Cardiology Flashcards

Question

What is uremic pericarditis?

Answer 1

Occurs in 6-10% of renal failure patients, typically in those w/ BUN >60mg/dl Most pts doe not present with classic electrocardiogram changes of pericarditis (eg diffuse ST segment elevations) Tx: hemodialysis leads to rapid resolution of chest pain and reduces size of any associated pericardial effusion

Answer 2

A common cause of LE edema. Presentation: varicose veins, skin discoloration, and medial skin ulceration, pitting edema is most common PE finding Initial treatment: conservative measures w/ leg elevation, exercise, and compression stockings

Answer 3

It is recommended as an initial stress test for diagnosis and risk stratification of most pts with suspected stable ischemic heart disease. Coronary angiography is performed in pts with high-risk findings on initial stress testing.

Answer 4

Hx of URI followed by sudden onset of cardiac failure Etiology: coxsackievirus B, parvovirus B19, HSV6, adenovirus, enterovirus Dx: echocardiogram - dilated ventricles with diffuse hypokinesia resulting in low EF (ie systolic dysfunction) Tx: supportive

Answer 5

A disease of noncaseating granuloma infiltration of the myocardium. Can result in serious arrhythmia (complete AV block*), cardiomyopathies, heart failure, and sudden cardiac death

Answer 6

Due to inflow from LA striking blood already in the LV causing reverberation of blood between LV walls. A low frequency diastolic sound heard just after S2 that is associated with LV failure. IV diuretics provide symptomatic benefits to patients with decompensated heart failure. Can be seen in viral myocarditis (+ pulmonary vascular congestion)

Answer 7

Due to aortic root dilation or congenital bicuspid valve Produces early diastolic decrescendo murmur It leads to increased LV end diastolic volume due to leakage of blood from the aorta back in the LV. Presentation: wide pulse pressure, "water hammer" pulse - rapid, abrupt upstroke followed by rapid collapse of the peripheral pulse, and LV enlargement L lateral decubitus position brings the newly enlarged LV closer to the chest wall and causes pounding sensation and increased awareness of the heartbeat

Answer 8

Diastolic and continuous murmurs are usually due to an underlying pathologic cause. Presence should prompt further evaluation w/ a transthoracic echocardiogram. Midsystolic murmurs in otherwise young, asymptomatic adults are usually benign and do not require further evaluation.

Answer 9

Commonly caused by ectopic foci w/in the pulmonary veins. | Tx: radiofrequency ablation in the PVs

Answer 10

Commonly involves a reentrant circuit around the tricuspid annulus.

Answer 11

Results from a reentrant circuit formed by 2 separate conducting pathways within the AV node.

Answer 12

An uncommon cause of dilated cardiomyopathy characterized by the development of heart failure during the last month of pregnancy (>36w) or w/in 5 months following delivery. Rapid onset systolic HF (dyspnea, cough, pedal edema) A fib with rapid ventricular rate is relatively rare in PPCM.

Answer 13

An elevated plasma BNP level has high sensitivity (>90%) for the diagnosis of CHF.

Answer 14

An arterial thrombus from the LV. [Acute limb ischemia: Arterial occlusion due to: embolus from cardiac source (LA thrombus due to a fib; LV thrombus following MI), infective endocarditis (septic emboli), thrombus from prosthetic valves]

Answer 15

Warmth, erythema, swelling, and tenderness.

Answer 16

Dx: preverterbral aortic calcifications on XR Confirm with an abdominal CT scan In pts w/ HD instability and signs and sxs consistent w/ an abdominal aortic aneursym (AAA) but w/o a known hx, a focused bedside u/s should be performed. A CT scan is helpful in symptomatic pts who are stable, while those who are unstable w/ a known history of AAA should undergo emergent repair.

Answer 17

Portends underlying pathologic cause including ventricular arrhythmias (due to MI) and outflow tract obstruction (eg aortic stenosis, HOCM) Presents with dyspnea on exertion, fatigue

Answer 18

Due to severe atherosclerosis of the L subclavian artery proximal to origin of vertebral artery; leads to reversal of blood flow in ipsilateral vertebral artery L more commonly affect than the R Presentation: ischemia in affected UE, vertebrobasilar ischemia (dizziness, ataxia, dysequilibrium) Lower brachial SBP (>15mm Hg) in affected arm, systolic bruit in supraclavicular fossa on affected side; 4th heart sound due to LVH from systemic HTN Dx: Dopper u/s or MRA Tx: statins, smoking cessation, stent placement

Answer 19

Common complication. Presentation: sternal wound drainage Soft tissue dehiscence occurs when superfical tissues (skin, muscle) separate. No signs of sternal instability or systemic illness. Local wound care/debridement with primary closure is indicated. Sternal dehiscence occurs w/ separation of edges of approx. sternum, may occur w/ or w/o soft tissue dehiscence; sternal instability + nonunion = "clicking" or "rocking" on sternal palpitation. surgical emergency requiring sternal rewiring to prevent cardiac trauma Dx: chest and sternal imaging

Answer 20

Should be suspected in pts w/ unexplained CHF, proteinuria, and LVH in the absence of hx of HTN. Presentation: proteinuria (>300mg/d), nephrotic syndrome (>3.5g/d), waxy skin, anemia, easy bruising w/ ecchymosis, early satiety, enlarged tongue, peripheral or autonomic neuropathy Increased ventricular wall thickness w/ normal or nondilated LV cavity

Answer 21

Parenteral vasodilator w/ quick onset and offset of action Metabolized to nitric oxide and cyanide ions Cyanide toxicity occurs in pts receiving prolonged infusion or higher doses of nitroprusside, most common in pts w/ renal insufficiency Presentation: altered mental status, lactic acidosis, seizures, and coma

Answer 22

Continuous flow murmur | Mildly accentuated peripheral pulses can occur

Answer 23

Pulmonary stenosis leads to harsh, crescendo-decrescendo systolic ejection murmur over LUSB RVH Over-riding aorta: single S2 due to normal aortic and inaudible pulmonary component VSD

Answer 24

ACE-i/ARBs Aldosterone antagonists (spironolactone, eplerenone) Beta blockers Aspirin + p2y12 receptor blockers (clopidogrel, prasugrel, ticagrelor) Statins

Answer 25

Development of AV block in pt w/ infective endocarditis should raise suspicion for perivalvular abscess extending into adjacent cardiac conduction tissues. Aortic valve endocarditis is assoc. w/ an increased risk of periannular extension of endocarditis.

Answer 26

Highly susceptible to pencillin and should be treated w/ IV aqueous penicillin G or IV ceftriaxone for 4 weeks. Oral abx are not recommended.

Answer 27

Warfarin or non-vit. K antagonist oral anticoagulants (eg apixaban, dabigatran, rivaroxaban) should be used to reduce the risk of systemic thromboembolism in pts w/ a fib and moderate to high risk of thromboembolic events (CHADVASC score >2).

Answer 28

Occurs 3-5d after an acute MI Presentation: sudden onset cardiogenic shock w/ sudden onset hypotension, biventricular failure, VSD-new harsh holosystolic murmur w/ palpable thrill at the L sternal border Does not cause rapid decompensation

Answer 29

``` Occurs 3-5d after an acute MI Leads to acute, severe MR Presentation: sudden onset hypotension, dyspnea, pulmonary edema Does not cause rapid decompensation Systolic murmur of MR is soft There is NO palpable thrill present ```

Answer 30

Transesophageal echocardiogram has excellent sensitiivty and specificity for the dx of aortic dissection and is preferred diagnostic study in pts w/ hemodynamic instability or renal insufficiency. CT angio and MR angio should be avoided in pts w/ moderate to severe kidney disease. Antiplatelet or anticoag therapy can increase the bleeding complications assoc. w/ aortic dissection (eg hemothorax, hemopericardium, propagation of dissection). NO FEVERS present.

Answer 31

Energy delivery is synchronized to the QRS complex to minimize the likelihood of the shock occurring during repolarization, which can precipitate ventricular fibrillation. Need a QRS complex present.

Answer 32

Provides a high-energy shock at a RANDOM point in the cardiac cycle (unsynchronized shock) and is indicated in pts w/ v fib or pulseless v tach.

Answer 33

``` AD congenital long QT syndrome caused by molecular defects in K channels Pts are at high risk of syncope, torsade de pointes, and sudden death Tx: refraining from vigorous exercise, avoiding meds that can lengthen the QT interval, maintaining normal levels of Ca, K, + Mg Beta blockers (propranolol) are class 2 antiarrhythmics and the TOC to blunt exertional HR and shorten the QT interval Syptomatic pts (lightheadness, palpitations) or those w/ a hx of syncope require beta blocker tx + long-term pacemaker placement. ```

Answer 34

Fatigue, exertional dyspnea, and LE swelling in the absence of pulmonary edema are consistent w/ right sided HF, the predominant manifestation of restrictive cardiomyopathy. Amyloidosis can cause a restrictive cardiomyopathy.

Answer 35

"Lone AF" is occasionally used for pts w/ paroxysmal, persistent, or permanent AF w/ no evidence of cardiopulmonary or structural heart disease. Pts w/ lone AF are generally <60y and have a CHADsVASc score of 0. Risk of systemic embolization in pts is low and anticoag therapy is not indicated.

Answer 36

Most common primary cardiac neoplasm, usually arises in the LA. Fragments of the tumor can dislodge and lead to systemic embolization (eg stroke, acute limb ischemia) Tumors may cause position-dependent obstruction of the mitral valve, leading to a middiastolic murmur and sxs of decreased cardiac output (eg dyspnea, syncope) Constitutional sxs (fever, wt loss) may be present.

Answer 37

A potent inotropic agent w/ a strong affinity for beta1 receptors and a weak affinity for beta2 and alpha1 receptors. Stimulates increased myocardial contractility leading to improved ejection fraction, reduced LV end systolic volume, and symptomatic improvement of decompensated HF. Increase in myocardial contractility allows for forward ejection of a higher volume of blood and results in decrease in LV end systolic volume.

Answer 38

Congenital malformation of the great vessels that encircle and compress the trachea and/or esophagus Respiratory symptoms incldue biphasic stridor that improves w/ neck extension Esophageal sxs: dysphagia, vomiting, difficulty feeding Dx: CT scan, all pts require direct laryngoscopy, bronchoscopy, and echocardiogram Tx: surgical division of structures creating the ring

Answer 39

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, bibasilar crackles, hypoxemia = pulmonary edema due to acute decompensated HF Due to LV systolic or diastolic function, uncontrolled HTN Tx: supplemental O2, IV furosemide

Answer 40

Alpha1 agonist which causes vasoconstriction In pts w/ decreased blood flow, vasoconstriction can result in ischemia and necrosis of distal fingers and toes Can also occur in intestines (resulting in mesenteric ischemia) or kidney (causing renal failure)

Answer 41

Cause of finger ischemia that typically progresses from pallor to cyanosis to erythema. Can be accompanied by pain and is usually due to cold exposure or stress.

Answer 42

Due to rapid accumulation of a small amount of fluid w/in a stiff pericardium, causing a sudden rise in intrapericardial pressure. Unlike subacute tamponade, the cardiac silhouette can be normal on CXR.

Answer 43

Immediately fatal. Rare instances: aortic rupture w/ bleeding into the L pleural space has been contained (by a hematoma) can present w/ L sided pleural effusion and hypotension. However, it would cause hypovolemic (rather than obstructive) hypotension w/ flat (rather than distended) neck veins.

Answer 44

Direct vascular smooth muscle relaxation causing systemic venodilation and an increase in peripheral venous capacitance Primary anti-ischemic effect mediated by systemic vasodilation and decrease in cardiac preload resulting in a decrease in LV end diastolic and end systolic volume which leads to a reduction in LV systolic wall stressand a decrease in myocardial O2 demand, resulting in relief of anginal sxs [coronary vasodilatoiin effect mechanism is not certain]

Answer 45

``` Supervised graded exercise program is the most useful intervention to improve functional capacity and reduce symptomatic claudication in pts w/ PAD. Antiplatelet agents (aspirin, clopidogrel) reduce overal cardiovascular mortality. Lipid lowering therapy w/ statin should also be given to all pts w/ clinically significant atherosclerotic cvd. ```

Answer 46

Chronic pulmonary emboli can lead to pulmonary HTN and subsequent right HF (cor pulmonale). [COPD is the most common cause of cor pulmonale; distant heart sounds due to inflated lungs Cor pulmonale = RHF from pulmonary HTN; gradual onset, but can present acutely (loud P2, tricuspid regurg, elevated JVP, peripheral edema, hepatomegaly due to hepatic congestion, ascites)] Presentation: right-sided murmurs, elevated JVP, bilateral peripheral edema, and hepatojugular reflux [XR: enlarged central pulmonary arteries and loss of retrosternal air space due to RVH EKG: right axid deviation, R BBB, RAH Right heart cath = gold standard for diagnosis; shows elevated CVP, mean arterial pressure >=25 w/o LH disease]

Answer 47

Or external pacing Indicated only for symptomatic bradycardia. Sx include: lightheadedness, presyncope, or syncope

Answer 48

A disease of non-caseating granuloma infiltration of the myocardium. Can result in serious arrhythmia (AV block most common), restrictive (early) + dilated (late) cardiomyopathy, valvular dysfunction, heart failure, and sudden cardiac death. Should be suspected in any young pt (<55) w/ unexplained 2nd or 3rd heart block or when EKG changes occur in pts w/ known or suspected systemic sarcoidosis

Answer 49

EKG: persistent ST segment elevation after a recent MI and deep Q waves in the same leads. Large VAs can lead to progressive LV enlargement, causing heart failure, refractory angina, vent. arrhythmias, mural thrombus w/ systemic arterial embolization or annular dilatioin w/ MR. Dx: echocardiography

Answer 50

Loud S1 Commonly due to rheumatic heart disease and presents w/ gradual and progressively worsening dsypnea or orthopnea. A fib is a common complication and can cause rapid decompensation in previously asymptomatic pts. Longstanding mitral stenosis can cause severe LA enlargement leading to compression of recurrent laryngeal nerve to cause persistent cough or hoarse voice and elevation of the L main stem bronchus seen on CXR.

Answer 51

Inability of sinoatrial node to generate an adequate heart rate Most common cause: age-related degeneration of the cardiac conduction system w/ fibrosis of the sinus node; ischemia and infiltrative cardiac disease (eg sarcoidosis, amyloidosis) are other potential causes Exercise testing demonstrates chronotropic incompetence (inadequate heart rate response to exercise) Mgmt: pacemaker Once a pacemaker is placed, rate-control meds (beta blockers) can be administered in pts w/ persistent paroxysmal tachyarrhythmias

Answer 52

Decreases w/ expiration | Increases w/ inspiration

Answer 53

Occurs due to myxomatous degeneration of the mitral valve leaflets and/or chordae tendinae. Nonejection clcik w/ a mid to late systolic murmur Third heart sound Most common cause of chronic MR.

Answer 54

Meds shown to improve long-term survival in pts w/ LV systolic dysfunction: beta blockers, ACE-i, ARBs, mineralocorticoid receptor antagonists, and in AA pts a combo of hydralazine and nitrates.

Answer 55

Initial therapy of patients w/ pulmonary edema and hypoxemia due to acute decompensated heart failure includes aggressive IV diuresis, O2 supplementation, and possible assisted ventilation.

Answer 56

RF: smoking Results from hyperreactivity of intimal smooth muscle, leading to intermittent coronary artery vasospasm. Resolves spontaneously w/in 15min. Commonly occurs during sleep. CCB (diltiazem, amlodipin) cause coronary artery vasodilatioin and are the preferred treatment.

Answer 57

Aspirin (+statins) are standard therapy in pts w/ atherosclerotic CAD Aspirin should be avoided in pts w/ vasospastic angina as it can inhibit prostacyclin production and worsen coronary vasospasm. Propranolol can worsen coronary vasospasm as well.

Answer 58

Hypotension and sycnope

Answer 59

Presents w/ recurrent chest pain and new or worsening EKG changes of ischemia (eg ST elevation) Can cause ventricular tachycaredia/fibrillation, which can degenerate further into asystole.

Answer 60

Occurs in pts w/ acute inferior wall MI due to occlusion of the proximal R coronary artery. Hypotension, shock, JVD, clear lung fields EKG: either an inferior MI and/or ST elevation in leads V4R-V6R

Answer 61

Occurs as a late (weeks to months) complications of acute ST segment elevation Characterized by scarred or fibrotic myocardial wall as a result of healed transmural MI Presentation: HF, refractory angina, ventricular arrhythmias, or systemic arterial embolism due to mural thrombus formed w/in aneurysm.

Answer 62

Mechanical complicatoin that usually occurs w/in 5d to 2w after an acute MI (usually anterior). Leads to hemopericardium and eventually cardiac tamponade Presentation: acute onset chest pain, profound shock, w/ rapid progression to pulseless electrical activity and death.

Answer 63

Prompt recognition and restoration of coronary blood flow w/ primary percutaneous intervention or fibrinolysis improves cardiovascular and overall long-term mortality in pt w/ ST elevation MI. No evidence of improved long term outcomes w/ interventions aimed at decreasing cardiac afterload (nitrates, intra-aortic balloon pump) Early use of beta blockers (w/in 24h) decreases myocardial contractility and can reduce myocardial O2 demand in MI, but immediate use of IV beta blockers (before PCI) does not improve outcomes and can exacerbate hemodynamic instability or HF.

Answer 64

Excessive alcohol intake (>2 drinks/d) or binge drinking (>=5 drinks in a row) is assoc. w/ increased incidence of HTN compared to nondrinkers. If medication for HTN is absolutely necessary CCB are preferred over beta blockers unless there are compelling indications for b (HF, axs LV dysfunction, post MI, hyperthyroidism, rate control in a fib).

Answer 65

An abnormal connection between the arterial and venous systems that bypasses the capillary beds Shunting of a large amount of blood through fistula decreases SVR, increases cardiac preload, and increases CO Presentation: widened pulse pressure, strong peripheral arterial pulsation (eg brisk carotid upstroke), systolic murmur, tachycardia, flushed extremities LV hypertrophies and PMI is displaced to the L EKG: LVH Pts have HF b/c circulation is unable to meet O2 demand of peripheral tissues

Answer 66

A form of distributive shock Leads to decrease in SVR (cardiac afterload) due to overal peripheral vasodilaton. Decreased (or low normal) pulmonary cap wedge pressure due to capillary leakage, which causes decreased preload Elevated mixed venous O2 saturation due to hyperdynamic circulatoin (as CO is increased in response to reduced SVR to maintain perfusion) w/ an inability of tissues to adequately extract O2 (may develop lactic acidosis from tissue hypoperfusions)

Answer 67

Decreased cardiac contractility from LV dysfunction causing poor pump function; Low cardiac output leads to high LVEV (preload) and a compensatory increase in systemic vascular resistance (afterload) Elevated RA pressures, PCWP due to volume overload and a compensatory elevation in SVR Pts experience dyspnea and hypoxemia due to pulmonary edema, and lung exam reveals bilateral crackles Decreased CO decreases tissue perfusion, which signals tissues to extract more O2 decreasing MvO2

Answer 68

A form of distributive shock in which CNS injury affects autonomic pathway and results in reduction in SVR. Bradycardia is classic (impaired sympathetic response) MvO2 is low (improved peripheral extraction due to lower flow) No underlying infection

Answer 69

A form of distributive shock that usually presents w/ hypotension from low aldosterone levels. Pts have low SVR w/ assoc. hyperkalemia and hyponatremia

Answer 70

The percentage of O2 bound to hemoglobin in blood returning to the right side of heart. Reflects the amount of O2 "left over" after tissues remove what they need.

Answer 71

Conduction system abnormalities, prolonged PR interval and intraventricular conduction delay (prolonged QRS complex duration) suggest bradyarrhythmia or high grade av block as cause of syncope AV block w/ assoc. bradyarrythmia can be intermittent Normal HR does not exlude bradyarrythmia due to intermittent nature of block EKG findings suggesting an arrhytmia as cause of syncope: inappropriate sinus bradycardia, sinoatrial block, sinus pauses, av block, nonsustained ventricular arrhythmias, and short or prolonged QTc interval.

Answer 72

Diastolic dysfunction caused by impaired myocardial relaxation or increased LV wall stiffness (decreased compliance) leading to increased LVEDP which is transmitted to the LA and pulmonary veins and capillaries = pulmonary congestion, dyspnea, and exercise intolerance. Pt w/ HF w/ preserved ejection fraction, often due to hypertensive heart disease, have typical manifestation of CHF w/ a normal LV EF and objective evidence of diastolic dysfunction. Impaired myocardial relaxation and/or increased LV wall stiffness leads to an increase in LVEDP.

Answer 73

Most common heart defect in Down Syndrome. Clinical features: HF in early infancy, a fixed split S2 (ASD), holosytolic murmur (VSD), holosystolic apical murmur depending on degree of AV valve regurgitation, and a systolic ejection murmur due to increased pulmonary flow from the ASD.

Answer 74

Likely to cause dehydration and are not recommended.

Answer 75

Normal 6-8cm.

Answer 76

Pt w/ WPW syndrome who develop a fib w/ a rapid ventricular rate should be treated w/ cardioversion or antiarrythmics such as procainamide. AV nodal blockers such as beta blockers, calcium channel blockers, digoxin, and adenosine should be avoided as they can cause increased conduction through the accessory pathway.

Answer 77

SEs: n/v/diarrhea, vision changes, arrhythmias Pts chornically taking digoxin should have close and routine monitoring of their digoxin levels Causes increased ectopy and increased vagal tone. Atrial tachycardia w/ AV block occurs from the combination of these two effects, and is relatively specific for digitalis toxicity. Digitalis toxicty does not cause atrial flutter, atrial fibrillation, Mobitz type II second degreee AV block (as this involves pathology of the conduction system below the AV node), and multifocal atrial tachycardia.

Answer 78

Uncommon cause of dilated cardiomyopathy that develops during last month of pregnancy or w/in 5 months following delivery dyspnea on exertion, LE edema, 3rd heart sound = decompensating HF due to PPCM Often assoc. w/ MR (holosystolic murmur) Dx: transthoracic echocardiogram shows dilated LV cavity w/ global systolic dysfunction and EF <45% can confirm dx Urgent or immediate delivery should be considered for pts w/ advanced HF or hemodynamic instability.

Answer 79

Refers to 2 strong systolic peaks of the aortic pulse from the LV ejection separated by a midsystolic dip. It can be palpated in patients w/ significant aortic regurgitation (w/ or w/o aortic stenosis), HOCM, and PDA.

Answer 80

Clear lungs on auscultation Nitrates should be avoided as venous dilation causes an abrupt decrease in RV preload and can lead to profound hypotension; diuretics (volume depletion), opiates (venous dilation) can do this as well To treat inadequate preload, give bolus w/ isotonic saline to increase RV preload and improve CO Inotropic agents (dopamine, dobutamine) may be needed for RV MI pts w/ persistent hypotension despite adequate fluid resuscitation.

Answer 81

Narrowing of the descending aorta that leads to a proximal arterial pressure load. Headaches, epistaxis Pts typically present w/ upper extremity HTN and diminished femoral pulses w/ brachial femoral delay. CXR reveals inferior notching of the 3-8th ribs due to pressure-induced enlargement of the intercostal arteries. Can develop L-sided cardiac enlargement Evaluate w/ simultaneous palpation of brachial and femoral pulses to asses for brachial-femoral delay Bilateral UE (supine position) and LE (prone position) BP measurement to evaluate for U an LE BP differential EKG shows sytemic long-standing HTN: high voltage QRS complexes, lateral ST segment depression, lateral T wave inversion Dx: echocardiogram

Answer 82

Often seen in ebstein congenital abnormality (apical displacement of the tricuspid valve w/ atrialization of the RV).

Answer 83

In severe, chronic aortic regurg, the LV responds to volume overload w/ eccentric hypertrophy to increase both LV compliance and contractility, allowing for an increase in stroke volume to maintain cardiac output. This allows for a temporary asymptomatic period. However, overwhelming wall stress eventually leads to symptomatic, decompensated HF.

Answer 84

Pain, pallor, poikilothermia (cool extremity), paresthesia, pulselessness, paralysis Due to thromboembolic occlusion ABI (ratio of SBP in ankle/arm) is used as a screening and/or diagnostic tool in pt w/ suspected peripheral arterial disease Acute limb threatening complication should be treated with anticoagulation, heparin, which prevents further thrombus propagation and thrombosis in distal arterial and venous circulation

Answer 85

Convential beta blockers (eg metoprolol, atenolol, propranolol) are assoc. w/ impaired glucose control and increased weight gain, likely via effects on skeletal muscle that lead to reduced insulin sensitivity. Therefore, these drugs are an unfavorable option for HTN mgmt in pts w/ or at high risk for type 2 DM.

Answer 86

Alpha 1 stimulation causes vasocontriction which reduces glucose uptake into skeletal muscles Alpha 2 decreases insuline release --> increased glucose levels in blood

Answer 87

Can be used in pts w/ profound bradycardia However, it fails to capture, and even adequate capture (w/ increases in HR) rarely results in improved cardiac output and BP in the setting of severe betablocker overdose.

Answer 88

Loss of intravascular volume decreases LV preload which leads to decreased CO; LV, decreased in size due to low filling volume, compensates by increasing ejection fraction Characterized by low BP and CO and a compensatory elevation in HR and SVR (in attempt to maintain CO). Central venous pressure and pulmonary capillary wedge pressure are low due to decreased intravascular blood volume. Cold extremities, flat neck veins

Answer 89

RF: prior cardiac surgery (eg CABG, cardiac valve surgery), mediastinal irradiation, tuberculosis, malignancy, or uremia -US: idiopathic or viral pericarditis, radiation tx, cardiac surgery, connective tissue disorders -World: TB Important cause of R HF Presentation: progressive peripheral edema, ascites, elevated jugular venous pressure, pericardial knock (middiastolic sound) Kussmal's sing: lack of typical inspiratory decline in central venous pressure Sharp x and y descents on central venous tracing XR: pericardial calcifications

Answer 90

vague chest discomfort Most thoracic aortic aneursyms are due to age related degenerative changes that lead to disruption of the aortic medial layer, resulting in loss of elasticity and consequent aortic dilation. XR: widened mediastinum, enlarged aortic knob, tracheal deviation

Answer 91

Characteristic EKG findings: short PR interval (<120s), slurred initial upstroke of the QRS complex (delta wave), and widening of the QRS complex w/ ST/T wave changes. WPW is due to an accessor pathway that bypasses the AV node and directly connects the atria to the ventricles.

Answer 92

Ventricular arrhythmias, including ventricular premature beats, nonsustained or sustained ventricular tachycardia, and ventricular fibrillaton are quite common in the immediate post MI period. Ventricular fibrillation is the most frequent underlying arrhythmia responsible for sudden cardiac arrest in the setting of acute MI. More than 50% occur in the 1st hour of sx onset. Reentry is the predominant mechanism responsible for ventricular arrhythmias in the immediate post infarction period.

Answer 93

The use of anticoagulants in pts w/ suspected aortic disessction and possible hemopericardiuim is contraindicated.

Answer 94

DM pt age 40-75 should be treated w/ statin therapy in addition to lifestyle modification and glucose control. Those w/ a 10y risk of atherosclerotic cardiovascular disease <7.5% should receive moderate intensity statin therapy. Those w/ a risk >7.5% should receive high intensity statin therapy.

Answer 95

Widely split S2, increased intensity of the pulmonic component of S2

Answer 96

Electrical alternans w/ sinus tachycardia is a highly specific sign for large pericardial effusion. This is due to the swinging motion of the heart in the pericardial cavity causing a beat to beat variation in QRS axis and amplitude. Pt w/ cardiac tamponade and HD compromise should have emergency pericardiocentesis.

Answer 97

The second most common type of AS, usually refers to congenital LVOT obstruction due to discrete or diffuse narrowing of ascending aorta Causes a systolic murmur similar to that seen in AS, but murmur is heard in R 1 ICS Pts may also have unequal carotid pulses, differential blood pressure in the UE (high pressure jet in ascending aorta) and a palpabel thrill in the suprasternal notch LVH and coronary artery stenosis These changes with increased in myocardial O2 demand during exercise can lead to subendocardial or myocardial ischemia leading to angina during exericse

Answer 98

Results from normal blood flow from a structurally normal heart. The intensity is typically grade I or II and decreases w/ standing and valsalva. Valsalva and standing - decrease venous blood return Benign murmurs are also early or mid-systolic in timing. Mgmt: observation and reassurance

Answer 99

Pt initially dx w/ HTN should have a detailed hx and physical. In addition, the following basic testing should be performed: u/a for occult hematuria and urine protein/creatinine ratio chemistry panel lipid profile (risk stratification for CAD) baseline EKG (to evaluate for CAD or LVH)

Answer 100

It can identify asymmetrical kidney size or small atrophic kidneys, which suggests primary renal disease. Dupex dopper u/s is also helpful in screening for RAS in pts w/ severe or resistant HTN. However, these imaging studies are done only if there is elevated serum creatinine or abnormal u/a.

Answer 101

ESR usually >50

Answer 102

Characterized by temporal dissociation of P waves and QRS complexes (atrioventricular [AV] dissociation). Pts w/ symptomatic 3rd degree AV block should be managed w/ temporary pacemaker insertion while undergoing further evaluation to identify and correct reversible causes. A permanent pacemaker is indicated if no reversible causes of heart block are found. Adenosine, beta blockers, and digoxin are contraindicated in complete heart block.

Answer 103

IV abx decrease the risk of septic emboli in pts w/ native valve infective endocarditis. Surgery can be considered in pts w/ significant valvular dysfunction, persistent/difficult to treat infection, or recurrent embolism.

Answer 104

``` The pressure in the superior vena cava (SVC) where catheter tip is located. Approximates RA pressures Low CVP (low preload): reflects hypovolemic or distributive shock Elevated CVP (high preload): reflects cardiogenic or obstructive shock Blunt cardic injury w/ myocardial dysfunction can cuase cardiogenic shock w/ elevated CVP and refractory hypotension ```

Answer 105

Small VSDs close spontaneously in 75% of children by age 2 w/ no long term sequelae.

Answer 106

symptomatic: occurence of TIA or stroke in distribution of affected artery w/in previous 6mo. Carotid endarterectomy is recommended for symptomatic pts w/ high grade carotid stenosis (70-99% for symptomatic lesions) Asymptomatic: carotid atherosclerosis w/o recent TIA or stroke. <80; managed medically (aspirin + statins)

Cardiology Flashcards

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