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Flashcards in Cardiology Deck (248):

reliability of a test is quantified using
maximal when?

CV coefficient of variation. standard deviation of repeated measurements divided by the mean.
maximal when random error is minimal


another name for validity of a test



sensitivity vs specificity

ability to identify true presence of a disease vs ability to identify true absence of disease


S3 sound (frequency, mech, occurs when?)

low frequency sounds occuring just after S2
associated with increased left vent ESV. (sudden deceleration of blood)
occurs in left ventricular systolic failure. and mitral valve regurge.
normal in athletes and children and pregnant women


bulging of intraventricular septum

occurs in cardiac tamponade,
bulging of septum into left vent. allows for increased volume in r. vent to allow for more blood to flow in
during inspiration this causes pulsus paradoxus


aortic valve sclerosis vs stenosis

sclerosis causes murmur (mid systolic)
stenosis causes S3 sounds which is indicative of l. vent. failure



a iron-chelator that prevents doxorubicin cardiotoxicity


why is it easier to hear a heart sound at lateral decubitus position when pt fully exhales?

b/c the volume in lung is decreased and heart is closer to the wall


what are valsalva maneuvers and positional changes used for in heart sounds? what effect do they have on MR, MS, hypertrophic cardiopathy, and MVP?

to increase or decreases blood flow to heart. helps to distinguish between systolic mummers (aortic stenosis vs mitral regurg and mitral valve prolapse)

increase blood to heart (Valsalva release, supine)
aortic stenosis-increase in sound
mitral regurg/ hypertrophic cardiomopathy- decrease in sounds
mitral valve prolaspe- decrease in sound, and later onset of opening click (sudden tensing of cordae tendineae)

decrease blood to heart (Valsalva maneuver-bearing down. standing up)
cardiomyopathy increases in sound (b/c afterload is decreased and LV vol is increased)
aortic stenosis- decrease in sound
mitral regrug-decrease in sounds
MVP- increase in sound and earlier onset of opening click


mitral valve prolaspe vs mitral valve stenosis

both have opening sounds: MVP-opening click
MS-opening snap
MS-diastolic murmur and MVP-mid-sysolic murmur


what effect does inspiration have on heart sounds?

increase intensity of all right heart sounds


causes of subacute endocarditis? how do you differentiate the two
acute endocarditis-valve it prefers

subacute- enteroccoccus (after GI/GU procedures) and s. viridans (after dental procedures)
enterococcus can grow in salt and s. viridans is optochin resistant. also viridans causes damage to already abnormal heart valves (congential, or rheumatic fever-high pressure valves first (mitral>aortic>>>tricuspid))

acute-s. aureus (tricuspid)


pulmonary complication of s. aureus endocarditis

septic emboli in lungs=multiple hemorrhagic pulmonary infarcts. hemorrhagic b/c of dual bloos supply (pulmonary and bronchial arteries)


myocardial hybernation vs myocardial stunning

-ischemia-induce reversible loss of contractile function, reversible with reperfusion (CABG or ballon angioplasty)
-less severe form of hibernation- (recovers after hrs to days), repetitive stunning can result in hibernation


ischemic pre-conditioning

development of resistance to infarction by cardiac myocytes previously exposed to repetitive non-lethal ischemia


ventricular remodeling

increased hemodynamic load results in changes in mass, volume, and shape of heart


ECG changes and associated problems:
prolonged QT
high voltage in precordial leads
prolonged QRS
absent P waves/variable R-R
ST elevation

-torsade the pointes
-ventricular hypertrophy
-ventricular dyssynchrony-a common cause is bundle branch block
-atrial fib


which wall of heart forms most of the anterior border

right ventricle


brain natriuretic peptide

released from ventricles in response to high pressure. like ANP
both activate guanylate cylase cause increase in cGMP leading to vasodilation (decrease BP). can also cause diuresis/natriuresis


marijuana- active ingredient, receptor, effects (5), immediate symptoms (2), detection time

contains THC, stimulates cannabinoid receptors to produce mild euphoria with laughing behavior, slowed reflexes, dizziness, impaired memory, and short term memory loss
-immediate symptoms-rapid heart rate and conjunctival injection
-can be detected up to 30 days after use


neuro drug that causes

-GHB (gamma hydroxybutyric acid), opiate, or benzodiazepine use
-ketamine (NMDA receptor antagonist)


when can pts information be disclosed to others? what act is responsible for this rule? are there any exceptions?

only when there is documented permission from the pt (even to spouse, loved ones etc...)
HIPAA (health insurance portability and Accountability act)
only exception is if the pt with incapacitated.


treatment of coagulase-negative staph infections. why no penicillin?

vancomycin with or without rifampin or gentamicin due to widespread antibiotic resistance of S. epidermis


effect of class IC anti-arrhythmics on QRS duration and QTc vs class III

class IC (i.e. flecainide* and propafenone) "Can I have Fries Please?"
-potent sodium blockers that prolong QRS interval at faster heart rates (use-dependence)

-class III (AIDS- amiodarone, ibutilide, dofetilide*, and sotalol)
-block outward repolarizing potassium current and demonstrate reverse use-dependence (slower the heart rate the more the Qtc is prolonged) no effect on QRS-depolarization has already passed


prospective/retrospective vs case-control

prospective/restrospective-selecting a group of ppl determining exposure status and then looking for development of disease from present to future (prospective) or past to present (retrospective)

-case control- picking ppl with diseases (case) and ppl without diseases (control) and look for previous exposures


which muscle is an arm flexor that lies deep to biceps and overlies median nerve and brachial artery. innervated by which nerve?

coracobrachialis- innervated by musculocutaneous


name two places where ulnar nerve can be damaged

hook of hamate (Guyon's canal), pisiform bone of wrist
medial epicondyl of the humerus "funny bone"


side effect of long and short nitrates (nitroglycerin and isosorbie dinitrate)

headaches HA


ECG if pacemaker is SA node, AV node or Purkinje fibers

-normal ECG
-mismatch of P and QRS wave, normal QRS wave shape
-abnormal QRS was shape


long term and short term adaptation to volume overload in left ventricle (i.e.aortic regurgitation). not concentric hypertrophy b/c?

-long term=increased preload (end diastolic volume)
-short term=increase heart rate
-eccentric hypertrophy results in increased forward LV stroke volume, concentric hypertrophy is response to increased pressure overload


growth of new sacromeres in concentric vs eccentric hypertrophy

-parallel growth, creates net vent. wall thickening and reduces ventricular size (decreased EDV)
-series growth, creates dilation of chamber, increases EDV


cardiac anomalies associated with:
Downs,Turners, DiGeorge, Friedreich's Ataxia, Marfan syndrome, Tuberous Sclerosis, kartagener's, infant of diabetic mother, congenital rubella, fetal alcohol syndrome

-endocardial cushion defects (ostium primum ASD, regurgitant AV valves)
-coarctation of aorta
-tetralogy of Fallot and interrupted aortic arch (poor lower extremetry pulse like coarctation + respiratory distress, cyanosis, and congestive heart failure early in life)
-hypertrophic cardiomyopathy
-cystic medial necrosis of aorta (aneurysms)
-valvular obstruction due to cardiac rhabdomyoma
-sinus invertus
-transposition of great vessels
-septal defects, PDA*, pulmonary art stenosis


sequele of a fib in patients with aortic stenosi

pt with aortic stenosis rely on atrial contraction to contribute to left ventricular filling. impairment can lead to decreased preload, cardiac output, hypotension, increased left atrial pressure, and acute pulmonary edema


exercising causes what effect on stroke volume?

increases due to increased EDV which increases more forceful systolic contractions (Frank-starling mechanism)


how do you relate Ohm's law to fluid flow through an system of cylinders of varying cross sectional area (cardiovascular systems)

V=IR (velocity=current*resistance)

-Total flow=Flow velocity*cross sectional area=constant


If blood flow is inversely related to cross sectional area. Then why is blood flow through capillaries slower than blood flow through aorta?

b/c capillaries are arranged in parallel. even though there individual cross sectional area is smaller than aorta collectively they're cross sectional area is larger than aorta


guess the pathogen:
1) 34-year old female with known mitral stenosis develops low-grade fevers and negative blood cultures
2) 45-year old male complains of fatigue and extertional dyspnea after a tooth extraction
3) 62- year old female has a persistent fever after being diagnosed with colon cancer
4) 64-year old male with repeatedly negative blood cultures has small mitral vegetation on transesophageal echocardiogram
5)29-year old male with a persistent fever has tricuspid vegitations and tricuspid regurgitation on transthoracic ECHO

1) acute rheumatic fever
2) strep viridans
3)strep bovis
4) culture negative endocarditis (Bartonella, Coxiella, Mycoplasma, Histoplasma, Chlamydia, and HACEK organisms (hameophilius, actinobacillus, cardiobacterium, eikenella, and kingella)
4) IV drug user, S. aureus


name and describe action potential phases of cardiac muscle

phase 4: resting potential (diastole) -90mv determined by K+ ions
phase 0: rapid depolarization; voltage-gated Na+ channels open and Na+ rushes in
phase 1: initial rapid repolarization; associated with rapid closure of Na+ channels
phase 2: plataeu; distintive feature of cardiac muscle; opening of L-type dihydropyrindine-sensitive Ca2+ and closure of some K+ channels
phase 3: late rapid reploarization; closure of Ca2+ channels and opening of K+ channels


chromosome game
22 (2 disorders)

long arm deletion-22q1 (DiGeorge syndrome or velocardiofacial syndrome)
NF2 gene mutation neurofibromatosis type 2


what composes the superior and inferior borders of the cardiac sihouette on right side?

-middle is right atrium
-inferior is IVC
-superior is SVC


triad of cardiac tampanode. same triad as what pulmonary phenomenon? how to distinguish between the two?

hypotension, tachycardia, and elevated central venous pressure.
-tension pneunothorax
-pulsus paradoxus (systolic pressure drops more than 10mmHg on inspiration)


afferent nerve of carotid sinus vs aortic arch baroreceptors?

-Hering's nerve, branch of CN IX hypoglossal
-CN X vagus


histology of acute cardiac transplant rejection vs chronic

-acute: dense mononuclear lymphocytic infiltrate with cardiac myocyte damage
-chronic: scant inflammatory cells and interstitial fibrosis


psycahitry technique of empathy vs support

-expression of understanding pt's feelings, " walk in the patient's shoes"
-expressing concern in interest for patient, not claiming to understand how pt feels


antihypertensive drug useful for pts with reflex tachycardia

nifedipine-causes vasodilation which may result in reflex tachycardia


-low pitched holosystolic murmur that accentuates during maneuvers that increase afterload (handgrip maneuver)
-systolic ejection murmur that decreases during manuvers that increase afterload and preload

-VSD (increased flow from left to right side of heart)
-hypertrophic cardiomyopathy (b/c increase of a and p attentuate the outflow obstruction by increasing left ventricular volume)


gallstone in ileum (gallstone ileus) vs gallstone in cystic duct or common bile duct (both called choledocolithiasis)

-large gallstones (>2.5 cm) in small instestine due to fistula b/t bowl and gallbladder (cholecystenteric fistula) air in gallbladder and biliary tree, symptoms of small bowel obstruction
- biliary colic, jaundice, cholangitis (fever, RUQ pain, and inspiratory pause during RUQ palpation (Murphy's sign)). no air in biliary tree


definitions of PWCP, LAEDP, LVEDP, and LVPSP?

-pulmonary capillary wedge pressure- estimate of left atrial end diastolic pressure (LAEDP) b/c LAEDP can't be measured.
-LVEDP=l. ventricular end diastolic pressure. nearly equal to LAEDP.
-LVPSP= left ventricular peak systolic pressure. larger value than PWCP and LVSP


values of PWCP, LVEDP, and LVPSP in
-mitral stenosis
-aortic stenosis
-dilated cardiomyopathy
-restrictive cardiomyopathy
-cardiac tamponade

-PCWP (LAEDP) is larger than LVEDP. LVPSP is normal
-LVPSP is elevated. PCWP (LAEDP) and LVEDP can be elevated but remain equal
-LVPSP is decreased. PCWP and LVEDP are equal.
-causes diastolic dysfunction. both PCWP and LVEDP are elevated and equal.
-PWCP and LVEDP are elevated and equal


presentation of SLE (sex, age, 4), cardiac complication and presentation. not aortic dissection because

-20-40 women; malar facial rash, photosensitivity, arthralgias, and proteinuria
-pericarditis. chest pain that radiates to neck and shoulders, pain with inspiration, and relieved by sitting up
-can also cause non-bacterial endocarditis (Libman-Sacks endocarditis). wart like lesion on any valve. presents with heart murmur and no other symptoms
-occur in pts with HTN, Marfan's and Elher''s-Danlos syndrome. abrupt severe tearing chest pain that radiates to back


cardiac deformity seen in
-Marfan's and Elher's Danlos
-infants with respiratory distress syndrome

-bicuspid valve
-VSD, and ASD,
-MVP b/c these are connective tissue disorders


wide, fixed splitting of S2 is? leads to damage where? surgery is done to prevent what irreversible complication?
not RVH or R atrial enlargement because

-characteristic sound of ASD
-can lead to chronic pulmonary HTN and damage to pul vessels
-Eisenmerger syndrome is late onset reversal of l-r shunt (to right to left causing cyanosis) due to increased pulmonary HTN
-surgery can to close ASD can lead to prevention of permanent Esienmerger
-not RVH or RAE b/c these are reversible


homocystinuria can lead to what cardiovascular complication? when should you think of this condition. which a.a is essential in this disorder?

-hypercoaguability and premature atherosclerosis
-young child with acute MI and increased serum methionine levels
-cysteine become an essential a.a b/t of defective cystathionine synthetase (can't make cysthationine for csythionase to convert to cysteine)


anterior uveitis

an inflammation of iris and can be caused by infectious processes such as Herpes, syphillus, and Lyme


which microbe produces dextrans from glucose? purpose of the dextran? should use antibiotic prophylaxis when? in which pt pop?

virdans sterptococci
-this allows them to colonize host surfaces such as dental enamel and heart valves. also helps to bind to *fibrin and plts* (this is why damage is needed b4 they can bind to valves-this is not the case for staph aureus)
-use antibiotic prophylaxis prior to dental work in pts with valvular abnormalities


which catheters transverse pulmonary artery?

-Swan-Ganz cath


name locations of leads in biventricular pacemaker?

-first 2 are placed in right atrium and right ventricle
-last one is placed in coronary sinus in AV groove on posterior aspect of heart.


gift policy, exceptions, how to respond?

as a rule physicians should maintain a general policy of not accepting gifts of significant monetary value from patient or their families.
-one time time are exception if given altruistically (not from psych pt) (cards, photographs, cookies)
-be sure to give proper amt of respect and gratitude when declining a gift


causes of restrictive cardiomyopathies, dysfunction type vs causes of dilated cardiomyopathy, dysfunction type?

-LV diastolic dsyfunction. amyloidosis, sarcoidosis, mets, inborn metabolic errors
-systolic dsyfunction. infectious myocarditis, cardiotoxic agents (alcohol, doxorubicin aka adriamycin, danuorubicin)


vaginal adenosis-def, caused by what toxins?

replacement of vaginal squamous epithelium with glandular columnar epithelium
-occurs in female children of women exposed to DES (diethlystilbestrol)


congenital disorder associated with co-arctation of aorta? look for what other symptoms?

also look for streak ovaries, amenorrhea, infertility, short stature, webbed neck, and low posterior hairline.


majority of LV blood flow occurs when?

-during diastole
-only 10% occurs during systole


fate of 2nd brachial cleft

-aka pharyngeal grooves is obilterated in normal human developement.
-persistance leads to brachial cleft cyst usually at angle of manidble and forms draining sinus tracts to skin


fate of 3rd brachial arch

-gives rise to tissues innervated by 9th CN, stylopharyngeus muscle, portions of hyoid bone, and posterior 1/3 of tongue


4th brachial arch becomes?

tissues innervated by superior laryngeal branch of 10CN including most of muscles of soft palate and pharynx, posterior 1/3rd of tongue
-exceptions (tensor veli palantini- CN V 1st arch) and stylopharyngeus (CN IX 3rd arch)


septum transversum-def, give rise to, vestige structure, what grows into here?

-mesoderm tissue that extends ventral to the gut tube from umbilicus to pericardium
-gives rise to myoblasts that form diaphragm
-exists as a vestige as the central tendon of diaphragm
-liver grows into septum transversum as outpouching of embryonal gut


which receptor is responsible fore calcium efflux prior to myocyte relaxation? not ryanodine receptor b/c?

Ca2+ ATPase (active transport to sequestion calcium within the sarcoplasmic reticulum) and Na/Ca2+ exchange (no ATP needed ratio of 3Na+/1Ca2+).
-voltaged dependent Ca2+ increase Ca2+ levels after AP, and Ca2+ stimulates ryanodine receptors allowing for more release of Ca2+ into cytoplasm from sarcoplasmic reticulium


role of calmodulin

-indirect contributor to calcium efflux from cell
-binds and activates plasma membrane Ca2+ ATPase, which removes Ca2+ from cell using ATP.


In a pt with CHF and HTN use what drug for long term? not thiazide diuretic b/c?

-ACE I (inhibits ANG II mediated LVH and remodeling) or beta blockers
-not hydrochlorothiazide b/c ACE I is better. use HCT for acute treatment of CHF and PE for symptomatic relief.


endothelial surface glycoproteins

mediate binding of immune cells to endothelium and migration in between cells


subendothelial collagen and subendothelial glycosamionglycans-found where? activate what? complication?

form subendothelial cap over central core of atherosclerotic plaque.
-activate plts and contribute to rapid thrombus formation
-can lead to MI


what role does RAS have in CHF

-can exacerbate it by increasing activation of sympathetic output to raise arterial resistance (afterload) making it's harder for failing heart to pump blood to tissues.


image of LV pressure vs LV volume curve due to
-AV shunt from AV fistula
-increase in cardiac contractility
-increased afterload
-decreased preload

-SV is larger due to increased preload (max LV vol increases). also afterload is smaller so max LV pressure is smaller
-increased systolic pressure (curve has higher LV pressure max) and increased SV (Min LV vol decreases)
-skinnier loop b/c increased afterload (LV pressure max increased) but decreased SV (Min LV volume increases)
-LV max doesn't change and decreased preload max LV volume to decrease.


early systolic murmur best heard over left lower sternal border that is accentuated by inspiration

tricuspid regurgitation


best place to hear
aortic valve

-second right intercostal space at right sternal border
-second left intercostal space at left sternal border
-fourth left intercostal space at lower left sternal border
-fifth left intercostal space, medial to mid clavicular line


inheritance of familial htpercholesterolemia

autosomal dominant


presystolic sound immediately preceding S1

S4 gallop
-requires normal atrial contraction and results from rapid emptying of atrial blood into ventricle with reduced compliance


increased flow velocity through aortic valve

would tend to produce murmur of aortic stenosis. occurs during systole


during which phase are papillary muscles placed under increased tension?

-ventricular systole (after S1)
-not during diastolic ventricular filling


hyperkalemia + anorexia, confusion, changes in color perception (blurry yellow vision). not spironolactone

digoxin- causes hyperK due to inhibition of Na/K pump leading to indirect in inhibition of Na/Ca2+ exchanger/anitport.
spironolaction would cause hyperK but not all the other symptoms


toxicities of digitoxin and ways to treat them-what predisposes to dig toxicity?

-Cholinergic- nausea, vomiting, diarrhea, blurry vision,
ECG abnormalitlies (AV block, V tach T wave inversion, increased PR and decreased QT, ST scooping)
-note hypoK leads to increased risk of toxicity b/c K+ binding site is where digitoxin binds
-slowy normalize K+ (insulin, kayexalate), cardiac pacer, anti-digitoxin Fab fragments, Mg2+, oral activated charcoal (esp in case of attempted suicide)


most common site of aortic injury in
-syphilis, vasculitis, HTN
-places where injury doesn't usually occur

-aortic isthmus- connection between ascending and descending aorta distal to left subclavian art. b/c it's fixed.
-where right brachiocephalic art branches off ascending aorta
-where coronary art come off aorta and descending aorta


how can digitoxin lead to v tach and death

-delayed afterpolarizations-occur after complete repolariztion of cardiac myocytes in states of hyperexitabilty
-dig causes hyperexitabilty by increasing Ca2+ levels in cystoplasm


how does digitoxin decrease AV nodal conduction vs how it increases cardiac contractility

-by increasing parasympathetic tone through direct stimulation of vagus nerve
-blocks Na/K and indirectly blocks Na/Ca2+ leading to increased Ca2+


how does LV dysfunction lead to Pulm HTN?

-reactive vasoconstriction secondary to pulmonary venous congestion and endothelial dysfunction
-hypoxia induced vasoconstriction and obliteration of pulmonary vascular bed
-left to right shunt increases volumen of flow and pressure in pulmonary arteries


normal pressures of
-right atrium
-right ventricle
-pulmonary art
-left atrium
-left vent



administration of (which has best bioavailability)
-isosorbide dinitrate
-isosoribide mononitrate

-oral (low bio due to 1st pass metabolism)
-oral (low bio due to 1st pass metabolism)
-oral (best bioavailabilty abt 100% despite oral route). isosorbide 5 mononitrate is active metalbolte of isosorbide dinitrate


important a.a derivatives
-Arginine (2)
-Glycine (2)
-Glutamate (3)
-Histidine (1)
-phenylalanine (1)
-tryptophan (3)

-NO; aspartate + arginine=Urea
-+Succinyl CoA=heme; arginine + SAM=creatine
-GABA;glutathione; + apartate=pyrimidines; +aspartate+glycine=purines
-serotonin-melatonin; niacin; thyroxine and melanin


how is NO synthesized? precursor can be used to help treat?

-from arginine by nitric oxide synthase
-arginine can play an adunct role in treatement of conditions that improve with vasodilation, like stable angina


acute mitral regurg vs chronic mitral regurg

-near normal LA compliance curves, pulm edema and HTN
-adaptive increase in LA volume and compliance (curve rotates down), less likely to have pul HTN but increased risk for atrial fib and mural thromboembolism
-both can have lower extremity edema and fatigue and exhaustion


which factors are most important determinates of coronary blood flow? vessel type? which is most important

-NO (most important) in large arteris and pre-arteriolar vessels. smooth muscle relaxation by cGMP second messenger system
-adenosine (comes from ATP) vasocdilatory element in small coronary arterioles


which bac can ferment mannitol

S. aureus


mc cause of acquired valvular dis. (esp in developing countries)? agent responsible? prophylactic prevention

-acute rheumatic fever
-untreated streptococcal pharyngitis (group A strep)
-treatment with penicillins


strep pyrogens can cause which two hypersensitivity rxn

rheumatic fever (molecular mimicry of M protein), causes damage to all three layers of heart
-glomerulonephritis (not nephrotic disease)


which is best indicator of mitral stenosis severity? not diastolic murmur intensity b/c? how can presystolic accentuation of murmur be used?
vs what is best indicator of mitral regurgitation. not holosystolic murmur intensity because

-S2 to opening snap time interval (shorter=more severe)
-diastolic murmur "rumble" can increase however there are too many variables (thoracic antaomy etc...)
- (transvalvular flow with left atrial contraction) presence or absence (severe and indicates possible a fib)
-left sided gallop
-intensity does not correlate well with regurgitant vol as larger orifices often present with softer murmurs


B1 def vs B12 defiency

-thiamine causes Wernicke-Korsakoff syndome, wet or dry beriberi in adults
-pernicious anemia


classic presentation of B12 def

-older, mentally slow woman of northern European descent who is "lemon colored" (anemic and icteric) has smooth shiny tongue (atrophic glossitis) and demostrates a shuffling gait


-forms of beriberi and presentation

infantile- 2-3months of age. cardiomegaly, tachy, cyanosis, dyspnea, vomiting
-adult has two types (wet and dry)
dry: symmetrical peripheral neuropathy accompanied by sensory and motor impairments esp of distal extremities
-wet: neuropathy + cardiac involvement (dilated cardiomyopathy, CHF, edema)


ways to affect ventricle to increase coronary blood flow

decrease wall tension, by decerasing afterload (systemic art dilation) or decreasing LV vol by decreasing preload (venous dilation- more blood in venous vasculature)


what supplies blood to areas distal to occluded vessel?coronary steal-def, drugs that can cause this?

-collateral microvessels
-phenomenon in which blood flow in ischemic areas is reduced due to arteriolar vasodilation in nonischemic areas
-adenosine and dipyridamole


meds with negative chronotropic effects

-beta blockers, non-dihydropyridine ca2+ channel blockers (verapamil, dilitazem)
-cardiac glycosides (digitoxin)
- amiodarone and sotalol
-cholingeric agonists (pilocarpine, rivastigmine)


nifedipine vs verapamil (mech and uses)

-dihydropyridine calcium channel blocker. minimal effect on SA node and cardiac conduction. vascular smooth muscle vasodilator. HTN, angina (Prinzmental), Raynaud's phenomenon
-non-dihydropyridine Ca2+ channel blockers (verapamil/diltiazem) causes decreased contractility by decreasing amt of intracellular Ca2+available within cardiomyocytes. HTN, angina, and a fib/flutter


toxic effect of combined beta blockers and verapamil

-combined use of non-dihydropyridine ca2+ channel blockers (verapamil and diltiazem) and beta blockers (atenolol) can have additive negative chronotropic effects causing severe bradycardia and hypotension


describe phases of action potential and pacemakers 0,3,4

0-upstroke: opening of L-type (long lasting) dihydropyrine sensitive ca2+ channels and slow influx of Ca2+ into cell
3-repolariztion: opening of K channels and efflux of K+ ions from cells in conjunction with closure of L-type Ca2+ channels
-4-pacemaker potential: spontaneous depolarization and occurs due to closure of K+ channels, influx of Na+, and opening of T (transient) and L (long lasting) type Ca2+ channels


how do adenosine and acetylcholine affect AP in cardiac pacemaker cells

-reduce rate of spontaneous depolarization (phase 4) by activating K+ channels (prolonging K+ flow) and inhibiting L-type Ca2+ channels (prolonging time it takes to reach threshold)


milrinone-mech, administraiton mode, toxicity

phosphodiesterase inhibitor that increases cardiac contractility and decreases both preload and afterload. given IV so reserved for short term use. associated with increased mortality


which beta blocker in particular has been shown to slow progression of CHF and reduce all-cause mortality in pts

carvedilol non specific alpha and beta blocker (beta blockade slows vent rate (decreased HR activation) and decreases afterload (decreased renin release)


Frank starling effect

-cardiac function curve (CO vs RA pressure)
-as cardiac muscle is increasingly stretched the CO increases up to a certain point


effect on cardiac function curve
-chronic anemia
-excessive hydration
-acute hemorrhage
-changes in TPR

-sharp decrease in CO leads to decreased slope and maximal height of line (ROTATES curve down)
-increase in CO (to meet metabolic demand) leads to increased slope and maximal height of line (ROTATES curve up)
-SHIFTS venous return curve to left (decreased mean systolic pressure=x-intercept)
-shifts venous return curve to right (increased mean systolic pressure which equals x-intercept)
-leads to left SHIFT of venous curve (leaky vessels decreases mean systolic pressure) and increase slope and maximum valve of cardiac function curve (increase HR ROTATES curve up)
-TPR changes effect ROTATION of BOTH cardiac and venous return curves. mean systolic pressure is unchanged so the x-intercept doesn't change. if TPR is decreased CO and venous return increase to compensate. if TPR goes down then CO and venous curves decrease


when does coronary sinus dilation occur?

increases in right atrial pressure such as pulm HTN


left ventricle forms which border of the heart?
-right atrium?
-right ventricle?
-left atrium

-apex and left border of heart on frontal chest X-ray
-along with SVC forms right lateral cardiac border on frontal chest X-ray
-anterior (sternal) surface and majority of inferior border
-majority of posterior surface (nxt to esophagus)


values of SV, ESV, EDV, and EF in increased

-SV increases so ESV decreases, and EF increases, EDV doesn't change
-SV increases, EDV increases and EF increases, ESV doesn't change
-SV decreases, ESV increases, and EF doesn't change (in heart that's able to compensate with increased pressure), EDV doesn't change


drugs that act by
-lowering threshold potential
-slow diastolic depolarization
-shorten the action potential
-reduce refractory period

-Class I (sodium blocking) and IV (calcium blocking) anti-arrhythmic drugs raise threshold potential of cardiac fast and slow response tissue respectively
-verapamil works by decreasing ca2+ ion influx during phase 0 and latter part of phase 4 and by decreasing cardiomyocyte contractility
-class IB antiarr drugs (lidocaine, tocainide, and mexiletine)
-class 1A (quinidine) and class III (amiodarone)


changes in EKG related to:
-occlusion of RCA
-occlusion of LAD
-occlusion of LCX
-occlusion of epicardial art

-90% transmural ischemia (ST elevation in leads II, III, avF as well as possible node dsyfunction (bradycardia)
-anteroseptal transmural ischemia (ST elevation in leads V1-V4)
-transmural ischemia of lateral wall of left ventricle (ST elevations in V5 and V6 possibly in I and aVL)
-rare and would cause subendocardial ischemia (ST DEPRESSION)


appetite supressants can lead to increased risk of? cardiac changes? complication?

-extended consumption of appetite suppressants like fenfluramine or phentermine is associated with pulm HTN
-pulm HTN can manifest as dyspnea on extertion and progress to cor pulmonade with RVH
-sudden cardiac death


describe atrial fib EKG finding. what is responsible for ventricular contraction rate? not Purkinje system b/c?

-absent P waves replaced by chaotic fibrillatory (f) waves, irregulary irregular R-R intervals, and narrow QRS complexes (narrow b/c of tachycardia)
-AV nodal refractory period prevents all atrial impulses from reaching ventricles
-this does not assume pacemaker activity when SA and AV nodes are functioning properly like in atrial fib


drug assocaited with disturbed color perception. most serious toxicity.

-ventricular dysrhythmias


mech of heavy calcification in pts who recently died?

cell necrosis causes dystrophic calcification. not associated with high levels of calcium in serum


factors that determine whether or not a coronary artery plaque will cause ischemic myocardial injury (i.e myocardial necrosis and scarring)

-major determinant is rate at which it occludes involved artery
-slowing developing plaques allow time for collateral that can prevent necrosis
-on the other hand a thin fibrous cap, a rich lipid core, and active inflammation in atheroma would decrease plaque stability


what is most common cause of death in young healthy individual. not endocardial thickening and non-compliant ventricular walls because?

-ventricular fibrillation caused by hypertrophic cardiomyopathy
-this describes findings in restrictive cardiomyopathy (RCM) caused by idiopathic, fibrosis, amyloidosis, or hemochromatosis. usually leads to CHF, not v tach, which is most common cause of death


irreversible or reversible cell injury?
-myofbril relaxation
-desaggregation of polysomes
-mitochondrial vacuolization aka
-dissaggregation of nuclear granules aka and other examples
-TG droplet accumulation aka
-glycogen loss

only mitochondrial vacuolization is irreverisble b/c now mito can't make ATP
-disaggregation of polysomes is dissociation of rRNA from mRNA
-disaggregation of nuclear granules is pyknosis (nuclear shrinkage) other reversible signs in nucleus are karyorrhexis and karyorrlysis
-TG droplet accumulation is aka fatty change


how does carcinoid syndrome affect the heart vs plasma homocysteine? increased levels of what in urine indicate carcinoid syndrome?

-high levels of serotonin and bradykinin can cause fibrosis and with can progress to pulmonic stenosis and restrictive cardiomyopathy.
-high homocysteine levels can contribute to arterial and venous thrombosis and atheroscleorsis
-look for high levels of serotonin in blood and it's breakdown product 5,hydroxyindoleacetic acid in urine


why does carcinoid syndrome affect only right side of heart?

b/c lung monoamine oxidase inactivates serotonin and bradykinin


time after MI: name major light microscopic changes
-0-4 hrs
-4-12 hrs
-1-5 days
-5-10 days
-10-14 days
-2 wks-2 month

-minimal change
-early coagulation necrosis (hypereosinophilia), edema, hemorrhage (punctate), wavy fibers
-coagulation necrosis and marginal contraction band necrosis
-coagulation necrosis and neutrophilic infiltrate
-macrophage phagocytosis of dead cells
-granulation tissue and neovascularization
-collagen deposition/scar formation


define pulsus paradoxus? what causes it? how it is measured?

-decrease in systolic BP greater than 10mmHg with inspiration
-acute cardiac tamponade, constrictive pericarditis, severe obstructive lung disease and restrictive cardiomyopathy
-inflating blood pressure cuff above systolic pressure and slowly releasing it. as cuff pressure is reduce Korotkoff sounds are first heat during expiration and then become audible during all phases. inspiration causes an increase in expansion in right ventricle but should have no effect on left ventricle. if a pt has cardiac tamponade then increased right ventricular pressure will push IV spetum into left ventricle resulting in decreased left heart diastolic vol and SV leading to decreased systemic blood pressure during inspiration=pulus paradoxus


COPD like asthma can present how and lead to what cardio complication? treat immediate symptoms with? why not cortocosteroids antihistamines b/c?

-shortness of breath, prolonged expiration, and prominent wheezing
-pulus pardoxus (b/c of increased cardiothoracic pressure)
-beta blockers for immediate relief (causing bronchial smooth muscle relaxation by increased cAMP)
-not steroids b/c they take hours to a few days to take effect
-antihistamines are not effective in bronchodilation just prevent hypersensitivity rxn


which drugs are useful in ischemic myocardium and post MI arrhythmias? what about ventricular tachy

class 1B (lidocaine and mexiletine)
-bind rapidly depolarizing and depolarized cells. ischemic myocardium is depolarized tissue.
-amiodarone has replace lidocaine in the management of v tachycardia


gross appearance of dilated cardiomyopathy or ischemic heart disease due to CHF
-diastolic dysfunction due to HTN
-hypertrophy cardiomyopathy

-look for dilation* of 1 or both ventricles, systolic dysfunction.
-look for concentric ventricular hypertrophy (all walls increased) and decreased left vent chamber size*
-look for asymmetric SEPTAL wall hypertrophy (greater than 1cm)* and outflow tract obstruction. also diastolic dysfunction


thiazide diuretics cause high levels which lipoprotein? not HDL?

LDL not HDL!, increased LDL leads to increased cholesterol*


why does MVP murur decrease with increased preload or afterload? why can sound of murmur increase with increased afterload when usually it decreases?

-both cause increased LV VOLUMES
-this causes leaflets to more to a more normal arrangment which allow proper closing of valve
-with severe MVP murrur is more holosystolic and increases with afterload b/c of higher LV PRESSURE however normally it decreases b/c of increase LV VOLUME


mc cause of MVP in developed? other 2 causes?

-sporadic myxomatous degeneration of mitral valve
-Marfan's and Ehler's Danlos
-both of these can lead to stretching and elongation of valve leaflets and chordae tendineae by chronic hemodynamic stress


papillary muscle dysfunction, ischemia, or dilated cardiomyopathy lead to what mitral valve problem?

mitral regurg?


inspiration has what effect on murmurs on right and left side of heart

-increases venous return to right side of heart. increases right sided murmurs
-decreases venous return to left heart and lift sided murmurs decrease


valsalva strain phase and abrupt standing have what effect on preload and afterload, which murmurs increase and which decrease?

-decrease both preload and afterload
-MVP and HCM increase (decreased LV vol)
-most other murmurs decrease b/c of decreased flow through stenotic or regurgitant valve


what effect does squatting have on preload and afterload? what abt passive leg raise? murmurs that increase and one that decrease?

-increases both after and preload by leg raise increases just preload
-both cause most murmurs to increase (through increased flow through stenotic or regurgant valve)
-both cause MVP and HCM to decrease b/c of increased LV volume


what effect does handgrip have on afterload and preload? murmurs that increase and murmurs that decrease

-increases afterload
-AR, MR and VSD all increase (increase LV and aortic pressures)
-HCM decreases b/c of increased LV volume
-AS decreases b/c of decreased transvalvular pressure gradient


why is skeletal muscle resistant to effect of calcium channel blockers?

-b/c it doesn't require an influx of extracellular calcium for excitation-contraction coupling
-cardiac and smooth muscle does depend on extracellular ca2+ to enter through voltaged gated L-type ca2+ channels-RyR mechanical coupling which is target of drug like verapamil


where are t-tubles found?

in skeletal and cardiac but not smooth muscle


def epitopes

-antigenic determinants
-human and bacterial epitope homology can lead to damage of "self" organs and tissue in an attempt to rid body of disease
mechanism of rheumatic fever


coronary art aneurysm-disease, presentation, treatment

sequela of Kawasaki disease (mucocutaneous lymph node syndrome)
-high fever, palmoplantar (hand foot) erythema and perlungual desquamation, oral muscosa "strawberry tongue" conjunctival inflammation, and cervical lymphadenopathy
-give aspirin even though child has flu like illnesses


number of phases of action potential in cardiac myocytes vs pacemaker cells. which phases do antiarrhythmics affect?

-4 phases (0,1,2,3,4) vs 3 phases (4,0,3)
-just the pacemaker ones, 4,0,3
-class 1 affects phase 0,
-class 3 affects phase 3
-class4 is affected by calcium channel blockers


when does loss of cardiac contractility occur after total ischemia? when can blood be restored? when injury irreversible?

-occurs within 60 seconds after onset of total ischemia
-less than 30 mins leads to restoration of blood flow (from ATP conversion to adenosine-vasodilator) which causes stunning as contractility gradually increases
-after 30 min injury is irreversible b/c adenosine stores depete


supine hypotension syndrome

-pregnant women >20wks gestation can experience compression of IVC by gravid uterus while in supine position
-reduces venous return, CO and can cause hypotension and syncope


where are beta 1 receptors found

-cardiac tissue
-renal juxtaglomerular cells
-not on smooth muscle (vs beta 2)


most common cause of hypertrophy cardiomyopathy vs causes of dilated cardiomyopathy. histological apperance

-60-70% of cases are familial, autosomal dominant (a beta-myosin heavy-chain mutation). look for large transeverse diameter of myocytes and haphazardly arranged myocytes and myocyte bundles with fibrosis
-ABCCCD (alcohol use, beriberi, coxsackie A, cocaine, chagas, doxorubicin, hemochromatosis and peripartum cardiomyopathy). nothing specific in particular however more of these causes are associated with an immune response so look for mononuclear cells and eosinophils, lymphs etc...


which antarrhythmic drug has both beta-adrenrgic and class 3 properties

sotalol. it prolongs both PR (atrial repolarization/conduction delay through AV node) and QT (period of ventricular repolarization as ventricles prepare for next beat) and causes bradycardia (beta blocker)


left ventricular outflow obstruction in hypertophic cardiomyopathy is caused by. murmur type? not aortic valve cusp and IV septum because

-causes a harsh holosystolic murmur.
-abnormal systolic anterior motion (SAM) of anterior leaflet of mitral valve towards a hypertrophied IV septum
-deform, fused, or calcified aortic valve cusp leads to aortic stenosis (crecendo-decresendo murmur). this is not associated with asymmetric septal hypertrophy


explain difference b/t murmur of VSD and hypertrophic cardiomyopathy

-both cause harsh holosystolic murmur
-VSD is heard best at tricuspid
-HCM is head best at left sternal border


triad of pericardial tamponade. association with acute MI

muffled heart sounds, elevated JVP, and profound hypotension
-can be caused by rupture of ventricular free wall 3-7 days after MI after coag necrosis, neutrophils, and enzymes have weakened the myocardium


ventricular septal rupture vs free wall rupture

-left to right shunting
-cardiac tamponade


compare and contrast dobutamine and nitroglycerin (myocardial oxy consumption)

-selective beta 1 with some alpha 1 and beta 2 activity. main effect is to increase contractility and O2 consumption
-nitroglycerin reduces myocardial oxygen consumption by decreasing preload via smooth muscle relaxation. can cause reflex tachycardia (b/c which would increase oxy consumption so treat this with beta blockers)


phase that class 1 drugs act on

-phase 0 and 3. increases AP duration and effective refractory period
-only in very fast depolarizing cells. decreases AP duration
-phase 0 only. increase refractory period in AV node minimal effect on AP duration


when is supravalvular stenosis seen

-mental retardation, peculiar facies, and systolic murmur from birth


presentation of severe aortic stenosis, best heard, mc cause presents when? bicuspid aortic stenosis presents when? what can cause mixed AS and AR? what can cause AR?

SAD (syncope, angina, and dyspnea)
-heard best at right second intercostal space and may radiate to carotids
-mc cause is senile calcific aortic valve degeneration in 7th decade vs
-calcification caused by bicuspid aortic valve which presents in 6th decade
-rheumatic fever
-infective endocarditis


fatality rate of lighting injuries, mc cause of death, why is thorough review of systems necessary? name effects on cardiac, neurologic, dermatologic, musculoskeletal, and other organ systems

-25% fatality rate
-occurs within 1st hr and is due to fatal arrhythmias and respiratory failure
-b/c a minor cutaneous involvement can mask major internal injury
-CV: cardiac arrest, arrhythmias
-NEURO: peripheral nerve damage, seizures, confusion, respiratory arrest, autonomic dysfunction
-DERM: lichtenberg figures (erthematous cutaneous marks in fern-leaf pattern)
-M/S: rhadomyolysis, bone fractures, compartment syndrome
-Other: cataracts (late sequelae), ruptured tympanic membranes, curling ulcers


name five T's of cyanotic congenitial heart disease. noncyanotic congential heart diseases

-tet of fallot, tricuspid atresia, transposition of great vessels, truncus ateriosis, total anomalous pulmonary venous return
-ASD, VSD, PDA, and aortic coarctation (note* can cause lower extremity cyanosis though in infantile form)


name mnemonic for class I antiarrhythmics. what effect do they have on inhibition of phase 0? effect on length of AP

class 1A-double quarter pounder (disopyramide, quinidine, and procainamide)
class 1B is lettuce, tomato, mayo (lidocaine, tocainide, mexiletine)
class 1C-more fries please (morcizine, flecainide, proafenone)
-weak (B), intermediate (A), strong (C)
-prolonged (A), shortened (B) no change (C)


is it possible to change ventricular refractory period?

not this muscle has fixed absolute and relative refractory period. can only affect pace maker cells


paroxysmal suprventricular tachycardia presents how?, most common cause, treat (drugs, maneuvers)

-common dsyrhthmia that occurs in pts with no other heart disease (young person in ER with papilatations)
-mc cause is re-entrant circuit in AV node
-treat with adenosine
-can also use carotid sinus massage and Valsalva


why should nitrates and phosphodiseterase inhibitors never be used together to treat eretile dsyfunction?

-risk of profound systemic hypotension
-nitrates are converted to NO by vascular smooth muscle cells and NO increases cGMP leading to SM relaxation. cGMP is metabolized by phosphodiesterase and inhibits to PDE can causes vasodilation


which precursor protein can leads localized amyloidosis in
-cardiac atria
-thyroid gland
-pancreatic islets
-cerebrum/cerebral blood vessels
-pituitary gland
-systemic multi-organ amyloid deposition

-atrial natriuretic peptide
-islet amyloid protein (amylin)
-beta amyloid protein
-immune globulin light chain


mc cause of in hospital death due to MI? mc complication of treatment?

-LV failure/cardiogenic shock
-coronary art fibrinolysis can cause systemic bleeding


murmur of pulmonary regurg- increases when?, pitch?, best heard where?

-early diastolic murmur, decrescendo
-increases with inspiration
-high pitched
-best herd over left 2nd and 3rd intercostal space


3 holosystolic murmurs

-tricuspid regurg
-mitral regurg
-septal defects


murmur of PDA- best heard, maximal intensity, symptoms, mc pt pop (2)

-continuous murmur best heard in left infracalvicular region
-max intensity at S2
-usually asymp if small and detected incidentally
-premature pts and cyanotic congenital heart disease


which artery supplies most of diaphragmatic surface of heart? not acute marginal branches

-posterior descending artery from RCA (80-90% of the time) supplies inferior wall of heart
-acute marginal branches (from RCA) supply wall of right vent provide collateral circulation to pts with LAD occlusion


LCX supplies

-lateral and posterior superior walls of left ventricle via obtuse marginal branches


LAD artery supplies

-anterior 2/3 of IV septum (septal branches)
-anterior wall of LV (diagonal branches)
-part of anterior pap muscle


diseases of corynebacteria
transmission/symptoms/pt pop
immunization produces antigen against

-diphtheria by colonizing respiratory tract and secreting diphtheria toxin
-respiratory droplets/coaslesing pseudomembrane fever, cervical adenopathy/developing countries but rare in developed countries
-AB (a=active (protein inhibitor) and B-bind (allows entry into cell)) exotoxin that inhibits protein synthesis by ADP-ribosylation of EF-2
-myocarditis/CHF and neurologic toxicity
-diphtheria toxoid
-IgG antibody against exotoxin B subunit


ventricular end diastolic vol and left ventricular end diastolic pressure in diastolic heart failure vs systolic heart failure

-LVEDV is normal
-LVEDV is increased
-both have increased LVEDP


phase 0 in non pacemarker cell is mediated by what vs pacemaker cell. which is at a high resting membrane potential

-non pace: sodium
-pace: Ca2+ (note this is the same ion for phase 0 in Purkinje cells too)
-pace are at higher potential so fast Na+ channels are inactivated


what determines dose required to maintain a steady state? how to calculate?

-maintenance does=Cpss x CL/ [bioavailabilty fraction]


formula for
-half life
-maintenance dose
-loading dose

-CPss x CL/{Bioavailability fraction]
-Vd x Cpss/ [Bioavailability fraction]


how long does it take to reach steady state?
bioavailability of drugs given IV
affect of renal or hepatic impairment on loading dose? maintenance dose

-4-5 half lives
-loading dose doesn't change but maintenance dose is decreased


etiology and morphology of:
coagulative necrosis
liquefactive necrosis
fat necrosis
caseous necrosis

-ischemic injury/tissue arch is preserved (lytic enzymes are denatured). annucleated cells
-bacterial infections, CNS infarct/viscous liquid mass, pus, abscess formation, CSF-filled spaces
-acute pancreatitis/lipases, saponification (chalky-white deposits)
-tuberculous infection or fungal/cheesy tan-white gross appearance granuloma


nitroglycerin's primary action vs secondary action

-venodilators causing decreased cardiac work by decreasing preload (decreased venous tension)
-dilatory effects on coronary arterioles


head bobbing with each heart beat is characteristic of which type of valvular defect? presents how? aka

-aortic regurg- increase amt of blood being ejected out of aorta (large LVSV and large regurgant SV, and large pulse pressure)
-water hammer pulses, de Musset sign


carotid pulses in aortic stenosis (2)

'pulsus parvus et tardus" delayed and prolonged pulses
-systolic vibrations or carotid "shudder" thrill can also be present


which drugs cause vasodilation of arterioles over veins? major side effect? give what to counter them?

-hydralazine and minoxidil
-reflex tachy and edema (activation of RAS)
-usually give in combination with sympatholytics and diuretics to counteract these effects


mc cause of native valve bacterial endocarditis in 15-60 year old age group?



mitral annulus calcification-def, complication, age

-loss of sphincteric action of annulus
-can lead to mitral valve regurg
-females, over age 60


mc acquired chorea of childhood

-Sydenham chorea from rheumatic fever


delayed S1 can indicate

delayed closure of tricuspid valve caused by right bundle branch block


-splitting of S2 that does not change with respiration
-systolic ejection murmur accentuated by standing
-early diastolic decresendo murmur decreased by amyl nitrite
-late diastolic murmur eliminated by a fib

-hypertrophic obstructive cardiomyopathy. it's AS if the murmur is decreased with standing
-aortic regurg (increases vasodilation, leads to reduced systemic art pressure)
-mitral and or tricuspid stenosis


be able to identify nitroglycerin molecule


describe xray of acute LV failure with pulmonary edema

-cardiomegaly (heart >1 hemithorax in size)
-pleural effusions
-Kerley B lines
-increased vascular shadowing "batwing" peri-hilum patter (alveolar edema bilaterally)


which of the heart defects is considered a variant of normal in an adult pt? not fenestrae in membranous ventricular septum

-patent foramen ovale is present in 20-30% of normal adults.
-seen frequently but not normal (defect in part just beneath AV valves)


what is aPTT used to monitor

unfractionated heparin


what effect does chronic AV shunt have on cardiac output and venous return curves?

decrease in TPR causes increased CO curve and right shift of venous return curve


what causes increased Ca and Na in cells during cardiac ischemia?

ATP deficiency leads to failure of Na/K pump and Ca-ATPase


where along nephron does drug act?
-carbonic anhydrase inhibitors
-osmotic diuretics
-loop diuretics
-thiazide diuretics
-potassium sparing diuretics

-acetazolamide- PCT
-mannitol- Descending loop of henle
-furosemide-thick ascending loop of henle
-potassium sparing diuretics-Na+ channel blockers/aldosterone receptor antagonists (spironolactone)-collecting duct


abnormal prominent v wave indicates

-mitral regurg


kussmal's sign

-raise in JVP during inspiration when it should usually drop (think when you breath in blood comes in)
-seen in constrictive pericarditis


labetalol vs isoproterenol

-non selective beta and alpha blocker
-selective beta 1 and beta 2 agonist


% of plaque obstruction in
-stable angina

-more than 75%


sound due to left ventricular hypertrophy? beat heard?

S4- low frequency at the end of diastole
-can also be caused by restrictive cardiomyopathy


describe pathogenesis of nonbacterial hypercoagulability? similar to which other disease? not metastases because?

-involves a hypercoagulable state, this leads to marantic endocarditis (cardiac valve vegetations from procoagulant effects)
-similar to Troussaeu's syndrome (migratory thrombophlebitis) which can be induced by disseminated cancers that release procoagulants
-mets rarely affect valves and would more likely involve pericardium or myocardium


what do endothelial cells release to prevent plt aggregation? aka, mech, opposes what molecule

-PGI2 aka prostacyclin* from prostagladin H2 by prostacyclin synthase
-it vasodilates, inhibits plt aggregation and increases vascular permeability
-opposes thromboxane A2


most common cause of death in MI? not embolic stroke b/c?

-v fib
-mural thrombosis with thromboembolism can occur only after after 48hrs


mc cause of fatigue and new onset murmur? can lead to what renal complication? not endotoxin-induced renal tubular injury b/c?

-bacterial endocarditis
-acute diffuse proliferative glomerulonephritis secondary to circulating immune complexes
-gram neg bugs rarely cause BE and acute tubular necrosis would cause sepsis not glomerulonephritis


effect of cGMP on SM

causes relaxation by inhbiting myosin light chain kinase which leads to myosin light chain dephosphorylation


example of exogenous pigment endocytosis

-urban-residing pts inhale carbon or coal dust that is taken up by macs in lung parenchyma "anthracosis"


lipofusin-product of what process? see in which cells? which population? color vs color of melanin?

-product of lipid peroxidation
-accumulates in aging cells (esp in pts with malnutrition and cachexia)
-melanin is dark brown to black


what is deposited in valves cause by bacterial endocarditis? not fibrosis b/c?

-the vegetations are fibrin and platelets
-fibrosis is uncommon in developed countries and leads to endocardial thickening (not valves) causing restrictive cardio


differential cyanosis restricted to lower body in a child indicates vs whole body cyanosis? not coarctation of aorta b/c? look for what instead?

-PDA with late onset reversal of shunt flow (Esienmergers) vs tetralogy of Fallot with reversal of flow
-COA limits lower body exercise but doesn't cause cyanosis in children and adults. instead look for BP discrepancy or heart failure in neonates


thickening >4mm and calcification of pericardium on CT vs calcifications in aorta vs thickening of IV septum indicates? possible causes of 1st disease? not viral myocarditis b/c?

-constrictive pericarditis
-ischemic heart disease
-hypertrophic cardiomyopathy
-constrictive peri can be caused by radiation, surgery, and TB
-viral myo does not cause pericardial thickening


mc adverse rxn of verapamil

-constipation, gingival hyperplasia, and bradycardia (1-3 AV block)


how does drug induced lupus present? (antibodies) which drugs (top 3). pts at risk?

-new lupus symptoms
-anti-nuclear antibodies (ANA) and anti-histone antibodies
-NO anti-dsDNA vs actual SLE
-drugs include procainamide*, hydralazine*, and isoniazid*, mincycline and quinidine
-slow acetylators are at high risk b/c this is how procainamide to metabolized


pts taking maintenance nitrates need to adjust their intake how to prevent what?

have nitrate free period every day to prevent tolerance


drug used to provoke coronary vasopasm in pts with Prinzmetal's variant (angina)? not morphine b/c. how to treat?

-ergonovine-argot alkaloid that constricts vascular smooth muscle by stimulating both alph and serotonergic receptors
-morphine is a vasodilator (use to treat ischmic pain during acute MI)
-calcium channel blockers and nitrates


define Janeway lesions-location, disease, mech, pain, pt pop

-small erythematous, sometime hemorrhagic macules that appear on soles of feet and palms
-seen in bacterial endocarditis
-caused by septic microembolic to cutaneous blood vessels
-emboli are fragments of infected intracardiac vegetations
-painless vs osler nodules
-pt with fever, fatigue and new holosystolic murmur with blowing quality


when is a wave absent

pts with at fib b/c of no atrial contraction


what is treatment for overdose with beta blockers? name intracellular signaling protein?

-activated GPCR on cadiac myocytes, causing activation of adenylate cylase and raising intracellular cAMP. this leads to calcium release from intracellular store and increased SA node firing


name two common congenital long QT syndromes and difference b/t them
-serious complicaition

-Jervell and Lange nielsen. autsomal recessive
-also look for neurosensory deafness
-Ramano-Ward syndrome-autosomal D, pure cardiac, no neurosensory problems
-can lead to long QT causing torsades de point


describe use dependence, which class of drugs demonstrate this?

-higher rates of depolarization lead to increased sodium channel blockade
-this is due to channels spending less time in closed (resting state).
-use dependent drugs only bind in open (activate) and both closed (inactivated) states.
-class 1 antiarrhythimics, 1C>1A>1B (class 1C has highest affinity and great use dependence than class 1B)


closed (resting) vs closed (inactivated state)

-closed resting is period right after (2-5ms) the second closed (inactivated state) from here the channel can be open (activated again)
-closed inactivated state occur in two phases fast (occur by closing of bottom gate) and slow (occurs by closing of internal gate after repolarization), in this state an AP won't depolarize channel as a refractory period must occur first leading to closed (resting) state


fick's prinicple

-co=o2 consumption/arteriovenous difference
-venous content comes from pulmonary artery
-arterial content comes from arteries


CO calculation using Hb and BSA

-(135 x BSA)/ [(13 x Hb) x (SaO2-SvO2)]


wht is used to measure metabolic rate?

respiratory quotient; usually 0.8


order of arteries involved in atherosclerosis

abdominal aorta, coronary, popliteal, internal carotid, circle of willis
-or large elastic then large or medium sized muscular arteries


prussian blue stain differentiate. what type of cells are they if positive? aka indicates what disease?

-iron from lipofusin
-siderophages aka heart failure cells. mac with hemosiderin
-LVH failure


effect of beta blockers on EKG

-slow conduction through AV node
-causes PR interval longation


s. aureus presentation in IV drug abusers vs non IVDU

-both will experience shaking chills (rigors), high fever, dyspnea on extertion and malaise.
-right sided endo with septic emboli into lungs causing pulmonary abcess
-rapid decompensation, heart failure, sepsis, septic emboli to brain and other end organs


coffee ground hemesis

-GI bleed. coffee color is due to exposure to gastric acid causing heme oxidation


Aschoff bodies and Antischokow cells. define and condition found in? later replaced by?

interstitial myocardial granulomas, caused by enlarged antischokow cells
-found in acute rheumatic carditis
-contain plump macrophages with abundant cytoplasm and central, round to ovoid nuclei with central slender ribbons of chromatin
-later replaced by scar tissue


acute-onset, mid chest pain that decreases with sitting up and leaning forward and pt has normal BP is? not restrictive heart disease or cardiac tampanode b/c? look for what instead?

-acute pericarditis. mc form is fibrinous or serofibrinou. look for pericardial friction rub
-restrictive heart disease takes years to develop
-tampanode would not have a normal BP. also look for Kussmal's sign, 3rd heart sound, pulsus paradoxus


dilated cardiomyopathy is diagnosed how?

-by exclusion
-rule of other causes of CHF like pericardial ds, valvular defect, coronary artery disease, cardiac rhythm disturbances


% of DCM that's genetic? caused my mutations where?

-mutations in cardiac myocytes cytoskeletal proteins (dystrophin) or mitochondrial enzymes


scattered cells within mucopolysaccharid stroma, abnormal blood vessels and hemorrhaging. triad

-atrial myxoma
-mid diastolic murmur best heard at apex, positional cardiovascular symptoms (syncope and dyspnea), embolic symptoms and large pedunculated mass in left atrium


nitroprusside acts on which vessels? causes what change in pressure volume curve

-short acting balanced venous and arterial vasodilator
-decreases preload and afterload
-curve shifts to left and max pressure decreases without change in SV


neurapraxia and it's relation to ortner syndrome

failure of nerve conduction due to compression injury
-mitral stenosis causing LA dilation sufficient enough to impinge on left recurrent laryngeal nerve (hoarseness and vocal cord paresis)


when is murmur of AR heard loudest? where?

-in early diastole when pressure gradient between aorta and left ventricle is maximal
-left sternal border with pt leading forward at end expiration


risk of torsades de pointes with amiodarone vs procainamide

-both can prolong QT interval by slowing phase 3 of ventricular repolarization myocardium
however amiodarone has no risk while procainamide does


mc cause of mitral stenosis
mc cause of mitral regurg
-mitral calcinosis has what effect on mitral valve?
what about 3rd syphilis and RA?

-chronic rheumatic heart disease
-bac endocarditis
-rarely has any effect
-these also rarely affect cardiac valves


MI in setting of normal coronary arteries=

-coronary arteritis, (can be seen in Chrug-Strauss syndrome due to vascular necrotizing granulomas)
-hypercoagulability with acute thrombosis (caused by Libman-Sacks endocarditis from SLE)
-coronary vasospasms


libman-sacks endocarditis-def, ds association, mech, pt pop

-verrucous endocarditis
-causes small cardiac vegetation in either side of valve
-look for acute coronary syndrome in young pt with normal coronary arteries


morphologic changes of aging in heart

-decrease left ventricular chamber apex to base dimensions
-development of sigmoid -shaped ventricular septum*
-myocyte atrophy with interstitial fibrosis (collagen)
-accumulation of cytoplasmic lipfusion pigment
-concentric hypertrophy of LV


like in order from highest to lowest organ susceptibility to infarcts

-CNS, myocardium, kidney, spleen, and liver.
-b/c liver has dual/and or collateral blood supply


what is mc cause of death in acute rheumatic heart failure? not mitral stenosis b/c?

-severe myocarditis
-not stenosis b/c it's takes years to develop


role of cAMP in cardiac muscle? in smooth muscle? metabolized by?

-activates protein kinase A
-increases calcium levels in heart
-inhibits myosin light-chain kinase (leading to relaxation in smooth muscle)


Wolff-Parkinson-White syndrome-def, presents, triad on EKG

-an accessory AV conduction pathway (Kent's bundle)
-can manifest as a recurrent paroxysmal supraventricular tachycardia
-ventricular pre-excitation on EKG presents as shorten PR interval, delta wave at start of QRS complex and widened QRS interval


orthopnea- def and sign of

supine dsypnea relieved by sitting up
-sign of LVH



-degrades ANG II
-describes multiple blood and tissue enzymes


where is ACE found

in endothelium of lungs


mc cause of splinter hemorrhages- look for what on exam?

-microemboli from valvular vege of bac endo
-look for regurg murur


endomyocardial fibrosis with prominent eosinophilic infiltrate-ds and pt pop

loffler syndrome can cause restrictive cardiomyopathy


explain hemodynamic consequences of mitral stenosis
-increased pressure between left atrium and left ventricle
-left atrial pressure and vol
-pulmonary venous and capillary wedge pressures
-Pul HTN
-right ventricular pressure and vol, with eventual right heart failure

-severe stenosis can decrease left ventricular filling and CO
-promotes atrial fib and mural thrombus formation
-pulmonary edema and alveolar hemorrhage
-decrease pulmonary vascular compliance due to vessel constriction and obliteration
-tricuspid regurgitation, increased venous pressure and peripheral edema


bifid carotid pulse with brisk upstroke

-"spike and dome"
-hypertrophic obstructive cardiomyopathy