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Step 1 Cardio Testwe
| Question | Answer |
|---|---|
| What artery typically supplies SA and AV node? | R coronary artery. |
| What supplies the inferior LV 80% of the time? 20%? | RCA via PD 80%, PD( posterior descending a.) from circumflew 20% |
| Where does a cronary artery occlusion most often happen? What does it supply | LAD (left anterior descending a) supplying the anterior inferior IV septum |
| When do coronary arteries fill? | diastole |
| What is the most posterior part of the heart? What can its enlargement cause? | eft atrium. enlargement= dysphagia (esophageal nerve), hoarseness (compression of left recurrent laryngeal n) |
| How do you calculate CO? How with regard to O2 content? | CO=SV x HR. CO = rate of O2 consumption/(arterial O2-venous O2) |
| How do you calculate Mean arterial P? | CO x total peripheral resistance= 2/3 diastolic P + 1/3 systolic P |
| How do you calculate pulse pressure? | systolic_P-distolicP |
| How do you calculate SV? | SV=CO/HR= EDV-ESV |
| In exercise why does CO initially increase? What happens if HR gets too high? | initially incr due to incr HR. if HR gets too high, distolic filling is incomplete and CO decr |
| How is CO maintained in early vs late stages of exercise? | SV early, HR late stages |
| What 3 factors control SV, and when does SV incr with their changes? | Contractility, Afterload, Preload. incr Preload, decr afterload, incr contractility incr SV |
| What is the effect of catecholamines on contractility and SV? | catacholamine incr activity of Ca++ pump in SR= incr contractility |
| What is the effect of extracellular sodium levels on contractility? WHy? | decr extracellular Na= decr Na/Ca++ exchanger= incr SV and contractility |
| How does digitalis effect intracellular Na+ and contraciltiy? | incr Na+, incr Ca++ causing an incr in SV and contracitly |
| What happens to SV in anxiety, exercise and pregnancy? A failing heart? | incr SV. failing heart = decr SV |
| What are 4 ways that incr the O2 demand of the myocardium? | 1. incr afterload 2. incr contractility 3. incr HR 4. incr Heart size (incr wall tension) |
| What is the effect on contractility and SV of a Beta 1 blockade? | decr cAMP leading to decr SV and contractility |
| What is the effect of acidosis, hypoxia, hypercapnea on SV and contractility? | decr contractility and SV |
| What is the effect of non dihydropyridine Ca++ channel blockers on SV and contractility? | decr contractility and SV |
| What is preload? | ventricular EDV |
| What is afterload? | mean arterial P, proportional to peripheral resistance |
| What is the effect on afterload or preload by an venodilator like nitroglycerin? | decr preload |
| What is the effect on afterload or preload by a vasodilator like hydralizine? | decr afterload |
| What are 3 ways that preload increases? | exercise, incr blood volume, excitement |
| To what is the force on cntraction of cardiac muscle proportional to? | end diastolic length of cardiac muscle (preload) |
| What are 3 things that increase the contractile state of the myocardium? | 1. circulating catecholamines 2. digitalis 3. SNS stim |
| What are 2 things which decr the contractile state of myocardium? | pharmacologic depressants, lost of myocardium |
| What are 2 ways to calculate ejection fraction? | EF= SV/EDV= (EDV-ESV)/EDV |
| What does EF help to measure, what is a normal level, and what happens to it in systolic HF? | index of ventricular contractility, EF decr in systolic HF |
| What is the relation of resistance to viscosity and radius of vessel/ | directly proportinal to viscosity, inversely related to radius^4 |
| What does flow equal? | Flow= Pressure/resistance |
| What vessels account for most of peripheral resistance and regulate capiallary flow? | areterioles |
| What is the total resistance of a set of vessels in series vs. paralllel? | series: R1+ R2 + R3.... parallel 1/totalR= 1/R1+ 1/R2+!/R3... |
| On what does blood viscosity mostly depend and what are 3 cases where it would be increased? | mostly determined by hematocrit. Viscosity incr in 1. polycythemia 2. hyperproteinemic states (myeloma) 3. hereditary spherocytosis |
| Exercise or an AV shunt would have what effect on total peripheral resistance? | decr |
| hemorrage would have what effect on total peripheral resistance? | incr |
| What part of the venous retrun curve represent the mean systemic pressure? | X intercept |
| What are the 5 stages of the cardiac cycle in the left ventricle? | 1. isovolumetric contraction 2. systolic ejection 3. isovolumetric relaxation 4. rapid filling 5. reduced filling |
| What happens in the LV in isovolumetric contraction with regard to valves and O2 consumption? | higherst O2 consumption. period b/w mitral valve closing and aortic vlave opening |
| What happens in LV during the systolic period valve wise? | period b/w aortic valve opening and closing |
| What happens in LV during isovolumetric relaxation valvewise? | period between aortic valve closing and mitral valve opening |
| What happens valvewise in the LV in the rapid filling and reduced filling stages? | rapid filling is just after mitral valve opening, reduced filling in just before mitral valve closure |
| What makes S1 and where is it loudest? | mitral and tricuspid closure. loudest at the mitral area |
| What makes S2 and where is it loudest? | closure of pulmonic and aortic valves. loudest at left sternal border |
| When is S3 heard? | early diastole during rapid ventricular filling |
| What situations is an S3 often heard? | early diastole during rapid ventricular filling. associated with incr filling P (MR CHF) and dilated ventricles (normal in children and prenant) |
| When is an S4 heard? | artial kick in late diastole |
| What situation ,makes an S4 and why? | associated with LV hypertrophy. LA must push against a still LV wall |
| What is the a wave in JVP? | atrial contraction |
| What is the c wave in JVP? | RV contraction (closed tricuspid bulges into atrium) |
| What is the v wave in JVP? | incr RA pressure due to filling against a closed tricuspid valve |
| What is the x descent in JVP? | atrial relaxation and downward displacment of closed tricuspid during ventricular contraction |
| What is the y descent in JVP? | blood flow from RA to RV |
| What is the split of S2, when is the split increased? | aortic closes before pulmonic. incr in inspiration |
| Pulmonic stenosis or right bundle branch block has what effect on S2 splitting? | wide splitting, wider than usual, P2 still moves out a little in inspiration |
| Atrial septal defect would have what effect on S2 splitting? | splitting would become wide and be unaffected by inspiration |
| What would the effect of aortic stenosis or left bundle branch block be on S2 splitting? | paradoxical splitting, P2 ahead of A2 but move closer together on inspiration |
| Why does normal splitting of S2 occur? | inspiration incr intrathoracic P, incr capcity of the pulmonary system. pulmonic valve clsoes later to accomidate more blood entering lungs. aortic vlave closese sooner due to decr return to the LH |
| What is the mechanism of widened splitting? | delay in RV emptying (pulmonic stenosis, RBBB). Delayed pulmonic sound regardless of breath. exaggeration of normal splitting |
| What is the mechanism of fixed splitting? | atrial septal defect leads to a left to right shunt and incr flow through pulmonic valve s/t regardless of breath, pulmonic closure is delayed |
| What is the mechanism of paradoxical splitting? | seen when LV is delayed in emptying ( aortic stenosis, LBBB). P2 before A2. On inspiration P2 moves closer to A2 (paradoxiaclly eliminating the split) |
| Where is the aortic area and what are 3 things best heard there? | upper left 2ndICS. aortic stenosis, flow murmur, aortic valve stenosis |
| Where is the pulmonic area and what are 2 things best heard there? | upper right 2nd ICS. systolic ejection murmurs: pulmonic stenosis, flow murmur (trial dseptal defect) |
| What are 3 things best heard on the left sternal border? | diastolic murmurs: aortic regurgitation, pulmonic regurgitation systolic: hypertrophic cardiomyopathy |
| Where is the tricuspid area and what are 4 things best heard there? | Left side 5th ICS, Pancystolic murmurs: tricuspid regurgitiation, ventricular spetal defect diatolic mumur: tricuspid stenosis, atrial septal defect |
| Where is the mitral area and what are 2 things best heard there? | apex. systolic mumur: mitral regurgitation distolic: mitral stenosis |
| A pulmonary flow murmur and a diastolic rmuble is a common presentation of? | atrial septal defect |
| What is the the effect of inspiration on heart sounds? | incr intensity of RH sounds |
| What is the effect of expiration on heart sounds? | incr intensity of left heart sounds |
| What is the effect of hand grip on vascular resitance and heart sounds? | increases systemic vascular resistance: incr mitral regurgitation, VSD systolic murmurs |
| What is the effect of a valsalva maneurver on venous return and heart sounds? | decr venous return. decreases intensity of most murmurs but incr MVP, hypertrophic cardiomyopathy murmurs |
| What is the effect of rapid squatting on venous return and afterload and how would it effect heart sounds? | incr venous return, incr afterload. decr MVP, HCM murmurs |
| What are the systloic Heart murmurs? | aortic/pulmonic stenosis. mitral/tricuspid reugrgitation |
| What are the distolic heart murmurs? | aortic/pulmonic regurgitation. mitral/tricuspid stenosis |
| Where and when is mitral regurgitation heard? | holocystolic. loudest at apex radiating toward axila |
| What cuases mitral regurgitation and what kind of maeuvers could be used to increase its intensity? | often due to ischemic HD, MVP, LV dilation. Can be increased by incr TPR (squatting, hand grip) or LV return (expiration) |
| Where and when is tricuspid regurgitation heard? | holocystolic blowing at tricuspid area radiating to Right sternal border |
| What causes tricuspid regurgitation and how might its sound be enhanced? | RV dilation, endocarditis, rheumatic fever. louder with incr RA return (inspiration) |
| Where and what is heard in aortic stenosis? | crescendo decrescendo systolic ejection murmur following ejection click. heard in aortic area radiating to carotids/apex |
| What type of carotid pulse might be seen in aprtic stenosis? | pulsus tardus et parvus. can lead to syncope |
| What causes aortic stenosis commonly? | age related calcification or congenital bicuspid aortic valve |
| What is heard where in a ventricular septal defect? | holosystolic, harsh murmur at tricuspid area |
| What is heard where is mitral vavle prolapse? | late systolic crescendo with midsystolic click (tensind of chordae tendinae) in mitral area |
| what causes an ejection click? | abrupt halting of valve leaflets as in aortic stenosis |
| When is mitral valve prolpase loudest and what might it predispose you to? | loudest at S2, can predispose to infective endocarditis |
| What causes mitral valve prolapse and what maneuvers might enhance it? | myomatous degenration, rheumatic fever, chordae rupture. enhanced by features withc decr venous return (standing, valsalva) |
| Where and what is heard in aortic regurgitation? | immediate, high pitched blowing diastolic murmur. wide pulse P if chronic, can present with bounding pulses amd head bobbing |
| What causes aortic regurgitation and what might decrease the intensity of the murmur? | often due to aortic root dilation, bicuspid aortic valve, rheumatic fever. vasodilators decrease the intensity of the murmur |
| Where and what is heard in mitral stenosis? | follows opening snap (aburpt halt in leaflet movement in diastole), delayed rumble in late diastole |
| What causes mitral stenosis and what can enhance the murmur? | often secondary to rheumatic fever. chronicall can lead to LA dilatio. enhanced by incr LA return (expiration) |
| What is heard where in patent ductus arteriosus murmur?> What causes it? | countinous machine like murmur. ludest at S2. can be due to congenital rubella or prematurity |
| What are the major differences between cardiac and skeletal action potentials? | 1. CM AP has plateau due to Ca++ 2. CM nodal cells spontaneus depolarize during diastole due to If channels 3. CM coupled to e/o by gap junctions |
| What is phase 0 of the cardiac AP and what is responsible? | rapid upstroke, VG Na+ channels open. |
| What is phazse 1 of the cardiac AP and what is responsible? | inital repolarization. inactivation of VG Na+ channels. VG K+ begin to open |
| What is phase 2 of the cardiac AP and what is responsible? | plateau, Ca++ influx thru voltage gatesd Ca++ balances K+ efflux. influx triggers more Ca++ release from SR leading to contraction |
| What is phase 3 of the cardiac AP and what is responsible? | rapid repolarization: massive K+ efflux due to opening of voltage gated slow K+ channels and closure of VG Ca++ channels |
| What is phase 4 of the cardiac and what is responsbile? | resting potential- high K+ permeability thru K+ channels |
| Where does the pacemaker AP occur? | SA and AV nodes |
| What is phase 0 of the pacemaker AP? | upstroke. opening of VG Ca++. Na+ channels are permanently inactive due to resting voltage of cells. this results in slowing thru AV node |
| Is there a plateau in the pacemaker AP? | no |
| What happens in phase 3 of the pacemaker AP? | inactivation of Ca++ channels and incr activation of K+ channels (K+ efflux) |
| What happens in phase 4 of the pacemaker AP? | slow diastolic depolarization: membrane slowly depolarizes as Na+ conductance increases(If not Ina). Slope of phase 4 determines the HR |
| What is the effect of adenosine/ACH on phase 4 of the pacemaker AP? | decr rate of diastolic depolarization= decr HR |
| what is the effect of catecholamines on phase 4 of the pacemaker AP? | incr depolarization rate= incr HR |
| What is the interaction of SNS and phase 4 of the pacemaker AP? | increases the liklihood that If channels are open |
| What does the P wave on ECG represent? | atrial depolarization |
| What does the PR interval on ECG represent? What's normal? | conduction delay thru AV node, <200msec normal |
| What does the QRS complex represent in ECG and whats normal? | ventricular depolarization. normal < 120msec |
| What does the QT interval on ECG represent? | mechanical contraction of the ventricles |
| What does the T wave on ECG represent? What if it's inverted? | T wave is ventricular depolarization. inversion implies recent MI |
| Where is atrial repolarization seen on ECG? | it isn't, its masked by the QRS complex |
| What does the ST segment on ECG represent? | isoelectric, ventricles are depolarized |
| What might cause a U wave on ECG? | hypokalemia, bradycardia |
| What is the relative speeds of conduction in deifferent parts of the heart? | Purkinje>atria>ventricles>AV node |
| What is the relative speeds of the pacemaker cells of the heart? | SA>AV>bundle of HIs/purkinje/ventricles |
| What is the normal conduction pathway in the heart? | SA-->atria--->AV--->common bundle-->LAF, bundle branches, purkinje fibers, ventricles |
| What is the normal pacemaker of the heart? | SA node |
| Why does the AV node have a delay? | allows time for ventricular filling |
| What is seen on ECG in torsade de pointes, and what can predispose someone to it? What happens if it progresses? | a V tac characterized by shifting sinusoidal waves. can progress to V fib. Anything which prolongs QT can predispose to torsades |
| What types of congenital conditions might cause Torsades? | long QT due to cardiac sodium or potassium channel defect. Also congenital deafness (Jervell and Lange-Nielsen syndrome) |
| What is seen on ECG in atrial fibrillation? | chaotic baseline, irreugularyl irregular QRS's, no discrete P waves |
| What can A fib lead to and how is it treated? | can result in atrial stasis and lead to stroke. Tx: beta blocker, Ca channel blocker, digoxin. prophylax for thromboembolism with warfarin |
| What is seen on ECG in atrial flutter? | rapid succession of back to back atrial depolarization waves. SAWTOOTH. |
| How do you Tx atrial flutter? | attempt to convert ot sinus rhythm: IA, IC, III antiarryhtmics |
| What is seen on ECG in 1st degree heart block? | prolonged PR, > 200 msec. Asx |
| What is seen on ECG of Mobitz type I (Wenckebach) heart block 2nd degree HB? | progressive lengthening of PR until a beat is droped ( P without a QRS). usually ASx |
| What is seen on ECG of Mobitz type II ) heart block second degree HB? | dropped beats not preceded by a change in PR interval. Pathologic. often 2 p waves to 1 QRS |
| What is seen on ECG in 3rd degree heart block? | atria and ventricles beating independently of e/o. P waves with no relation to QRS's. atrial rate faster than ventriuclar |
| What infection could cause 3rd degree HB and how is it tx? | Lyme can cause it. All 3rd degree HB needs a pacemaker |
| What is seen in ECG in Ventricular fibrillaton? | completely erratic rhythm with no identifiable waves. pt is clinically dead |
| What is atrial naturetic peptide and what are its systemic effects? | released from atria in response to incr blood volume and atrial P. causes vascular relaxation |
| What is the effect of atrial naturetic peptide on the kidneys? | constricts efferent arterioles, dillates afferent (cGMP), promoting diuresis and helps to escape from aldosterone |
| What does the aortic arch respond to? how does it communicate with the CNS? | responds only to incr BP, transmits to CNS via vagus n. |
| What does the carotid sinus respond to, how does it communicate with the CNS? | responds to both high and low BP, transmits via glossopharyngeal n. to n. solitaris of medulla |
| How does hypotension lead to vasoconstriction, incr HR, and incr contractility? | hypoTN--->decr MAP-->decr stretch-->decr afferent barorecetpr firing-->incr efferent SNS firing, decr PSNS firing-->vasoconstriciton, incr HR, incr contractiltiy, incr BP |
| When is a response to hypotensioon key? | sever hemmorrhage |
| How does carotid massage decr HR? | incr P on carotid a--> incr stretch--->incr afferent baroreceptor firing---> decr HR |
| what are the peripheral blood chemoreceptors and what do they respond to? | carotid and aortic bodies. repsond to decr PO2(<60mmHg), incr PCO2, decr pH of blood |
| What are the central chemoreceptors and what do they respond to? | respond to changes in pH and P CO2 of brains ISF, which are influenced by arterial CO2. dont respond to PO2 |
| What is Cushing reaction? | caused by central chemorecptors. incr ICP contricts arterioles-->cerebral ischemia-->HTN-->reflex bradycardia |
| What is Cushing's triad? | hypertension, bradycardia, respiratoyr depression |
| What organ has the largest share of systemic cardiac output? | liver |
| Which organ has the highest blood flow per gram of tissue? | kidney |
| Which organ has the largest arteriovenous O2 difference? How does this impact how its perfused? | heart, because O2 extraction is always close to 100%. incr O2 demand is met by incr blood flow not incr O2 extraction |
| What is normal LA pressure? | <12 |
| What is normal LV pressure? | 130/10 |
| What is normal Ra pressure? | <5 |
| What is normal RV pressure? | 25/5 |
| What is normal pulmonary a pressure? | <25/10 |
| What is normal aortic P? | 130/90 |
| What does PCWP approximate, what is its relation to LV in mitral stenosis? | approximates LA pressure, in MS PCWP>LV. measured with Swan Ganz catheter |
| What is autoregulation? | how blood flow in an organ remains constant over wide range of perfusion pressures |
| What is the reaction to hypoxia in the lungs vs other tissues? | causes constriction in lungs but vasodilation everywhere else |
| What are the key factors determining autoregulation in the heart? | local metabolites: O2, adenosine, NO |
| What are the key factors determining autoregulation in the brain? | local metabolites: CO2 (pH) |
| What are the key factors determining autoregulation in the kidneys? | myogenic and tubuloglomerular feedback |
| What are the key factors determining autoregulation in the lungs? | hypoxia causes vasoconstriction |
| What are the key factors determining autoregulation in SM | local metabolites: lactate, adenosine K+ |
| What are the key factors determining autoregulation in the skin? | SNS most important, temperature controle |
| What is Pc in Starling forces, what does it do? | capillary P, pushes fluid out of capillary |
| What is Pi in Starling forces, what does it do? | interstiatial fluid P, pushes fluid into capillary |
| What is pi c in Starling forces, what does it do? | plasma colloid oncotic P, pulls fluid into capillary |
| What is pi i in Starling forces? What does it do? | interstitial fluid colloid oncotic O, pulls fluid out of cappilary |
| What is the Starling equation for net filtration? | Pnet= (Pc=Pi) - (pi c - pi i) |
| What is Kf? | fluid constant |
| How do you calculate net fluid flow with Starling? | NFF=Pnet (Kf) |
| heart failure has what effect on starling forces? | incr capillary P, incr Pc causing edema |
| nephrotic syndrome or liver failure has what effect on Starling forces? | decr plasma protein, decr pi c, get edema |
| What effect do toxin, infections, or burns have on Starling forces? | incr capillary permeabilty, icr Kf, edema |
| What effect does lymphatic blockage have on Starling forces? | incr ISF osmotic P, incr pi i, causing edema |
| What are some common etiologies of dilated cardiomyopathy? | ABCCCD: alcohol abuse, we Beri beri, coxsackie B virus, chronic Cocaine use, Chagas, doxorubicin toxicity. also hemochromatosis, peripartum |
| In what part of the heart cycle is the dysfunction in dilated cardiomyopathy? | systolic |
| What are the key findings in dilated cardiomyopathy? | S3, dilated heart, baloon appearance on CXR |
| What is the mech of Hypertrophic cardiomyopathy? | hypertrophied Iv septum is too close to mitral valve leaflet, leading to outflow tract obstructuion. can cause systolic murmur and syncopal episodes |
| What are the most common etiologies of hypertrophic cardiomyopathy? | familial AD. also friedrichs ataxia. cause of sudden death in young athletes |
| What are the key findings in hypertrophic cardiomyopathy? | normal sized heart, S4, apical impulses, systolic murmur. Concentric hypertrophy Tx: beta blocker or nondihypdropyridime Ca++ channel blocker. (verapamil) |
| What part of the heart cycle is principally affected by hypertrophic cardiomyopathy? | diastole |
| What part of the heart cycle is principally affected in restricitve cardiomyopathy? | diastole |
| What are some major causes of retrictive cardiomyopathy? | sarcoidosis, amyloidososi, post radiation fibrosis, endocardial fibroelastosis, Loefllers syndrome (eosinophillic inflitrate), hemochromtosis |
| what causes cardiac dilation in CHF? | greater ventricular end diastolic fx |
| What cause dyspnea on exertion in HF? | failure to incr CO in exercise |
| What sided HF are pulmonary edema and nocturnal dyspnea indicative of and what is the mech? | LHF. incr pulmonary venous P--> pulmonary venous distention. get hemosiderin laden macrophages in lungs |
| What sided Hf is orthopnea indicative of and what is the mech? | incr venous return in supine position exacerbates pulmonary vascular congestion |
| What sided HF is hepatomegaly evidence of and what is the mech? | RHF. incr central venous P--> incr resistance to portal flow. rarely leads to cardiac cirrosis |
| What sided Hf is ankle or sacral edema evidence of and what is th mech? | incr venous P = fluid transudation |
| What sided HF is JVD evidence of and what is the mech? | RHF. via incr venous P |
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tjs2123
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