Step Up To Medicine Cardiology

Front 1

Most common cause of endocarditis in a native valve

Back 1

Strep viridans

Front 2

most common cause of early (within 60 days of surgery) endocarditis on a prosthetic valve? late (>60 days after surgery) endocarditis?

Back 2

early--> staphylococci (e.g. staph epidermidis- skin bact)
late--> streptococci

Front 3

Atrial fibrillation

Back 3

irregularly irregular rhythm with absent p waves

Front 4

most common cause of right sided endocarditis

Back 4

S. aureus (often seen in IV drug users)

Front 5

complications of endocarditis

Back 5

1. cardiac failure
2. myocardial abscess
3. various solid organ damage from showered emboli
4. glomerulonephritis

Front 6

What should you always suspect in a patient with fever and new onset murmur?

Back 6

endocarditis

Front 7

Janeway lesions vs oslers nodes

Back 7

Janeway lesions- painless erythematous lesions on palms and soles-- symptom of endocarditis
Osler's nodes- painful raised lesions on fingers, toes and feet

Front 8

Roth spots

Back 8

oval, retinal hemorrhages with clear, pale center seen in endocarditis

Front 9

Is TEE or TTE better in the diagnosis of endocarditis?

Back 9

Transesophageal Echo (TEE)

Front 10

What should be given to any patient with cardiac valve disease undergoing GI/GU/dental procedures?

Back 10

amoxicillin as endocarditis prophylaxis

Front 11

Diagnosis of endocarditis (Duke's Criteria)

Back 11

Need 2 Major, 1 major + 3 minor or 5 minor

Major = sustained bacteremia, endocardial involvement (vegetation, abscess, valve perforation) or New onset valve regurgitation

Minor = predisposing condition (abnormal valve), fever, vascular phenomena (septic arterial or pulmonary emboli, mycotic aneurysms, Janeway lesions), immune mediate phenomena (glomerulonephritis, oslers nodes, roth spots), positive blood cultures, positive echo

Front 12

Tx for endocarditis

Back 12

IV (parenteral) antibiotics based on culture results for extended periods (4-6 weeks)

If culture negative, but high clinical suspicion, treat empirically with penicillin or vancomycin plus an aminoglycoside (e.g. gentamycin, neomycin etc) until organism can be isolated.

Front 13

4 parts to Tetralogy of Fallot

Back 13

1. Pulmonary Stenosis
2. Right Ventricular Hypertrophy (secondary pulm stenosis)
3. Overriding Aorta
4. Ventricular Septal Defect (VSD)

Front 14

Non-bacterial thrombotic endocarditis (Marantic endocarditis)

Back 14

associated with debilitating disease such as metastatic cancer
- sterile deposits of fibrin and platelets form along the closure line of cardiac valve leaflets
- vegetation can embolize to brain or periphery
- heparin may be used but NOT proven effective

Front 15

Nonbacterial Verrucous Endocarditis (Libman Sacks Endocarditis)
1. associations
2. what is it?
3. treatment

Back 15

- typically involves the AV valves in individuals with SLE
- characterized by formation of small warty vegetations on BOTH sides of valve leaflets +/- regurgitation murmurs
- rarely gives rise to infective endocarditis but can be a source of systemic emboli
- Tx: treat underlying SLE + anticoagulation

Front 16

5 congenital cyanotic Heart Diseases

Back 16

early cyanosis- Terrible Ts
1. Truncus Arteriosus- one trunk arising from RV and LV
2. Transposition of Great Vessels- Pulmonary artery and aorta arise from wrong sides of the heart
3. Tricuspid Atresia
4. Tetralogy of Fallot
5. Total Anomalous Pulmonary Venous Connection

Front 17

Atrial Septal Defect
1. most common type
2. pathophysiology

Back 17

1. ostium secundum- central portion of the septum
2. oxygenated blood from the LA goes thru ASD into RA which leads to increased pulm. blood flow and inc work of right side of heart. As the shunt size inc, RA and RV dilatation occur. Pulm HTN is a serious sequelae, but RARE in ASD

Front 18

Clinical course of ASD

Back 18

Patients are usually asymptomatic until middle age (age 40). thereafter sx may begin-- exercise intolerance, dysnpea on exertion, and fatigue
- if mild patients may have a normal life span

Front 19

Luetic Heart
1. Cause
2. demographic
3. features
4. treatment

Back 19

1. complication of syphilitic aortitis-- usually affecting men in the 4th to 5th decade of life.
3. aneurysm of aortic arch with retrograde extension that causes Aortic Regurg plus stenosis of aortic branches
4. IV penicillin and surgical repair

Front 20

Mycotic aneurysm
1. definition
2. Blood Cultures
3. Treatment

Back 20

1. aneurysm resulting from damage to the vessel wall secondary to infection
2. Blood cx are positive in most cases
3. IV abx plus surgical excision

Front 21

Acute Arterial Occlusion
1. Pathophysiology
2. Most common site

Back 21

1. Acute occlusion is usually caused by an embolus, although rarely from an in situ thrombosis
2. most common site = common femoral artery

Front 22

most common sources of emboli in acute arterial occlusion

Back 22

1. Heart - 85% (Afib is the most common cause, post-MI stasis, endocarditis, myxoma)
2. Aneurysms
3. Atheromatous plaque

Front 23

Clinical Features of Acute Arterial Occlusion

Back 23

6 Ps
1. Pain
2. Pallor
3. Polar
4. Pulselessness (use doppler US to assess)
5. Paresthesia
6. Paralysis

Front 24

Diagnosis of Acute arterial Occlusion

Back 24

1. Arteriogram to define site
2. ECG to look for MI or Afib (sources)
3. Echo to evaluate heart valves, clots, MI

Front 25

Compartment Syndrome
1. definition
2. treatment

Back 25

Compression of nerves, blood vessels, muscle etc inside an enclosed space/compartment within the body

tx: fasciotomy to relieve pressure

Front 26

Treatment of Acute Arterial Occlusion
1. main goal
2. how long can skeletal muscle survive without perfusion?
3. What if there is paralysis or paresthesia?

Back 26

Immediate anticoagulation with IV Heparin and emergent embolectomy via cutdown or fogarty balloon-- if this fails then bypass. Treat compartment syndrome as necessary
1. main goal it to assess viability of tissues and salvage the limb
2. skeletal muscle can tolerate 6 hours of ischemia- perfusion should be re-established within this time
3. if paralysis or paresthesia are present then amputation is probably necessary

Front 27

Treatment of Rheumatic Fever
1. prevention
2. acute treatment
3. pts with h/o RF
4. rheumatic heart dz

Back 27

1. Treat strep pharyngitis with penicillin or erythromycin (if pen allergy) to prevent it
2. Acute Rheumatic Fever = NSAIDs
3. pts with h/o RF should get abx before all GI/GU/dental procedures-- amoxicillin or erythromycin
4. treat valvular disease as indicated

Front 28

Diagnosis of Acute Rheumatic Fever

Back 28

Jones criteria: 2 major, 1 major and 2 minor

Major
1. Migratory polyarthritis
2. Eyrthema marginatum- pink rings on the trunk that come and go
3. cardiac involvement- pericarditis, CHF, valve disease
4. subQ nodules- Aschoff nodules
5. chorea

Minor
1. fever
2. inc ESR
3. polyarthralgias
4. h/o s. pyogenes infection (positive ASO titer -antistreptolysin O antibodies)
5. h/o rheumatic fever
6. prolonged PR

Front 29

Causes of hypertensive emergency

Back 29

1. Medication non-compliance
2. cocaine, LSD, methamphetamine
3. Alcohol withdrawal
4. hyperaldosteronism- inc aldo --> inc reabsorption of sodium and water, inc secretion of K+
5. Cushings syndrome- inc cortisol secretion
6. eclampsia- seizure in pre-eclampsia
7. vasculitis
8. pheochromocytoma
9. Non-compliance with dialysis

Front 30

Treatment of aortic dissection
1. Medical for all
2. Type A vs Type B

Back 30

Initiate medical treatment- IV Beta blockers to decrease HR and force of LV Ejection, Nitropusside or Nitroglycerin to decrease blood pressure to below 120 mmHg

2. For Type A (proximal aorta dissections) - surgery is indicated as cardiac tamponade may develop
For Type B (distal dissections)- medical management only unless pt is unstable

Front 31

Best Tests for Aortic Dissection
1. stable pt
2. unstable pt

Back 31

1. TEE and CT
2. TEE at the bedside

Front 32

Aortic Dissection
1. definition
2. types-- Stanford

Back 32

1. tear in the inner wall of the aorta causes blood to flow between vessel/intimal wall layers, forcing them apart
2. Type A- involves ascending aorta +/- arch- may spread retrograde into heart--> tamponade
Type B- involves descending aorta or arch

Front 33

Hypertensive Emergency Treatment
1. over 1st 1-2 hours
2. if severe? (how do you define severe?)
3. if less immediate danger?

Back 33

1. reduce MAP by 25% in the 1st 1-2 hours. The goal is NOT immediately to achieve normal BP, but to get the patient out of danger and then gradually reduce it
2. if SEVERE (DBP > 130 mmHg) or hypertensive encephalopathy --> IV agents such as nitroglycerin, nitroprusside, or labetalol (alpha and beta antagonist) are appropriate
3. If in less immediate danger - oral agents such as captopril, clonidine, labetalol, or diazoxide

Front 34

Clinical features of Patent Ductus Arteriosus (PDA)

Back 34

1. Maybe asx
2. signs of HF
3. loud P2- sign of pulm HTN
4. LVH ( L--> R shunt)--> Left heart has to pump against increased PVR
5. continuous machinery murmur at 2nd ICS (both systolic and diastolic)
6. Wide Pulse pressure (SBP-DBP)
7. Differential cyanosis- lower extremity clubbing- toes are more likely to be cyanotic than fingers

Front 35

Complications of VSD

Back 35

1. Heart Failure
2. Endocarditis
3. Progressive Aortic Regurgitation
4. pulm HTN and shunt reversal (R-->L) = Eisenmenger's syndrome

Front 36

Symptoms of hypertensive emergency

Back 36

severe headache, visual disturbances, and altered mental status (AMS)

Front 37

Complications of aortic coarctation

Back 37

1. Severe HTN
2. rupture of cerebral aneurysms (inc flow/pressure above coarctation)
3. infective endocarditis
4. aortic dissection

Front 38

Treatment of PDA
1. if pulm HTN absent
2. if PHTN present or R--> L shunt

Back 38

1. surgical ligation if there is NO PHTN
2. if severe PHTN or R-->L shunt do not correct PDA-- this is a contraindication

Front 39

What are the leading causes of death in adults with a PDA (2)?

Back 39

Heart failure and infective endocarditis

Front 40

What is PDA associated with (3)?

Back 40

Congenital rubella syndrome
High altitude
Premature births

Front 41

Treatment of VSD
1. when indicated
2. what needs to be given as ppx
3. for asx pts with a small defect?

Back 41

1. surgical repair when pulmonary to systemic blood flow ratio is greater than 1.5:1 or 2:1 (same as with ASD)
2. endocarditis prophylaxis (amoxicillin, or erythromycin if allergy)
3. surgery is not indicated

Front 42

Non-cyanotic congenital heart diseases (4)

Back 42

1. ASD
2. VSD
3. PDA
4. Coarctation of the Aorta - narrowing of the aorta

Front 43

Signs of VSD
1. type of murmur
2. what happens to murmur with valsalva
3. other sx
4. what happens to pulm component of S2 as Pulmonary Vascular Resistance inc?
5. What causes AR when a VSD is present?

Back 43

1. harsh, blowing holosystolic murmur with thrill (blood crossing VSD)-- the smaller the defect, the louder the murmur
2. murmur decreases with valsalva and handgrip (decreased return of blood to heart- decreased preload)
3. sternal lift from RV enlargement
4. As PVR increases the pulm component of s2 increases in intensity
5. Aortic Regurgitation- flow through VSD creates low pressure zone leading to AV prolapse by venturi effect

Front 44

Clinical features of superficial thrombophlebitis vs chronic venous insufficiency vs DVT

Back 44

superficial thrombophlebitis- local tenderness and erythema along course of superficial vein

CVI- aching of lower extremities worse at end of day, relieved by elevation of the lefts and worsened by recumbency. May see edema, pigmentation and ulcers

DVT- usually asymptomatic, but may calf pain, and unilateral swelling

Front 45

Diagnosis of superficial thrombophlebitis vs chronic venous insufficiency vs DVT

Back 45

superficial thrombophlebitis- clinical dx

CVI- clinical dx

DVT- duplex US, D-Dimer to r/o

Front 46

Treatment of superficial thrombophlebitis vs chronic venous insufficiency vs DVT

Back 46

superficial thrombophlebitis- analgesics, monitor for spread or cellulitis

CVI- leg elevation, avoid long periods of standing, elastic stockings, and if ulcers present then Unna boot and wet to dry dressings

DVT- anticoagulation

Front 47

Systemic Inflammatory Response Syndrome (SIRS)
1. criteria
2. sepsis
3. septic shock
4. multi-organ dysfunction syndrome (MODS)

Back 47

Characterized by 2 or more of the following
Temperature >38 or <36 C (fever or hypothermia)
HR >100 or <60 bpm
hyperventilation (rate >20 bpm or PaCO2 > 32 mmHg)
tachycardia (HR >90 bpm)
inc WBC count (>12,000 cell/hpf) or dec WBC count (<4,000 cell/hpf) or >10% band form (immature cells)

Sepsis- when blood cultures are positive + SIRS (two sets of blood cultures must be taken from two sites before abx are given)

Septic shock- decreased blood pressure due to sepsis despite fluid resuscitation

Multiorgan dysfunction syndrome- usually leads to death

Front 48

What is the most common primary cardiac neoplasm?

Back 48

atrial myxoma

Front 49

Atrial myxoma
1. definition
2. benign or malignant?
3. complications
4. causes
5. protypical presentation
6. tx

Back 49

1. benign gelatinous growth that is usually pedunculated and usually arising from the interatrial septum in the region of the fossa ovalis
2. benign
3. can embolize leading to metastatic disease or can cause relative valvular dynfunction
4. most are sporadic put some autosomal dominant cases have been reported
5. fatigue, fever, syncope, palpitations, malaise, low pitched diastolic murmur that changes with body position (diastolic plop)
6. tx- surgical excision

Front 50

patient presents with fatigue, fever, syncope, palpitations, and malaise. On exam you hear a low pitched diastolic murmur that changes with body position. What do they most likely have?

Back 50

Atrial myxoma- benign primary cardiac tumor

Front 51

General characteristics of cardiac neoplasms
1. primary vs metastatic more likely?
2. if metastatic where are the most likely primaries?

Back 51

1. primary cardiac neoplasms are rare, 75% are from mets
2. sites of primaries = lungs, breast, skin, kidney, lymphomas, kaposi's sarcoma (HHV-8) in AIDS pts

Front 52

Treatment of neurogenic shock

Back 52

1. judicious use of IV Fluids = mainstay
2. vasoconstrictors but be cautious
3. put patient supine or in trendelenburg position (head down)
4. maintain body temp

Front 53

Clinical features of neurogenic shock
- skin
- Urine output
- HR and BP?
- CO, SVR and PCWP

Back 53

- warm, well perfused skin (vasodilation)
- decrease urine output or nl
- decreased HR and BP (but can be tachy)
- C.O. is nl to decreased, dec SVR, PCWP is nl to decreased

Front 54

Neurogenic shock- general characteristics
1. mechanism
2. causes

Back 54

failure of the sympathetic nervous system to maintain adequate vascular tone (sympathetic denervation leading to decreased epi and norepi)
- causes include spinal cord injury, severe head injury, spinal anesthesia, pharmacologic sympathetic blockade
- characterized by peripheral vasodilation with dec SVR
- dec CO, SVR, and PCWP

Front 55

Definition of cardiogenic shock
1. SBP and Urine output criteria

Back 55

SBP <90mmHg and urine output <20 cc/hr with adequate LV filling pressure

Front 56

What is the most common cause of death in the ICU?

Back 56

septic shock

Front 57

1. diagnosis of septic shock
2. treatment of septic shock

Back 57

1. clinical diagnosis, confirmed by blood culture but blood cultures are commonly negative
2. IV antibiotics broad spectrum at max doses, surgical drainage if necessary (depending on source of infection), fluids to inc BP, pressors if BP remains low despite aggressive fluid fluids (1st dopamine, 2nd norepi)

Front 58

Clinical features of septic shock
1. skin

Back 58

- manifestations related to the cause of sepsis (pneumonia, UTI, peritonitis etc)
- signs of SIRS
- dec BP, oliguria, lactic acidosis
- fever or hypothermia
- hypothermia is more common in the very young, elderly or debilitated or ICH- don't have immune response that leads to the fever

Front 59

Septic shock
1. definition
2. causes
3. progression
4. presentation
5. complications

Back 59

1. decreased BP induced by sepsis that persists despite adequate fluid resuscitation
2. causes- pneumonia, pyelonephritis, meninigitis, abscess, cholangitis, cellulitis, peritonitis
3. Progression- SIRS --> sepsis--> septic shock --> multiorgan dysfunction
4. Severe decrease in SVR secondary to peripheral vasodilation, nl to increased C.O. (due to inc HR and maintained SV), warm extremities, dec EF secondary to decreased contractility
5. complications- ARDS, acute tubular necrosis (ATN), Disseminated Intravascular Coagulopathy (DIC)--form a bunch of clots then start hemorrhaging because you have used up all your clotting factors, multi-organ failure, death

Front 60

Treatment of hypovolemic shock

Back 60

1. Airway and Breathing- pts in severe shock and circulatory collapse generally require intubation and mechanical ventilation
2. Circulation- if hemorrhage- apply direct pressure +/- transfusion. IV hydration - pts with class I usually do not require IV fluids, class II benefits, and class III and IV require fluid resuscitation. Give fluid bolus and continuous infusion and then reassess
3. For non-hemorrhagic shock- do not transfuse. Crystalloids with electrolyte replacement is adequate

Front 61

What is the only type of shock where PCWP/LA filling pressure is increased?

Back 61

cardiogenic shock

Front 62

Clinical features of cardiogenic shock

Back 62

1. Altered mental status (AMS)
2. dec BP
3. inc HR
4. engorged neck veins (JVD) - inc venous pressure
5. pulmonary congestion (LVF)

Front 63

Cardiogenic shock
1. general characteristics
2. causes

Back 63

1. occurs when the heart is unable to generate enough C.O. to maintain tissue perfusion. Defined as SBP< 90 mmHg with urine output <20 cc/hr + adequate PCWP/LA filling pressure
2. After acute MI - most common cause
- cardiac tamponade (compression of the heart)
- tension pneumothorax (compression of the heart)
- arrhythmias
- massive PE --> RVF
- myocardial disease (cardiomyopathies, myocarditis)

Front 64

What is the most effective method of monitoring response to treatment in hypovolemic shock?

Back 64

measuring urinary output (UOP)

- also helpful are pulmonary catheter +/- central line

Front 65

Hypovolemic shock
1. general characteristics
2. causes

Back 65

1. Primary pathophysiology- dec effective circulatory volume (ECV) leads to dec preload and dec CO
2. Rate of volume loss is important- the slower the loss then the greater the compensatory mechanisms
3. patients with signs of medical commorbidities (esp cardiac) may be unable to compensate physiologically
4. there are 4 classes depending on the severity of the volume loss
5. causes
- hemorrhage- trauma, GI bleed, retroperitoneal
- non-hemorrhagic- lots of vomiting, severe dehydration, severe diarrhea, burns, 3rd spacing in bowel obstruction

Front 66

Treatment of the cardiogenic shock

Back 66

1. ABCs- airway, breathing and circulation
2. Identify and treat underlying cause
a. Acute MI- MONAH (standard), Aggressive revascularization with PTCA or CABG
b. tamponade- periocardiocentesis/surgery
c. surgery for valve issues
d. treat arrythmias
3. Vasopressors - dopamine = 1st, dopamine and dobutamine = 2nd, Norepi and epi if severe
4. Afterload reduction - Nitroglycerin or Nitroprusside- not usually indicated because they exacerbate hypotension but may be used later with vasopressor
5. IV fluids are likely harmful because of elevated LV pressures. Patients may actually need diuretics
6. Intra-aortic balloon pump (IABP) - dec afterload, inc CO, dec myocardial demand

Front 67

Diagnosis of cardiogenic shock

Back 67

1. ECG- ST elevation or arrythmia
2. Echo- mechanical compression of heart, valve disease, estimate EF, pericardial effusion
3. Hemodynamic monitoring-- Swan Ganz catheter (pulm artery catheter) to measure PCWP, PA pressure, CO, Cardiac Index, SVR, keep CO > 4 L/min (nl = 5 L/min), Cardiac Index > 2.2, and PCWP < 18 mmHg

Front 68

Surgical Treatment for peripheral vascular disease (PVD)
1. indications
2. methods

Back 68

1. rest pain, ischemic ulcerations (tissue necrosis), severe symptoms refractory to conservative treatment
2. options = surgical bypass graft is most common and has a 5 yr patency of 70% or angioplasty

Front 69

Causes of Abdominal Aortic Aneursym

Back 69

MULTIFACTORIAL- most cases = atherosclerotic weakening of the aortic wall

- Predisposing factors = trauma, HTN, vasculitis, smoking, and a positive family history
- syphilis + connective tissue abnormalities (E.g. Marfans, Ehler's Danlos) are associated with thoracic aneurysms but they may involve the lower aorta as well

Front 70

Rupture of AAA
1. triad of findings
2. Other symptoms

Back 70

1. Abdominal pain, hypotension, palpable pulsatile mass - ruptured AAA --> emergent laporotomy with further diagnostic tests
2. circulatory collapse, syncope, pre-syncope secondary to sudden hemorrhage, n/v

Front 71

Treatment of unruptured AAA vs ruptured AAA

- what is the normal size/diameter of the infrarenal Aorta?

Back 71

1. unruptured AAA- depends on the size. If the diameter > 5 cm or symptomatic then operate (synthetic graft). If asymptomatic and <5 cm diameter, treatment is controversial, but periodic imaging is recommended to F/U growth (NO SAFE SIZE EXISTS)
- consider life expectancy of patients vs risk of surgery and lengthy recovery
2. ruptured-- emergery laporotomy
3. nl = 2 cm

Front 72

Peripheral Vascular Disease (PVD)
1. definition
2. typical patients
3. sites of occlusion/stenosis

Back 72

1. PVD = atherosclerotic disease of the lower extremities
2. patients with PVD usually have co-existing CAD (with CHF, or h/o MI etc) plus other chronic medical problems like diabetes or lung disease
3. most common site is the superficial femoral artery (in Hunter's canal), popliteal artery, aortoiliac occlusive disease

Front 73

Prognosis of peripheral vascular disease (PVD)

Back 73

1. If the patient has intermittent claudication- good prognosis
2. patients with rest pain or ischemic ulcers have the worst prognosis (especially if they are diabetic or are smokers)

Front 74

Treatment of Peripheral Vascular Disease (PVD)

Back 74

- Diabetics have an amputation rate 4x higher than others
- Conservative management for intermittent claudication includes: 1) smoking cessation- cannot be over-emphasized), 2) graduated exercise program (walk to point of claudication, rest then continue), 3) foot care (especially in diabetics), 4) Atherosclerotic RF reduction (dec HLP, HTN, weight, and improve glycemic control), 5) avoid extremes of temperature (esp extreme cold), 6) aspirin, 7) Trental (pentoxyfylline)- lowers blood viscosity

Front 75

Diagnosis of Peripheral Vascular Disease
1. most common
2. other
3. gold standard

Back 75

1. Ankle-Brachial Index (ABI) - ratio of SBP at ankle vs arm (nl >/= 1.0, claudication ABI < 0.7, Rest pain ABI < 0.4)
2. pulse volume recordings - excellent assessment of segmental perfusion/non-invasive using pressure cuffs
3. gold standard - arteriography - contrast in vessels + radiographs- helps locate PVD- only needed if surgery/revascularization is being considered

Front 76

1. What is a normal ABI?
2. when does claudication begin (what ABI)?
3. When does rest pain begin (what ABI)?

Back 76

1. > 1.0 mmHg
2. <0.7 mmHg
3. < 0.4 mmHg

ABI = ankle-branchial index = SBP in ankle/SBP in arm (brachial artery)

Front 77

Signs of peripheral vascular disease (PVD) on physical exam

Back 77

1. dec or absent pulses
2. muscular atrophy
3. dec hair growth
4. thick toenails
5. dec skin temp
6. ischemic ulceration (usually on toes)- localized skin necrosis secondary to trauma that does NOT heal
7. tissue infarction/gangrene (end stage disease)
8. pallor of elevation and rubor of dependency

Front 78

Diagnosis of Atrial Septal Defect

Back 78

1. Transesophageal Echo is diagnostic (better than TTE)
2. CXR - may show large pulmonary arteries (secondary to inc blood flow) - inc pulmonary vascular markings
3. ECG- RBBB, right axis deviation, atrial abnormalities such as AFib or Aflutter

Front 79

Complications of ASD

Back 79

1. pulmonary HTN- common in > 40 yo
2. Eisenmenger's disease - irreversible pulmonary HTN leads to shunt reversal (R--> L shunt), HF and cyanosis
3. Right sided HF
4. atrial arrhythmias-- esp Afib
5. Stroke secondary to paradoxical emboli or afib

Front 80

Clinical features of ASD

Back 80

1. Mild Systolic Ejection murmur at pulmonary area secondary to inc blood flow
2. wide fixed splitting of S2 due to inc pulm blood flow and delayed closure of the Pulm Valve
3. diastolic flow "rumble" murmur - inc blood flow across the tricuspid valve
4. if advanced - signs of RVF - ascites, hepatomegaly, JVD etc

Front 81

What does fixed splitting of S2 indicate?

Back 81

ASD

Front 82

Treatment of ASD

Back 82

1. surgical repair when pulm to systemic blood flow ratio > 1.5 : 1 or 2.0 : 1 OR if the patient is symptomatic

Front 83

What is the most common congenital cardiac malformation?

Back 83

VSD

Front 84

What is a paradoxical embolus?

Back 84

DVT forms and instead of traveling to the lungs and causing a PE is transverses the ASD to the brain causing stroke

Front 85

Symptoms of Peripheral Vascular Disease (PVD)

Back 85

1. Intermittent claudication- cramping leg pain that is reliably reproduced by the same walking distance (relieved by rest or dangling legs over the bed)
2. Rest pain (continuous) - usually felt over distal metatarsals, often prominent at night-- awakens patient from sleep. Hanging foot over the bed or standing relieves the pain due to extra perfusion to ischemic areas - using gravity. This suggests severe ischemia such that frank gangrene may occur without intervention

Front 86

Peripheral Vascular Disease (PVD) Risk Factors

Back 86

1. Diabetes Mellitus - prevalence markedly increased
2. smoking
3. CAD
4. HLP
5. HTN
6. hyperhomocystinemia

Front 87

Diagnosis of AAA

Back 87

1. US = test of choice to evaluation both location and size of aneurysm - 100% sensitive
2. CT Scan - 100% sensitive, but is more expensive and more time consuming- should only be used if patient is hemodynamically stable
3. Abd Xray - may show calcification of dilated segment -- allowing measurement of aortic diameter. Quick method of diagnosis but a negative study is not helpful-- cannot r/o

Front 88

Grey-Turner's sign vs Cullen's sign

Back 88

Both are signs of acute pancreatitis or retroperitoneal bleed

Grey Turner's sign - ecchymosis on back or flanks

Cullen's sign - ecchymosis around the umbilicus (U in cullens and umbilicus)

Front 89

Clinical features of AAA

Back 89

- Usually asymptomatic and discovered incidentally on exam or radiologic study for another reason
- may have a sense of abd fullness
- +/- pain, usually in hypogastrium (below umbilicus) + lower back- throbbing
- pulsatile mass of exam
- symptoms suggest expansion or impending rupture
- sudden onset of severe pain in back or lower abd with radiation to groin or buttocks/legs --> rupture (may see grey turner's or cullen's signs)

Front 90

Abdominal Aortic Aneurysm
1. definition
2. where is it most common?
3. average age of diagnosis
4. women or men most likely afflicted?

Back 90

1. abnormal localized dilatation of the aorta
2. between the renal arteries and iliac bifurcation (infrarenal aorta)
3. incidence increase with age. They are rare before 50. Average age at the time of diagnosis is 65-70 yo
4. much more common in men

Front 91

Right-sided vs left-sided endocarditis

Back 91

Right-sided is more likely in IV drug users (s. aureus)- due to injection into the venous system-- then infection goes back to the Right heart

Left-sided is more commonly due to infection of a damaged or prosthetic valve-- usually caused by s. viridans, a less virulent organism than s. aureus

Front 92

Infective Endocarditis
1. definition
2. acute vs subacute

Back 92

1. infection of heart valves that can be acute or subacute
2. acute- usually caused by s. aureus (virulent), on a normal heart valve, if no treatment then death occurs in < 6 weeks
subacute- less virulent organisms (s. viridans or enterococcus), usually on damaged valves. If untreated then death may occur in > 6 weeks

Front 93

Rheumatic heart disease

Back 93

Complication of untreated S. pyogenes pharyngitis - acute RF is immunologically mediated process that may progress to rheumatic heart disease with chronic valvular abnormalities

The most common valve problem = mitral stenosis, but there may be AV or TV issues as well

Front 94

Hemodynamic changes in hypovolemic shock by class (% blood lost, pulse inc, SBP dec, pulse pressure (SBP- DBP) dec, cap refill dec, RR inc, CNS sx, UOP)
1. Class I
2. Class II
3. Class III
4. Class IV

Back 94

1. Class I - 10-15% blood lost, normal pulse, normal SBP, normal pulse pressure, normal cap refill, normal RR, no CNS sx, UOP is normal
2. Class II - 20-30% of blood lost, pulse > 100, normal SBP, dec PP, delayed cap refill, mild inc in RR, anxious, UOP = 20-30 cc/hr
3. Class III - 30-40% blood lost, pulse > 120 bpm and weak, dec SBP, dec PP, delayed cap refill, marked tachypnea, confusion, UOP = 20 cc/hr
4. Class IV - > 40% blood lost, pulse > 140 bpm or non-palpable, marked decrease in SBP and PP, absent cap refill, marked tachypnea, lethargy/ coma, and negligible UOP

Front 95

Hypertensive Emergency
1. definition
2. vs urgency

Back 95

1. SBP > 220 +/- DBP > 120 mmHg in addition to end-organ damage- immediate treatment is indicated
2. urgency - inc BP alone without end-organ damage = hypertensive urgency rarely requires emergency treatment and can be managed with attempts to lower the BP over a 24 hour period

Front 96

When patients present with markedly inc blood pressure what is it critical to access for?

Back 96

Signs of end-organ damage
1. Eyes- papilledema (swelling of the optic disc)
2. CNS - AMS or ICH -- hypertensive encephalopathy may develop (confusion etc)
3. Kidneys- renal failure or hematuria
4. Heart - unstable angina, MI, CHF with pulmonary edema, aortic dissection
5. Lungs- pulmonary edema

Front 97

Treatment of hypertensive URGENCY

Back 97

Lower blood pressure gradually with ORAL agents over the course of 24 hours

Front 98

Diagnosis of aortic coarctation
1. ECG findings
2. CXR findings

Back 98

1. ECG- LVH
2. CXR- notching of the ribs due to inc flow through the collaterals. Figure 3 appearance due to indentation of the aorta at the site of coarctation with dilation before and after the stenosis

Front 99

Diagnosis of PDA
1. CXR findings
2. Echo findings

Back 99

1. CXR- inc pulm vasc markings, dilated pulm arteries, enlarged cardiac silhouette, sometimes calcifications of the ductus arteriosus
2. Echo- PDA +/- turbulent blood flow`

Front 100

Pathophysiology of PDAs

Back 100

- large L--> R shunt results in Right Hear volume overload, PHTN, and RHF (ascites, HSM, JVD etc)
- cyanosis is a late finding
- may eventually see reversal of blood flow (R-->L)

Front 101

Treatment of Aortic Coarctation

Back 101

- Standard treatment is surgical decompression
- percutaneous balloon aortoplasty is also an option in selected cases

Front 102

Coarcation of the Aorta
1. definition
2. associations

Back 102

1. narrowing/occlusion of aorta usually at origin of Left subclavian near the ligamentum arteriosum --> leads to obstruction between the proximal and distal aorta thus leading to inc afterload
2. associated with Turner syndrome

Front 103

Diagnosis of VSD
1. ECG findings
2. CXR
3. Echo findings

Back 103

1. biventricular hypertrophy predominates when the PVR is high
2. CXR- enlargement of the pulm artery, enlargement of the cardiac silhouette. As the PVR increases the L--> R shunt decreases and heart size decreases but PA size increases
3. VSD

Front 104

Pathophysiology of VSD

Back 104

1.Blood flows from LV (high pressure) into the RV (low pressure) through the VSD. this leads to inc pulm blood flow. As long as pulmonary vascular resistance (PVR) is lower the systemic vascular resistance (SVR) then flow is L --> R. If PVR > SVR then shunt becomes R --> L
2. Large defects leads to PHTN

Front 105

Clinical features of aortic coarctation

Back 105

- HTN in upper extremities and hypotension in the lower extremities
- well-developed upper body with under-developed lower hald
- mid-systolic murmur heard best over the back
- sx- HA, cold extremities, claudication with exercise and fatigue

Front 106

treatment of shock (general)

Back 106

1. ABCs - airway, breathing and circulation
2. Except for cardiogenic and sometimes neurogenic shock-- give large boluses of IV Fluids

Front 107

What signs/symptoms are common to all forms of shock?

Back 107

- decreased BP
- oliguria
- tachycardia - compensatory due to low BP
- AMS

Front 108

Initial approach to the patient in shock
1. findings supportive of different types of shock
2. initial steps to treatment

Back 108

1. Focused H & P - fever and infection site--> septic shock
- trauma, GI bleeding, vomiting--> hypovolemic shock
- h/o MI, angina or heart disease --> cardiogenic shock
- JVD --> cardiogenic shock
- spinal injury or neuro deficits --> neurogenic shock
2. Stabilize and determine the cause- 2 large bore IVs, central line and art line, b. fluid bolus 500-1000cc, c. blood draw - CBC, elec, CR, BUN, PT/PTT, type and cross, d. ECG, CXR, e. pulse ox, f. vasopressors (dopamine or epi if unstable DESPITE fluids), g, if NOT sure what the cause is then do pulmonary catheter or echo

Front 109

Shock - general characteristics
1. definition
2. presentation
3. changes seen to what?

Back 109

1. underperfusion of tissues-- medical emergency. Supply does not meet demand
2. decreased BP plus malfunction of underperfused organ systems (lactic acidosis, renal -anuria/oliguria, CNS dysfunction (AMS)
3. C.O., SVR and volume status (assessed by JVP and PCWP) -- these vary depending on the type of shock

Front 110

treatment of superficial thrombophlebitis
1. need anticoag?
2. localized thrombophlebitis?
3. severe thrombophlebitis?
4. need for abx? if septic thrombophlebitis?

Back 110

1. No anticoagulation needed-- rarely causes PE
2. localized thrombophlebitis --< mild analgesic (aspirin) is all that is required-- continue activity
3. severe thrombophlebitis (with pain and cellulitis) - a. bed rest, elevation, hot compresses, b. onse symptoms resolve -- ambulation and elastic stockings, c. no abx unless suppurative-- need adequate drainage, d. septic thrombophlebitis-- usually due to infection of IV cannula -- remove and start IV abx

Front 111

Superficial thrombophlebitis
1. general characteristics
2. clinical features

Back 111

1. Vichow's triad is implicated (stasis, endothelial injury and hypercoaguable state). UE - at IV sites, LE - assoc with varicose veins (in greater saphenous system) - secondary to stasis of blood flow
2. pain and tenderness, induration, plus erythema long the course of vein. Tender cord may be palpated

Front 112

Perforating veins

Back 112

- connect superficial and deep venous systems
- valves allow flow from superficial to deep systems but not vice versa

Front 113

Prognosis of VTach

Back 113

- prognosis depends on presence of heart disease and whether VTach is sustained or non-sustained
- VTach after a MI leads to a poor prognosis especially if sustained
- If there is no underlying heart condition, then there is a good prognosis.

Front 114

Non-Sustained VTach

Back 114

-Brief self-limited runs of VTach
- usually asymptomatic
- when CAD and LV dysfunction are present, it is an independent risk factor for sudden cardiac death so do a thorough cardiac work-up in patients with non-sustained VT

Front 115

Torsades de pointes (TdP)

Back 115

- rapid polymorphic VT
- dangerous arrhythmia that often can lead to VFib
- associated wtih many factors that prolong QT interval (e.g. congenital, TCAs, anticholinergics, electrolyte abnormalities, ischemia)
- IV Magnesium stabilizes heart while you treat the underlying cause

Front 116

Sustained VTach definition

Back 116

- persists in absence of intervention
- lasts longer than 30 seconds and is almost always symptomatic
- often associated with marked hemodynamic compromise (dec BP or ischemia)
- LIFE THREATENING
- can progress to VFib

Front 117

Causes of VTach (6)- which is most common

Back 117

1. CAD with prior MI = most common cause
2. Active ischemia, hypotension
3. cardiomyopathies
4. congenital defects
5. prolonged QT syndrome
6. Drug toxicity

Front 118

Ventricular Tachycardia definition

Back 118

- rapid and repetitive firing of 3 or more PVCs in a row at a rate between 100-250 bpm
- AV dissocation present (i.e. sinus P waves continue with their cycle unaffected by Vtach)
- originates below the bundle of His

Front 119

Treatment of Wolff-Parkinson-White Syndrome

Back 119

1. Radio-frequency catheter ablation of one arm of the re-entrant loop
2. Avoid drugs active on the AV node (e.g. digoxin) because they may accelerate conduction through the accessory pathway (type IA + IC antiarrhytmics are better choices)

Front 120

ECG diagnosis of WPW syndrome

Back 120

- narrow complex tachycardia, short PR interval + DELTA WAVE (upward deflection seen before the QRS complex)

Front 121

Wolff-Parkinson-White (WPW) syndrome- definition

Back 121

- accessory conduction pathway from atria to ventricles causes premature ventricular excitation because it lacks the delay seen in the AV node.
- May lead to paroxysmal tachycardia by 2 mechanisms
a. orthodromic reciprocating tachy - impulse through AV node (anterograde) -- depolarizes ventricles -- retrograde impulse through accessory pathway redepolarizes the atrai -- re-entry loop (no delta waves)
b. supraventricular tachy (afib or aflutter)-- usually AV node only allows certain impulses through accessory pathway but everything gets through allowing for inc HR and hemodynamic instability

Front 122

Treatment for paroxsymal SVT

Back 122

1. Vagal maneuvers --> block re-entry mechanism by delaying AV conduction
2. Pharmacologic Treatment- IV adenosine - agent of choice. Short duration, that decreases sinoatrial activity and AV nodal activity. IV verapamil and IV esmolol or digoxin.
3. Direct Current Cardioversion if drugs are not effective or patient is unstable
4. Prevention- digoxin usually is the drug of choice. Verapamil or beta-blockers are alternatives. Radiofrequency catheter ablation of either the AV node or the accessory tract

Front 123

Side effects of adenosine

Back 123

- Headache
- flushing
- shortness of breath
- chest pain
- n/v

Front 124

Causes of paroxsymal Vtach (PVST)

Back 124

1. ischemic heart disease
2. digoxin toxicity= PVST with 2:1 ratio is most common
3. AV node re-entry
4. atrial flutter with RVR
5. AV reciprocating tachy (accessory pathway)
6. excessive caffeine intake or EtOH

Front 125

Most common cause of Supraventricular Tachycardia (SVT)

Back 125

AV nodal re-entrant tachycardia

Front 126

Paroxsymal supraventricular tachycardia (PVST) pathophysiology (2 types)

Back 126

1. most commonly due to re-entrant tachycardia. 2 pathways (one fast and one slow), within the AV node- re-entrant circuit is in AV node. It is initiated or terminated by PACs. ECG shows narrow QRS complexes with no discernable p-waves. The p-waves are buried in the QRS complex
2. orthodromic AV re-entrant tachycardia- an accessory pathway between atria and ventricles that conducts retrograde. Initiated or terminated by PACs and PVCs. ECG shows narrow QRS complexes with p-waves that may or may not be seen. Re-entrant circuit is longer