Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Cardio_Kaplan
| Question | Answer |
|---|---|
| Global measure of systolic function | Stroke Volume |
| Mitral valve stenosis associated with? | Rheumatic fever |
| Late diastolic rumbling murmur | Rheumatic fever - mitral valve stenosis |
| What is the cause of the scarring of the valves in Rheumatic fever? | M protein - Ag's similar to heart and joints so when make Ab's agnst Grp A strep, make Ab's against heart (own tissue) - Antigenic Mimicry |
| MC symptom in Rheumatic Fever? | Polyarthritis |
| MV valvular lesion in Rheumatic Fever? | Mitral Regurgitation (MS takes 10 yrs to develop) |
| High pitched blowing diastolic murmur in right 2nd ICS? | Aortic regurgitation |
| Long QT interval seen in what? | Torsades de pointes |
| How are afferent firing and HR related? | inversely - if decrease afferent firing, increase HR and vice versa |
| Positive rate of change of pressure? | isometric contraction |
| When is a sarcomere the longest and when is it the shortest in the cardiac cycle? | longest at end of diastole. shortest at end of systole. |
| Vessels that have highest drop in pressure? What is this due to? | arterioles - have highest resistance |
| How is velocity and cross-sectional area related? | inversely |
| What happens when CN 9 and 10 are stimulated? | decreases sympathetic tone and increases parasympathetic tone leading to bradycardia w/ hypotension |
| What causes the wide pulse pressure in arteriosclerosis? | decreased compliance - increase SBP and decrease DBP |
| What has the highest ratio of wall cross-sectional area to lumen cross-sectional area? | arterioles |
| What increases within an hour after exercise? | VEGF - for endothelial cells to survive |
| What happens when you remove a circuit from parallel resistance? | increase total resistance of circuit |
| Net filtration pressure eqn? | (Pc-Pi) - (Pi c - Pi i) = (cap hydrostatic - interstitial hydrostatic) - (capillary osmotic - interstitial osmotic) |
| What changes occur when a kidney is removed? | increase TPR, no change in arterial pressure, decrease total RBF |
| Where is the mean linear velocity of RBC the lowest? | capillaries - low velocity allows time for oxygen to diffuse to tissues |
| What happens when the sympathetic nervous system is activated? | constrict veins and venules will increase MCFP (mean circulatory filling pressure) which will increase venous return and cardiac output |
| What's given for A fib. after initial stabilization (e.g. w/ Diltiazem) and initial anticoag w/ Heparin? | Warfarin |
| SE of metoprolol? | dyslipidemias (b1 receptor causes increase lipolysis) |
| What is a SE of WPW and A fib patients if give Digoxin? | Ventricular fibrillation |
| MOA of cocaine? | block reuptake of NE |
| SE and class of atenolol? | bradycardia and 3rd degree AV block - selective B1 blocker |
| SE of Doxorubicin? | Dilated cardiomyopathy |
| SE of Bleomycin? | Pulmonary toxicity |
| If a patient given drug X which causes increase BP and reflex bradycardia, then given drug Y which increases HR but not BP, then given drug X again and BP is increased without an increase in HR, what is drug X and Y? | X = alpha-1 agonist = NE (vasoconstricts causing increase BP with reflex bradycardia) Y = M2 blocker on heart = Atropine (increase HR but not BP) X again = will increase BP but no reflex bradycardia b/c of Atropine |
| What drugs can cause long QT syndrome? | class 1a and class 3 antiarrhythmics - also quinidine, procainamide, sotalol, amiodarone, disopyramide, dofetilide, phenothiazines, TCA |
| MOA of Amlodipine? | Class 4 CCB that inhibits calcium influx across vascular smooth muscle more than cardiac muscle |
| What happens when a patient is given Epinephrine then Phentolamine? | Epinephrine reversal - Epi (a1, a2, b1, b2) inc VC (a1) which inc BP. When given Phentolamine (a1, a2 blocker), b1 and b2 receptors enhanced causing VD (b2) which will dec BP |
| DOC for pregnant women with chronic HTN (DBP >100 mmmHg)? | Methyldopa |
| MOA of Digoxin and what used for? | decreases conduction through AV node and depresses SA node - treats A fib esp when vent rate increased and indicated for CHF and A flutter |
| Tx for atrial arrhythmias without evidence of heart failure? | BB (Esmolol and Metoprolol) and CCB (Verapamil and Diltiazem) |
| Tx for diabetic nephropathy and hyperuricemia? | ACEI - controls HTN and slows renal disease |
| Drug that will maintain PDA? | PGE1 analog Alprostadil |
| MOA of Minoxidil? | decrease SBP and DBP and opens K ATP channels on vascular smooth ms and pancreatic B cells |
| Lab findings for Niacin (B3) and SE? | decrease VLDL, LDL, TG and increase HDL. MC SE = facial flushing (tx w/ ASA) |
| MOA of Losartan? | inhibits Angiotensin II at ATI receptor (AT II = Na+ retaining hormone in PCT and DCT) --> increase renal Na+ excretion |
| MOA of Amiodarone? | class III w/ Ia properties - blocks K+ channels, prolongs repol, widens QRS, prolongs QT interval --> torsades |
| Amiodarone is used to treat? | refractory V. tach and SVT |
| How does increasing the sympathetic system at the arterioles increase BP? | NE released enhancing a1 R stimulation - Gq -> PIP2 hydrolysis via PLC -> IP3 & DAG -> IP3 diffuses thru cytoplasm releasing Ca2+ which binds calmodulin -> complex + MLCK -> P myosin light chains -> M + A interact -> sm ms contraction -> inc BP |
| What does increasing cAMP do? | muscle relaxation via B2 R (Epi) -> via protein kinase A inactivates MLCK -> prevents M + A interaction -> sm ms relaxation |
| What does increasing cGMP do? | relaxes and VD by dephosphorylating (deactivating) myosin light chains |
| Systolic anterior motion (SAM) of mitral valve indicates what pathology? | Hypertrophic Cardiomyopathy |
| Tx of HCM | Metoprolol, Atenolol, Propranolol |
| What are the SE of carbonic anhydrase inhibitors (Acetazolamide)? | hypokalemia, metabolic acidosis, alkaline urine |
| Which diuretics increase urine K+? | all except K+-sparing diuretics |
| How do CA inhibitors cause metabolic acidosis? | decrease HCO3- reabsorption |
| What symptoms occur when a patient has low serum K+ concentration? | arrhythmias and paralysis |
| What happens when a patient has high serum K+ concentration (> 6.0 mEq/L)? | peaked T waves, wide QRS, arrhythmias |
| MOA of PDE5 inhibitors? | prevent cGMP breakdown by inhibiting cGMP phosphodiesterase |
| What do PDE5 inhibitors (sildenafil) treat? | erectile dysfunction (inc blood flow in corpus cavernosum), pulmonary arterial HTN (inc pulmonary artery relaxation) |
| Drug associated with inducing gout? | HCTZ (HyperGLUC: hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia) |
| What patients should not be given HCTZ? | Patients with sulfa allergy and with diabetes mellitus |
| Symptoms of CHF? | fatigue, exertional and nocturnal dyspnea, S3 gallop |
| Tx of CHF to prevent ventricular remodeling? | ACEI - dec AT II levels which dec NE levels -> circle of sympathetic and RAAS activation blocked |
| What does an excess in nitric oxide cause and how is it treated? | Methemoglobinemia. Treat w/ high flow O2 and methylene blue. |
| What symptoms will nonselective beta blockers (i.e. propranolol) mask? | tachycardia and hypoglycemia - b2 inc glucagon release & glycogenolysis to inc glucose -> block results in hypoglycemia -> beta blockers bind adrenoreceptors blocking NE & Epi -> inhibit sympathetic response (tachycardia) |
| What are the functions of a1 and b1 receptors? | a1 - inc arterial pressure (BP), b1 - inc inotropic state (contractility) and SV |
| SE of Digoxin? | arrhythmia, paroxysmal atrial tachycardia w/ 2:1 block, blurry yellow vision, vent tachyarrhythmia, torsades (inc K+) |
| Which beta blockers are B1 selective and which are nonselective? Exceptions? | A thru M = B1 selective. N thru Z = beta nonselective. Except C (Carvedilol) and L (Labetolol). |
| Beta-1 selective blockers are indicated for which group of patients? | asthmatics |
| What electrolyte imbalance increases the risk of Digoxin toxicity? Which drugs should be avoided in these patients? | hypokalemia. diuretics. |
| Patients w/ PCKD should be given what drug? | ACEI - dec ang II (overproduced in these pxs due to inc renin prod) - result is dec BP & increase renal blood flow via efferent arteriole thus is renoprotective for HTN pxs. |
| What patients should avoid Verapamil (1st gen CCB)? | CHF pxs b/c of negative inotropic effects |
| Which drugs are CI in angina due to its high myocardial O2 consumption? | Partial beta-agonists - Pindolol and Acebutolol |
| Which drugs decrease myocardial oxygen requirements during exertion and stress? How? | Beta blockers - reduce HR, myocardial contractility, and BP |
| What drug is used to treat ventricular arrhythmias and can cause SLE-like syndrome? | Procainamide (class 1a) - stabilizes cardiac membranes and depresses AP phase 0 |
| How does nitroglycerin work? | dilates arteries and veins which decrease resistance reducing arterial BP thus decreasing LVEDV and LVESV. |
| MOA of Digoxin? | inhibits Na+/K+ ATPase -> indirect inhibition Na+/Ca2+ exchanger/antiport -> inc Ca2+ -> positive inotropy. Also stimulates vagus nerve. |
| MOA of thiazide and thiazide-like diuretics? | inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of nephron -> dec Ca2+ excretion |
| What drug affects the afferent arteriole and should not be given in pxs w/ renal failure? | NSAIDs - dec PG production - PG dilates afferent arteriole (inc RBF, inc GFR, FF constant) |
| Hi serum CKMB indicates what kind of infarct? | MI (subendocardial infarct) rather than angina b/c in angina there is not sufficient myocardial damage for release of CKMB |
| What effect does an increase in adenosine have on the heart? | increases coronary blood flow |
| How does aortic stenosis affect coronary blood flow? | high peak systolic pressure compresses coronary vessels more than normal causing systolic BF to dec and coronary diastolic BF to inc |
| What happens to arteries and arterioles when BP is increased? | hypertrophy of vessels causing inc thickness of vessel wall w/o much change in vessel radius inc wall-to-lumen ratio of vessel - loss of arterioles occurs from inc BP |
| Px with fever, positional chest pain noted on leaning forward, and friction rub w/ diffuse ST elevations | Dressler syndrome (autoimmune) - fibrinous pericarditis |
| ST elevations with (+) cardiac enzymes | Transmural MI |
| Px w/ trauma from a knife wound is most likely to experience what heart condition? | Right heart failure from AV fistula -> inc venous return to heart -> inc resting CO -> inc venous hydrostatic pressure -> inc JVP -> S3 heart sound -> RVH -> dec compliance RV -> right heart failure |
| What supplies the anterior part of the LV and anterior 2/3 of interventricular septum? | Left anterior descending artery |
| What supplies the posteroinferior part of LV and posterior 1/3 of interventricular septum, RV, posteromedial papillary ms in LV and AV and SA nodes? | Right coronary artery |
| What supplies the lateral wall of the left ventricle? | left circumflex coronary artery |
| What would give a normal EKG reading but produces pain during physical labor? | Stable angina |
| What would give a normal EKG reading but occurs at rest? | Prinzmetal's variant angina |
| MC manifestation of coronary artery disease? | Angina pectoris |
| Subendocardial ischemia with ST-segment depression? How relieved? | Stable angina. Resting or nitroglycerin. |
| Vasospasm with transmural ischemia and ST-segment elevation? What drugs does it respond to? | Prinzmetal's angina. Nitroglycerin and CCB (vasodilator). |
| Patient with BP of 160/50 indicates what? | wide pulse pressure - aortic insufficiency (AR) - retrograde flow from aorta to LV - vol overload of LV inc SV (Frank Starling) |
| MCC of acute aortic regurgitation? | infective endocarditis |
| What happens in CHF? | activate RAAS -> Na+ and H2O retention -> inc hydrostatic pressure -> edema -> S3 -> CHF -> inc venous return -> inc RA pressure |
| Consequence of mural thrombus to systemic circulation? | stroke from thromboembolism |
| Blowing diastolic murmur, large SV, wide pulse pressure? | aortic regurgitation |
| Severely anemic patient will develop what kind of symptoms? | tachycardia, inc SV (inc SBP), wide PP, cold hands, inc arteriolar diameter (dec DBP) |
| Patient has a wide pulse pressure and a HR of 30-45 bpm. This suggests what pathology? | Complete heart block |
| Bedridden patient w/ sudden chest pain and dyspnea? | pulmonary embolus arising from femoral vein thrombosis |
| Patient has decreased ankle pulse and increased peripheral vascular resistance. This suggests what pathology? | arteriosclerotic occlusive disease |
| Patient w/ bicuspid aortic valves has midsystolic murmur radiating to neck. This indicates what pathology? | aortic stenosis |
| Px w/ perihilar infiltrates has ankle edema, dyspnea, low BP and inc BUN. Pathology? | CHF |
| Pathogenesis of atherosclerotic disease? | injury to endothelial lining of vessels |
| Patient presents w/ worsening chest pain that occurs at rest or w/ minimal exertion. ST depression on EKG. Pathology and pathogenesis? | Unstable angina - thrombosis of coronary artery w/ disrupted atherosclerotic plaques |
| Px presents w/ aphasia, hemiparesis, paresthesias, loss of vision, and loss of consciousness that resolves within 24 hours. This suggests what pathology? | Transient ischemic attack - brief, reversible episode of neuro dysfxn due to focal ischemia (occlude 1 artery by thrombus or embolus) |
| 4-8 weeks post MI, patient is at risk of what MI complication? | ventricular aneurysm |
| Px on autopsy w/ a blood clot appeared to have alternating white lines on microscopy. This indicates patient developed this when? | Premortem thrombus |
| What is the difference btwn Goodpasture's ds and Wegener's granulomatosis? | Goodpasture's not associated w/ nasal symptoms whereas Wegener's is. |
| Patient w/ Marfan's has defect in? | fibrillin |
| Patient is an elderly w/ ring-like calcifications. This patient has what disease process? | Monckeberg arteriosclerosis |
| Patient presents with tendon xanthomas. Labs indicate increased LDL above 190 mg/dL and cholesterol levels. This indicates what disease? Pathophysiology? | Familial hypercholesterolemia (type II) - receptor mediated endocytosis is defective |
| Patient w/ heart transplant is at risk for what serious complication? | graft vascular disease (graft arteriosclerosis) |
| Px presents w/ hamartomas, adenoma sebaceum, ash leaf spots, cardiac rhabdomyomas and renal angiomyolipomas. This suggests what pathology? | Tuberous sclerosis |
| Px w/ sudden cardiac death. What is the underlying factor? | Ischemic heart ds -> ventricular fibrillation |
| Amyloid protein associated with acute phase reactant (i.e. Rheumatoid arthritis) | AA protein |
| Amyloid protein seen in familial and old fogies | AF |
| Amyloid protein associated with light chain and lymphoma | AL |
| Amyloid protein associated w/ the endocrine system | AE |
| What does an increase in AST alone indicate? | myocardial infarction |
| What is a frequent fatal complication that can occur the 1st week after MI? | rupture of free LV wall |
| What is a common complication that occurs in pxs w/ beta thalassemia major? | CHF from accumulated iron of frequent blood transfusions |
| Px w/ thickened blunted cardiac valve leaflets w/ fibrous bridging btwn valve leaflets and calcifications has what pathology? | Acute rheumatic fever |
| Young px presents w/ ejection click/systolic click. What is pathology? | bicuspid aortic valve (aortic stenosis) |
| Px experiences repeated episodes of exercise-induced substernal chest pain. What is the pathology and pathophysiology? | stable angina pectoris - gradual loss of myocytes - small patches of fibrosis and vacuolization of damaged myocytes typically in subendocardial locations which are poorly perfused |
| Px has history of being IV drug abuse user. Px at risk of what pathology which is commonly caused by what bacteria? | Acute bacterial endocarditis - Staph aureus |
| Duodenal atresia seen commonly in which pxs? Pathophysiology? | Down's - inadequate migration of neural crest cells |
| Pathophysiology of aortic stenosis? | MCC by calcification of normal or bicuspid valves |
| Opening snap | Mitral stenosis |
| How is HDL (good cholesterol) increased? | exercise, wine, estrogen |
| Where is HDL synthesized? | liver and SI |
| Functions of HDL? | removes cholesterol from plaques for disposal in liver |
| What are diet-derived triglycerides? | chylomicrons |
| What do CMs need to be synthesized in the intestinal epithelium and for assembly and secretion? | apo-B48 |
| What transports liver-synthesized triglyceride in the blood and requires apo-B100 for assembly and secretion? | VLDL |
| What causes turbidity in plasma? | hypertriglyceridemia |
| What transports cholesterol in blood? | LDL |
| Increased LDL due to decreased LDL receptors describes what? | type II hyperlipoproteinemia |
| Premature CAD and stroke, tendon xanthomas, and xanthelasma describe what? | familial hypercholesterolemia (type II hyperlipoproteinemia) |
| Deficiency of apoE and increased liver uptake of chylomicron remnants and IDL describes what? | type III hyperlipoproteinemia (familial dysbetalipoproteinemia) |
| Palmar xanthomas in flexor creases and increased risk for CAD describes what? | familial dysbetalipoproteinemia ("remnant disease") |
| Increased VLDL and the MC lipid disorder describes what? | type IV hyperlipoproteinemia (familial hypertriglyceridemia) |
| What are the acquired causes of type IV hyperlipoproteinemia? | excess alcohol intake, progesterone in OCP, DM |
| Eruptive xanthomas (yellow, papular lesions) and increased risk for CAD and peripheral vascular disease describes what? | type IV hyperlipoproteinemia (familial hypertriglyceridemia) |
| Deficiency of apo B-48 and B-100 with deficiency of CM, VLDL, and LDL, and decrease in serum cholesterol and triglyceride describe what? | apolipoprotein B deficiency (abetalipoproteinemia) |
| Marked decrease in vitamin E, malabsorption from chylomicrons accumulating in villi, and ataxia, hemolytic anemia with thorny RBCs (acanthocytes) describes what? | abetalipoproteinemia |
| What is the formula for CO? | rate of O2 consumption/(arterial O2 content - venous O2 content) |
| What is the formula for MAP? | CO * TPR |
| What is another formula for MAP? | 2/3 diastolic pressure + 1/3 systolic pressure |
| What is the formula for pulse pressure? | systolic pressure - diastolic pressure |
| What is proportional to SV? | pulse pressure |
| What is the formula for SV? | CO/HR = EDV-ESV |
| During exercise, CO increases initially as a result of what? | increase in SV |
| After prolonged exercise, CO increases as a result of what? | increase HR |
| If HR is too high (e.g. ventricular tachycardia), what happens? | diastolic filling incomplete and CO decreases |
| What is SV affected by? | CAP = contractility, afterload, preload |
| When is SV increased? | increase preload, decrease afterload, or increase contractility |
| Contractility (and SV) increase with what? | catecholamines (inc activity of Ca2+ pump in SR), inc intracellular Ca2+, decrease extracellular Na+ (dec Na+/Ca2+ exchanger activity), digitalis (inc intracellular Na+ resulting in inc Ca2+) |
| Contractility (and SV) decrease with what? | B1 blockade, HF, acidosis, hypoxia/hypercapnea, non-dihydropyridine Ca2+ channel blockers |
| SV increases in what events? | anxiety, exercise, and pregnancy |
| What does a failing heart have? | decrease SV |
| Myocardial O2 demand is increased by what? | inc afterload (~arterial pressure), inc contractility, inc HR, inc heart size (inc wall tension) |
| What does preload equal? | ventricular EDV |
| What does afterload equal? | MAP (proportional to peripheral resistance) |
| Example of venodilators? | nitroglycerin |
| Example of vasodilators? | hydralazine |
| What do venodilators decrease? | preload |
| What do vasodilators decrease? | afterload |
| What does preload increase with? | exercise (slightly), blood volume (overtransfusion), and excitement (sympathetics) |
| What is force of contraction proportional to? | initial length of cardiac muscle fiber (preload) |
| What stimulates the contractile state of myocardium? | circulating catecholamines, digitalis, sympathetic stimulation |
| What inhibits the contractile state of myocardium? | pharacologic depressants, loss of myocardium (MI) |
| What is the formula for EF? | SV/EDV = EDV-ESV/EDV |
| What is EF an index of? | ventricular contractility |
| What is the normal EF? | >=55% |
| What is resistance directly proportional to? | viscosity |
| What is resistance inversely proportional to? | radius to the 4th power |
| What accounts for most of TPR and regulates capillary flow? | arterioles |
| What does viscosity depend mostly on? | hematocrit |
| Viscosity increases in what? | polycythemia, hyperproteinemic states (e.g. multiple myeloma), hereditary spherocytosis |
| What does an isolated decrease in CO indicate? | decrease contractility that is not due to decrrease preload (VR unchanged) - action of negative inotropic drug and to myocardium inhibiting contraction such as MI |
| On the venous return curve, what does the x-intercept mean? | mean systemic pressure |
| In the phases of the left ventricle of the cardiac cycle, what is the period of isovolumetric contraction? | period between mitral valve closure and aortic valve opening; period of highest O2 consumption |
| In the phases of the left ventricle of the cardiac cycle, what is the period of systolic ejection? | period between aortic valve opening and closing |
| In the phases of the left ventricle of the cardiac cycle, what is the period of isovolumetric relaxation? | period between aortic valve closing and mitral valve opening |
| In the phases of the left ventricle of the cardiac cycle, what is the period of rapid filling? | period just after mitral valve opening |
| In the phases of the left ventricle of the cardiac cycle, what is the period of reduced filling? | period just before mitral valve closure |
| Loudest at apex and radiates toward axilla? | mitral regurgitation |
| Loudest at tricuspid area and radiates to right sternal border? | tricuspid regurgitation |
| Is often due to ischemic heart disease, mitral valve prolapse, or LV dilation? | MR |
| Is due to RV dilation or endocarditis? | TR |
| Crescendo-decrescendo systolic ejection murmur following ejection click (EC)? | aortic stenosis |
| LV>>aortic pressure during systole? | aortic stenosis |
| Where does aortic stenosis radiate to? | carotids/apex |
| Pulses weak compared to heart sounds is called what? | pulsus parvus et tardus |
| What is aortic stenosis often do to? | age-related calcification |
| Holosystolic, harsh-sounding murmur loudest at tricuspid area? | VSD |
| Late systolic murmur with midsystolic click? | mitral prolapse |
| What is the most frequent valvular lesion loudest at S2? | mitral prolapse |
| What can mitral prolapse predispose to? | infective endocarditis |
| Wide pulse pressure when chronic refers to what? | aortic regurgitation |
| High-pitched "blowiing" diastolic murmur describes what? | aortic regurgitation |
| Follows opening snap? | mitral stenosis |
| Delayed rumbling late diastolic murmur? | mitral stenosis |
| What is the pressure during diastole in mitral stenosis? | LA>>LV |
| What does mitral stenosis often occur secondary to? | rheumatic fever |
| Continuous machine-like murmur describes what? | PDA |
| Where is PDA loudest at? | S2 |
| Irregularly irregular with no discrete P waves describes what? | atrial fibrillation |
| "Sawtooth" appearance describes what? | atrial flutter |
| How do you treat atrial fibrillation? | warfarin (Coumadin) |
| What is used in atrial flutter? | class IA, IC, or III antiarrhythmics |
| What is the PR interval in 1st degree AV block? | >200 msec |
| What is the PR interval in 2nd degree AV block (Mobitz type 1 (Wenckebach))? | progressive lengthening of PR interval until a beat is "dropped" |
| What do dropped beats not preceded by a change in the length of the PR interval? | Mobitz type II |
| How is Mobitz type II often found? | 2:1 block where 2 P waves to 1 QRS response |
| Atria and ventricles beat independently describes what? | 3rd degree (complete) AV block |
| Coarctation of the aorta can result in what? | aortic regurgitation |
| Antiarrhythmic that inhibits cyp3A4? | amiodarone |
| In neonates, blood flows how in PDA? | aorta to pulmonary artery |
| What are the blood oxygen tension values in PDA? | only pulmonary artery is increased (aorta, vena cava and LV are normal) |
| What can myomectomy do? | complete heart block |
| Where is right bundle branch block seen? | ventricular hypertrophy or if conduction delayed through right bundle |
Created by:
eandres1
Popular USMLE sets