatic Fever showing fusion of aortic valve commissures = fish mouth appearance

Front 210

Aortic Stenosis

Definition? Caused by? See in?

Back 210

-Narrowing of aortic valve orifice

-Usually due to fibrosis and calcification from wear and tear

1. presents in late adulthood (>60 yo)

2. Bicuspid aortic valve increases risk and hastens disease onset; normal valve has 3 cusps >> fewer cusps >> increased wear and tear on each cusp

-Can also arise as a consequence of chronic rheumatic valve disease

---coexisting mitral stenosis and fusion of the aoritc valve comissures distinguis rheumatic disease from wear and tear

Front 211

Aortic Valve

Back 211

-Aortic Valve Stenosis

Front 212

Aortic Stenosis

Initial Presentation? Describe the murmur.

Back 212

-Cardiac compensation >> prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-descresendo murmur is heard

-LV > aortic pressure during systole

-loudest at heart base - 2nd ICS

-radiates to carotids

- soft S2; would probably hear S4

Front 213

Aortic Stenosis

What changes the intensity of the murmur?

Back 213

-intensity increases with expiration, and increased preload of the ventricle

-Decreased blood in the ventricle decreases the intensity of the murmur b/c less blood has to move across the valve

-differentiates from hypertrophic cardiomyopathy

Front 214

Aortic Stenosis

Complications & associated presentations? Treatment?

Back 214

-concentric LVH >> can progress to cardiac failure

-Angina, dyspnea and syncope w/ exercise - limited ability to increase blood flow across stenotic valve >> decreased perfusion of the myocardium & brain

-Microangiopathic hemolytic anemia - RBCs damaged (producing schistocytes) while cross calcified valve

-Pulsus parvus et tardus: pulses are weak with a delayed peak (delayed rate of rise in carotid pulse)

-Treatment: complications >> valve replacement

Front 215

Aortic Regurgitation

Definition? Causes? most common cause?

Back 215

-Backflow of blood from the aorta into the LV during diastole

-Arises due to:

---Aortic root dilation: most common cause is isolated ARD; pulls on valves, increases space between them >> regurgitation

------can be caused by syphilitic aneurysm and aortic dissection

---bicuspid valve

---Valve damage: caused by infectious endocarditis/rheumatic fever

Front 216

Aortic Regurgitation

Clinical Features? Describe the Murmur

Back 216

1. High-pitched, early, blowing diastolic decrescendo murmer

2. Hyperdynamic circulation due to increased pulse pressure

---pulse pressure = difference between systolic & diastolic pressures

---Diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume - seen in chronic cases

---presents with bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse), head bobbing

3. Results in LV dilation and eccentric (one aspect) hypertrophy (due to volume overload) - so S3 & S4 also

Front 217

Aortic Regurgitation

How can the intensity of the murmur be altered? Treatment and how do you know when its absolutely time for treatment?

Back 217

-Hand grip increases the intensity of the murmur

-expiration

-Vasodilators decrease the intensity

-Treatment: LV dysfunction >> valve replacement

---Austin flint murmur - anterior leaflet of the mitral valve is dripping blood (on side of outflow tract of the aorta) >> immediate valve replacement

Front 218

Mitral Valve Prolapse

Definition? Prevalence?

Back 218

-Ballooning of mitral valve into left atrium during systole

-seen in 2-3% of US adults - most frequent valvular lesion

Front 219

Mitral Valve Prolapse

Causes by/ Etiology? Seen In?

Back 219

-Due to myxoid degeneration (accumulation of ground substance - excess of dermatan sulfate) of the valve making it floppy, rheumatic fever, or chordae rupture

-Etiology mostly unknown

-Seen in Marfan Syndrome and Ehlers-Danlos syndrome

Front 220

Mitral Valve Prolapse

Describe the Murmur. What affects its intensity?

Back 220

-Presents with incidental mid-systolic click (sudden tensing of chordae tendinae) followed by regurgitation murmur (late systolic crescendo)

-best heard over the apex

-loudest just before S2

-Usually asymptomatic/benign

-Click and murmur become softer with squatting due to increased systemic resistance decreases LV emptying (closer to S2)

-murmur/click occurs earlier w/ standing/ valsava maneuver/anxiety due to increase in venous return (S1)

Front 221

Mitral Valve Prolapse

Complications? Treatment?

Back 221

-Complications are rare but include: infectious endocarditis, arrhythmia, severe mitral regurgitation

-Treatment: valve replacement

Front 222

Mitral Regurgitation

Definition?

Back 222

-Reflux of blood from the LV into the L atrium during systole

Front 223

Mitral Regurgitation

Caused by? Seen in?

Back 223

-Usually arises as a complication of mitral valve prolapse

-Other causes: LV dilatation (left-sided cardiac failure), infective endocarditis (can damage valve leaflets), acute rheumatic heart disease (vegetations on valve; most common one involved), papillary muscle rupture after MI

Front 224

Mitral Regurgitation

Clinical Features and Complications?

Back 224

-Holosystolic, high-pitched "blowing" murmur

-loudest at apex

---can get louder with squatting (increased systemic resistance decreases LV emptying), hand grip (increased TPR) and expiration (increased return to L atrium)

-Results in volume overload and left-sided failure

Front 225

Tricuspid Regurgitation

Describe the Murmur. What changes its intensity? Causes?

Back 225

-holosystolic, high-pitched blowing murmur

-loudest at tricuspid area and radiates to right sternal border

-enhanced by maneuvers that increase RA return (inspiration)

-Commonly caused by RV dilation

-Also caused by rheumatic fever and infective endocarditis

Front 226

Mitral Stenosis

Definition? Caused by?

Back 226

-Narrowing of the mitral valve orifice

-Usually due to chronic rheumatic valve disease

-chronic MS can result in LA dilation

Front 227

Mitral Stenosis

Describe the murmur.

Back 227

-Opening snap (due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips) followed by a late diastolic rumble

-decreased interval between S2 and OS correlates w/ an increase in severity

-LA > LV during diastole

-Enhanced by maneuvers that increase LA return (expiration)

Front 228

Difference in Mitral Valve involvement in Acute vs. Chronic Rheumatic Fever

Back 228

-Acute: causes mitral regurgitation

-Chronic: causes mitral stenosis

Front 229

Mitral Stenosis

Clinical Features/Complications?

Back 229

-Volume overload >> dilatation of left atrium >>:

---pulmonary congestion w/ edema and alveolar hemorrhage

---pulmonary HTN >> R sided HF

---atrial fibrillation (caused by stretching of atrium >> damage to conducting system) w/ associated risk of mural thrombi

-NO ventricular hyerptrophy... it had decreased volume actually

Front 230

Back 230

-Mural Thrombus

-Complication of mitral stenosis (from a fib)

Front 231

Endocarditis

Definition? Most Common Cause?

Back 231

-Inflammation of the endocardium that lines the surface of the cardiac valves

-Usually due to bacterial infection

-Most common cause: Steptococcus viridans - low virulence organism that infects previously damaged valves (chronic rheumatic heart disease & mitral valve prolapse) - mitral valve most commonly involved

Front 232

Streptococcus viridans & Endocarditis Pathogenesis

Back 232

-most common cause

-low-virulence - infects previously damage valves

-Results in small vegetations that do not destroy the valve (subacute endocarditis)

1. Damaged endocardial surface develops thrombotic vegetations (platelets and fibrin)

2. Transient bacteremia >> trapping of bacteria in vegetations

-Prophylactic antibiotics decrease risk

Front 233

Staphylococcus aureus & Endocarditis

Seen In? What other organisms can you see as the cause of endocarditis in this population? Pathogenesis?

Back 233

-most common cause in IV drug abusers - can also see Pseudomonas and Candida

-High-virulence organism that infects normal valves, most commonly tricuspid valve

-Results in large vegetations on previously normal valves that destroy the valve (acute endocarditis) - rapid onset

Front 234

Staphylococcus epidermidis & Endocarditis

Back 234

-endocarditis of prosthetic valves

Front 235

Back 235

S. aureus endocarditis

-large vegetations sitting on valve >> acute endocarditis

Front 236

Streptococcus bovis & Endocarditis

Back 236

associated with endocarditis in patients with underlying colorectal carcinoma

Front 237

HACEK organisms

Back 237

Haemophilus

Actinobacillus

Cardiobacterium

Eikenella

Kingella

-associated w/ endocarditis w/ negative blood cultures

Front 238

Endocarditis

Clinical Features

Back 238

1. Fever - due to bacteremia

2. Murmur (new or worsening)- due to vegetations on valve

3. Septic Embolization of Vegetations (Type III HS -immune complex)

---Janeway lesions - erythematous nontender lesions on palms and soles

---Osler nodes - tender lesions on fingers or toes

---Splinter hemorrhages in nail bed

---Roth spots - white spots on retina surrounded by hemorrhage

---glomerulonephritis can be seen

4. Anemia of chronic disease - due to chronic inflammation

Hint 238

FROM JANE

Front 239

Endocarditis

Lab Findings

Back 239

-Positive blood cultures

-Anemia of chronic disease (decrease Hb, decreased MCV, increased ferritin (b/c of hepcidin), decreased TIBC, decreased %saturation)

-TEE detects lesions on valves

Front 240

Nonbacterial thrombotic endocarditis

Back 240

-sterile vegetations that arise in association with hypercoagulable state or underlying adenocarcinoma

-vegetations arise on mitral valve along lines of closure >> mitral regurgitaiton

Front 241

Libman-Sacks Endocarditis

Back 241

-due to sterile vegetations that arise in association with SLE

-vegetations present on the surface & undersurface of the mitral valve >> mitral regurgitation

Front 242

Complications of Endocarditis

Back 242

chordae rupture, glomerulonephritis, suppurative pericarditis, emboli

Front 243

Dilated Cardiomyopathy

Definition? Commonality?

Back 243

-Dilation of all 4 chambers of the heart

-most common form (90% of cases)

Front 244

Dilated Cardiomyopathy Complications & Presentation

Back 244

-Results in systolic dysfunction (ventricles can't pump) >> biventricular CHF

-Complications: Mitral & Tricuspid regurgitation, arrhythmia, eccentric hypertrophy (sarcomeres added in series)

-Presentation: heart failure, S3, dilated heart on echocardiogram, balloon appearance of heart on CXR

Front 245

Back 245

-Dilate cardiomyopathy - all 4 chambers massively dilated

Front 246

Dilated Cardiomyopathy Causes

Back 246

Most commonly idiopathic; others:

-Genetic mutations (AD)

-Myocarditis - usually due to coxsackie A or B >> characterized by lymphocytic infiltrate of the myocardium >> chest pain, arrhythmia w/ sudden death, or HF (dilated cardiomyopathy late complication if they survive the acute phase) - other virses: influenza, adeno, echo, CMV, HIV

-Alcohol Abuse

-Drugs - doxorubicin, cocaine

-Pregnancy - late pregnancy or weeks to months after childbirth >> develop HF due to dilated cardiomyopathy

-Hemochromatosis

-Chaga's Disease

Front 247

Dilated Cardiomyopathy Treatment

Back 247

Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, implantable cardioverter defibrillator (ICD), heart transplant.

Front 248

Heart Biopsy

Back 248

Myocarditis >> dilated cardiomyopathy

-notice the lymphocytic infiltrate

Front 249

Hypertrophic Cardiomyopathy

Definition? Cause?

Back 249

-Massive hypertorphy of LV, often septa predominance

-Usually (60-70% of cases) due to genetic mutations in sarcomere proteins (B-myosin heavy chain mutation); most common AD

-rarely associated with Friedrich ataxia

Front 250

Hypertrophic Cardiomyopathy

Clinical Features? Biopsy

Back 250

1. Decreased cardiac output - LVH >> diastolic dysfunction & S4

2. Sudden death due to ventricular arrhythmias

---hypertrophic cardiomyopathy is a common cause of sudden death in young athletes

3. Syncope with exercise - subaortic hyerptrophy of the ventricular septum >> functional aortic stenosis

4. Biopsy: myofiber hypertrophy with disarray

Front 251

Heart Biopsy

Back 251

Hypertorphyic Cardiomyopathy

- Disorganization with myocytes in every direction instead of in line

-myofibrillar disarray and fibrosis

Front 252

Hypertrophic Cardiomyopathy Treatment

Back 252

Cessation of high-intensity athletics,

use of β-blocker or non-dihydropyridine calcium channel blockers (e.g., verapamil). ICD if patient is high risk.

Front 253

Obstructive Hypertrophic Cardiomyopathy

Back 253

-hypertrophied septum is too close to the anterior mitral valve leaflet >>outflow obstruction >> dyspnea >> syncope

Front 254

Back 254

Hypertrophic Cardimyopathy

-concentric ventricular hypertrophy

Front 255

Restrictive Cardiomyopathy

Defintion?

Back 255

Decreased compliance of ventricular endomyocardium that restricts filling during diastole

Front 256

Restrictive Cardiomyopathy

Causes?

Back 256

-Amyloidosis, Sarcoidosis, Hemochromatosis, Endocardial Fibroelastosis (children - have a dense layer of fibrosis and elastic tissue in the endocardium >> can't stretch when heart expands)

-Loeffler Syndrome - endomyocardial fibrosis with an eosinophilic infiltrate and eosinophillia >> fibrosis of the endo- and myo- cardium

Front 257

Restrictive Cardiomyopathy

Presentation

Back 257

-dyastolic dysfunction >> Presents as CHF

-Classic finding = EKG w/ low QRS amplitude despite thick myocardium (especially with amyloid)

Front 258

Myxoma

Definition? Seen in? Where? Complication?

Back 258

-Benign mesenchymal tumor w/ gelatinous appearance and abundant ground substance on histology

-most common primary cardiac tumor in adults

-Usually forms a pedunculated mass in the left atrium (ball valve obstruction of the atrium) that causes multiple syncopal episodes due to obstruction of mitral valve

-Can also embolize b/c soft >> fever

Front 259

Rhabdomyoma

Back 259

-Benign hamartoma of cardiac muscle

-Most common primary cardiac tumor in children

---associated with tuberous sclerosis

-Usually arises in the ventricle

Front 260

Metastasis to Heart

From where? Involves what part of the heart? Causes what?

Back 260

-Metastatic tumors are more common in the heart than primary tumors

----common metastases to the heart: breast & lung carcinoma, melanoma, and lymphoma

-Most commonly involves pericardium >> pericardial effusion

Front 261

Heart embryology

Truncus arteriosus

Back 261

Ascending Aorta & pulmonary trunk

Front 262

Heart embryology

Bulbous cordis

Back 262

Smooth parts (outflow tract) of the left and right ventricles

Front 263

Heart embryology

Primitive Atria

Back 263

Trabeculated part of the left and right atria

Front 264

Heart embryology

Primitive Ventricles

Back 264

Trabeculated part of the left and right ventricles

Front 265

Heart embryology

Primitive pulmonary vein

Back 265

smooth part of the left atrium

Front 266

Heart Embryology

Left horn of the sinus venosus

Back 266

Coronary Artery

Front 267

Heart Embryology

Right horn of the sinus venosus

Back 267

smooth part of the right atrium

Front 268

Heart Embryology

right common cardinal vein and right anterior cardinal vein

Back 268

SVC

Front 269

What is the first organ to form in embryo?

Back 269

The heart is the first functional organ in vertebrate embryos

Front 270

When does the heart start beating?

Back 270

week 4

Front 271

Heart Embryology

Cardiac Looping

What is it? When does it start?

Back 271

-primary heart tube loops to establish left-right polarity

-begins in week 4 of gestation

Front 272

Kartagener Syndrome

What is it? Complications?

Back 272

-It is a defect in dynein >> primary ciliary dyskinesia

-In terms of cardiac embryology, it is a defect in L-R dynein which affects L-R symmetry >> dextrocardia

-It can also affect the lungs mimicing CF, and cause infertility

Front 273

Heart Embryology

Septation of the Atria

Back 273

1. Septum primum grows towards the endocardial cushions, narrowing the foraman primum

2. Foramen secundum forms in septum primum; foraman primum disappears

3. Septum secundum develops foraman secundum maintaining the L-to-R shunt

4. Septum secundum expands to cover most for foraemen secundum forming residual foramen ovale

5. Remaining septum primum forms valve of foramen ovale

6. Septum primum & septum secundum fuse to form the atrial wall

7. Foramen ovale usually closes soon after birth due to increase in LA pressure

Front 274

Patent Foramen Ovale

What is it? Treatment? Complications?

Back 274

-caused by failure of septum secundum and septum primum to fuse after birth

-most are left untreated

-can cause paradoxical emboli

Front 275

Heart Embryology

Vetrincular Formation

Back 275

1. Muscular ventricular septum forms; Opening is the interventricular foramen

2. Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form the muscular interventricular septum, closing the interventricular foramen

3. Growth of the endocardial cushions separetes atria from the ventricles and contributes to atrial septation and membranous portion of interventricular septum

Front 276

Ventricular Septal Defect

Back 276

-Most commonly occurs in the membranous septum

-acyanotic at birth due to left-to-right shunt

Front 277

Heart embryology

Outflow tract formation

Back 277

-truncus arteriosus rotates

---neural crest & endocardial cell migrations >> truncal and bulbar ridges that spiral and fuse to form the aorticopulmonary septum >> ascending aorta and pulmonary trunk

Front 278

Heart embryology

Conotruncal abnormalities

Back 278

-Transposition of the great vessels

-Tetralogy of Fallot

-Persistent truncus arteriosus

Front 279

Heart Embryology

Valve development

Back 279

-Aortic/pulmonary: derived from the endocardial cushions of the outflow tract

-Mitral/tricuspid: derived form the fused endocardiacl cushions of the AV canal

Front 280

Heart Embryology

Valve Abnormalities

Back 280

stenotic, regurgitant, atretic (tricuspid atresia), displaced (Ebstein anomaly)

Front 281

Fetal erythropoiesis

Back 281

-Yolk sac (3-8 weeks)

-Liver (6 weeks - birth)

-Spleen (10-28 weeks)

-Bone marrow (18 weeks to adult)

Hint 281

Young Liver Synthesizes Blood

Front 282

Fetal hemoglobin development

What is special about HbF

Back 282

-Fetal Hemoglobin (HbF) = alpha2gamma2

---HbF has higher affinity for O2 b/c 2,3-BPG can't bind >> right curve shift, facilitating unloading of O2 form HbA across the placenta

-Adult Hemoglobin (HbA) = alpha2beta2

Hint 282

Alpha always; gamma goes, becomes beta

Front 283

Fetal circulation

vein vs artery O2 saturation

Back 283

-Blood in umbilical vein has PO2 of 30 mmHg and is 80% saturated with O2

-Umbilical arteries have low O2 saturation

Front 284

Fetal circulation

Shunts

Back 284

1. Blood entering the fetus through the umbilical vein is conducted via the ductus venus into the IVC to bypass hepatic circulation

2. Most highly oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body

3. Deoxygenated blood entering the RA from the SVC goes: RA >> RV >> main PA >> patent ductus arteriosus >> descending aorta due to high fetal pulmonary artery resistance and low O2 tension

Front 285

What happens in fetal circulation when the first breath is taken?

Back 285

Breath >>:

1. decreased resistance in pulmonary vasculature >> increased LA pressure vs. RA pressure >> closure of foramen ovale (now called fossa ovalis)

2. increased O2 (from respiration) and decreased protaglandins (from placental separation - PGE2 comes from placenta) >> closes ductus arteriosus >> DA remant = ligamentum arteriosum

Front 286

What keeps the PDA open?

What closes it?

Back 286

-PGE1 and 2 keep it open

-Indomethacin can help close

Front 287

Follow fetal circulation from placenta through fetus

Back 287

1. oxygenated blood from placenta >> umbilical vein >> ductus venosus >> IVC >> RA >> foramen ovale >> LA >> aorta to brain & down descending also (most oxygenated blood to brain) >> descending aorta >> umbilca arteries >> placenta

2. deoxygenated blood from SVC >> RA >> SV >> pulmonary trunk >> through PDA >> descending aorta

Front 288

Fetal-postnatal derivatives

Umbilical Vein

Back 288

Ligamentum teres hepatis - contained in falciform ligament

Front 289

Fetal-postnatal derivatives

Umbilical artery

Back 289

Medial umbilical ligaments

Front 290

Fetal-postnatal derivatives

Ductus arteriosus

Back 290

Ligamentum arteriosum

Front 291

Fetal-postnatal derivatives

Ductus venosus

Back 291

Ligamentum venosum

Front 292

Fetal-postnatal derivatives

Foramen ovale

Back 292

Fossa ovalis

Front 293

Fetal-postnatal derivatives

Allantois

Back 293

Urachus - median umbilical ligament

---urachus is part of the allantoic duct between the bladder and the umbilicus

---Urachal cyst/sinus is a remnant

Front 294

Fetal-postnatal derivatives

Notochord

Back 294

Nucleus pulpous of intervertebral disc

Front 295

Right coronary artery

supplies what? infarction leads to?

Back 295

-supplies SA & AV nodes

-infarct can cause nodal dysfunction (bradycardia or heart block)

-infarct affects posterior wall, posterior septum, and posterior papillary muscles of the LV (via PDA) (can lead to rupture and valvular insufficiency)

Front 296

Acute marginal artery

Comes off what? Supplies what?

Back 296

-from RCA

-supplies right ventricle

Front 297

What does right-dominant circulation mean? What is its prevalence?

Back 297

-PDA arises from RCA

-85% of the population

Front 298

What does left-dominant circulation mean? What is its prevalence?

Back 298

-PDA arises from LCX

-8% of the population

Front 299

What does co-dominant circulation mean? Prevalence?

Back 299

-PDA arises from RCA & LCX

-7% of the population

Front 300

Most common sight of coronary artery occlusion

Back 300

LAD

Front 301

Coronary blood flow peaks when?

Back 301

in early diastole

Front 302

Left Circumflex artery supplies what?

Back 302

lateral and posterior walls of the left ventricle

Front 303

Left Anterior Descending Artery supplies what?

Back 303

supplies anterior 2/3 of the interventricular septum, anterior papillary muscle, and anterior surface of the left ventricle

Front 304

Left marginal artery arises from?

Back 304

LDA

Front 305

Posterior descending artery supplies what?

Back 305

posterior 1/3 of the interventricular septum and posterior walls of the ventricles

Front 306

What is the most posterior part of the heart? What can enlargement cause?

Back 306

-left atrium is the most posterior portion of the heart

-enlargement can cause dysphagia (compression of esophagus) or hoarseness (compression of recurrent laryngeal, a branch of the vagus)

Front 307

Cardiac Output (equation)

Back 307

=stroke volume x heart rate

Front 308

Stroke volume equation

Back 308

= End-diastolic volume - end-systolic volume

proportional to pulse pressure

Front 309

Ejection Fraction equation

Back 309

= stroke volume/ end-diastolic volume

Front 310

Fick Principle

Back 310

CO = rate of O2 consumption / (arterial O2 content - venous O2 content)

Front 311

Mean arterial pressure equation

Back 311

MAP = CO x TPR

MAP = 2/3 diastolic pressure + 1/3 systolic pressure

Front 312

Pulse pressure

Back 312

= systolic pressure - diastolic pressure

proportional to stroke volume & inversely proportional to arterial compliance (C=v/p)

Front 313

Describe exercise in terms of CO, HR, and SV

Back 313

-Early stages of exercise: CO maintained by increased HR and increased SV

-Late stages: CO maintained by increased HR only; SV plateaus

Front 314

What happens to diastole with increased HR? Consequences?

Back 314

-increased HR >> shortened diastole >> less filling time >> decreased cardiac output (ventricular tachycardia)

Front 315

What causes an increased pulse pressure?

Back 315

hyperthyroidism, aortic regurgitation, arteriosclerosis, obstructive sleep apnea (increased sympathetic tone), exercise (transient)

Front 316

What causes a decreased pulse pressure?

Back 316

aortic stenosis, cardiogenic shock, cardiac tamponade, advance heart failure

Front 317

What affects stroke volume?

Back 317

-SV affected by contractility, afterload, and preload

-SV increases with an increase in contractility, an increase in preload, and/or a decrease in afterload

Hint 317

SV CAP

Front 318

What causes an increase in contractility?

Back 318

-also causes an increase in SV

-Catecholamines (increase activity of Ca2+ pump in SR)

-increased intracellular Ca2+

-decreased extracellular Na+ (decreases activity of Na+/Ca2+ exchanger)

-Digitalis - blocks Na+/Ca2+ pump

Front 319

What causes an changes in stroke volume?

Back 319

-Increase in SV: anxiety, pregnancy

-Decrease in SV: heart failure

Front 320

Myocardial O2 Demand

Back 320

-increase in afterload

-increase in contractility

-increase in HR

-increase in ventricular diameter (increases wall tension)

Front 321

What causes a decrease in contractility?

Back 321

-results in decreased SV

-B1-blockade (decreases cAMP)

-heart failure w/ systolic dysfunction

-acidosis

-hypoxia/hypercapnia (decreases PO2/PCO2)

-non-dihydropyradine Ca2+ channel blockers

Front 322

How is preload approximated? What affects it?

Back 322

-Preload is approximated by ventricular EDV

-Depends on venous tone and circulating blood volume

---thus venodilators (nitroglycerine) decrease preload

Front 323

How is afterload approximated? Equation associated? What affects it?

Back 323

-afterload approximated by MAP

-Relation of LV size and afterload:

---Laplace's Law: Wall tension = (pressure x radius) / (2 x wall thickness)

---LV hypertrophies in response to increased afterload

-vasodilators (hydralazine) decrease afterload (arterial)

-ACE inhibitors & ARBs decrease preload and afterload

-Chronic HTN (increased MAP) >> LV Hypertrophy

Front 324

How does the ventricle respond to increased afterload? Equation?

Back 324

-LV compensates for increased afterload by thickening (hypertrophy) to decrease wall tension

-Laplace's Law: Wall tension = (pressure x radius) / (2 x wall thickness)

Front 325

Ejection Fraction

Equation? Normal? What happens to it in heart failure?

Back 325

EF = SV/EDV = (EDV - ESV) / EDV

-left ventricular EF is an index of ventricular contractility

-normal ≥ 55%

-Systolic HF - EF decreases

-Diastolic HF - EF normal

Front 326

Force of contraction is proportional to...

Back 326

-end-diastolic length of cardiac muscle fiber (pre-load)

Front 327

What causes increase in contractility?

Back 327

catechoalmines (exercise), digoxin

Front 328

What causes a decrease in contractility?

Back 328

loss of myocardium (MI), B-blockers, Ca-channel blockers, dilated cardiomyopathy

Front 329

Starling curve

What does it describe? Relationships?

Back 329

-describes increases in CO or SV in response to an increase in venous return or end-diastolic volume

-increases in contractility increase CO for any level of end-diastolic volume

Front 330

Blood flow can be expressed by which equation? Describe the components of this equation.

Back 330

Q = change in pressure/ resistance

CP = MAP - RA pressure / TPR

-analagous to Ohm's law

-pressure gradient drives flow from high to low pressure

-Resistance is directly proportional to viscosity and vessel length and inversely proportional to radius to the 4th power

-Arterioles account for most of TPR as they are the site for highest resistance >> they regulate capillary flow

Front 331

Equation for Resistance

Back 331

Front 332

Systemic Circulation exhibits what type of resistance?

Back 332

-Parallel resistance - exhibited by each organ system

1/Rtotal = 1/R1 + 1/R2

-total resistance less than any individual artery

-each time you add an artery to the system, you decrease total resistance

Front 333

Circulation within an organ exhibits what type of resistance?

Back 333

-Series resistance - exhibited by arrangement of vessels withing a given organ

Rtotal = Rarteries+ Rarterioles + R3caps

-arterioles contribute largest proportion of resistance

-pressure decreases as blood flows through a series

Front 334

What causes changes in viscosity?

Back 334

-depends on mostly on Hct

-increased by: polycythemia, hyperproteinemic state (multiple myeloma), aHereditary spherocytosis

-decreases in anemia

Front 335

Inotropy & Cardiac/Vascular Function Curve

What affects inotropy?

Back 335

-inotropy = change in contractility >> altered CO for a given RA pressure (preload)
1.Increased by: catechoalmines, digoxin
2.Decreased by: uncompensated HF, narcotics overdose

Front 336

Inotropy & Cardiac/Vascular Function Curve

What affects inotropy?

Back 336

-inotropy = change in contractility >> altered CO for a given RA pressure (preload)

1.Increased by: catechoalmines, digoxin

2.Decreased by: uncompensated HF, narcotics overdose

Front 337

Venous Return & Cardiac/Vascular Function Curve

What affects venous return?

Back 337

-Changes in circulating volume or venous tone >> altered RA pressure for a given CO

-MSP (x-intercept) changes w/ volume & venous tone

3. venous return increased by: fluid infusion, sympathetic activity

4. decreased by: acute hemorrhage, spinal anesthesia

Front 338

Total Peripheral Resistance & Cardiac/Vascular Function Cruve

What affects TPR?

Back 338

-changes in TPR >> altered CO for a given RA pressure, but MSP is unchanged

5. TPR increased by: vasopressors

6. TPR decreased by: exercise, AV shunt

Front 339

Exercise effects on inotropy, TPR, CO

Back 339

Exercise >> increased inotropy and decreased TPR to maximize CO

Front 340

HF effects on inotropy, TPR, CO

Back 340

HF >> decreased inotropy >> fluid retention to increase preload and maintain CO

Front 341

Pressure volume loops and cardiac cycle

Normal cycle/loop? When do you hear heart sounds?

Back 341

1. isovolmetric contraction - period between mitral valve closing and aortic valve opening; highest O2 consumption - S1 at beginning

2. Systolic ejection - period between aortic valve opening and closing - S2 at end

3. Isovolumetric relaxation - period between aortic valve closing and mitral valve opening

4. Rapid filling - mitral valve opens - S3 at beginning

5. Reduced filling - just before mitral valve closes - S4 at end

Front 342

Pressure volume loops and cardiac cycle

What does increased contractility do to the loop?

Back 342

- increased SV >> larger steeper part 2 >> increased EF & decreased ESV

Front 343

Pressure volume loops and cardiac cycle

What does increased afterload due to the loop?

Back 343

= increased aortic pressure >> decreased SV and increased ESV

Front 344

Pressure volume loops and cardiac cycle

What does increased preload due to the loop?

Back 344

= increased venous return >> increased SV

Front 345

S1 heart sound

What is it? Loudest where? What else is happening at this time?

Back 345

-mitral & tricuspid valve closure

-loudest in mitral area

-Concurrent events: isovolumetric contraction (end of QRS)

Front 346

S2 heart sound

What is it? Loudest where? What happened between S1 & S2? What else is happening at this time?

Back 346

-aortic and pulmonary valve closure >> dicrotic notch

-loudest at left sternal border

-Between S1 & S2: LV pressure rose & peaked, ventricles repolarized (T wave)

-Concurrent events: LV pressure & volume decreased, isovolumetric relaxation

Front 347

S3 heart sound

What is it? Normal? What else is happening at this time?

Back 347

-in early diastole during rapid ventricular filling

-associated with increased filling pressures (CHF, mitral regurge)

-more common in dilated ventricles (volume overload)

-normal in children & pregnant women

Front 348

S4 heart sound

What is it? Normal? What else is happening at this time? Associated with?

Back 348

-S4 = atrial kick in late diastole

-high atrial pressure

-associated with ventricular hypertrophy >> LA must push against stiff LV wall (decreased compliance)

-associated with HTN

-can also occur with volume overload

Front 349

Jugular venous pulse (describe points on the wave)

Back 349

-a wave = atrial contraction

-c wave = RV contraction (closed tricuspid valve bulging into atrium)

-x descent = atrial relaxation and downward displacement of tricuspid valve during ventricular contraction; absent in tricuspid regurgitation

-v wave = increased atrial pressure due to filling against closed tricuspid valve

-y descent = blood flow from RA to RV

Front 350

Normal splitting of heart sounds

Back 350

-inspiration >> decreased thoracic pressure >> increased venous return to RV >> increased SV >> increased ejection time >> delayed closure of pulmonic valve

-decreased pulmonary impedance (increased capacity of pulmonary circulation) also occurs during inspiration, also contributing to delayed closure

Front 351

Wide splitting of heart sounds

Back 351

-seen in conditions that delay RV emptying (pulmonic stenosis, RBBB)

-delayed RV emptying >> delay in pulmonic sound regardless of breath

=exaggeration of normal splitting

Front 352

Fixed splitting of heart sounds

Back 352

-ASD >> L to R shunt >> increases RA volumes >> increases RV volumes >> increased flow through pulmonic valve so that regardless of breath, closure of pulmonic valve delayed

Front 353

Paradoxical splitting

Back 353

-seen in conditions that delay LV emptying (aortic stenosis, LBBB)

-P2 occurs before A2 >> inspiration >> P2 moves closer to A2 paradoxically eliminating the split

Front 354

Auscultation of Heart

Aortic Area: what will you hear here?

Back 354

Systolic murmur: aortic stenosis, flow murmur, aortic valve sclerosis

Front 355

Auscultation of Heart

Pulmonic Area: what will you hear here?

Back 355

Systolic Ejection murmur: pulmonic stenosis, flow murmur (physiologic murmur - ASD from increased flow)

Front 356

Auscultation of Heart

Left Sternal border: What will you hear here?

Back 356

-Diastolic murmur: aortic regurgitation, pulmonic regurgitation

-Systolic murmur: hypertrophic cardiomyopathy

Front 357

Auscultation of Heart

Tricuspid Area: What will you hear here?

Back 357

-Pansystolic murmur: tricuspid regurgitation, VSD

-Diastolic murmur: tricuspid stenosis, ASD (rumble due to increased flow)

Front 358

Auscultation of Heart

Mitral Area: What will you hear here?

Back 358

-Systolic murmur: mitral regurgitation

-Diastolic murmu: mitral stenosis

Front 359

Systolic murmurs

Back 359

-aortic/pulmonic stenosis

-mitral/tricuspid regurgitation

-VSD

Front 360

Diastolic murmurs

Back 360

-aortic/pulmonic regurgitation

-mitral/tricuspid stenosis

Front 361

Bedside Maneuver: Heart Sounds

Inspiration

Back 361

-increases intensity of right heart sounds

Front 362

Bedside Maneuver: Heart Sounds

Hand grip

Back 362

-causes increased systemic vascular resistance

-increased intensity of MR, AR, and VSD murmurs

-decreased intensity of AS, hypertrophic cardiomyopathy murmurs

-MVP: increased murmur intensity, later onset of click/murmur

Front 363

Bedside Maneuver: Heart Sounds

Valsalva (phase II), standing

Back 363

-decreases venous return

-decreased intensity of most murmurs (including AS)

-increased intensity of hypertrophic cardiomyopathy murmurs

-MVP: decreased murmur intensity, earlier onset of click/murmur

Front 364

Bedside Maneuver: Heart Sounds

Rapid Squatting

Back 364

-increased venous return, increase preload, increased afterload with prolonged squating

-decreased intensity of hypertrophic cardiomyopathy murmurs

-increased intensity of AS murmur

-MVP: increased intensity of murmur, later onset of click/murmur

Front 365

Ventricular (Bundle of His, Purkinje Fibers) Action Potential Phase 0

Back 365

Phase 0 = rapid upstroke and depolarization; voltage gated Na+ channels open (increase in conductance)

Front 366

Ventricular (Bundle of His, Purkinje Fibers) Action Potential Phase 1

Back 366

Phase 1 = initial repolarization - decreased conductance/ inactivation of VG Na+ channels & VG K+ channels begin to open (increase in conductance)

Front 367

Ventricular (Bundle of His, Purkinje Fibers) Action Potential Phase 2

Back 367

Phase 2 = plateau - Ca2+ influx through VG Ca2+ channels balance K+ efflux; Ca2+ influx triggers release of Ca2+ from SR >> myocyte contraction

Front 368

Ventricular (Bundle of His, Purkinje Fibers) Action Potential Phase 3

Back 368

Phase 3 = rapid repolarization - massive K+ efflux due to opening of VG slow K+ channels and closing of VG Ca2+ channels

Front 369

Ventricular (Bundle of His, Purkinje Fibers) Action Potential Phase 4

Back 369

Phase 4 = resting membrane potential - high K+ permeability through K+ channels; about -85mV (close to K+ equilibrium potential)

Front 370

Contrast cardiac action potentials to skeletal muscle action potentials

Back 370

In contrast to skeletal muscle:

-cardiac muscle AP has a plateau due to Ca2+ influx and K+ efflux; myocyte contraction is due to Ca-induced-Ca release from the SR

-cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity of the If channels (slow mixed Na+/K+ inward current)

-cardiac myocytes are electrically coupled to each other by gap junctions

Front 371

Pacemaker Action Potential Phase 0

Back 371

Phase 0 = upstroke of AP - opening of VG Ca2+ channels; Fast VG Na+ channels are permanently inactivated b/c of the less negative resting voltage of these cells
-results in slow conduction velocity that is used by the AV node to prolong transmission from the atria to the ventricles

Front 372

Pacemaker Action Potential Phase 0

Back 372

Phase 0 = upstroke of AP - opening of VG Ca2+ channels; Fast VG Na+ channels are permanently inactivated b/c of the less negative resting voltage of these cells

-results in slow conduction velocity that is used by the AV node to prolong transmission from the atria to the ventricles

Front 373

Pacemaker Action Potential Phase 3

Back 373

Phase 3 = inactivation of Ca2+ channels and increased activation of K+ channels >> efflux of K+

Front 374

Pacemaker Action Potential Phase 4

What affects this phase?

Back 374

Phase 4 = slow diastolic depolarization; membrane potential spontaneously depolarizes as Na+ conductance increases (If different from INa in phase 0 of ventricular AP)

-accounts for automaticity of SA and AV nodes

-slope of phase 4 determines HR

-Ach/adenosine decrease rate of depolarization and thus decrease HR; Catecholamines increase rate of depolarization increasing HR

-Sympathetic stimulation increases chance that If is open >> increased HR

Front 375

ECG

P wave

Back 375

-atrial depolarization; repolarization is hidden by QRS

Front 376

ECG

PR interval

Back 376

-conduction delay through the AV node >> allows ventricular filling (100 msec delay)

-normally <200 msec

Front 377

ECG

QRS complex

Back 377

-ventricular depolarization

-normally <120 msec

Front 378

ECG

QT interval

Back 378

-mechanical contraction of the ventricles

Front 379

ECG

T wave

Back 379

-ventricular repolarization

-inversion may indicate MI

Front 380

ECG

ST segment

Back 380

-isoelectric, ventricles depolarized

Front 381

ECG

U wave

Back 381

-caused by hypokalemia and bradycardia

Front 382

Speed of conduction

Back 382

Purkinje > atria > ventricles > AV node

Front 383

Pacemakers of the heart

Which is dominant?

Back 383

SA > AV > bundle of His / Purkinje fibers / ventricles

SA node is the pacemaker of the heart has inherent dominance with slow phase of upstroke

Front 384

Conduction through the heart

Back 384

SA node >> atria >> AV node >> common bundle >> bundle branches >> Purkinje fibers >> ventricles

Front 385

Torsades de pointes

What is it? Complication?

Back 385

-polumorphic ventricular tachycardia characterized by sinusoidal wave forms on ECG

-can progress to ventricular fibrillation

Front 386

What Causes Torsades de pointes?

Back 386

-long QT predisposes to it

-Caused by drugs, decreased K+, decreased Mg2+, others

-Drugs: Sotalol, Risperidone (antipsychotics), Macrolides, Chloroquine, Protease Inhibitors (-navir), Quinidine (class Ia, class III), Thiazides

Hint 386

Some Risky Meds Can Prolong QT

Front 387

Congenital long QT syndrome

Back 387

-Inherited disorder of myocardial repolarization, typically due to ion channel defects

-Increased risk of sudden cardiac death due to torsades de pointes

-Includes; Romano-Ward Syndrome & Jervell and Lang-Neilsen Syndrome

Front 388

Romano-Ward Syndrome

Back 388

-autosomal dominant, pure cardiac phenotype >> congenital long QT syndrome

Front 389

Jervell and Lange-Nielsen Syndrome

Back 389

-autosomal recessive congenital long QT syndrome that also causes sensorineural deafness

Front 390

Wolff-Parkinson-White syndrome

What is it? Pathogenesis & Presentation? Complications?

Back 390

-most common type of ventricular pre-excitation syndrome

-abnormal fast accessory conduction pathway form atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node >> ventricles begin to partially depolarize earlier >> characteristic delta wave w/ shortened PR interval on ECG

-May lead to reentry circuit >> supraventricular tachycardia

Front 391

Back 391

Atrial Fibrillation

Front 392

Atrial fibrillation

What is it? Complications

Back 392

-chaotic and erratic baseline (irregular irregular) with no discrete P waves in between iregularly spaced QRS complexes

-can lead to atria stasis >> thromboembolic stroke

Front 393

Atrial fibrillation

Treatment?

Back 393

-rate control

-anticoagulation

-pharmacologic or electrical cardioversion

---glycosides (digoxin)

---Na+ channel blockers (Quinidine, Procainamide, Disopyramide)

---B-blockers

---K+ channel blockers (amiodarone...)

---Ca2+ channel blockers

Front 394

Back 394

Atrial Flutter

-a rapid succession of back to back identical atrial depolarization waves

-identical appearance gives risk to "sawtooth" appearance on EKG

Front 395

Atrial Flutter

Treatment?

Back 395

-Pharmacological cardioversion: class IA, IC, or III antiarrhythmics

-Rate control: B blockers, or Ca channel blocker

-Definitive treatment = ablation

Front 396

What is it? Complications?

Back 396

Ventricular Fibrillation

-a completely erratic rhythm with no identifiable waves

-Fatal arrhythmia without immediate CPR and defibrillation

Front 397

AV block

Definition? What does it look like on ECG? Treatment?

Back 397

-1st degree block w/ PR interval > 200ms

-benign and asymptomatic >> no treatment necessary

Front 398

Mobitz type 1 block

Other names? Definition? What does it look like on ECG? Treatment?

Back 398

-2nd degree block/ Weckenbach block

-progressive lengthening of the PR interval until a beat is dropped (P wave not followed by QRS)

-Usually asymptomatic

Front 399

What is this?

Back 399

AV / 1st degree block

Front 400

What is this?

Back 400

2nd degree block (Mobitz type I) (Weckenbach)

Front 401

What is this? Definition? Complications?

Treatment?

Back 401

Mobitz type II

-dropped beats that are not preceded by a change in the PR interval

-often found as a 2:1 where there are 2 or more P waves to 1 QRS response

-may progress to a 3rd degree block

-treat with a pacemaker

Front 402

What is it?

Back 402

Mobitz type II

Front 403

What is this? Definition?

Back 403

3rd degree (complete) heart block

-the atria and ventricles beat independently of 1 another

-Both P waves and QRS complexes are present, but the P waves bear no relation to the QRS complexes

-the atrial rate is faster than the ventricular rate

Front 404

Treatment of 3rd degree heart block

What can cause it?

Back 404

-Treatment: pacemaker

-Lyme Disease can result in a 3rd degree heart block

Front 405

Atrial natriuretic peptide

When/where is it released? What does it do?

Back 405

-released from atrial myocytes in response to increased blood volume and atrial pressure

-Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule

-Constricts efferent renal arterioles and vasodilates afferent renal arterioles via cGMP, promoting diuresis and contributing to the aldosterone escape mechanism

Front 406

B-type (brain) netriuretic peptide

What is it? What does it do? What is it used for clinically?

[NT-proBNP?, normal levels BNP and associated disease levls]

Back 406

-released from ventricular myocytes in response to an increase in tension

-similar physiological actions to ANP, w/ an increased half life

-BNP blood tests used for diagnosing HF (good NPV) - esp. used for assessing acute decompensation and monitoring response to rx - better than using Framingham guidelines as a predictive factor

-recombinant form (nesiritide) for treatment of HF

-normal NT-proBNP rises with age and declining renal function

-no HF: BNP = 100 pg/dL; non-cardiac dyspnea = 346 pg/dL; Acute HF = 675 pg/dL

Front 407

Aortic arch receptors transmit via? to? in response to?

Back 407

Aortic arch transmits via the vagus nerve to the solitary nucleus of the medulla in response ONLY to increases in BP

Front 408

Carotid sinus receptors transmit via? to? in response to?

Back 408

Carotid sinus (dilated region at carotid bifurcation) transmits via the glossopharyngeal nerve to the solitary nucleus of the medulla in response to BOTH increases and decreases in BP

Front 409

Response of Baroreceptors to Hypotension

Back 409

Hypotension >> decrease arterial pressure >> decrease in stretch >> decrease in afferent baroreceptor firing >> increased efferent sympathetic firing and decrease efferent parasympathetic firing >> vasocontriction, increased HR, increased contractility, and increased BP

-important response for severe hemorrhage

Front 410

Carotid massage

Back 410

increased pressure on carotid sinus >> increase stretch >> increase afferent baroreceptor firing >> increased AV node refractory period >> decreased HR

Front 411

Cushing reaction

Back 411

-triad: hypertension, bradycardia, respiratory depression

-increased intracranial pressure constricts arterials >> cerebral ischemia and reflex sympathetic increased in perfusion pressure (HTN) >> increased stretch >> reflex baroreceptor-induced bradycardia

Front 412

Chemoreceptors

Where are they & what stimulates them?

Back 412

-Peripheral: carotid and aortic bodies - response to decreases in PO2 (< 60 mmHg), increases in PCO2, and decreased pH of blood

-Central: stimulated by changes in pH and PCO2 of brain interstitial fluid, which are influenced by arterial PCO2

---do NOT directly respond to PO2

Front 413

What organ has the largest blood flow? largest share of CO? highest blood flow per gram of tissue? largest arteriovenous difference in O2?

Back 413

-Largest blood flow: Lung - 100% of cardiac output

-Largest share of CO: liver

-Highest blood flow: kidney

-The heart has the largest difference in arteriovenous O2 b/c extraction is about 80%.

Front 414

How is increased O2 demand met by the heart

Back 414

-the heart has the largest difference in arteriovenous O2 b/c extraction is 80%

-increases in O2 demand must be met by an increase in coronary artery blood flow, NOT by an increase in extraction of O2

Front 415

Normal heart pressures

Back 415

-PCWP is a good approximation of LA pressure

-in mitral stenosis PCWP > LV diastolic pressure

-pressures are measured with a pulmonary artery catheter (Swanz-Ganz catheter)

Front 416

What is autoregulation?

Back 416

How blood flow to an organ remains constant over a wide range of perfusion pressures

Front 417

Factors Determining Heart Autoregulation

Back 417

Local metabolites are vasodilatory - CO2, adenosine, NO

Front 418

Factors Determining Brain Autoregulation

Back 418

Local metabolies are vasodilatory - CO2 (pH)

Front 419

Factors Determining Kidney Autoregulation

Back 419

Myogenic and tubuloglomerular feedback

Front 420

Factors Determining Lung Autoregulation

Back 420

pulmonary vasculature is unique in that hypoxia causes vasoconstriction so that only well-ventialted areas are perfused

-in all other organs, hypoxia causes vasodilation

Front 421

Factors Determining Skeletal Muscle Autoregulation

Back 421

Local metabolites - lactate, adenosine, K+, H+, CO2

Front 422

Factors Determining Skin Autoregulation

Back 422

Sympathetic stimulation is the most important - for temperature control

Front 423

Starling forces that determine fluid movement across capillary membranes

Back 423

- Pc = capillary hydrostatic pressure - pushes fluid out of capillary

- Pi = interstitial fluid pressure - pushes fluid into capillary

- pi c = plasma colloid pressure - pulls fluid into capillary

- pi i = interstitial colloid pressure - pulls fluid out of capillary

Front 424

Net filtration pressure across a capillary

Back 424

P[net] = [(Pc -Pi) - (pi c - pi i)]

Front 425

Net fluid flow in a capillary

Back 425

Kf = filtration constant

Jv = net fluid flow = (Kf)(Pnet)

Front 426

Edema definition & causes

Back 426

Edema is excess fluid outflow into the interstitium. Commonly caused by:

- increased capillary pressure due to HR

- decreased plasma protein due to nephrotic syndrome and/or liver failure

- increase capillary permeablity = increase Kf caused by infection, toxins, burns

- increased interstial fluid colloid osomotic pressure cause by lymph blockage

Front 427

Congenital Cardiac Defect(s) associated with

22q11 syndrome

Back 427

-Truncus arteriosus

-Tetralogy of Fallot

Front 428

Congenital Cardiac Defect(s) associated with

Down Syndrome

Back 428

-ASD

-VSD

-AV septal defect (endocardial cushion defect)

[Tetralogy of Fallot]

Front 429

Congenital Cardiac Defect(s) associated with

Congenital Rubella

Back 429

-septal defects

-PDA

-pulmonary artery stenosis

Front 430

Congenital Cardiac Defect(s) associated with

Turner Syndrome

Back 430

-infantile coarctation of the aorta

-bicuspid aortic valve

Front 431

Congenital Cardiac Defect(s) associated with

Marfan Syndrome

Back 431

-MVP

-thoracic aortic aneurysm and dissection

-aortic regurgitation

Front 432

Congenital Cardiac Defect(s) associated with

Infant of Diabetic Mother

Back 432

Transposition of the great vessels

Front 433

Signs of Hyperlipidemia

Back 433

Xanthomas, Tendinous xanthoma, corneal arcus

Front 434

Back 434

Due to hyperlipidemia

A. Xanthomas

-plaques or nodules composed of lipid-laden histiocytes in the skin

B. Xanthelasma - xanthomas on the eyes - very common

Front 435

Tendinous xanthoma

Back 435

-lipid deposit in tendon, especially Achilles

-due to hyperlipidemia

Front 436

Back 436

Due to hyperlipidemia

Corneal arcus

-lipid deposits in the corney, appear early in life with hypercholesteremia

-common in the elderly - arcus senilis

Front 437

Cardiac Dilation is Caused by?

Back 437

-greater ventricular end-diastolic volume

Front 438

Dyspnea on exertion is caused by?

Back 438

Failure for CO to increase during exercise

Front 439

Acute peridcariditis

Presentation? Types & their causes?

Back 439

Commonly presents w/ sharp pain, aggravated by inspiration, & relieved by sitting up and leaning forward. Presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression.
-Fibrinous—caused by Dressler syndrome, uremia, radiation. Presents with loud friction rub.
-Serous—viral pericarditis (often resolves spontaneously); noninfectious inflammatory diseases (e.g., rheumatoid arthritis, SLE).
-Suppurative/purulent—usually caused by bacterial infections (e.g., Pneumococcus, Streptococcus). Rare now with antibiotics.

Front 440

Causes what? Findings?

Back 440

Compression of heart by fluid (e.g., blood, effusions) in pericardium, leading to decreased CO. Equilibration of diastolic pressures in all 4 chambers.
Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), increaesd HR, pulsus paradoxus, Kussmaul sign. ECG shows low-voltage QRS and electrical alternans (due to “swinging” movement of heart in large effusion).

Front 441

Pulsus paradoxus

What is it? Caused by?

Back 441

-Decrease in amplitude of systolic blood pressure by ≥ 10 mmHg during inspiration.

-Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup.

Front 442

Treatment for Primary (essential) hypertension

Back 442

Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers

Front 443

Treatment of Hypertension with CHF

Back 443

Diuretics, ACE inhibitors/ARBs, β-blockers (compensated CHF), aldosterone antagonists.

β-blockers must be used cautiously in decompensated CHF and are contraindicated in cardiogenic shock.

Front 444

Treatment of Hypertension with diabetes mellitus

Back 444

ACE inhibitors/ARBs. Calcium channel blockers, diuretics, β-blockers, α-blockers.

ACE inhibitors/ARBs are protective against diabetic nephropathy.

Front 445

Ca channel blockers

Names? Use of each?

Back 445

Amlodipine, nimodipine, nifedipine (dihydropyridine); diltiazem, verapamil (non-dihydropyridine).

Use:

-Dihydropyridine (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud phenomenon.

-Non-dihydropyridine: hypertension, angina, atrial fibrillation/flutter.

-Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).

Front 446

MOA of Ca channel blockers

Back 446

-Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reduce muscle contractility.

-Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.

-Heart—verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle). `

Front 447

Ca channel blockers toxicity

Back 447

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation.

Front 448

Hydralazine

Use?

Back 448

Use: Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa.

Frequently coadministered with a β-blocker to prevent reflex tachycardia.

Front 449

Hydralazine MOA

Back 449

increased cGMP >> smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.

Front 450

How do you treat a hypertensive emergency?

Back 450

-Commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.

Front 451

Nitroprusside

MOA? toxicity?

Back 451

Short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)

Front 452

Fenoldopam

MOA?

Back 452

Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. decreases BP and increases natriuresis.

Front 453

Nitroglycerin, isosorbide dinitrate

Use? MOA?

Back 453

-Use: Angina, acute coronary syndrome, pulmonary edema.

-MOA: Vasodilate by increasing NO in vascular smooth muscle >> increase in cGMP and smooth muscle relaxation. Dilate veins >> arteries. Decrease preload.

Front 454

Nitroglycerin, isosorbide dinitrate

Toxicity?

Back 454

Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache, “Monday disease” in industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure.

Front 455

Antianginal therapy goals and determinants

Drugs used?

Back 455

Goal—reduction of myocardial O2 consumption (MVO2) by decreasing 1 or more of the determinants of MVO2: end-diastolic volume, blood pressure, heart rate, contractility.

Use nitrate, B blockers, or a combination of the 2

Front 456

Nitrates in antianginal therapy

Effects?

Back 456

-Overall, they affect the preload

-decrease end-diastolic volume

-decrease blood pressure

-increase contractility (reflex response)

-increase HR (reflex response)

-decrease ejection time

-decrease MVO2

Front 457

B blockers in antianginal therapy

Effects?

Back 457

-Overall, they affect afterload

-increase end-diastolic volume

-decrease blood pressure

-decrease contractility

-decrease HR

-increase ejection time

-decrease MVO2

Front 458

Nitrate + B blockers in antianginal therapy

Effects?

Back 458

-no effect or decrease in end-diastolic volume

-decrease blood pressure

-little/no effect on contractility

-decreased HR

-little/no effect on ejection time

-very decreased MVO2

Front 459

Aternates to nitrats and/or B blockers in antianginal therapy?

Back 459

Calcium channel blockers—nifedipine is similar to nitrates in effect; verapamil is similar to β-blockers in effect.

Front 460

What is contraindicated for antianginal therapy?

Back 460

Pindolol and acebutolol—partial β-agonists contraindicated in angina.

Front 461

lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

Class? MOA? Effects? Toxicity?

Back 461

-Class: HMG-CoA reductase inhibitors

-MOA: Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor [>> decreased hepatic cholesterol pool >> increased expression of hepatic LDL receptors >> increased uptake of LDL & IDL >> decreased availability of LDL and IDL for uptake by arterial macrophages[

-Effects: greatly decreases bad cholesterol, low increase on good cholesterol, low decrease on triglycerides

-Toxicity: Hepatotoxicity (increased LFTs), rhabdomyolysis (esp. when used with fibrates and niacin)

Front 462

Niacin (vitamin B3)

Class? MOA? Effects? Toxicity?

Back 462

-Class: vitamin - lipid-lowering agent

-MOA: Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

-Effects: medium decrease in bad cholesterol, medium increase in good cholesterol, low decrease in triglycerides

-Toxicity: Red, flushed face, which is decreasedby aspirin or long- term use; Hyperglycemia (acanthosis nigricans); Hyperuricemia (exacerbates gout)

Front 463

cholestyramine, colestipol, colesevelam

Class? MOA? Effects? Toxicity?

Back 463

-Class: bile acid resins >> lipid-lowering agent

-MOA: Prevent intestinal reabsorption
of bile acids; liver must use cholesterol to make more

-Effects: medium decrease in bad cholesterol, slight increase in good cholesterol, slight increase in triglycerides

-Toxicity: Patients hate it—tastes bad and causes GI discomfort, decreases absorption of fat-soluble vitamins, Cholesterol gallstones

Front 464

ezetimibe

Class? MOA? Effects? Toxicity?

Back 464

-Class: cholesterol absorption blocker

-MOA: Prevent cholesterol absorption at small intestine brush border

-Effects: medium decrease of bad cholesterol, no effect on good cholesterol or triglycerides

-Toxicity: Rare increased LFTs, diarrhea

Front 465

gemfibrozil, clofibrate, bezafibrate, fenofibrate

Class? MOA? Effects? Toxicity?

Back 465

-Class: Fibrates

-MOA: Upregulate LPL >> increased TG clearance, Activates PPAR-α to induce HDL synthesis

-Effects: low decrease in bad cholesterol, low increase in good cholesterol, great decrease in triglycerides

-Toxicity: Myositis (increased risk with concurrent statins), hepatotoxicity (increasedLFTs), cholesterol gallstones (esp. with concurrent bile acid resins)

Front 466

Digoxin

Class? bioavailability/metabolism?

Back 466

-Class: cardiac glycoside

-75% bioavailability, 20–40% protein bound, t1/2 = 40 hours, urinary excretion.

Front 467

Digoxin

MOA? Clinical Use?

Back 467

-MOA: Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. increased [Ca2+]i >> positive inotropy. Stimulates vagus nerve >> decreases HR.

Front 468

Digoxin

Toxicity?

Back 468

-Cholinergic—nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). ECG—increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block.
-Can lead to hyperkalemia, which indicates poor prognosis.
-Factors predisposing to toxicity—renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase), verapamil, amiodarone, quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites).

Front 469

Treatment of Digoxin Toxicity

Back 469

Antidote: Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+.

Front 470

Class I antiarrhythmics

What are they (class) and what is their general mechanism?

Back 470

Na+ channel blockers -

Slow or block/decrease conduction (especially in depolarized cells). Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized [e.g., tachycardia]). Hyperkalemia causes increased toxicity for all class I drugs

Front 471

Class Ia antiarrhythmics

Names? MOA?

Back 471

Quinidine, Procainamide, Disopyramide

-MOA: Na+ channel blockers - Increase AP duration, increase effective refractory period (ERP), increase QT interval.

Front 472

Class Ia antiarrhythmics

Use? Toxicity?

Back 472

-Use: Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

-Toxicity: Cinchonism (headache, tinnitus, psychosis with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de pointes due to increased QT interval.

Front 473

Class Ib antiarrhythmics

Names? MOA?

Back 473

Lidocaine, Mexiletine

-MOA: Na+ channel blockers - Decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Phenytoin can also fall into the IB category.

Front 474

Class Ib antiarrhythmics

Use? Toxicity?

Back 474

-Use: Acute ventricular arrhythmias (especially post- MI), digitalis-induced arrhythmias. IB is Best post-MI.

-Toxicity: CNS stimulation/depression, cardiovascular depression.

Front 475

Class Ic antiarrythmics

Names? MOA?

Back 475

Flecainide, Propafenone. “Can I have Fries, Please.”

-MOA: Na+ channel blocker - Significantly prolongs refractory period in AV node. Minimal effect on AP duration.

Front 476

Class Ic antiarrythmics

Use? Toxicity?

Back 476

-Use: SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

-Toxicity: Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart disease.

Front 477

Class II antiarrhythmics

Names? their Class?

Back 477

Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

-B blockers

Front 478

Class II antiarrhythmics

MOA?

Back 478

MOA: Decrease SA and AV nodal activity by decreasing cAMP & Ca2+ currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive— increasing the PR interval. Esmolol very short acting.

Front 479

Class II antiarrhythmics

Toxicity? Treatment of toxicity?

Back 479

Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.

Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor agonist activity).

Treat overdose with glucagon.

Front 480

Class III antiarrhythmics

Names? Their Class? MOA? Use?

Back 480

Amiodarone, Ibutilide, Dofetilide, Sotalol

-Class: K+ channel blockers

-MOA: increases AP duration, increases ERP. Used when other

antiarrhythmics fail. increases QT interval.

-Use: Atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone, sotalol)

Front 481

Class III antiarrhythmics

Toxicity?

Back 481

-Sotalol—torsades de pointes, excessive β blockade.

-Ibutilide—torsades de pointes.

-Amiodarone—pulmonary fibrosis, hepatotoxicity, hypothyroidism/ hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF).

-Remember to check PFTs, LFTs, and TFTs when using amiodarone.

Amiodarone has class I, II, III, and IV effects and alters the lipid membrane.

Front 482

Class IV antiarrhythmics

Names? Their Class? MOA? Use?

Back 482

Verapamil, diltiazem

-Class: voltaged gated Ca2+ channel blockers

-MOA: decreases conduction velocity, increases ERP, increases PR interval

-Use: Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation

Front 483

Class IV antiarrhythmics

Toxicity?

Back 483

Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression).

Front 484

Adenosine

Class? MOA? Use? Toxicity?

Back 484

-Class: antiarrhythmics

-MOA: increases K+ out of cells >> hyperpolarizing the cell and decreasing ICa.

-Use: Drug of choice in diagnosing/abolishing supraventricular tachycardia.

-Very short acting (~ 15 sec).

-Adverse effects include flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.

Front 485

Mg2+

Back 485

-Class: antiarrhythmic

-Use: Effective in torsades de pointes and digoxin toxicity.

Front 486

How can you tell which side of the heart the abnormal heart sound or murmur is on?

Back 486

all right sided heart sounds and murmur increase in intensity with inspiration

Front 487

What risk do all congenital heart defects have in common?

Back 487

infective endocarditis

Front 488

CABG

What do they use?

Back 488

Saphenous vein - will be come fibrosed over time (usually about 10 yrs) due to it become arteriolized

Can also use internal mammary artery - lasts longer

Front 489

Blood Pressure =

Back 489

BP = CO x TPR

Front 490

Hypertension is an important modifiable risk factor for..

[lecture]

Back 490

Stroke, MI, renal failure, CHF, progressive atherosclerosis, Dementia*

Front 491

J curve

[lecture]

Back 491

The threshold for which there is evidence that lowering the blood pressure outweighs the potential risks of treatment

-lower the BP too low is just as bad as having BP too high (think in terms of diabetes glucose levels)

Front 492

[How low should BP be lowered?]

Back 492

-chronic kidney disease + proteinuria = 130/80

-Diabetes = 140/90

-General population = 150

-Uncomplicated HTN = 140/90 (AHA)

-HTN + Angina = 130/80 (AHA)

-HTN + High risk CAD = 130/90 (AHA)

Front 493

[Proper BP Reading techniques]

Back 493

-In office: 2 readings, 5 min. apart, sitting in chair (arm @ heart); confirm in contralateral arm

-Ambulatory: possible white coat HTN; Dipping Pressure: BP drops over night 10-20% >> those that don't dip = poor cardiovascular diagnosis

-Self measurement: important for monitoring response to therapy and can evaluate white coat HTN; can also see masked HTN when it is high at high home and low in the clinic;135/85 @ home = HTN

Front 494

[Potential Indications for ambulatory BP monitoring]

Back 494

-unusualy variability of BP

-possible white coat HTN (10-15% of pts) - may be precursor to sustained HTN

-nocturnal HTN

-drug-resistant HTN

-determining efficacy of drug treatment over 24 hrs

-HTN in pregnancy

-symptomatic hypotension on meds, suggesting that patient may be normotensive

-episodic HTN or autonomic dysfunction

it helps to identify abnormalities, as well as normal circadian rhythm/failure of BP to decrease the 10-20% at night

Front 495

[Factors that may increase probability of white coat HTN]

Back 495

-office BP of 150-159/90-99

-female sex

-not smoking cigarettes

-HTN of recent onset

-limited # of office BP readings

-normal left ventricular mass

Front 496

[Goals of Hypertensive therapy]

Back 496

-reduce CVD mortality and morbidity

-treat to BP <140/90 or BP 130/80 in patients with diabetes or CKD

-achieve ABP in persons ≥ 50 yo

Front 497

[Treatment of HTN]

Back 497

-start with thiazide diruetics for most, but comorbidities are good reason to use other drug classes (also look at age, race, hx, efficacy, adverse rxns)

-most pts will need 2 or more drugs to control it - monotherapy effective <40% of patients

-If BP is ≥20/10 mmHg over target goal, start with 2 drugs, one of which should be thiazide diuretics (stage 2 HTN or higher)

-reduce BP by 10-15%, minimize side effects, favor longer acting meds, be willing to change

-combing drugs to lower BP w/ less side effects improve compliance, more rapidly achieves BP goal, and shows improved CV outcomes

-after BP stable, follow up every 3-6 months

Front 498

[General Classes of antihypertensive drugs, indications for their use depending on comorbidities, etc., contraindications, and side effects]

Back 498

Front 499

[Most common factor contributing to resistant HTN & most appropriate treatment]

Back 499

-non-adherence to therapy or inadequate dosing may cause patients to appear resistant to therapy

-the most common factor contributing to resistant HTN in compliant patients is excess Na/volume

-longer acting diruetics like hydrochlorathiazide are more appropriate for resistant HTN than shorter acting agents like furosemide

-other contributors to resistant HTN: obesity, sleep apnea, cigarette smoking, panic attacks

Front 500

[Prognosis of HF]

Back 500

-5 yr mortality rate = 50%

Front 501

[High Output Cardiac Failure Causes & their Presentation]

Back 501

-wide pulse pressure, bounding pulse, flow murmur

-Anemia: pallor

-Hyperthyroidism: A Fib w/ RVR

-Systemic AV Fistula: continuous murmur

-Berberi: wasting, malnutrition

-Paget's disease

Front 502

[DDx of of PHTN: WHO Classifications]

Back 502

-Group I: PAH - Idiopathic, Familial, associated w/ other diseases

-Group II: PHTN associated w/ L heart disease

-Group III: PHTN associated w/ lung disease (COPD, OSA, etc.)

-Group IV: PHTN associated with thromboembolitic disease

-Group V: miscellaneous (sarcoidosis, scleroderma, CREST, etc.)

Front 503

[R sided failure signs due to pericardial disease]

Back 503

-Elevated JVP, + Kussmaul's sign

-pericardial knock

-pulsus alternans

-pulsus paradoxus

-unexplaned ascites

Front 504

[R sided failure signs due to PHTN]

Back 504

-Increased P2

-Murmurs: PI, TR, diastolic rumble

-Respiratory variation of S3 or S4

-Elevated JVP, +HJR

-Hepatomegaly

-Pedal edema

Front 505

[Framingham criteria for HF]

Back 505

-2 major or 1 major +2 minor criteria

-Major: PND, orthopnea, elevated JVP, rale, S3, cardiomegaly, +HJR

-Minor: ankle edema, night cough, DOE, hepatomegaly, pleural effusion, HR > 120

Front 506

[NYHA Functional Class for HF Assessment]

Back 506

-Class I: symptoms with greater than normal exertion (no limitation of normal physical activity); Stage B & C

-Class II: symptoms with normal exertion; Stage C

-Class III: symptoms with restricted activity, comfortable at rest but less than ordinary activity >> symptoms; Stage C

-Class IV: symptoms at rest; some Stage C, mostly D

Front 507

[NYHA Stages & Phenotypes of HF]

Back 507

-Stage A: at risk for HR but w/o structural disease or symptoms of HF (pts w/ HTN, atherosclerosis, DM, obesity, metabolic syndroms, using cardiotoxins, family hx)

-Stage B: Structural heart disease, but without symptoms - Class I (pts w/ previous MI, remodeling including LVH & low EF, asymptomatic valvular disease)

-Stage C: Structural heart disease, with prior or current symptoms - Class I, II, III (pts w/ known structural heart disease w/ signs & symptoms)

-Stage D: Refractory HF requiring specialized interventions - Class IV (pts with marked HF symptoms, recurrent hospitalizations despite GDMT)

Front 508

[Cardiac MRI]

Back 508

- need for a biopsy is obviated by cardiac MRI; routine biopsy is not recommended

- it provides unique info related to cardiac pathology

- delayed enhancement >> ischemia vs. scar

- complex congenital heart disease

- Concern - impaired renal function (CrCl < 30)

Front 509

[Summary of Evidence of Statin Trials]

Back 509

-every trial showed decreased DV event rate

-any statin is better than non

-more potent/higher doses are better than lesser

-NNT much larger for primary prevention than in secondary prevention trials

-statin plus another lipid-lowering drug, is not better than statin alone

Front 510

[Why are statins so good?]

Back 510

-dramatic decreased in LDL

-decreased in small, dense LDL

-Pleiotropic: anti-inflammatory, increased eNOS activity, plaque stabilization

Front 511

[Statins recommended for:]

Back 511

-known CVD

-Age >40-75 if: DM or LDLc 70-189 mg/dL, LDL > 190 mg/dL, 10 yr estimated CVD risk >7.5%

Front 512

[Heart Pressures]

Back 512

-RA: 0-5

-RV: 30/5

-PA: 30/10

-PCWP = LA: about 8 (normally about equal to PA pressure; if going into HR, >25 mmHg)

-LV: 120/8

-Aorta: 120/80

Front 513

[SVR & PVR equations]

Back 513

SVR= [(MAP - RAP)/CO] x 80

PVR = [(MPAP - PCWP)/CO] x 90

Front 514

[Cardiac Indices and Associated PA saturations]

Back 514

-70% saturation (normal) = 3 L/min cardiac index (normal)

-50% saturation = 2 L/min cardiac index

-30% saturation = 1 L/min cardiac index

Front 515

[Hemodynamic chart from lecture w/ associated pressures and pathology]

Back 515

Pathologic States:

-loss of volume >> low pressures & high resistance

-Septic Shock >> low pressure & low resistance

-Cardiogenic shock >> low pressures, high filling pressures (PCWP, LVEDP)

Front 516

[Hemodynamics in acute MI]

Back 516

-Normal Hemodynamics: PCWP <18 mmHg, CI > 2.2

-Pulmonary Congestion: Warm & Wet >> PCWP > 25 mmHg, CI > 2.2

-Peripheral Hypoperfusion: Cold & dry >> PCWP < 10 mmHg, CI < 2.2

-Pulmonary Congestion & Peripheral Hypoperfusion: Cold & Wet >> PCWP > 25 mmHg, CI < 2.2

Front 517

[What defines a shunt as significant?]

Back 517

-Qp/Qs ≥ 1.5 (normal = 1) >> L to R shunt

-Qp = blood flow through pulmonary circuit

-Qs = blood flow through systemic circuit

Front 518

CHA2DS2 VASC Score

Back 518

-CHF/LV dysfunction - 1 pt

-Hypertenion - 1 pt

-Age >75 - 2 pts

-Diabetes Mellitus - 1 pt

-Stroke, TIA, Thromboembolism - 2 pts

-Vascular disease - 1 pt

- age 65=75 - 1 pt

-Sex (female) - 1 pt

Front 519

[Grading of Angina Pectoris -CCS]

Back 519

-Class I: ordinary physical activity doesn't cause angina; agina occurs with strenuous/rapid/prolonged exertion

-Class II: slight limitation of ordinary activity - angina w/ climbing flight of stairs or w/ walking > 2 blocks, walking or climbing stairs rapidly, uphill or after meals, strong emotional rxn, cold, wind, or during first few hours of waking

-Class III: Marked limitations of normal activity; angina occurs w/ walking 1-2 blocks or climbing one flight of stairs normally

-Class IV: Inability to carry out any physical activity without symptoms; angina may occurs at rest

Front 520

[JNC 8 summary for treatment/ prevention of ischemic heart disease]

Back 520

-≥ 60 yo, treat when BP ≥ 150 systolic or 90 diastolic

-< 60 yo, treatment initiation and goals are 140/90, use in pts with ≥ 18 yo w/ CKD or diatbets

-nonblack pts w/ HTN, initial treatment should be thiazide diuretic, CCV, ARB, or ACE inhibitor; general black popularion: use thiazide diuretic or CCB

-pts ≥ 18 yo w/ CKD, initial or add on therapy should include ACE inhibitor or ARB

Front 521

[TIMI Score of UA/STEMI]

Back 521

predicts 30 day mortality rate after MI

-Aged ≥ 65 yrs

-≥ 3 CAD risk factors

-prior CAD (>50% stenosis)

-aspirin in last 7 days

-≥ 2 anginal events in ≤ 24 hrs

-ST deviation

-elevated cardiac markers (CK-MB or troponin 1)

Front 522

[Summary of inpatient meds for MI patients]

Back 522

-aspirin + 2nd antiplatelet (clopidogrel) + GpIIb/IIIa inhibitors

-unfractionated heparing or enoxaparin

-high dose stain

-Beta blocker

-ACE I (if BP tolerates)

-send them home on aspirin, clopidogrel, beta blockers, ACE I, and statin

Front 523

Treatment of HF

Stage A

Back 523

Goal: Prevention

-ACE I or if untolerant of ACE I >> ARB for patients with vascular disease or DM

Front 524

Treatment HF

Stage B

Back 524

Goal: prevent HF symptoms, prevent further remodelling

-ACE I or ARB if intolerant to ACE I (should be used in all esp. w/ reduced EF)

-Beta blockers if hx of MI or ACS and reduced EF OR just reduced EF regardless of hx

-statins should also be used in those patients with hx of MI or ACS - prevent symptomatic HF and cardiovascular events

-ICD placement in those at ≥ 40 days post MI, EF ≤30%, on appropriate medical therapy, and have a good survival outlook

-Nondihydropyridine CCB may be harmful in asymptomatic pts w/ low LVEF and no symptoms after MI

Front 525

Treatment of HF

Stage C

Back 525

Systolic HF - Goals: control symptoms, educate, prevent hospitalization & mortality; exercise training, Na restriction, CPAP for those with sleep apnea, cardiac rehab

-diuretics for fluid retention

-ACE I or ARB + Beta Blockers for all

-Aldosterone Antagonists if GFR > 30mL/min if EF <35%, or post MI w/ EF <40%

-Add loop diuretics if volume overloaded

-Add Hydral-Nitrates if African American

-ICD therapy same as for Stage B; CRT also considered

Diastolic HF - Goals: control symptoms, improve HRQOL, prevent hospitalization & mortality; Na restriction, exercise therapy

-diuresis to relieve congestive symptoms, repurfusion?

Front 526

Treatment of HF

Stage D

Back 526

Goals: control symptoms, improve HRQOL, reduce hospital readmissions, establish pts' end of life goals

-fluid restriction

-IV Inotropic support if cardiogenic shock (systolic dysfunction)

-heart transplant

-chronic inotropes

-temporary or permanent MCS - VADS used as bridge to transplant

-palliative care and hospice

-ICD deactivation

Front 527

Treatment of Hospitalized HF Patient

(decompensated HF)

Back 527

-Loop diuretics for volume control (high dose then taper >> followed by Beta blocker at low does after stabilized volume >> thrombosis prophylaxis

-monitor electrolytes, BUN, Cr during titration of meds

-if diuresis inadequate, increase dose or add 2nd line diuretic like thiazide; low dose dopamine can be attempted, and nitro (if patient stable) can be attempted to help with diuresis