Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

410 Cards in this Set

  • Front
  • Back
describe the pathology of coagulative necrosis
- seen in acute MI
- denaturation of proteins due to fall of pH and lack of H2O
describe the pathology of liquifactive necrosis
- occurs with infection, esp with abscesses
- digestion of proteins by hydrolases released by microorganisms and/or neutrophils
describe the pathology of fat necrosis
- characteristic of acute pancreatitis
- relase of lipases from the pancrease -> digestion of peripancreatic and omental fat -> saponification -> chalky white areas
describe the pathology of fibrinoid necrosis
- occurs in inflammatory processes involving arteries (arteritis)
- necrosis of media and intima, with effacement of structural components ->also deposition of plasma derive fibrin
what usually precedes vfib?
- vtach
- degeneration of VT restuls in multiple small wavelets of reentry that constitute the VF rhythm
what is the major cause of mortality in acute myocardial infarction?
- vfib
what do you see on the ECG for vfib?
- chaotic irregular appearnace without discrete QRS waveforms
how do you treat vfib?
- prompt electrical defibrillation
how can VT be distinguished from supraventricular tachycaria (SVT)?
- wide QRS in VT
- narrow/normal QRS in SVT
what is the difference in experiencing VF within the first 48 hours after MI vs. after the first 49 hours of acute MI?
- within 48 hours: no change in prognosis of survivors
- after 48 hours: reflects severe LV dysfucntion -> associated with high subsequent mortality
what causes ventricular ectopic beats, VT, and VF during an acute MI?
- reentrant circuits
- enhanced automaticity of the ventricular cells
what can be given to prevent VF in the ischemic setting?
- IV lidocaine (class IB antiarrhythmic)
- not indicated in routine management of acute MI patients b/c of side effects
define syncope
Light-headedness or fainting caused by insufficient blood supply to the brain.
what are the different systolic murmurs?
1. systolic ejection murmurs
2. pansystolic murmurs
3. late systolic murmurs
what is S1?
- ventricular contraction
- closure of the tricuspid and mitral valves
what is S2?
- closing of the pulmonic and aortic valves
name some systolic ejection murmurs
- aortic stenosis
- pulmonic stenosis
name some pansystolic (holosytolic) murmurs
- mitral regurgitation
- tricuspid regurgitation
name some late systolic murmurs
- mitral valve prolapse
describe the systolic ejection murmur
- A or P valve stenosis
- begins after S1 and terminates at or before S2
- crescendo-decrescendo
which murmurs may be preceded by an ejection click?
- aortic and pulmonic stenosis -> systolic ejection murmur.
describe the characteristics of a pansystolic/holosystoic murmur
- regurg of blood across incompetent mitral or tricuspid valve or through a VSD
- uniform in intesity throughout systole
- the smaller the VSD, the LARGER the murmer
what are the different types of diastolic murmurs?
- early decrescendo murmurs
- mid to late rumbling murmuers
describe the characteristics of late systolic murmurs
- begin in mid to late systole and continue to S2
- mitral regurg due to mitral prolapse
- usually preceded by midsystolic click
what causes early diastolic murmers?
- regurgitant flow through the A or P valve (A is more common in adults)
- early decrescendo
- starts at S2; may not continue all the way to S1
desribe the characteristics of mid to late diastolic rumbling murmers
- turbulent flow across a stenotic mitral or tricuspid valve
- opening snap after S2
- slight crescendo before S1
what causes a continuous murmur?
- patent ductus arteriosus
what causes a to-and-fro murmer?
- aortic stenosis and regurg
- pulmonic stenosis and regurg
define: atresia
A condition in which an opening or passage for the tracts of the body is absent or closed.
Fragile X syndrome and cardiovascular disease
- breakpoint at q27.3 on the X chr
- increased risk for mitral valve prolapse
Fragile X sydrome prevalence
- mental retardation (about as common as Down's Syndrome)
what are the phenotypic traits associated with Fragile X in childhood?
- large head circumference at birth
- perinatla complications (premie, asphyxia, seizures)
- increase in Sudden death syndrome
- Later in life: mental retardation (esp. language), ADD or autism
- conncetive tissue disorders (lax skin and joints, flat feet, large ears)
what are the phenotypic traits associated with Fragile X after puberty?
- long narrow face with prominent jaw and nasal bridge
- macro-orchidism
- cardio: Mitral valve prolapse and aortic root dilation
what cardiovascular conditions can you see with Down's syndrome?
- atrial septal defect
- ventricular septal defect
tricuspid atresia
- congenital cardiac malforamtion limiting flow into the right ventricle
what are common clinical manifestations of PE?
- hypoxia (V/Q mismatch)
- normal CXR
- tachycardia
- delirium in older patients
Describe Borrelia burgdorferi
- causes lyme disease
- spirochetal illness (tick borne)
describe the clincial presentation of lyme disease
- erythmea migrans in early stages
- late stages: disseminated disease- fever, chills, migratory muscle and joing pains, cardiac involvement
describe the cardiovascular changes during lyme disease
- atrioventricular block
- in first degree AV block, the PR interval is >0.21 sec, but the P wave always precedes the QRS complex
what can E. coli cause?
- UTIs and abdominal infections
what can neisseria gonorrhea cause?
- pelvic inflammatory disease
- STDs
what can ricketsia rickettsiii cause?
- rocky mountain spotted fever
- tick transmitted
- patients present with headache, fever, and centripetal rash (petechial)
what can staphlococcus aureus cause?
- gram postiive
- scalded skin syndrome
- toxic shock sydrome
- abscess formation
- endocarditis
- food poisoning
describe what happens in severe endocarditis caused by staph aureus
- abcess formation
- cardiac arrhythmia
- murmur
list the components of the AV conduction system
- AV node
- bundle of His
- L and R bundle branches
what is 1st degree AV block?
- prolonged PR interval (>0.2 sec; >5 small boxes)
- 1:1 relationship with QRS complexes is preserved
- block is within AV node
what can cause reversible 1st degree AV block?
Reversible causes:
- heightened vagal tone, transient AV node ischemia, drugs that depress conduction (digitalis, B-blockers, Ca channel antagonists)
what can cause irreversible (structural) 1st degree AV block?
Structural causes:
- MI and chronic degenerative diseases ofthe conduction system (comes with aging)
describe 2nd degree AV block
- intermittent failure of AV conduction
- some P waves are not followed by a QRS complex
what are the two types of 2nd degree AV block?
1. Mobitz type I (Wenckebach block)
2. Mobitz type II
describe Mobitz type I AV block
- aka Wenckebach block
- a type of 2nd degree AV block
- degree of AV delay gradually increases until an impulse is completely blocked
- ECG shows progressive increase in the PR intervals
what causes Mobitz type I AV block?
- impaired conduction in the AV node
- usually benign: seen in children, athletes, and people with high vagal tone
- can also occur during an acute inferior wall infarction
how do you treat Mobitz type I AV block?
- usaully not necessary to treat
- IV atropine or isoproterenol
- if not helped, can implant a pacemaker
describe a Mobitz type II AV block
- 2nd degree AV block
- more dangerous
- sudden and unpredictable loss of AV conduction without gradual lengthening of PR interval
- wide QRS
what is high grade AV block?
- a block that persists for two or more beats
- a Mobitz type II block
what causes a Mobitz type II AV block?
- conduction block beyond the AV node (in the bundle of His or in the Purkinje system)
- MI involving the septum or chronic degeneration of His-Purkinje system
what can a Mobitz type II AV block progress to?
- a 3rd degree AV block without warning
- usually treated with a pacemaker
describe 3rd degree AV heart block
- complete heart block
- complete failure of conduction between atria and ventricles
what causes 3rd degree AV block?
- acute MI
- drug toxicity (e.g. digitalis)
- chronic degeneration of conduction pathways
- a type of AV dissociation
how does adult polycystic kidney disease cause hypertension?
- cysts impair perfusion of glomeruli -> renin secretion by juxtaglomerular complexes
- treated by ACE inhibitors
name some Ca channel blockers, and describe their role in managing hypertension
- nifedipine, verapamil, ditiazam
- block Ca entry into cells -> inhibits vascular smooth muscle contraction
name some centrally acting sympatholytics, and describe their role in managing hypertension
- clonidine
- stimulate a2 receptors -> reduce sympathetic outflow
name some nitrates, and describe their role in managing hypertension
- nitroglycerin
- release NO in smooth muscle cells -> stimulate guanylate cyclase -> increase in cGMP levels -> sm muscle relaxation and vasodilation
name some thiazide diuretics, and describe their role in managing hypertension
- hydrochlorothiazide
- acts on the early distal tubule. does not direct address hypertension
what type of hypertension medicine can block the symptoms of hypoglycemia?
beta-adrenergic blockade
- e.g. propranolol (non-selective B-blocker) can even potentiate insulin-induced hypoglycemia
what are the symptoms of hypoglycemia?
- tachycardia
- blood pressure changes
- ACE inhibitor that can be safely used in treating hypertension of diabetics
- Ca-channel blocker that can be safely used in treating hypertension of diabetics
- Methyldopa, in its active metabolite form, leads to increased alpha-2 receptor-mediated inhibition of SNS, allowing PSNS tone to increase -> decrease in TPR and CO
- however, side effect profile make it so that they're generally only used on patients unresponsive to ACE inhibitors and Ca channel blockers
- a1 adrenergic antagonist that can be safely used in treating hypertension of diabetics
- however, side effect profile make it so that they're generally only used on patients unresponsive to ACE inhibitors and Ca channel blockers
what are the units for vascular resistance?
what is the normal resting CO?
- 6L/min
what is normal mean circulatory filling pressure (MSFP), and what causes elevated MSFP?
- aka mean systemic filling pressure
- 7+ mmHg
- elevated MSFP can be caused by increased retention of salt and water
what is the mean systemic filling pressure?
- the pressure that exists in all parts of the circulation when the heart has stopped and blood volume is redistributed in all the systems
how do you find the MSFP on a cardiac function curve?
- it's where the venous return curve intersects the x-axis
how do you calculate CO from the Fick equation?
CO = O2 consumption / (arterial O2 content - venous O2 content)
what is the most common complication of tPA (tissue plasminogen activator)
- hemorrhage
describe the mechanism of tPA on acute MI
- produced by recombinant DNA technology
- known as 'clot buster'
- binds to fibrin in a thrombus -> converts entrapped plasminogen to plasmin -> initiates fibrinolysis -> thrombus dissolution
what is tPA indicated for?
- acute MI
- acute ischemic stroke
- PE
what are the two types of bleeding that can be caused by tPA?
1. internal bleeding involving the GI, GU, respiratory tracts, and intracranial sites
2. superficial bleeding
what is significant about the fact that tPA is made by recombinant technology?
- incidence of anaphylactic reactions is very low, since it's essentially the same as the tPA produced by the body
what are some RARE side effects of tPA administration?
1. anaphylactic reaction
2. cardiac arrhythmia (secondary to thrombolysis with reperfusion)
3. hypotension
4. thrombosis
describe the initial response to vascualr injury
- brief period of arteriolar vasoconstriction (from reflex neurogenic mechanims and secretion of endothelin
what is the sequence of events for clot formation?
1. initial arteriolar vasoconstriction
2. primary hemostasis
3. secondary hemostasis
4. permanent plug formation
primary hemostasis during clot formation
- highly thrombogenic ECM is exposed -> activates platelets -> release of secretory granules -> recruitment of additional platelets -> formation of hemostatic plug
secondary hemostasis during clot formation
- tissue factor is also exposed at site of injury -> activation of coagulation cascade -> thrombin activation -> thrombin converts circulating soluble fibrinogen to insoluble fibrin -> local fibrin deposition.
- thrombin also induces further platelet recruitment and granule release
permanent plug formation in clot formation
- polymerized fibrin and platelet aggregates form a solid permanent plug
- at this point, counterregulatory mechanisms (tissue plasminogen activator tPA) is set in motion to limit the plug to the site of injury
what is thoracic outlet syndrome?
- broad term for a group of disorders where there is compression of neurovascular bundles
which artery is compressed when you see pain in upper extremity and tingling/numbness in the 4th and 5th digits of the hand?
- subclavian artery
- compressed between the scalenus anterior and cervical rib (throacic outlet syndrome)
what are predisposing factors for thoracic outlet syndrome?
- presence of a cervical rib
- repetitive motion
- poor posture
what is a cervical rib?
extra rib located above the normal first rib
- can cause thoracic outlet syndrome due to compression of the brachial plexus or subclavian artery
- Compression of the brachial plexus may be identified by weakness of the muscles around the muscles in the hand, near the base of the thumb.
- Compression of the subclavian artery is often diagnosed by finding a positive Adson's sign
what is a positive Adson's sign?
Adson's sign is seen during abduction and external rotation at the shoulder, where there is loss of the radial pulse in the arm. It can be a sign of thoracic outlet syndrome.
what are the clincial features of an abdominal aortic aneurysm?
- pulsatile abdominal mass
- foci of calcium
- usually caused by severe atherosclerosis
what vascular complications can arise from congenital weakness of vessels?
berry aneurysms, esp in the cerebral vessels of the circle of Willis
what vascular complications can arise from cystic medial necrosis?
- dissecting aneurysms, esp in Marfan's sydnrome
what vascular complications can arise from syphilis?
syphilitic aneurysms involving the aortic root as it leaves the heart
what vasculra complications can arise fro vasculitis?
- aneurysms in small arteries
what is cisplatin? what are its side effects?
- an alkylating agent used for the treatment of metastatic testicular and ovarian tumors in combination with other agents
- can cause severe bone marrow supression and renal toxicity
what is methotrexate? what are its side effects?
- antimetabolite and folic acid antagonist
- side effects: mucosities, GI ulcer, hepatotoxicity, BM supression, and pulmonary toxicity
when is methotrexate used?
- pediatric ALL
- burkitt's lymphoma
- non-hodgkin's lymphoma
- breast, head, neck and small cell lung cancer
what is carmustine (BCNU)? and what are its side effects?
- alkylating agent used for Hodgkin's disease and other lymphomas
- side effects: delayed myelosuppression and pulmonary toxicity
what is bleomycin? what are its side effects?
- anticancer antibiotic
- does NOT cause BM suppression
- pulmonary toxicity
which chemotherapeutic agents cause pulmonary toxicity?
1. bleomycin
2. busulfan
3. carmustine (BCNU)
4. methotrexate
when do you use bleomycin?
- treatment of sqamous cell carcinomas of the head, neck, penis, cervix, and vulva
- used for several types of lymphomas
what causes dilated/congestive cardiomyopathy?
- lessened contractile function of the L, R, or both ventricles
- frequently results in CHF
what are the classic symptoms of congestive cardiomyopathy?
- orthopnea
- paroxysmal nocturnal dyspnea
- nocturia
- tachycardia
- pulmonary rales
- S3
what drugs are associated with the development of congestive cardiomyopathy?
- anthracycline antibiotics: doxorubicin and daunomycin
(higher incidence with doxorubicin therapy)
what is doxorubicin used for?
- antibiotic antineoplastic agent used for:
- sarcomas
- multiple myeloma
- malignant lymphoma
- acute leukemia
- ovarian, breast, testicular, gastric, bladder, and throat cancer
what are the causes of amaurosis fugax?
five distinct causes of transient monocular blindness: 1. embolic
2. hemodynamic
3. occular
4. neurologic
5. idiopathic
what is the pathology underlying the causes of amaurosis fugax?
- atheromatous disease of the internal carotid or ophthalmic artery, vasospasm, optic neuropathies, giant cell arteritis, angle-closure glaucoma, increased intracranial pressure, orbital compressive disease, a steal phenomenon, and blood hyperviscosity or hypercoagulability
name CN 9
what happens when you sever the glossopharyngeal afferent fibers to the carotid sinus?
- hypertension and tachycardia
- medulla thinks that there is a loss in BP -> baroreceptor reflex -> increased sympathetic outflow and decreased parasympatehtic outflow
from where does CN IX carry afferent info to the medulla?
what happens with increased firing?
- from the carotid sinus
- the medulla believes that there is increased blood pressure
from where does CN X carry afferent info to the medulla?
what happens with increased firing?
- from the aortic arch baroreceptors
- the medulla believes that there is increased blood pressure
which vascular layer do a1 receptors present on?
- the smooth muscle layer
what happens to smooth muscle when you stimulate its a1 receptor?
- inrease in intracellular [Ca] via PI hydrolysis -> smooth muscle contraction
what is phosphatidylinositol? what happens upon its hydrolysis?
- a minor phospholipid component in the cytosolic side of eukaryotic cell membranes
- Upon hydrolysis, they yield 1 mole of glycerol, 2 moles of fatty acid, 1 mole of inositol and 1, 2, or 3 moles of phosphoric acids.
where in the vessel is the endothelial cell located?
- in the intima of the arteriole
what do endothelial cells produce?
- Nitric oxide (aka endothelial cell relaxing factor) is made from arginine
what is another name for NO?
- endothelial cell relaxing factor (EDRF)
what lays outside the smooth muscle cells of the arteriole?
- adventitia
tell me more about the adventitia
- the connective tissue that surrounds an artery: tunica adventitia, b/c it's extraneous to the artery.
- whether an organ is covered in adventitia or serosa depends upon whether it is peritoneal or retroperitoneal:
* peritoneal organs are covered in serosa (a layer of mesothelium, the visceral peritoneum)
* retroperitoneal organs are covered in adventitia (loose connective tissue)
what happens if you give a nonselective b-blocker to an asthmatic?
- e.g. propranolo
- may result in bronchoconstriction
where do b1 receptors predominate?
- heart
where do b2 receptors predominate?
- lung
what is a mnemonic for remembering the b1 selective blockers?
- cardioselective
1. acebutolol
2. betaxolol
3. esmolol
4. atenolol
5. metoprolol
what is labetalol?
- blocks a1, b1, b2
- used for treating hypertensive emergencies
- used for hypertension of pheochromocytoma
what is nadolol?
- blocks b1 and b2
- very long half life (14-24 h)
what is prazosin?
- blocks a1
- used for hypertension
what is timolol?
- blocks both b1 and b2
- used for open-angle glaucoma
what percentage of total body blood volume is found in the veins and venules?
- 64% (nl: 3200mL)
what accounts for occlusion distal to the aortic arch in young people?
- coarctation of the aorta
what accounts for occlusion distal to the aortic arch in old people?
- severe atherosclerosis of the abdominal aorta
- iliac system
- femoral system
in coarctation of the aorta, where is there decreased flow?
- decreased flow through the descending aorta, off of which most of the intercostal arteries orginate
where does the first intercostal artery originate?
- aka supreme intercostal artery
- originates off the subclavian artery at the costocervical trunk
do the vertebral arteries supply the intercostal muscles?
- no
what comes off the subclavian artery?
- internal mammary artery, which feeds the intercostal arteries
where do most of the intercostal arteries originate from?
- the descending aorta
- exception: the first intercostal artery, which originates from the subclavian artery at the costocervical trunk
how do you calculate total peripheral resistance (TPR)?
- think V = IR
- or (mean arterial pressure - right atrial pressure)/ CO
- right atrial pressure is assumed to be 0mmHg
what do you assume right atrial pressure to be?
- 0 mmHg
what is the ostium primum?
- the gap that exists while the septum primum is growing towards the endocardial cushions.
- when the septum primum is done growing, the ostium primum is completely closed
what is a primum type atrial septal defect?
- failure of the septum primum to fuse completely -> persistent ostium primum
when does the ostium secundum form?
- it forms within the septum primum before the ostium primum closes
what happens if you don't have formation of the ostium secundum?
- embryonic death
- no communication from R -> L atrium so embryo doesn't get oxygenated blood
which septum is pushed against which after birth?
- valve of the foramen ovale (septum primum) is pushed against the septum secondum due to increased L atrial pressure
what is probe patency?
- when the fushion of the valve of the forament ovale and the septum secondum is not achieved
does the septum secundum fuse with the endocardial cushions?
- no
describe the genetics of familial hypercholesterolemia
- autosomal DOMINANT condition due to mutation in the receptor for LDL
what happens if you're heterozygous for familial hypercholesterolemia?
- 3x elevation in plasma cholesterol and increased incidence of atherosclerosis
what are the clinical presentations of a homozygous patient for familial hypercholesterolemia?
- numerous xanthomas
- 6x elevation in plasma cholesterol
- due in their 20s-30s from MI or cerebral infarction
what can a penetrating wound of the aorta cause?
- an aneurysm, that can erode into the vena cava -> large AV fistula
why would you have an increase in the mean systemic filling pressure when you have an AV fistula?
- there is decreased BP b/c of decreased resistance (in the microcirculation)
- decrease in BP causes increased sympathetic reflexes -> increased MSFP
what would you most likely find in a ventricle that has been scarred by MI?
- ventricular aneurysm
where are ventricular aneurysms most likely to develop?
- in large transmural infarctions affecting the free wall of the L ventricle
when does creatine kinase peak after infarction?
- 18 hours
when does AST peak after infarction?
- 24 hours
when does LDH peak after infarction?
- 36 hours
when does troponin I peak after infarction?
- will persist for up to 10 days
what is fibrinous pericarditis?
- common complication of the earliest stages of transmural infarction
- invovles the visceral pericardium by inflammatory reaction the necrotic myocardium
- usually resolves spontaneously after a few days
what is the most common primary cardiac tumor of adults?
- ATRIAL myxoma
- usually a single lesion in the L atrium that can INTERMITTENTLY obstruct the mitral valve
what are atrial myxomas composed of?
- scattered mesenchymal cells in a prominent myxoid background
what is benign glandular tissue suggestive of?
- adenoma
- not usually found in heart
what is densely packed smooth muscle suggestive of?
- leiomyoma
- not usually found in heart
what is densely packed striated muscle suggested of?
- rhabdomyoma
- most common primary cardiac tumor in children
what is the most common primary cardiac tumor in children?
- rhabdomyoma
what is malignant glandular tissue suggestive of?
- carcinoa
- can be metastatic to the heart, but does nto cause a ball-valve obstruction
arterioles account for what percentage of the TPR?
what is the sequence of events that follows irreversible ischemic injury?
- necrosis of parenchymal cells
- inflammatory reaction
- granulation tissue
- scar healing
what are the histologic changes that happen 1 hour after ischemia?
- no morphologic change indicative of necrosis
what are the histologic changes that happen 12 hours after ischemia?
- (applicable only to irreversible ischemia)
- myocytes appear intensely eosinophilic and wavy
- no inflammatory reaction yet
what are the histologic changes that happen 1 day after ischemia?
- PMNs infiltrate the infarcted tissue beginning at 1 day and peaking 2-3 days after injury
define histiocyte
a macrophage that is found in connective tissue
what comes after PMNs invade necrotic tissue?
- lymphocytes and histiocytes
what are the histologic changes that happen 5 days after ischemia?
- early formation of granulation tissue: reabsorption of necrotic myofibers by histiocytes and proliferation of small blood vessels
what are the histologic changes that happen 10 days after ischemia?
- advanced granulation tissue
- fibroblasts, small blood vessels, and residual chronci inflammatory cells in a matrix of young collagen matrix
- ACE inhibitor
- reduces mortality associated with MI
- can cause a dry cough
how do ACE inhibitors reduce the mortality associated with MI?
- decrease the amount of ventricular remodeling afer infarction and reduce risk of CHF
- can also diminish risk of 2nd heart attack
what is a common side effects associated with ACE inhibitors?
- can also cause:
- headache
- diarrhea
- fatique
- nausea
- dizziness
what are the side effects associated with asprin?
- increased bleeding time
- GI bleeding
- tinnitus
what are the side effects associated with metoprolol?
- b1 antagonist
- hypoglycemia
- peripheral vasoconstriction
- CNS side effects
what are the side effects associated with procainamide?
- group IA antiarrhythmic
- antimuscarinic and direct depressant effects on heart
- drug induced lupus erythematous
what are the side effects associated with warfarin?
- oral anticoagulant
- cause bleeding at therapeutic doses
- bone defects in developing fetus
by how much can blood flow increase in exercising skeletal muscle?
20 fold
- greater increase than any other tissue in the body
- results from local vasodilators on arterioles
what happens to oxygen concentration in skeletal muscle during exercise?
- decreases
- oxygen is utilized more rapidly than it can be delivered by blood
what happens during oxygen deficiency in skeletal muscle during exercise? what is secreted?
- vasodilator metabolites: adenosine, CO2, lactic acid, and others to accumulate in the tissues
what lab value can you use to differentiate infarction from angina?
- high serum CK-MB values
- in infarction, can be 6x that of the upper limit of normal
what conditions indicate a subendocardial infarction? what do you see on the ECG?
- subendocardial: most likely in the setting of known, prolonged, severe hypotension
- occurs during poor perfusion complicated by increased demand or transient vasospasm
- ECG: equivocal. some degree of S-T segment depression over several leads
which muscle layer of the heart is most vulnerable to ischemia?
- the subendocardial muscle b/c it is farthest away from the arterial supply
what conditions indicate a transmural infarction? what do you see on the ECG?
- not specifically expected in the setting of shock
- produces characteristic ECG changes that are very localized to a few leads
what do you see in lab values for unstable angina?
- may be slight increase in cardiac enzymes, but usually, this is less than 2x the upper limit of normal
what do you find in the children with rhabdomyoma?
- tubers
- rhabdomyoma are common in children with tuberous sclerosis
what is tuberous sclerosis?
proliferation of small benign tumors in the brain, as well as on the face and eyes, and in the kidneys, lungs, and other organs. Seizures and mental retardation are associated with the disturbance in brain function.
what are berry aneurysms associated with?
adult polycystic kidney disease
what is glioblastoma multiforme?
- high grade astrocytoma
- relatively common childhood CNS malignancy
- not associated with cardiac tumors
embolization of which type of cardiac tumor causes CNS infarction?
- atrial myxomas, NOT rhabdomyomas
- tumor of the cerebellum seen in children
- more common in adults rather than children
- usually benign that grow at the periphery of the brain
- may compress the brain, but does not pentrate it
what is sydenham chora associated with?
- rheumatic fever
what is the most appropriate treatment for a patient with paroxysmal atrial tachycardia?
- digitalis
- a cardiac glycoside that slows conduction through the AV node via parasympathetic actions
- can be blocked by atropine
- blocks cardiac muscarinic receptors, thereby increasing conduction through the AV node
- increases conduction by stimulating sympathetic autonomic ganglia and the adrenal medulla
- increases conduction by stimulating cardiac B receptors
- acts centrally to decrease vagal tone -> increases AV conduction
what electrolyte disturbances can be seen with ACE inhibitors?
- hyperkalemia and mild hyponatremia
- can also cause neutropenia, anaphalactoid reactions, angioedema, chronic cough, and fetal abnormalities
what are some risk factors for hyperkalemia?
- renal insufficiency, diabetes mellitus, use of potassium containing products
what electrolyte level is not affected by ACE inhibitors?
phosphate blood levels
what are ACE inhibitors used for?
- hypertension
- heart failure
- diabetic neuropathy
what drug class does enalapril belong to?
ACE inhibitor
what is Dressler's syndrome?
- autoimmune disease
- causes fibrinous pericarditis with fever and pleuropericardial chest pains several WEEKS after MI
what does the p wave represent?
- the depolarization of the R atrium, followed by the depolarization of the L atrium
- where is the P wave best visualized?
- lead II: the one that runs most parallel to the flow of current through the atria from the SA to AV node
what happens on the ECG when you get a bundle branch block?
- prolongs depolarization and widens the QRS complex
- QRS: 0.1-0.12 - incomplete BBB
- QRS: >0.12 - complete BBB
what are BBBs associated with?
- coronary artery disease
- ischemia
- damage to heart conduction system
what are the five major criteria for the diagnosis of RF?
1. carditis
2. migratry polyarthritis
3. subcutaneous nodules
4. Sydenham's chorea
5. erythema marginatum
what are the minor criteria for the diagnosis of RF?
1. fever
2. arthralgia
3. elevated actue phase reactants
4. prolonged PR interval
describe the clinical symptoms of aortic dissection
- acute and severe chest pain that radiates to the back
what diseases are associated with pericardidits?
1. viral syndromes
2. connective tissue diseases
3. fenal failure
4. MI
5. tumor invasion of the pericardium
where does the electrical activity begin in left anterior fascicular block (LAFB)? ECG changes?
- activation begins at the post papillary muscle and then spreads ot the rest of the ventricle
- initial depolarization will be downwards
- no widening of the QRS
where does the electrical activity begin in left posterior fascicular block (LPFB)? ECG changes?
- L ventricualr activation starts at teh base of the anterior papillary muscle
- no widening of the QRS
what do you see on the ECG after a transmural MI?
- the hallmark of a transmural MI is a pathologic Q wave
- Q waves are wider and deeper
- width > 1small box
- depth > 25% of the total QRS
- ST elevation
do pathologic Q waves disappear over time?
- no
what do you see on the ECG for a posterior wall myocardial infarction?
- no pathologic Q waves
- instead, you see taller than normla R waves in V1 and V2
what do subendocardial MIs generate on the ECG?
- aka non-Q wave infarctions
- no Q waves
- ST depression (and/or T wave infersion)
what happens to TPR if you remove an organ, and why?
- TPR goes up, because organs are arranged in parallel
what happnes to the following when you remove a kidney:
1. arterial pressure
2. CO
3. pulmonary blood flow
4. total renal blood flow
arterial pressure: no change
CO: decrease
pulmonary blood flow: equat to CO, decrease
total renal blood flow: decrease
what do juxtacapillary receptors (J receptors) do?
- sense changes in oxygenation
- will stimulate rapid shallow breathing during pulmonary congestion
what is paroxysmal nocturnal dyspnea (PND)?
- severe breathlessness that awakens the patient from sleep 2-3 hours after going to bed
- caused by gradual reabsorption of lower extremity edema -> increased venous return to heart and lungs
why do you get nocturnal cough (possibly hemoptysis) during congestive heart failure?
- it's simply a symptom of pulmonary congestion
- hemoptysis may result from rupture of engorged bronchial veins
what is the Cheyne-Stokes respiratory pattern?
- periodsof hyperventilation separated by intervals of apnea
- seen in advanced cheart failured
- caused by the delay in circulating getting to the respiratory center of the brain for normal feedback
what causes S4?
- S4 is a late diastolic sound that results from the forceful atrial contraction into a stiffened ventricle
- commonly seen in states of decreased left ventricular compliance (left heart failure)
what clinical signs might you see for a patient in right heart failure?
- right ventricular heave from RV enlargement
- right sided S3 or S4 gallop
- murmer of tricuspid regurge (from RV enlargement)
- distention of jugular veins
- hepatic enlargement
- edema
- pleural effusion
why does pleural effusion occur in both right and left sided heart failure?
- pleural veins drain into both the systemic and pulmonary venous beds
how do you uncover pleural effusion on physical exam?
- dullness to percussion over the posterior lung lobules
what clinical findings may present during left heart failure?
- pulmonary rales
- rhonchi and weezing
- PMI is more lateral
- S2 (pulmonic) is louder than normal
- early diastolic S3
- late diastolic S4
what are the four extra diastolic heart sounds?
- Opening snap
- S3
- S4
- pericardial knock
what causes the opening snap? which valve is it more common for? Describe the timing.
- caused by opening of mitral or tricuspid valves during M or T valvular stenosis
- more common in MS
- the interval to P2 is closer in more severe MS
what causes S3? when is it pathologic? what does it mean when you see it in its pathologic state?
- results from tensing of the chordae tendinae during rapid filling of the ventricle
- normal in children
- pathologic in middle-aged adults -> volume overlaed from CHF or increased flow from M or T regurge
what is a pathologic S3 also known as?
- a ventricular gallop
what causes S4? what sort of disease states does it indicate?
- the atrium contracting against a stiffened ventricle
- usually indicates decreased ventricular compliance (from ventricular hypertrophy or MI)
what is S4 also known as?
- an atrial gallop
what defines Afib?
- chaotic rhythm with atrial rate so fast (360-600 discarges/min) that discrete P waves can't be seen on the ECG
- only some of the depolarizations are conducted to the ventricles -> irregular rhythm
what is the average ventricular rate in untreated AF?
- 160 bpm
what is AF associated with and why?
- large R or L atria
- the atria need to enlarge to allow for a greater probablity of reentrant circuits
in which types of patients do you see AF?
- hypertension
- alcohol intoxication
- thyrotoxicosis
- pulmonary disease
- right after cardiothoracic surgery
why are AFs dangerous?
1. rapid ventricalar rates may compromise cardiac output -> pulmoanry congestion and hypotension
2. absence of organized atrial contraction promotes blood stasis -> thrombi -> stroke
what are the three treatment avenues for AF?
1. ventricular rate control
2. attempts to restore sinus rhythm
3. assessment for the need for anticoagulatin to prevent thromboembolism
what drugs are given to reduce ventricular rate in AF?
- beta blockers or Ca channel antagonists (diltiazem, verapamil)
- digitalis is usually not as effective
what drugs are give to restore sinus rhythm in AF?
- vardioversion back to sinus rhythm can be attemted by giving:
1. class IA, IC, or III antiarrythmic drugs
2. electrical cardiversion
- drugs have bad side effects
what do you do for patients with asymptomatic AF?
- simply continue with chronic anticoagulation therapy, b-blockers, Ca channel blockers or digoxin
what are class 1A drugs used for?
- atrial fib/flutter
- paroxysmal SVT
- v tach
what are class 1b drugs used for?
- v tack
- digitalis-induced arrhythmias
what are class 1c drugs used for?
- atrial fib
- paroxysmal SVT
what are class II drugs used for?
- atrial or ventricular premature beats
- paroxysmal SVT
- artial fib/flutter
- ventricular tach
what are class III drugs used for?
- v tach (amiodarone and sotalol)
- atrial fib abd flutter
- bypass-tract mediated paroxysmal SVT (amiodarone)
what are class IV drugs used for?
- paroxysmal SVT
- atrial fib and flutter
- multifocal atrial tach
name class IA drugs
- quinidine
- procainamide
- disopyramide
name class IB drugs
- lidocaine
- tocainide
- mexiletine
- phenytoin (DPH)
name class 1C drugs
- flecainide
- propafenone
name class II drugs
- b-blockers
- propranolol
- esmolol
- metoprolol
name class III drugs
- K channel blockers- prolong repolarization
- amiodarone
- sotalol
- bretylium
- ibutilide
- dofetilide
name class IV drugs
- Ca channel blockers
- verapamil
- diltiazem
how are patients with afib initially stabilized?
- given diltiazem (Ca channel blocker)
atropine and heart rate
- a muscarinic cholinergic antagonist -> increase HR
what is propylthiouracil? what is it used for?
- treats hyperthyroidism
- inhibits thyroid peroxidase and diminishes peripheral iodination of T4 to T3
what is cystic hygromas?
- lymphatic malformations resembling hemangiomas
what congenital disease can cause cystic hygromas?
- turners sydrome
what malformations are associated with turner's syndrome?
- coarctation of the aorta
- cystic hygroma
- pulmonary stenosis
what is turner's syndrome?
- complete or partial monosomy of X chr
- hypogonadims in phenotypic females
what is the prevalence of turner's syndrome?
- most common sex chromosome abnormality in females
- 1:2000 liveborn females
how do turner's sydrome girls present during infancy?
- lymph stasis -> edema of the dorsum of the hand and foot, and swelling of the nape of the neck (from a cystic hygroma)
- as they get older, the swelling goes down, but leave bilateral neck webbing
what heart conditions are seen in turner's sydnrome babies?
- coarctation of the aorta
- bicuspid aortic valve
- cardiovascular problems are most important cause of mortality
what happens to turner's syndrome children at adolescence?
- failure to develop normal secondary sex characteristics
- shortness of stature
what is the single most important cause of primary amenorrhea?
- turner's syndrome
turner's syndrome and autoimmune disease
- 50% of patients develop autoantibodies against the thyroid gland -> hypothyroidism
in what sort of patient would you see aortic dissection or cystic medial necrosis of the aorta?
- marfan's patients
in what type of child would you see early severe aortic atheroscleroris?
- DM
- familial hyperlipidemia (xanthomas, elevated serum lipids)
where do mural thrombi develop?
- over a previously infarcted segment of myocardium, esp with the infarct is large and a ventricular aneurysm develops
what is electromechanical dissociation?
- in EMD, a normal potential is transmitted through the myocardium, but no blood is sent to the circulation
- may occur from pericardial tamponade, massive PE, or toxins that prevent normal cardiac contraction
what does electromechanical dissociation cause?
- sudden death
what is the pressure gradient across the circulation, used for calculating TPR?
(mean arterial pressure - right atrial pressure)
what two structures does the ductus arteriosus connect? which direction is blood flow before birth? after birth?
- the LEFT pulmonary artery and the aortic arch
- before birth: L pulm a -> aorta
- after birth: aorta -> L pulm a
name two class IB drugs used for v tach
- blocks Na channels -> shortens action potential duration
- lidocaine
- tocainide
- mexiletine
- produce moderate suppression of SA automaticity and AV node conduction
what is esmolol?
- class II antiarrhythmic
- ultrashort acting b-1 adrenergic blocking agent (cardioselective)
what are disopyramide and procainamide?
- class IA antiarrhythmics
- decrease myocardial excitability, conduction velocity, contractility, and automaticity
what is the clinical progression of aortic dissection?
- pain that radiates to the back, and which moves downwards as the dissection progresses
- aortic branch involvement causes weakening of wrist pulses
- hypertension
describe the histologic observations of cystic medial necrosis
- focal fragmentation of elastic elements
- deposition of myxoid material
- formation of small cleft-like or cystic spaces
what types of vessels does polyarteritis nodosa effect?
- medium sized vessels (smaller than the aorta)
what is supraventricular tachycardia (SVT)?
a rapid rhythm of the heart in which the origin of the electrical signal is either the atria or the AV node. These rhythms require the atria or the AV node for either initiation or maintenance. This is in contrast to ventricular tachycardias, which are tachycardias that are not dependent on the atria or AV node.
what are the different types of supraventricular arrhythmias?
- sinus bradycardia
- sinus tachycardia
what causes sinus bradycardia?
- excess vagal stimulation
- SA nodal ischemia, usually from inferior wall MI
what causes sinus tachycardai?
- pain, anxiety, heart failure, drugs (nitrates, dopamine), or intravascular volume depletion
what do you see clinically during acute infective endocarditis?
- splinter hemorrhages in nail bed
- petechia in skin and mucoase
- all due to microscopic septic emboli
how does acute infective endocarditis cause sudden death?
- MI from septic embolus in the coronary circulation
what types of infections cause acute and subacute infective endocarditis?
- acute: staph aureus (IV drug user); high mortality
- subacute: strep viridans
how do you get subacute infective endocarditis?
- infection with streptococci viridans
- arises in patients with previously malformed or damaged valves
- associated with slower course, and better prognosis
what is the clinical presentation of carcinoid syndrome?
- episodic flushing of skin
- cramps
- nausea
- vomiting
- diarrhea
what bioactive products are produced by carcinoid tumors?
- serotonin
- kallikrein
- bradykinin
- histamine
- prostaglandins
- tachykinins
what inactivates 5-HT and bradykinin in the lungs (for carcinoid tumors)
how can you get fibrosis of the endocardium from carcinoid syndrome on the left side of the heart?
- pulmonary carcinoids
- huge levels of circulating 5-HT so not all of it is inactivated
- a patent foramen ovale
what is libman-sacks endocarditis?
- non-infective form of endocarditis
- associated with SLE
- vegetations are small and regularly aligned along the valvular margins
what is nonbacterial thrombotic endocarditis associated with?
- aka marantic endocarditis
- disseminated neoplasm
- increase coagulability
- lesions are small vegetations similar to libman-sacks endocarditis
rank the velocity of blood flow
aorta > vena cavae > large veins > small arteries > arterioles > small veins > venules > capillaries

- capillaries have the largest cross sectional area
- we also assume that the VC has a larger cross sectional area than the aorta
how do you distinguish a VSD from a patent ductus arteriosus?
- while a patient DA initially causes L -> R shunting, as pulmonary vascular resistance increases, a R -> L shung can occur
- will not see increased O2 sat in R ventricle
- continuous 'machinery' murmur
how do you distinguish a VSD from a patent foramen ovale?
- a patent foramen ovale is a slitlike opening that would not account for the systolic murmer heard in VSD
what is niacin? what does it do?
- vitamin B12. used for hyperlipidemia
what is niacin's effects on LDL?
- LDL reductions occur in 5-7 days (max effect in 3-5 wks)
what is niacin's effect on triglycerieds and VLDL?
- triglycerides and VLDL reduced by 20-40% in 1-4 days
what is niacin's effect on HDL?
- increases HDL by 20%
when is niacin prescribed?
- for adjunctive therapy in patients with elevated cholesterol and triglycerides when diet and exercise are inadequate
what is the most common side effect of niacin?
- generalized flushing and sensation of warmth in face
- can persist even after discontinued therapy
what are less common side effect of niacin?
- hepatotoxicity
- tachycardia
- hypoalbuminemia
- hyperglycemia
- nausea
- vomiting
- hyperuricemia
- glucose intolerance
- pruitus
- PUD, dry skin
what are some symptoms associated with cocaine use?
- generalized tonic-clonic seizures
- restlessness, irritability
- nausea and headache
- tachycardia
- elevated BP
how does cocaine cause hypertension and tachycardia?
- blocks norepi uptake -> increase a1 stimulation (systemic vasoconstriction); increase b1 stimulation (increase HR, and inotropic state)
what happens with b2 stimulation?
- vasodilation in the skeletal muscle vasculature -> decreased BP
how do amphetamines work?
- increase norepi release ->increase BP
what is Kawasaki syndrome?
- mucocutaneous lymph node sydrome
- leading cause of acquired heart disease in children in the US
what are the cardiovascular complications from Kawasaki syndrome?
- affects small, medium, and large arteries
- transmural inflammation and variable necrosis
- 20% of children have damage to coronary vessels -> coronary artery aneurysms
what causes sudden death in children with Kawasaki syndrome?
- ruputure of the coronary artery aneurysms
(1-2% of cases)
what sort of congenital disease is berry aneurysms associated with?
- polycystic kidney disease
what is kawasaki disease associated with?
- mucocutaneous lymph node syndrome
- acute but self-limited disease manifested by fever, conjunctival and oral erythema
- erosion, edema of hands and feet
- erythema of palms of soles
- skin rash with desquamation
- enlargement of cervical lymph nodes
name the large vessel vasculitis diseases
- giant cell (temporal arteritis)
- takayasu arteritis
name the medium-sized vessel vasculitis diseases
- polyarteritis nodosa
- kawasaki disease
name the small vessel vasculitis diseases
- wegerner granulomatosis
- churg -stauss syndrome
- microscopic polyangiitis
giant cell (temporal) arteritis
- granulomatous arteritis of the aorta and its major branches (esp extracranial branches of the carotid: temporal a)
- patients > 50yrs
what is associated with giant cell (temporal) arteritis?
- polymyalgia rheumatica
takayasu arteritis
- granulomatous inflammation of the arota and its major branches
- usually in patients < 50
polyarteritis nodosa
- classic polyarteritis nodosa
- necrotizing inflammation of medium-sized or small arteries without glomerulonephritis or vasculitis in arterioles, capillaires, or venules
what are congenital AV fistulas associated with?
- limb swelling and hypertrophy
- visible pulsations (large fistulas)
- varicose veins
- warmer than the non-affected extremity
what happens to the hematocrit levels in the veins of patients with an AV fistula?
- normal: venous hematocrit is greater than arterial hematocrit b/c of a 'chloride shift' into RBCs as they pass through the circulation
- with an AV fistula, this increase in hematocrit is diluated
what is the chloride shift?
in RBCs, synthesis of carbonic acid by CA produces HCO3- and a free proton. Bicarbonate freely diffuses out of the red blood cell, but the proton does not as cell membranes are impermeable to cations.
- to maintain electrical neutrality, Cl- ions move into the cell from the plasma: this is the chloride shift or Hamburger's phenomenon .
why is venous hematocrit slightly higher than arterial hematocrit?
- chloride shift:
- The osmotic effect of the extra and Cl- in venous RBCs causes the venous RBC volume to increase slightly.
what is Type I hyperlipidemia? prevalence?
- very rare
- due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2, resulting in elevated chylomicrons in plasma (hypertriacylglycerolemia)
- prevalence is 0.1% of the population.
what are the different names for Type I hyperliidemia?
- Buerger-Gruetz syndrome
- primary hyperlipoproteinaemia
- familial hyperchylomicronemia
what are chylomicrons? where are they synthesized?
- made in the intestinal mucosal cells
- carry dietary triacylclycerol, cholesterol, fat-soluble viamins, and CE to the peripheral tissues
what is Type IIa hyperlipidemia?
- familial hypercholesterolemia
- mutation either in the LDL receptor gene on chr 19 or the ApoB gene.
- characterized by tendon xanthoma, xanthelasma and premature cardiovascular disease.
define: xanthelasma
A yellow, fatty spot or bump on the inner corner of either the upper eyelid, the lower one or both eyelids, often caused by a lipid disorder such as high cholesterol.
define: xanthoma
a skin problem marked by the development (on the eyelids and neck and back) of irregular yellow nodules; sometimes attributable to disturbances of cholesterol metabolism
what is Type IIb hyperlipidemia?
- high VLDL levels are due to overproduction of substrates, including triglycerides, acetyl CoA, and an increase in B-100 synthesis.
- may also be caused by the decreased clearance of LDL.
- Prevalence: 10%
* Familial combined hyperlipoproteinemia (FCH)
* Secondary combined hyperlipoproteinemia (usually in the context of metabolic syndrome)
what is Type III hyperlipidemia?
This form is due to high chylomicrons and IDL (intermediate density lipoprotein). Also known as broad beta disease or dysbetalipoproteinemia, the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL (β-VLDL). Prevalence is 0.02% of the population.
what is Type IV hyperlipidemia?
This form is due to high triglycerides. It is also known as hypertriglyceridemia (or pure hypertriglyceridemia). Prevalence is 1% of the population.
what is Type V hyperlipidemia?
This type is very similar to type I, but with high VLDL in addition to chylomicrons.
briefly, type 2b hyperlipidemia
- elevation in both cholesterol and triglycerides in the form of LDL and VLDL
briefly, type 3 hyperlipidemia
- elevations of triglycerides and cholesterol in the form of chylomicron remnants and IDL
briefly, type 5 hyperlipidemia
- elevations of triglycerides and cholesterol in the form of VLDL and chylomicrons
which bacteria is associated with endocarditis with carcinoma of the colon and other colonic diseases?
- streptococcus bovis, a Group D streptococcus
- up to 50% of patients with S. bovis bacteremia have underlying colonic malignancies
- 25-50% of S. bovis bacteremia is associated with endocarditis
what does streptococcus agalactiae cause?
- maternal and neonatal bacteremia and neonatal meningitis
- normal flora of the GI and female genital tracts
what does strep pneumoniae cause?
- leading cause of community acquired pneumonia
- meningitis in adults
- otitis media in children
- sinusitis
how can you get spontaneous peritonitis?
- s. pneumoniae in children with ascites from nephrotic syndrome
what condition predisoposes patients to severe S. pneumo infections?
- asplenia
which patients are more susceptible to S. pneumo infections?
- sickle cell anemia
- multiple myeloma
- alcoholism
- hypogammaglobulinemia
what is the leading cause of invasive bacterial respiratory disease in patients with AIDS?
- S. pneumo
what does strep pyogenes cause?
- bacterial pharyngitis
- complications: paratosillar abscesses, otitis media, sinusitis
what is giant cell arteritis associated with?
- polymyalgia rheumatica
what do patients with polyarteritis nodosa get?
- 30% get hepatitis B antigenemia
what is polyarteritis nodosa?
- systemic necrotizing vasculitis that can be difficult to diagnose, since the vascular involvement is widely scattered
how do patients with polyarteritis nodosa present?
- low grade fever
- weakness
- weight loss
- abdominal pain, hematuria, renal failure, hypertension, and leukocytosis
- can be fatal if untreated!
what can produce a right to left shunt?
persistent truncus arteriosus
what is persistent truncus arteriosus?
- failure of the aorticopulmonary septum to form
- a single truncus arteriosus receives blood from both the right and left ventricles
- the septum between the ventricles is also not well formed
what is amlodipine?
- a calcium channel blocker
- used for mild to moderate hypertension and angina
- selectively blocks Ca influx across myocytes withotu changing serum calcium concentrations
what is terazosin?
- an a1 adrenergic receptor blocker
- used for hypertension and benign prostatic hypertrophy
what is enalapril
ACE inhibitor
- used for hypertension and CHF
what does b1 receptor blockade cause? what does b2 receptor blockade cause?
- b1: negative inotropinc and chronotropic effects on heart
- b2: bronchoconstriction
what is loeffler endocarditis?
- a restrictive cardiomyopathy
- you have endomyocardial fibrosis with myocyte necrosis and a prominent eosinophilic infiltrate
- aka endomyocardial fibrosis with hypereosinophilia syndrome
- caused by heart toxicity from proteins in eosinophil granules designed for paracyte killing
which proteins contribute to loeffler endocarditis?
- eosinophil ribonuclease
- eosinophil major basic protein
why do you get hypereosinophilia in loeffler endocarditis?
- often idiopathic
- sometimes caused by parasitic infection
how do you do dye from loeffler endocarditis?
- heart failure
- arrhythmia
- massive emboli from the damaged endometrium
what is the prognosis for loeffler endocarditis?
- originally poor, but now, b/c of early diagnosis, is helping
- you go in with open-heart surgery to resect the fibrous tissue
what does alcoholic cardiomyopathy produce?
- a dilated heart
what do you see with severe cardiac amyloidosis?
- restrictive heart disease
- red extracellular deposits on biopsy
what do you see with endocardial fibroelastosis?
- restrictive heart disease
- disease of YOUNG children
what do you see with idiopathic subaortic stenosis?
- hypertrophic cardiomyopathy
define cardiomyopathy
- heart disease resulting from a primary abnormality in the myocardium (not from ischemic heart disease, hypertension or valvular heart disease)
what are the three types of cardiomyopathy?
- dilated cardiomyopahty
- hypertrophic cardiomyopathy
- restrictive cardiomyopathy
which forms of cardiomyopathy are most common?
- dilated is most common
- restricitve is least common
define dilated cardiomyopathy
- progressive cardiac dilation and contractile (systolic) dysfunction
- dilated LA and LV
- usually also see hypertrophy (LV)
what is the LF ejection fraction for dilated cardiomyopathy?
< 40%
what causes dilated cardiomyopathy?
- idiopathic
* alcohol (15%)
* peripartum (nutritional deficit)
- genetic (~30%)
* myocarditis
what is associated with dilated cardiomyopathy?
- ischemic heart disease
- valvular heart disease
- hypertensive heart disease
- congenital heart disease
how does myocarditis cause dilated cardiomyopathy (DCM)?
- infection with coxsackievirus B has been found in DCM tissues
- don't know if myocarditis causes DCM or vice versa
how is alcohol or other toxicities associated with dilated cardiomyopathy?
- ethanol toxicity or secondary nutritional disturbance may cause myocardial injury
describe some clinical features of dilated cardiomyopathy
- usually affects people between 20-50 yrs
- slow progressive progression
- SOB, easy fatigability, poor exercise capacity
- may slip into a decompensated state
- secondary MR and abnormal rhythms are common
- embolism from intracardiac thrombus may occur
define restrictive cardiomyopathy
- primary decrease in ventricular compliance -> impaired ventricular filling during diastole
- easily confused with constrictive pericarditis or HCM
simple note:
- CONstrictive PERIcarditis
- REstrictive MYOcarditis
describe the morphology of a restrictive myocarditis heart
- ventricles are normal, slightly hypertrophied
- dilated LA
- biopsy will help you pinpoint the etiolgy
what are the different types of restricitive cardiomyopathies?
1. Endomyocardial fibrosis
2. Loeffler endomyocarditis
3. Endocardial fibroelastosis
endomyocardial fibrosis
- occurs in children, young adults in africa, and other tropical areas
- firbosis of ventricular endocardium and suebdocardium
- involves Tricuspid and mitral valves
- ventricular mural thrombi sometimes develop
loeffler endomyocarditis
- also marked by endomyocardial fibrosis
- large mural thrombi
- not restricted to a geographical area
- release of toxic products of eosinophils is thought to initiate endocardial damage
endocardial fibroelastosis
- focal or diffuse fibroelastic thickening involving the mural left ventricular endcardium
- most common in first 2 years of life
- often appears with congenital heart anomalies or AV obstruction
what happens when you have aortic stenosis on the cardiac PV diagram?
- peak systolic pressure in the LV increases
- increases stroke work output
- increases myocardial demand
- increase coronary artery flow during diastole
how do you determine stroke work from a PV diagram?
- its the area enclosed
what happens when you increase the oxygen demand of the heart?
- you increase the O2 consumption by the heart
- decrease O2 content of venous outflow from heart
- decrease O2 tension in the myocardium
how much O2 is normally used in the coronary circulation?
what happens to coronary vessel blood flow when there is increased peak systolic pressure from aortic stenosis?
- more compression on coronary vessels during systole
what is idiopathic hypertrophic subaortic stenosis
- usually seen in young adults
- autosomal dominant genetic predisposition may be present
what are clinical symptoms of idiopathic hypertrophic subaortic stenosis?
- dyspnea
- angina
- dizziness
- sometimes asymptomatic until sudden death during strenous exercise
what causes sudden death in idiopathic hypertrophic subaortic stenosis?
- aortic outlet becomes occluded as a result of muslce contraction
- infective endocarditis of the damaged mitral valve and a fib can also occur
define hypertrophic cardiomyopathy
- aka idiopathic hypertrophic subaortic stenosis (IHSS)
- aka hypertrophic obstructive cardiomyopathy
- hypertrophy
- abnormal DIASTOLIC filling
- 1/3 of cases: intermittent ventricular outflow obstruction
what do you see morphologically with idiopathic hypertrophic subaortic stenosis?
- disproportionate thickening of the ventricular septum
- endocardial thickening or mural plaque formation in the left ventricular outflow tract
what do you see histologically with idiopathic hypertrophic subaortic stenosis?
1. extensive myocyte hypertrophy
2. disarray of bundles of myocytes
3. interstitial and replacement fibrosis
what is the genetic cause of idiopathic hypertrophic subaortic stenosis?
- mutation in one of several genes that encode proteisn that are part of the sarcomere
- disease of force generation
what are teh basica physiologic abnormalities seen in idiopathic hypertrophic subaortic stenosis?
- reduced chamber size
- impaired diastolic filling of LV
- 25% of patients have dynamic obstruction to LV outflow
what do you auscultate for idiopathic hypertrophic subaortic stenosis?
- harsh systolic ejection murmur from outflow obstruction
what is cardiac amyloidosis?
- can appear with systemic amyloidosis
- deposits occur in the venrticles and atria
what are the different types of cardiac amyloidosis?
1. senile cardiac amyloidosis (SCA)
2. systemic senile amyloidosis with cardiac involvement
3. isolated atrial amyloidosis
what is monckeberg arteriosclerosis?
- aka medial calcific sclerosis
- disease of the elderly
- no inflammation
- no occlusion of vessel lumen
- ring like calcifications in the media of medium to small arteries
what is hyaline arteriolosclerosis?
- affects small arteries and arterioles
- thickens vessel walls
- luminal narrowing
- do not calcify
- associated with hypertension and DM
what is hyperplastic arteriolosclerosis?
- affects small arteries and arterioles
- thickens vessel walls
- luminal narrowing
- do not calcify
- associated with hypertension and DM
what are the two types of arteriolosclerosis?
1. hyaline
2. hyperplastic
what are the three symptoms you see in Wegener granulomatosis?
1. acute necrotizing granulomas of the Upper resp/lower resp tract
2. necrotizing or granulomatous vasculitis affecting small ro medium-sized vessels
3. focal necrotizing, often crescentic, glomerulitis