cardio Flashcards
acute mitral regurgitation findings
increased preload, decreased afterload, normal contractile function, increased ejection fraction, decreased forward stroke volume.
chronic mitral regurg
compsetaory LA enlargement allows the LA to recieve regurgitant volume at lower filling pressure, preventing pulmonary edema. volume overload also causes the LV to undergo eccentric hypertrophy which is good at first but eventually causes dysfunction of contractiliy
pulmonary hypertension clinical findings
question showed thickening of the RV.
progressive dyspnea
complication is cor pulmonale and right sided signs
pulmonary hypertensino causes
Pulmonary arterial hypertension (primary) - idiopathic (sporadic) - hereditary Pulmonary hypertension (secondary) -left heart failure - chronic lung disease ∨. or hypoxia - chronic pulmonary embolisms
pulmonary arterial hypertension histology
intimal hyperplasia and fibrosis, medial hypertrophy, and formatino of capillary tufts
severity of mitral stenosis
determined by (s2) a2-to-opening snap time
as things get worse and more stenotic, the left atrial pressure rises, this causes increased forceful filling of the left ventrile and a soon snap
complication of mitral stenosis?
right sided HF
most specific sign for LHF
orthopnea
what causes endocarditis on damaged valves?
damaged valves (eg MVP or rheumatic fever) cause turbulent flow.
This causes a sterile fibrin-platelet nidus to develop.
usually happens on the atrial surface of AV valves or ventricular surface on semilunar valves
bactermia of any cause can seed nidus
staph aureus can adhere to damaged or non damaged valves
vegetations become macroscopic
purpose of inverse relationship of hr and stroke volume
decrease heart rate? stroke volume increase helps maintain the cardiac output (because of increased filling)
what can worsen mitral regurgitation?
increased preload?
what can cause an s3?
functional mitral regurgitation in heart failure
what can make functional s3 go away?
dieuretic (lady had acute heart failure and murmur was gone the next morning)
what can cause rupture of the chrodae tindinae?
infective endocarditis or acute MI
what can cause infranodal (morbitz type II) second degree or third adegree av block?
LAD infarction
what would cause v1-v4 st evelations?
PROXIMAL lad
what causes v5 and v6
LCX dugh, but also possibly lead 1 and avl.
what would cause v1-v6 and possibly 1 and avl?
an occlusion of left main coronary artery
what would cause an increase in v1 - v2?
i think a distal lad?
what can cause s4?
it can be benign in elderly, just from age related decrease in ventricular compliance
the louder it is though, the more likely it is pathological
can be caused from long standing hypertension, or from restrictive cardiomyopathy
it is never normal in young adults, unlike the s3
secondary causes of MVP
marfarn
ehlers danlos
osteogenesis
what what demostrate severity of mitral regurgitation?
presense of an s3
large volume of regurgitant flow reenters the left ventrilce causing s3
so heart failure can lead to mitral rerurgit -> s3
or mitral regurgi can cause s3 by itself
a man with chronic stable angine and s4, with echo showing hypokinesia and has lvef 35 percent. undergoes cabg -> 10 days after surgery increased LVEF. Cause?
Hibernating mycocardium
myocardium decrease their metabolism, etc to prevent necrosis but comes at cost of lost contractility
transient MI iscehmia in experient shows increase in cell size. why?
because increase in na and c due to failure of the na k atpase and sarcoplasmis reticulum ca atpase.
increased ions draws in free water
a woman with chronic atypical chest pain has near total occlusion of LAD, why no necrosis?
collaterals that could form due to slow growth rate
important factors in determintation if a plague will rupture
thin fibrous cap, rich lipid core, active inflammation (macs release metalloproteinases which degrade collagen)
thoughts on diastolic dysfunction
you have decreased co in both systolic and decrease, i think BB was trying to say its just the worse component in diastolic is the increased LVEDP and volume.
Remember PV loop cv physiology.
So the heart cant fill, lower preload, lower stroke volume, even though the heart contractility is normal.
I think these mechanics are true for restrictive cardiomyopathies, contrctive pericarditis (uworld q gave me all this thinking), and tamponade
pathogenesis of atheroscleoris
fatty streak to fibrofatty atheroma
begins with endothelial dysfunction from various causes (next card)
leads to increased permeability and monocyte/lymphocyte adhession and migration into intima. endothelial denudation allows for platelets to adhere
growth factors from monocytes and platelets stimulated SMC migration and proliferation into th eintima
increased permeability allows LDL to come in and be phagocytosed by macs and smcs to become foam cells
chronic infallmatory state of macs/lymphocytes with cytokine release maintains things
foam cells die, release their lipid contents (inlcuding oxdized ldld) into extracellular matrix.
endothelial insults in atherogenesis
HTN (hemodynamic) hyperlipidemia smoking diabetes homocysteine
toxings (alcochol)
viruses
immune reactions
BMPR2 mode of inheritance
AD
features of PAH
i
first insult is inheriting BMPR2
second insult involves
ncreased endothelin (vasoconstrictor)
Decreased NO (vasodilator), and prostacyclin (vasodilator and platelet inhbitor)
get dyspnea and fatigue -> cor pulmonale which results in exertional angina and typical right sided failure symptoms
why would you get pulmonary htn in obstructive sleep apnea?
hypoxic vasconstriction
patient with murmur and bilateral knee swelling as a kid
mitral regurge and had rhematic fever as a kid
a man has a stemi with II, III, and avf elevations. he has clear lungs on ascultation and has persistent hypotension and JVD … whats going on?
Key to spot this. II, III, avf with clear lungs and persistent hypotension
This man as a LV inferior wall myocardial infarction that is complicated by RV infarcation (can occur with inferior infarction).
Lungs are usually clear unless major LV dysfxn too (more common with LAD)
Even though the heart has plenty of contractility, RV dysfxn has caused decreased LV preoload. Also RV dilation and increased RV diastolic pressures cause bulge of the interventricular septum, further imparing output.
Swan ganz would show decreased PCWP and increased CWP accompanied by decreased CO.
I think an inferior infarcation without RV infarction would have similar swan ganz as LAD infarcation but not as severe because inferior doesnt cause severe LV dysfxn usually.
LV anterior wall infarct (LAD) -
much more liekly to causes LV systolic dyfxn than inferior infarct.
Causes decrease CO, elevated left sided filling pressures (PCWP increased), and pulmonary edema (crackles on ascultation).
initially the central venous pressure may be normal, but persistenly elevated left sided pressures may lead to right sided heart failure and causes elevated central venous pressures.
take note of septic shock
said increased CO and decreased PCWP and CVP is characteristic of septic shock (distributive)
when does tricuspuspid close on JVP tracing?
Fa makes it look like in trough between a and ac wave
BB said at C wave peak
calcifications and thickened pericardium on ct
contrstrictive pericarditis
constrictive pericarditis clinical features
progressive dyspnea, chronic edema, ascites (uworld pushed this with abdominal distenstion)
remember kussmall sign and jvd from BB
never mentioned decreased CO
So i am sure you get low CO in hypertrophic cardiomyopathy, restrictive cardiomyopathy, tamponade and diastolic dysfxn from htn, but unsure about constrictive pericarditis
a man on autopsy found to have enlarge left atrium, increase myocardial mass, and increased wall thickness. cause?
long standing HTN (aortic stenosis wasnt a choice)
could aortic stenosis left to diastolic dysfunction?
one more causes of eccentric hypertrophy
MI
one can happen to person with COPD?
get an acute exacerbation with pulsus paradoxus. (dyspnea, prolonged expiration, and bilateral wheezing, hyperinflated lungs and flattened diaphragm).
can causes pulsus paradoxus in the abscence of pericardial disease
what infiltrate in coagulative necorsis?
leukocytes and cellular digestion
hepatic angiosarcoma can be casues by and marker
arsenic, thorotrast, polyvinyl chloride.
cells express cd31
how can you test stress testing?
i think coronary artery vasodilation or by dobutamine
coronary steal phenomenon
i think its collateral microvessels forming between major major epicardial vessels (eg lad and rca).
Say lad is occluded, well it gains collaterals and the arterioles are already maximally dilated.
if you use a vasodilator the arterioles of the rca would become dilated and “steal” blood flow away.
Caused by “coronary arteriolar vasodilation.
more info about atherslcerosis
endothelial cell injury casues VCAM to be upregulated.
this allows monocytes and t lymphocytes to adhere to endothelium and infiltrate the intima.
endothelium platelets and leukocytes release factors like PDGF and FGF that recruit the medial smooth muscle cells
macs make metalloproteinases that degrade extracelluar matrix, causeing a large soft lipid rich core with thinning of the fribrous cap -> propensity to rupture.
three major causes of stenosis
bicuspid valve with calcifcation
normal valve with calcifiocation
rheumatic fever
when would you hear the high frequency sound in mitral regurg?
right as mitral opens on wiggers
not (mid diastolic) thats the low pithched rumble which doesnt sound mid to me
things that move calcium out of the cardiac mycote for relxation to begin
both the na/c exchanger and the ca atpase
what would make an aortic regurge pt more comfortable?
sleeping on their right side
stroke volume increased how in AR
enlargement of chamber and eccentric hypertrophy
precordial impulse in AR
hyperdynamic and displaced laterally and downward
how does heart get more o2?
by increasing flow because percent oxygen extraction really cant be increased much
so regulated mostly by local hypoxia and metabolites in FA, not sympathetics
heart failure principles
redcued CO leads to a temporary drop in BP with compensatory neurohumoral stimualtion (eg raas, sympathetics, adh)
good for cardiac response initially, meaintains BP for tissue perfusion, increased preload, chronitropy and inotropy. venous and arterial constriction.
bad in the long run though.
increased afterload impedes CO
RAAS casues fluid retention with peripheral and pulmonary edema (congestive heart failure)
deletreious cardiac remodeling due to hemodynamic (increased preload and afterload) and neurohormal stimulation (ang II, aldosterone, and catecholamine exposure)
how is s3 best heard?
left lateral decubitis at end expiration
why would a kidney appear shrunken compared to another kidney?
oxygen and nutrient deprivation from unilateral renal artery stenosis
increased risk with diabetes
swan ganz inc dilated and restrive cardiomyopathy
relatively similar increased in LVEDP and PCWP for different reasons. One systolic dysfunctino and the other is diastoli
a man has redness and pain in right arm, nsaids helps, mild lukocytosis
trousseau syndrome
hypercoagulable state due to thromboplastin like substance made by cancer cells (pancreas, colon, lung)
casued by superficial venous throbosis
chostocondritis features
usually occurs with repetitive activity
reproduced with palpation
pericarditis often foolows?
URI syndrome
differential diagnosis for chest pain: CAD
substernal
radiation to arm, shoulder, jaw
preciptiated by exertion
relieved by nitroglycerin
differential diagnosis for chest pain: pulmonary/pleuritic (pleurisy, pneumonia, pericarditis, PE)
sharp/stabbing pain
worse with inspiration
pericarditis: worse when laying flat
PE, pneumothorax: respiratory distress, hypoxia
differential diagnosis for chest pain: aortic (dissection)
sudden, sever tearing pain
radiates to back
eldery men
HTN and atherscleortic risk factors
differential diagnosis for chest pain: Gi/esophageal
nonexertional, relieved by antacids
upper abdominal and substernal
assoicated with regurgitation, nausea, dysphagia
nocturnal pain
differential diagnosis for chest pain: chest wall/msk
persistent/ and or prolong pain
worse with movement or change in position
often follows repetitive activity
an iv drug user develops aortic valve endocarditis and devlops a fistula form the aortic root to venctricle. what is blood flow pattern?
continous flow from the aortic root to the right ventricle
pressures always higher on the left side!
see swan ganz diagram if confused
in eldery why does the aortic valve become calcified?
its due to the hemodynamic stress causing cell necrosis and dystrophic calcification
what is aortic sclerosis
signs like benign calcified aortic valve (not stenosed but can progress)
pericardial inflmmation overlying the necrotic segment of myocardium post mi
pericarditis is a reaction to the transmural inflammation
inflammation affects the adjacent and parietal pericardium
localized to that area, extension of the inflmmation
treat with 1 to 3 days of aspirin therapy
pericardial inflammatino due to autoimmune reaction to necrotic tissue post mi
dresslers
leukocytocis can be seens
diffusely inflammed tissue
treat with aspirin nsaids and or glucocorticoids
a cause of restrictive cardiomyopathy you didnt know
transthyretin
what determines LV end diastolic pressure?
the amount of blood in the chamber and the compliance
features of diastolic heart failure
uworld certainly acts like LV end diastolic volume would be normal, but i would think it would be decreased at least a bit leading to the decreased stroke volume and CO -> leads to all the activation of sympathetics and adh and raas
causes of edema in both types of heart failure
one you have fluid backing up into the pulmonary and systemic circulation, and two you have increased ecf from RAAS
diastolic HF characterized by
normal LV ejection fraction, normal LV end diastolic volume, and elevated LV filling pressures
a man has sudden SOB and chest tightness. has a history of noncomliant htn. bibasilar crackles. bp is 195/115
htn emergency
treated with nitroglycerin mechanism -> myosin dephosphorylation
a diabetic taking lisinopril has try cough
give a sartan
man gets treated for afib and devlops lightheadedness, weakness, and presyncope.
he has sinus bradycardia, qt prolongation, self resolved torsades was cause of symptoms
he was on sotalol
his afib was giving him palpitations and chest pressure, and were paroxysmal. why he started the meds.
a woman gets pneumonia and then devlops hypotension and lactic acidosis. she is treated with norepi IV and tissues around IV blanch and become cold and hard. What should you inject?
the norepinephrine has extravasated and is causing intense alpha 1 effects
block with phentolamine
features of an aging heart
decreased ventricular size bcause decreased length. decreased length causes heart to take a sigmoid shaped with the basilar portion bulging into the LVOT. there is increased interstitial connective tissue (collagen), often with amyloid deposition. inside cardiac cells there is lipofuscin.
diagram showed enlarged left atrium
actions of ANP.BNP
Increased GFR, decrease proximal Na resorption, decrease renin secretion
skeletal muscle contraciton
apparently there is still some influx of Ca and uworld called the channel L type, but said you didnt need the influx
systemic illnesses precipitatting atrial fib
heart failure, hypertension, hyperthyroidism
special waves in afib
fibrillatory waves (f aves)
high voltage QRS?
hypertrophy
adult type coartaction of the aorta complication
rupture berry of aneurysm -> both due to HTN and congenital association.
spontaenous ICH in adults
av malformation, ruptures cerebral aneuryms, abuse of sympathomiment drugs like cocain
epigastric pain and vomiting coffee ground emesis
peptic ulcer disease
person in hypovolemic shock physiology
increase in sympathetics and RAAS
increased contractilty and HR
contrstriction or arteriolar beds maintain end organ beds and causes cool extremities
constriction of veins helps maintain preload
increased Na and h20 resorption heps maintain volume
point of IV infusion in hypovolemic shock?
increase preload -> increase sarcomere end diastolic length -> stroke volume via frank starling
signs in hypotension
hypotension and tachycardia
other effects of IV saline ifusion in shock
no decrease hr, decrease renin levels, decrease tpr, decrease contractin velocity of heart (also because decreased sympathetics)
greatest difference between o2 in aorta and ??
coronary sinus
coronary circulation 3 special features copraed to other circulations
- perfused in diastole because the strong contraction (worst at subendocardium) contracts coronary vessels
- myocardial o2 extraction is very high
- therfore the only way to increase o2 because increased demand is through increased flow
a child has no mumur at birth but that you can hear it two weeks later. harsh holosystolic heard best at mid to lower sternal border
VSD (most common defect)
small vsds have murmur, takes time to show because the PVR has not increased yet. most close by themselves
large VSDs cause HF and failure to thrive and diaphoresis with feeding. usually have no murmur. can lead to eisenmenger syndrome
2 possible causes of systolic HF
ischemic heart disease or dilated cardiomyopathy
both lead to dilation is 1 or both ventricles
man has signs of HF dies, shows dilated heart, causes of problem?
systolic dysfunctin from either dilated cardiomyoapthy or ishmicc heart diseae
the point is you are supposed to be able to differentiate from hypertensive heart disease,, or HCM which would be diastolic problems
cor pulmonale findings
thickening of right heart with eventually dilation as the heart begins to fail
a man has a DVT and gets repurfused, he has a rise in creative kinase, why?
because of reperfusion injusry dmaging the cell membranes
cycle between RAAS and CHF
cant pump blood to kidneys to RAAS increased -> increased TPR and less blood flow to kdineys. Viscious cycle
also increases water retention increasing preload and worsening CHF
remember sympathetics are going too
both left and right HF ultimately lead to
decreased CO
a man is describe as having aortic stenosis, a month later he comes back and has bad hypotension and pulmonary edema, what happenes??
Afid happened, these patients need the atrial quick because of their concentric hypertrophy. without it in afib they get pulmonary edema and hypotension (acute onset HF)
need cardioversion
explain why the RVOT is most important in determining the severity of tetraology of fallot
its because the increased resistance to flow pushes deoxygenated blood from the right ventricle to the left ventricle
tet spells are caused by the same thing, but are a sudden increase in RVOT
a man with COPD has some right venricle dysfxn and increase in CV but not peripheral edema, why not
lymphatics are compensating
causes of non inflammatory edema
- elevated cappillary hydrostatic pressure (CCB, venous thrombosis, right sided HF)
- Decreased ocotic pressure - nephrotic syndrome, sever liver disease, malnutrion
- Na and water retention - increases hydrostatic pressure and decreased oncotic pressure. occurs in acute and chronic kidney problems, congestive HF
- Lyphmatic obstruction - filriasis, invasive malignancies, iatrogenic etiologies (lymph node dissection)
a man dies and heart has intracytoplasmic granules that are tinged yelloweish brown
lipofuscin is the product of free radical injury and lipid perodidation.
frequency of atherosclerosis
abdominal aorta > coronary arteries > popliteal arteries > internal carotids > circle of willis
a woman had fatigue, malaise, low grade fevers and devlops sudden onset right side weakness and pseech difficulty
embolic stroke from sub acute endocarditis
remember major cause is MVP with regurge in US and rheumatic fever is still important cause in devloping nations
an afib what determines rate of ventricular response?
av node refractory period
libman sachs endocarditis (verrucous endocarditis)
to me same thing, just means larger sterile platelete thrombus.
most often associated with SLE and antiphospholipid syndrome i think
is a subtype of NBTE (marantic endocarditis)
NBTE
associated with malignancy (mucinous), autoimmune (sle, antiphospholipid), and sepsis (dic)
paltelet rich thrombi with strands of fibrin, immune complexes, monouclaear cells (whit thrombus). no nacteria
more likely to embolize and cause infarction
a woman has a feeling of heaviness in her veins when standing still for long periods. works as a cashier for 20 years
varicose veins and she is at increased risk of skin ulcerations
risks include standing, age gretare than 50, and mulptiple pregancies
increased venous pressure causes lose of vein tensile strength and dilation -> incompetent valve -> further dilation -> vicious cycle
superficial venous thrmobosis that do not embolize but are painful, stasis dermatitis, skin ulcerations, poor wound healing, and superficial infections are all complications
stress uclers are venous stasis ulcers and occur over the medial malleolus
a man has multiple episodes of syncope and unle who died suddenly
passing out from the ventricular tachycarida and possible v fib, right?
uworld said torsdades can cause syncope, seizures, sudden cardiac death
congenital qt vs wolf
i remember something like wolf rarely causes vfib and death and congenital qt often does. do i remember this right?
typical cases of qt prolongation
family history of sudden death
young patient with reccurent “seizures” actually passing out from torsades
uworld said syncopes, seizures, sudden cardiac death
motor vechiles accident with blunt chest trauma causes?
cardiac tamponade
lupus thing
serositis: pleurisy, pericarditis, peritonitis
viral myocarditis vs pericarditis
both have ekg changes, one has pleuritic chest pain, i think the other has probably more heart attack like pain, myocarditis has elevated enzymes,
dilated cardiomyopathy is a late phase complication of viral myocarditis
tamponade is a complication of acute pericarditis, but ihave never heard of myocarditis causing that (u world agreed with me)
also can get either following an upper URI
feature of tamponade
tachycardia along with the hypotension, clear lungs
isolated systlic hypertension caused by?
increased arterial stiffening (aka decreased compliance) of the aorta and major vessels. seen in people over 60
ISH can also be seen in AR, anemia, and hyperthyroidism
a woman who has an MI with st elevations in v2-v5 dies on the 5th day…. what was the causes?
profound hypotension due to rupture of the free wall of the anterior ventricle (this is where it usually occurs) leading to hempericardium -> cardiac tamponase -> profound hypotension and shock
what would an inhibitor of the metalloproteinase neprilysin do?
increases natruetric peptides -> cauing diuretic, natriuetic, and vasodilatory effects
improves outcomes in HF
what does mitral regurgitation show on cathertization (wiggers)
V wave
what provides a major proliferative stimuli for the cellular components of an atheroma?
platelets, they adhere to the enothelium when it becomes dysfunctional.
the platelets release PDGF (also released by macs and endothelial cells) is chemotactic for smc
plaeteles also release tgf b that causes smcs to migrates and to make collagen
a man who has an MI dies one the way to the hospital, cause?
ventricular fibrillation
SCD can be caused by sustained VF/VT most often VF resulting in hemodynamic collapse.
Most common cause of death from SCD in the first 48 hrs following mi
ecg changes in MI
peaked T waves occur first (localized hyperkalemia), st segment elevation follows in minutes to hours, within hours to days can see q waves
an old lady has aortic stenosis, why?
extensive valve calcificatino with impaired leaflet mobility
a man is found unresponsive under a tree during a thunderstorm, he has fern lead pattern markings, what is the most likely cause of death
cardiac arrythymia
marfan syndrome people most likely to die from?
aoritc dessection
what causes the slurred upstroke in wpw?
preexcitation
type of tachycardia in wpw?
av rentrant tachycardia
age for aortic atenosis in bicuspid aortic valve vs senile calcific stenosis
50 vs >65
what does ANP ultimately do?
lowers BP
limits NA resorption in the PCT and inner medullary collecting duct
restricts aldosterone secrtion
aniamals have mexomatoud degeneration with pooling of proteoglycans in the media layer what are they at risk for?
aortic aneuryms or dissection. describing cystic medial degerneation where you get fragmentation of the elastic tissue in the media
factors that increase renin
dieuretics (volume depletion -> low flow), acei, arbs
a man buttons his shirt and has an episode of lightheadness, whats the problem?
he has carotid sinus hypersensitivity and has stimulated the glossopharyngeal nerve
a man who is 23 has sudden onset of palpitations that started at his desk. what is going on and how to treat
he has paroxysmal supraventricular tachycardia, AVNRT, treat with vagal maneuver (eg carotid sinus massage) to increased AV nodal refractory period
features of atrioventricular canal defect
failure of fushion of the endocardial cushionions causes ostium premum and vsd and a single av valve.
lots of left to right shunting, av regurgitaiotion leads to HF
small pulmonary emboli cause what kind of infarction?
small wedge shaped and hemmorahgic
a 23 yearold old man notes reccurent sever nosebleeds and is found to have spider like lesions on his oral and nasal mucosa, face, and arms what does he have?
osler weber syndrome (heriditary hemmorach talgatasia) autosomal dominant.
get telangistasia in the skin as well as the mcous membranes of the lips, orophrayxn, respiratory tract, and gi tract, and urinary tract
rupture can lead to epistaxis, gi bleeds, or hematuria
what should decrease when you exercise?
tpr (not systolic pulmonary pressure)
ecg in a 32 year old woman reveals a dilated coronary sinus, whats going on?
anything that increases right atrial pressure can dilates the sinus.
most common cause is pulmonary htn
a man has infective endofcarditis of the aortic valve and later gets aortic regurg but has no symptoms, why?
because its chronic sever aoritc regurg where there was long term increase in backflow and preload causing eccentric hypertophy which allowed for an INCREASE IN STROKE VOLUME.
pts with acute AR have a small ventricular cavity that cannot significantly increase forward stroke volume to accomadate for the regurg. leads to decline is CO and acute pulmonary edema
a man has HF, what would be higher in the pulmonary vein than in the pulmonary artery?
ATII
acetylcholine infusion during cardiac stress testing causes?
a reaction with arginine
cardiac manefestations in lupus
acclerated atherslcerosis and MI
small arteries (arteroiles ) and arterioles can also show vasculits with fibrinoid necrosis
libman sacks endocarditis
a man has left sided heart failure, why is there an increase in pulmonary htn
and vasoconstriction due to pulmonary venous constriction
fluid back up causes HTN and damage to the edothelium, get less NO and more endothelium, leads to increased vascular tone with increased smooth muscle proliferation (medial hypetrophy) and collagen and elastase deposition (intimal thickening and fibrosis)
diastoli heart failure values for lvedp, lvedv, lv ejection fraction
increased, normal, normal
said that the heart would have near normal CO and stroke volume with increased LVEDP -> gets transmitted back and causes symptoms
ishemic consequences in the myocaridum
when flow is occluded,
you get glycolysis and buildup of waste products (lactate)
the depletion of atp and build up of toxins (lactate) result in loss of contractility in about 60 seconds
within 30 minutes loss of contractile fxn is irreversible
if blood is returned before 30 minutes contractility will return but not immediately (myocardial stunning)
a 35 year old man has progressive signs of heart failure over the last two weeks. he had an episode of fever, runny nose, and myalgias recently. what would you find on echo?
dilated ventricles with abnormal systolic ventricular fxn
he has dilated cardiomyopathy in the setting of viral myocarditis
a man has a 2 month history of HF signs, you hear an s3, where best and what does it represent?
left lateral decubitis in the apex and represents increased left venrticular end systolic volume which occurs in left ventricular systolic failure
VERAMPMIL WOULD slow what in pacemaker cells?
the T type ca channels slowing spontaneous depolarization
would also block L type channels and in the cardiac myocytes this would cause decreased excitation contraction coupling
2 3 avf means?
most likely infarct in the inferior wall of the left ventricle
a man exercises, what is the critical thing limiting coronary perfusion?
the shortening of diastole
a man presents with flan discomfort and red urine. he recently had an iscehmic stroke. he has elevated ldh. urine microscopy shows many red cells. whats going on?
a fib
ldh represents cell necrosis
when does SCD happen in HCM?
while exercising
action of nitropreusside
balanced arterolar and venous dilator
so decreases lvedp (preload) and mean systolic intraventricular pressure (afterload)
because both of these happen stroke volume is maintained
a 22 yo female compains of worsening dyspnea and low grade fevers. SOB is worse when laying down. she has a low pitched mid diastolic rumble at the cardiac apex. ecg shows a large pedunculated mass. what would histoogy show?
scatterd cells within a mucopolysachharid stroma
can get CVS or embolic symptoms
a woman has mitral stenosis, what would indicate the aortic valve was involved too?
increased left ventricular diastolic pressure, which is normally normal or decreased in MS.
rhematic fevef involvement of aortic valve typically causes combined stenoiss and regurge both of which cause an increase in LV diastolic pressure
mitral stenosis by itself causes increased PCWP, pulmonary HTN, decreased pulmonary vascular complicance, right ventricular dilation, and functional tricuspid regurge.
dilated left atrium and or afib can promote thrombus formatino
cardiac amyloidosis
could be AL amyloidosis, mutated transthyretin (familial ATTR amyloidosis), wild type transerythtin (senile systemic amyloidosis)
histology would show amorphous and acellular pink material around normal myocardium
congo red stain clssicicaly shows apple green birefriengrence under plane polarize light
aortic stenosis in a 54 year old man caused by?
bicuspid aortic valve
a man has third degree heart block, what is causing the ventricle to fire
AV node
the SA node is causing the atria to contract
a boy who had a sore throat three months ago develops rapid irregular jerking movements in his face arms and legs, what is he at risk for devloping?
he has syndenham chorea (cross reaction with basal ganglia)
he is at risk for VALVULAR DISEASE
some features of kawasaki disease
- bilatersl non edudative conjuctival injection (erythema) (conunctival injection with no exudates)
- cerival lymphadenopathy
- fissured erythemaotus lips, strawberry tongue
- extremity changes: edema of the hands and feet, erythema of the palms and soles, deaquamtion of the fingertips
- rash: on extremities and spreads to trunk (centripitellay)
a man has a rupture of an atheroma and an MI, what enzyme would be active to have caused this?
increased in metalloproteinases secreted by MACs cause large necrotic core and small thin fibrous cap.
plaque stability most important factor is strenght of fibrous cap, not size
