jdlevenson's version from 2015-06-21 02:56


MI/ Cell Injury
Question Answer
Final stage of MI/ injury process is collagen deposition, which happens () after MI and is what type of collagen2 weeks- 2months after MI and involves collagen type 1 (Type 3 for granulation tissue preceding it at 10-14 days)
Cartilege in bone marrow blood vessels and lymphaticsType 3
Ruptured LV free wall happens how long after MI3-7 days
Ruptured LV free wall happens as result ofCoag necrosis, neutrophil inflammation, and enzymatic lysis of connective tissue have weakened the infarcted myocardium (mean 4-5 days; range 1- 10). Transmural MIs.
Ruptured LV free wall results inPericardial tamponade. Recall this prevents venous return leading to systemic hypotension.
Rupture of chordae tendonaie associated withInfective endocarditis and MI
Diseases that cause myocardial fibrosisSarcoidosis, muscular dystrophy, dermatomyositis, and scleroderma.
Major determinant of whether or not a plaque will cause ischemic MI?Rate at which it occludes the involved artery; slower the rate, the more opportunity for collaterals that would prevent myocardial necrosis. Small anastomotic vessels progressively dilate.
What are intracellular signs of irreversible injuryVacuoles and phospholipid contiang amorphous densities within mitochondria signifies irreversible injury and permanent inability to make ATP via oxidative phosphorylation. HOWEVER, mitochondrial swelling** may be reversible.
Signs of reversible injuryMyofibril relaxation (corresponds with ATP depletion and lactate accumulation), disaggregation of polysomes, disaggregation of nuclear granules and clumping of chromatin, TG droplet accumulation (especially in hepatocytes), and glycogen loss (may be completely depleted within 30 minutes of onset of severe ischemia).
Most common cause of sudden cardiac death/ SCDCAD
SCD definitionCardiac arrest within 1 hour of precipitating event
During prehospital stage, most common cause of death from MICardiac arrhythmia, generally V. Fib (and V. Tach)
During in-patient stage, most common cause of death from MIVentricular failure/ cardiogenic shock, complicates 10-15% of cases.
After MI, patient can die from mural thrombi—when?48 hours after MI
After MI, when does ventricular free wall rupture happen 3-7 days -> cardiac tamponade, extracardiac obstructive shock, and if its interventricular, hypotension and biventricular failure
How quickly after onset of total ischemia will loss of cardiomyocyte contractility occur60 seconds.
Ischemic injury of <30 minutes to cardiac myocytes leads toMyocardial stunning; reversible contractile dysfunction with contractility gradually returning to normal over next hours and days SO NOT IMMEDIATELY RESTORED (and length of time before it is restored depends on how long the ischemia lasted). After 30 minutes, irreversible damage.
Within seconds of total ischemia, what changes in cardiac myocyteAerobic to anerobic; total ATP levels remain normal until during first few minutes of ischemia, though they are depleted from areas of high metabolic demand like ETC pumps.
Persistent ischemia leads to depletion of ATP and...Adenosine, the breakdown product and also from intracellular stores. After 30 minutes, adenosine 50% lost at which point it can no longer maintain homeostasis.
Myocardial hibernation vs stunningStunning is less severe, more acute form of ischemia induced reversible loss of contractile function (brief ischemic episodes <30 minutes following by reperfusion; recovery is over hours to days) whereas hibernation is chornic form with repetitive ischemia or persistent hypoperfusion leading to chronic but reversible loss of contractile function where myocardial energy metabolism may be reduced but there is sufficient ATP to prevent contracture; can recover with CABG or balloon and it may takes hours or even months
Ischemic preconditionDevelopment of resistance to infarction by cardiac myocyetes exposed to repetitive non-lethal ischemia.


Question Answer
Bicuspid heart valves associated withTurner syndrome. Turner syndrome is most associated with bicuspid heart valve; however, there may also be coarctation of the aorta.
Bicuspid heart valves have what riskStenosis, insufficiency and infection, particularly infective endocarditis from abnormal leaflet structure and turbulent flow.
Early systolic high frequency click over right 2nd interspace?Bicuspid heart valve; aortic ejection sound. As bicuspid progresses and calcifies, may lead to aortic stenosis*** and regurgitation.
Bicuspid aortic valve accelerates normal aging process so that aortic stenosis occurs in () instead of ()Occurs in 6th and 7th decade instead of 8th or 9th
PDA most associated withPremature infants, particularly those with Respiratory distress syndrome. It may also be seen in an infant with coarctation of the aorta and congenital rubella infection. And fetal alcohol syndrome.
Coarctation of aorta may be associated withPDA and or Berry aneurysms of Circle of Willis; berry aneurysms with coarctation are very prone to rupture because of HTN in the branches of aortic arch proximal to the coarct (including carotids)
Patients with adult type of aortic coarctation usually die fromHTN associated complications including LVF, ruptured dissecting aortic aneuryms and intracranial hemorrhage
Coarctation of aorta presentationLimited lower extremity exercise tolerance
PD of PDA derived from6th aortic arch
PDA leads to L-> R or R->L ?In utero, right to left. Necessary. In infants etc when pulmonary BP drops, left to right. And then, over time with resultant pulmonary hypertension and pulmonary vascular sclerosis, increased pulmonary vascular resistance and reversal of shunt flow -> back to RIGHT TO LEFT causing differential cyanosis.**
Differential cyanosisthink PDA post pulmonary vascular sclerosis, increased pulm vasc resistance and reversal of shunt flow across the ductus.
Why is PDA a problem?Left to right shunt -> progressive RVH and/ or LVH and then HF.
Left infraclavicular thrill and continuous machine-like murmurPDA. A/w congenital rubella infection and prematurity and fetal alcohol syndrome.
Older patient with PDA?Not PGE but surgical ligation.
Mid-systolic click and late systolic murmurMVP. Most common in general and especially among EHDS and Marfan.
MVP occurs fromElongation and redundancy of valve leaflets and chordae tendineae. Mid-systolic click is from sudden tensing of chordae tendineae as they pulled taut by the ballooning valve leaflets
Defects in mitral valve connective tissue proteins -> Myxomatous degeneration ->Stretching and elongation of valve leaflets and chordae tendoneae
Mid-systolic ejection murmur best heard over right intercostal spaceAS
Fixed splitting of second heart soundASD
Aortic stenosis causesAbnormal valve with calfication (like bicuspid valve), calficied normal valve or rheumatic heart disease. Calcified aortic valve is most common in US and results from degenerative/ senile calcinosis.
Aortic stenosis presentationAsymptomatic -> dizziness with exertion, syncope, dizziness, angina or heart failure.
Holosystolic murmur vs crescendo decrescendoHolosystolic – VSD vs Cresc-Decresc – AS.
Severe aortic stenosis can lead to what complicationsSevere hypotension and acute pulmonary edema; the concentric hypertrophy of LV decreases its compliance and makes it super dependent on normal atrial contraction for LV filling; without normal atrial contraction, LV filling can decrease to point of producing hypotension and then the acute pulmonary edema.
Severe AS and acute atrial fib, treatment?Cardioversion.
Rheumatic fever, in adults it commonly presents as? Whereas in children?In adults- MS and in children – MR
Rheumatic fever can lead to Sydenham chorea. How long after? If you have Sydenham chorea, then...1-8 months after and if so then increased risk of chronic rheumatic disease
Infective endocarditis, FROM JANEFever, Roth Spots, Osler nodes (ouch), Murmur, Janeway lesions (small macular erythematous or hemorrhagic nontender lesions on palms and soles) Anemia Nail hemorrhage (splinter or flame shaped) Emboli
What is cause of sydenham choreaAutoimmune reaction involving anti-streptococcal antibodies that cross-react with basal ganglia**
Oh snap I am a medical studentOpening snap at beginning of diastole- Mitral Stenosis
Best indicator of severity of mitral stenosis?A2 to OS interval. The higher the early diastolic LAP, the closer the OS will be towards A2. More severe the stenosis, higher the steady state LAP in eraly diastole and shorter the A2-OS interval. a
Shorter interval between A2 and OS for MS is more or less severe?More severe. Recall, OS is from the abrupt tensing of the valve leaflets as the mitral valve reaches its maximum diameter during forceful opening -> Pressure in LA will increase -> pressure causes the valve to open more forcefully, hence shorter interval.
Orthopnea is fairly specific for LHF but may also be fromMS*
Blowing systolic murmur heard best at cardiac apex with radiation to axillaMR
Mitral regurgitation, the amount of blood that goes to LV vs LA is dependent on...?Left Ventricular afterload. Vasodilators will decrease amount of regurgitant flow and so increase the forward-to-regurgitant volume ratio.
Chronic MR will lead to what adaptive changeIncreased compliance of LA from thinning of wall and dilation
Chronic MR (and resulting adaptations) leads to what new riskLess prone to pulmonary HTN and edema but more prone to AFib and mural thromboembolism
Rheumatic fever affects which heart valves the mostMitral > Aortic >>> Tricuspid (whereas for infective endocarditis, less likely in higher blood flow valves? ReVIEW)
ARF is caused by molecular mimicry; antigens on GAS/ M protein activates B and T cells that become autoreactive against homologous self-antigens in the heart and CNS.
Question Answer
Recurrent untreated strep pharyngitis will lead to...Faster onset and increased severity of rheumatic heart disease due to increase autoimmune activity.
S3, ventricular gallop, literally heard whenImbalance between force of blood rushing into ventricles and the ability of the ventricles to accommodate that blood flow; can occur (1) when force is really high and ventricular compliance is normal, (2) normal filling rate when ventricular compliance is low, (3) blood flowing into an overfilled ventricle with high end-systolic volume
S3 heard with what physical maneuverBELL of diaphragm since it’s a low frequency sound and in LEFT LATERAL DECUBITUS position and also listen when they exhale. Recall S3 -> left ventricular systolic failure.
Increase venous return will bring out (via valsalva release, laying supine)Aortic stenosis
Less venous return (valsalva, standing) will bring outHCM and or MVP
S3 is heard in some young patients and well trained athletes but in older patients it is pathologically a sign ofLeft ventricular systolic failure. Recall S3 occurs during diastole as atrioventricular valves open.
S4, end of diastole just before systole, fromDecreased left ventricular compliance (usually just associated with old age) and associated with restrictive cardiomyopathy and left ventricular hypertrophy, especially as the sound gets louder. Thought to correspond to atrial contraction and sound of blood striking stiff left ventricle.
S4 is always pathologic whenIn younger patients


Question Answer
S3 normal inChildren, young adults, pregnancy
S4 normal inHealthy older adults
S3 fromTurbulent blood flow to the ventricles due to increased volume; heard during rapid filling of ventricles in diastole; ventricular gallop**
S4 fromheard immediately after atrial contraction phase as blood is forced into a stiff ventricle; atrial gallop**
S3 pathology inage >40; HF, restrictive cardiomyopathy; high output states (thyrotoxicosis, pregnancy)
S4 pathology inyoung adults, children; ventricular HT; acute MI i.e. rise in end-diastolic pressure following atrial contraction
You can have mitral annular and aortic valve calcifications inSystemic hypertension