Uworld Cardio II Flashcards
76 yo severe midsternal chest pain, diaphoresis. PMH significant HTN, type 2 diabetes, asymptomatic right carotid artery stenosis. BP 120/70, PULSE 75. Lungs clear to auscultation, ECG ST segment elevations > 1mm II, III, aVF. Patient immediately receives alteplase and low dose beta blocker, single dose of IV morphine. several hours later, patient found comatose with asymmetric pupils, irregular breathing. Most likely cause of condition? A. carotid artery thrombosis B. dissection of ascending aorta C. interventricular septum perforation D. intracerebral hemorrhage E. myocardial reperfusion injury F. opioid overdose G. pulm embolism
D. intracerebral hemorrhage
chest pain, diaphoresis, history atherosclerosis and type 2 DM => acute coronary syndrome
ECG => STEMI
Myocardial reperfusion via percutaneous coronary intervention or fibrinolysis within 12 hours of symptom onset
PCI preferred b/c of lower rates if intracerebral hemorrhage and recurrent MI, but not available at all institutions.
fibrinolytics- tenecteplase, alteplase improves clinical outcomes
contraindications- GI bleeding, recent surgery
alteplase- bind fibrin, convert plasminogen to plasmin in thrombus (clot) => hydrolyze bonds => clot lysis => restoration of coronary arterial blood flow. most common adverse effects = hemorrhage
signs of intracerebral hemorrhage => decreases levels of consciousness, asymmetric pupils, irregular breathing
A. carotid artery thrombosis => ischemic stroke, fluctuating symptoms, periods of improvement; treatment with thrombolytics, ICH more likely than thrombotic stroke
B. aortic dissection- severe, tearing chest pain radiates to interscapular area- HTN, Marfan/EDS- WIDENED MEDIASTINUM
C. IV septum perf => left to right shunt, acute heart failure symptoms; chest pain, dyspnea, cardiogenic shock, harsh holosystolic murmur on left sternal border
E. Referfusion of ischemic myocardium => paradoxical cardiomyocyte dysfunction (reperfusion injury)- patients treated with PCI, thrombolytics, coronary artery bypass grafting, arrhythmias, myocardial stunning, myocyte death
F. Opioid overdose- small constricted pupils (miosis), resp depression (
10 yo boy has tetralogy of Fallot. When there are episodes of severe dyspnea and cyanosis, the child assumes a squatting position. What is the mechanism by which the squatting relieves child’s symptoms?
A. decreasing left ventricular workload
B. decreasing pulm blood flow
C. decreasing pulm vascular resistance
D. improving lung compliance
E. increasing systemic vascular resistance
E. increasing systemic vascular resistance
TOF
-VSD
-overriding aorta
-Pulm stenosis
-RVH
pulm stenosis + overriding aorta => low ratio of systemic vascular resistance to pulm vascular resistance => allows deox blood to take low resistance route to systemic circulation => acute hypoxemia - Tet spell
squatting => increases SVR w/o changing PVR => forces higher proportion of RV output to enter pulm circulation and oxygenate pulm cap beds => increase arterial oxgen concentration, relieving tet spell
- lung compliance is not changed
- does not impact PVR
1 day old infant harsh, holosystolic murmur. born 39 weeks gestation to 36 yo, no prenatal screening. no family history of genetc or chromosomal disorders. flat facial profile, protruding tongue, small ears. most likely occurred prior to conception? A. chromosomal deletion B. chromosomal translocation C. gene inactivation D. meiotic nondisjunction E. trinucleotide repeat expansion
D. meoitic nondisjunction
-chromosmes fail to separate, one or more daughter cells pass on with extra copy of chromosome.
-increasing maternal age, particularly OVER/EQUAL TO 35 => elevated risk of nondisjunction likely due to cumulative oxidative stress, depletion of available mature oocytes, shortening of oocyte telomeres.
Most common: trisomy 21; Edwards 18; least common Patau 13
Prader-Willi/Angelman
E. Trinucleotide repeat expansions => dysregulate protein production => huntington, myotonic dystrophy, fragile X
33 yo immigrated to US severe SOB and hemoptysis. diastolic murmur. Chest Xray => severe pulm vascular congestion and edema. Admitted to hospital, treated with diuretics, feels better. but in hospital, develops right-sided hemiparesis. what additional finding most suggestive of combined disease involving mitral and aortic valves rather than exclusive mitral involvement?
A. increased left ventricular diast pressure
B. increased pulm artery pressure
C. increased pulm capillary wedge pressure
D. reduced pulm vascular compliance
E. right ventricular dilation
F. tricuspid regurgitation
A. increased left ventricular dias pressure
Mitral stenosis- cardiac and pulm pressures prox to stenotic mitra lvalve markedly elevated.
diastolic pressure in LV usually near normal or decreased
if there is increased LV diastolic pressure in person with suspect MS, aortic valve is also dysfunctional
Rheumatic heart disease- aortic stenosis and regurg => increase LV diastolic pressure
predispose to infective endocarditis even if valve is functionally normal
right-sided hemiparesis => embolsm- originated from atrial mural thrombus secondary to atrial dilation from MS, endocarditis related valvular vegetation
B and D. severe isolated MS => increase pulm artery pressure (pul HTN) backward tranmission of elevated pulm cap wedge pressure
longstanding pulm HTN => reduced pulm vascular compliance due to endothelial mediated pulm vasoconstriction, reactive hypertrophy of arterial muscle layer, partial obliteration of pulm cap bed
C. isolated MS significant elevation in left atrial pressure tarnsmitted to pulm veins and capillaries, increase pulm cap wedge pressure; wedge pressure only reflects LA end diast pressure, not left ventricular end diastolic pressure
E and F. RV dilation MS resulting pulm HTN severe enough to cause right heart failure => tricuspid regurg complication
34 yo acute myelogenous leukemia, chemotherapy with doxorubicin. progressive exertional dyspnea and orthopnea.
A. RV overload B. focal myocardial scarring C. restrictive cardiomyopathy D. hypertrophic cardiomyopathy E. dilated cardiomyopathy F. pericardial fibrosis
Anthracyclines- daunorubicin, doxorubicin, epirubicin, idarubicin chemotherapeutic agents associated cardiotoxicity via generation of free radicals
Dilated cardiomyopathy- cumulative dose dep, months after discontinuation of drug. swelling of sarcoplasmic reticulum morphologic sign of early stage of doxorubicin-associated cradiomyopathy- loss of cardiomyocytes- myofibrillar dropout- biventricular CHF- dyspnea on exertion, orthopnea, peripheral edema
most effective method of preventing doxorubicin cardiomyopathy is dexrazoxane- iron chelating agent decreases formation of oxygen free radicals by doxorubicin, etc.
A. RV overload- cor pulmonale- fatigue, dyspnea on exertion, peripheral edema. accentuation and splitting of pulm component of S2, distended neck veins, hepatomegaly with hepatojugular reflux. RV failure
C. Restrictive cardiomyopathy- hemochromatosis, amyloidosis, sarcoidosis, radiation therapy
D. Hypertrophic cardiomyopathy- aut dom mutation of beta myosin heavy chain
B. focal myocardial scarring commonly results following myocardial infarction
F. pericardial fibrosis- follows cardiac surgery, radiation therapy, viral infections of pericardium
46 yo woman has mitral regurg. What would increase the ratio of forward flow volume to regurgitant flow volume in this patient?
A. decreasing heart rte
B. decreasing lfet ventricular afterload
C. decreasing left ventricular preload
D. increasing left ventricular contractility
E. increasing left ventricular volume
B. decreasing left ventricular afterload
mitral regurg w/ left sided heart failure
patints with mitral regurg, some blood in left ventricle forward pumped trough aortic valve- forward stroke volume
some is forced backward through incompetent mitral valve- regurgitant stroke vlume
amount flows forward determined by left ventricular afterload
afterload decreases => resistance to blood flow into aorta is reduced = blood flow away from left atrium and toward aorta => increasing forward-to-regurgitant volume ratio
arterial vasodilator therapy reduce left ventricular afterload, reduce heart failure symptoms in patients with mitral regurg, though surgery remains definitive treatment
A and E. primary decrase in heart rate => increase LVEDV (preload) b/c increased increased diastolic filling time- reciprocal interaction between heart rate and stroke volume allows cardiac output and afterload to be maintained following mild to moderate solated decrease in heart rate. increased preload worsen mitral regurg if degree of regurg dep on left ventricular size
C. Left ventricular preload reduction => decrease regurg flow fraction if degree of mitral valve incompetence is volume dep. non-volume dep causes of mitral regurg (congenital defects, annular calcification) would not be affected. steady-state afterload unlikely to be significantly affected due to compensatory increases in heart rate and systemic vascular resistance
D. increase in LV contractility => increases total stroke volume => increase afterload => increase fraction of total stroke volume going toward regurg flow; people recommend chronic beta blocker therapy for patients with significant mitral regurg
43 yo comes in with nausea and vomiting and left-sided chest pain. History of dyslipidemia and HTN. Patient’s mother died from MI age 51. ECG and cardiac biomarkers are normal. She’s scheduled for exercise stress test. During the test, which of the following parameters is likely to be the most similar between the systemic and pulmonary circulation?
A. arterial oxygen content B. arterial resistance C. blood flow per minute D. diastolic arterial pressure E. driving pressure for blood flow F. mean arterial pressure
To maintain blood flow throughout body, blood flow (mL/min) in pulm circulation must closely match blood flow in systemic circuit. Exerise and rest as circulatory system is continuous circuit.
exception: bronchial circuit- supplies oxygen and nutrients to pulm parenchyma from systemic cculation but drains mostly to the left atrium as opposed to the right atrium (right to left shunt partially indep circuit).
10 yo boy comes in because he has lots of restlessness and involuntary jerking. no meds, vaccinations up to date. sore throat 3 mo ago. rapid, irregular jerking movements involving face, arms, legs. patient at greatest risk for developing which of the following?
A. deforming polyarthritis B. early dementia C. parkinson disease D. renal failure E. valvular heart disease
E. valvular heart disease
acute rheumatic fever
epidem: endemic in developing countries
pathogenesis: molecular mimicry: anti-group A streptococcal antbodies attack host antigens on cardiac and neuronal tissue approx 2-4 weeks after acute pharyngitis
clinical features: acute/subacute- migratory arthritis, pancarditis, sydenham chorea; chronic- mitral regurg/stenosis
prevention: prompt treatment of strep pharyngitis with penicillin
Sydenham chorea- hyperkinetic extrapyramidal movement disorder, most common acquired chorea of childhood. 1-8mo after group A beta hemolytic strep infection. delayed onset autoimmune reaction involing anti-streptocccal antibodies that cross react with the basal ganglia.
A. migratory polyarthritis is an early manifestation of acute rheumatic fever, generally transient and rarely ever deforming
B. early onset alzheimer dementai associated with down syndrome, increased expression of amyloid precursor protein on chromosome 21
C. Parkinson is extrapyramidal hypokinetic movement disorder consisting of tremor, rigidity, akinesia, postural instability. jerking extremity movements not seen in parkinson unless its levodopa overdose
D. Poststrep glomerulonephritis occurs following infection with specific nephritogenic strains of group A strep. nephritis manifests within 1-6weeks, self limited. renal failure not part of clinical syndrome associated with acute rheumatic fever
Discuss the changes in the cardiac and venous return curves of the following conditions: A. chronic arteriovenous fistula B. acute gastrointestinal bleed C. phenylephrine infusion D. myocardial infarction E. anaphylaxis
A. chronic AV fistula- increase cardiac output (increase height of cardiac function curve), decreased TPR (increased slope of cardiac and venous curves), increased mean systemic pressure (right shift of venous curve); acutely, AV fistula => decrease in TPR => increased cardiac output and increased venous return. over time, sympathetic nervous system and kidneys compensate for chronic fistula by increasing cardiac contractility, vascular tone, circulatin blood volume
B. acute GI bleed => sharp decrease in circulating blood volume and shift venous return graph to the left
C. a phenylephrine infusion increases symp tone => vasoconstriction, increase TPR => decreased cardiac output from increased afterload along with decreased venous return
D. MI => isolated decrease in CO with no change in blood volumes or venous return
E. anaphylaxis- widespread venous and arteiolar dilatation along with increased capillary permability and third-spacing of fluids => significant drop in venous return.
