Usmle Step 2: Cardiology Qbank

Front 1

Gold standard of diagnosis/follow-up of abdominal AA

Back 1

Abdominal U/S (nearly 100% sensitivity and specificity)

- may consider abdominal CT if can add valuable info when differential dx of patient's abdominal pain is broad (contraindicated in renal dz and has poor visualization of aortic branch origin)

Front 2

Dilated cardiomyopathy due to alcohol - expected findings?

Back 2

Thrombocytopenia, macrocytosis, and elevated transaminases all suggestive of alcoholism

Total abstinence from alcohol is the mainstay of alcoholic cardiomyopathy management and it may reverse this condition if it is employed earlier in the course of the dz

Front 3

transient ST elevations on ECG, chest pain that wakes one up during sleep

Back 3

Prinzmetal's angina

Greatest risk factor? epidemiology? tx?

Hint 3

Greatest risk factor = smoking (often lack other cardiovascular risk factors

Other sx - young females

Tx: nitrates or Ca channel blockade; avoid aspirin and non-selective beta blockers bc they can promote vasoconstriction

Front 4

Indications for digoxin use

Back 4

1) increase contractility in pts with CHF

2) rate control agent in pts with afib or flutter

Front 5

Good marker for hypovolemia

Back 5

Increased BUN/creatinine ratio (although not very specific)

Front 6

JVP distension and new-onset RBBB

Back 6

Massive PE (likely in a postoperative patient)

Also syncope (due to hypotension), tachycardia

Front 7

ECG findings of MI

Back 7

ST elevations, T wave inversions, Q wave changes

Front 8

Which drugs have been shown to have a mortality benefit when given as secondary prevention?

Back 8

Aspirin, beta blockers, ACEi, lipid-lowering statin drugs

additionally, clopidogrel should be prescribed to all pts with unstable angina/non-ST elevation MI, as well as patients who are post PCI

Front 9

Hypertensive urgency vs Hypertensive emergency

Back 9

Urgency: severe HTN (usually greater than or equal to 180/120) with no sx or acute end organ damage

Emergency: severe HTN with acute, life threatening end organ complications
- malignant: severe HTN with retinal hemorrhages, exudates, or papilledema
- hypertensive encephalopathy: severe HTN with cerebral edema and non-localizing neurologic sx and signs

Front 10

severe N/V after returning from a party. Also complaining of CP more intense than any other previously experienced.

Exam reveals injected conjunctivae and bilateral dilated pupils. Pleural fluid has elevated amylase content.

Dx?

Back 10

Esophageal Perforation - Boerhaave's syndrome (spontaneous esophageal rupture)

classic presentation is acute, severe chest or epigastric pain after an episode of retching. Fever and dyspnea are common (not hematemesis)

pleural fluid will have high amylase concentration, low pH, and may contain particles of food

Front 11

Digitalis (ie digoxin) toxicity

Back 11

1) increases ectopy - Atach
2) increases vagal tone and decrease conduction through AV node --> AV block

- results in atrial tachycardia with AV block --> specific for digitalis toxicity

Front 12

How to distinguish Atach vs Aflutter

Back 12

A tach --> slower atrial rate: 150-250 bpm as opposed to 250-350 bpm

Front 13

Characteristics of aortic stenosis murmur

Back 13

1) Harsh systolic murmur over right sternal edge

2) Only left sided heart murmurs increase on expiration

3) S4 due to left ventricular hypertrophy (forceful atrial contraction against thick, non-compliant ventricle)

4) radiation to carotids

5) tardus et parvus

Indicators for surgery?

Hint 13

symptomatic --> "SAD"
Syncope
Angina
Dyspnea

Front 14

Complications of venous insufficiency

Back 14

Lower extremity edema,
stasis dermatidis
ulceration

Front 15

Amiodarone side effects

Back 15

check PFTs, LFTs, and TFTs

It's a K+ channel blocker - increase AP duration, increase ERP; used when other antiarrythmics fail; increase QT interval

Front 16

Beta blockers such as metoprolol are relatively contraindicated in what patients?

Back 16

obstructive lung dz (ie asthma/COPD), but CAN be used in restrictive lung dz

Front 17

Explain the significance of S3

tx?

Back 17

low frequency diastolic sound -- associated with LV failure (can be normal in well-trained athletes and younger individuals)

Intravenous diuretics provide symptomatic benefits to patients with decompensated heart failure

Front 18

Indicators of cocaine abuse

Back 18

EKG changes of myocardial ischemia: ST depression and T wave inversion

tx of cocaine related cardiac ischemia?

Hint 18

Benzos - reduce anxiety and hypertension/tachycardia

Aspirin - retards thrombus formation

Nitrates - being a vasodilator, will be beneficial for the cocaine-induced coronary artery vasoconstriction (pure alpha blockers and Ca channel blockers may be added if desired)

- pure beta blockers would be contraindicated - may aggravate cocaine-mediated vasoconstriction

Front 19

Young healthy patient develops CHF - name sx of CHF and what might have caused this?

Back 19

sx: PND, DOE, peripheral edema, hepatomegaly, cardiomegaly, bilateral pleural effusions, S3

likely due to myocarditis (viral infection, particularly Cocksackie B virus, is the most common cause

Front 20

Clues of aortic dissection

Next best step in management?

Back 20

- Intense, retrosternal pain that radiates to the back of the chest, along with normal EKG = strongly suggestive; also presence of early diastolic murmur, characteristic of aortic regurg
- blood pressure may be different in both arms due to dissection

- preferred diagnostic tool = TEE
- can also use MRI and CT, but these are time consuming

-

Front 21

Indications for adenosine

Back 21

useful in initial diagnosis and management of pts with narrow-QRS-complex tachycardia

- slows the sinus rate, increases AV nodal conduction delay, or can cause transient block in AV node conduction.
- useful in identifying P waves to clarify dx of Aflutter or Atach
- can terminate paroxysmal SVT by interrupting the AV nodal reentry circuit -

Front 22

SVT - what does this mean?

common sx?

Back 22

any tachycardia originating above the His-bundle

-includes sinus tach, multifocal Atach, Aflutter, Afib, AVNRT, AVRT, and junctional tachycardia

sx: palpitations, dizziness, lightheadedness, SOB, diaphoresis, CP, presyncope, syncope

Front 23

Indications for IV nitroglycerine

Back 23

- myocardial ischemia
- pulm edema
- hypertensive urgency

Front 24

Pt with systolic-diastolic abdominal bruit; hx of HTN and atherosclerosis

Back 24

strongly suggestive of renal artery stenosis (up to 85% of patients)

particularly if HTN is difficult to control despite use of multiple medications

Front 25

Differential for blood pressure measured differently in both arms

Back 25

If with CP, consider aortic dissection

If greater in R arm than L - coarctation (if coarctation is proximal to left subclavian artery origin)

Secondary to subclavian atherosclerotic dz

Front 26

Signs of R ventricular infarction

Back 26

Signs of inferior MI - ST segment elevation in leads II, III, and aVF (inferior leads) and ST segment depression in leads I and aVL (left-most leads)

PE: hypotension, JVD, clear lung fields

side: preload dependent and should be treated with IV FLUIDS, not preload reducing meds like nitrates and diuretics

Front 27

Describe how diastolic dysfunction may lead to Afib? What is it commonly caused by?

Back 27

HTN is classic cause

Chronically elevated LV diastolic pressures cause LA dilatation, which in turn can lead to atrial fibrillation

Tx = diuretics and BP control

Front 28

Describe causes of high-output HF

Back 28

Anemia, hyperthyroidism, beriberi, Paget's dz, and AV fistulas

Front 29

When do you suspect hyperparathyroidism?

Back 29

uncommon cause of secondary HTN --> "stones, bones, abdominal moans, psychiatric groans"

look for muscle weakness, recurrent nephrolithiasis, neuropsychiatric sx, and hypercalcemia

Front 30

Signs of coarctation of the aorta

Back 30

H/A, epistaxis, and blurred vision, elevated BP in upper extremities, possible "to-and-fro machinery murmur" over posterior chest, brachial femoral pulse delay on exam

Front 31

Hypothyroidism can cause _____

Back 31

HTN!

Front 32

Most important factors in improving pt survival?

Back 32

adequate bystander CPR
prompt rhythm analysis
defibrillation

Front 33

Causes of Afib

Back 33

Cardiac: HTN, acute ischemia, HF, myopericardial inflammation, valve dz, and surgery

Pulmonary: any acute lung dz (eg PNA), PE, and hypoxia

Metabolic: catecholamine surges and hyperthyroidism

Drugs: alcohol, cocaine, amphetamines, and theophylline

Front 34

signs of Cushing's syndrome

Back 34

chronically elevated systemic corticosteroids

typical changes include: central obesity, DM, PROXIMAL MUSCLE WEAKNESS, psychosis, thin skin, and osteoporosis

Front 35

Hypogonadism, arthropathy, DM, and hepatomegaly

Back 35

Hereditary hemachromatosis

Front 36

Three most common causes of aortic stenosis

Back 36

senile calcific aortic stenosis

bicuspid aortic valve (majority of patients under 70 yrs old)

rheumatic heart dz

Front 37

How to identify AR on exam and what is the primary medical therapy?

Back 37

high pitched, blowing descrescendo diastolic murmur best heard at 3rd rib, intensified with handgrip

Tx: afterload reduction with ACEi or Ca channel blockade (nifedipine)

Front 38

Treatment for premature atrial beats

Back 38

benign and neither require any F/U or tx

Front 39

Best lifestyle interventions in patients newly diagnosed with stage I hypertension

Back 39

Obese patients: weight loss

Non-obese patients: diet high in fruits and veggies, followed by a low salt diet

(smoking has little effect on blood pressure reduction, but significantly reduces CV dz)

Front 40

What new heart sound may be appreciated following acute MI?

Back 40

S4 --> ischemic damage in setting of MI may lead to diastolic dysfunction and a stiffened LV, resulting in an atrial gallop

Front 41

Ascending aortic aneurysm vs Descending? Cause?

Back 41

Ascending: most often due to cystic medial necrosis or connective tissue disorders

Descending: usually due to atherosclerosis

Front 42

What do you expect in HOCM PE and epidemiology?

Back 42

Syncope in a young patient with crescendo-decrescendo murmur at the lower left sternal border is most likely due to HOCM.

What is the inheritance pattern?

Hint 42

Autosomal dominant

Front 43

Tx of pericarditis?

Back 43

NSAIDs

Front 44

Thiazide diuretics side effects (metabolic + electrolyte)

Back 44

Metabolic: hyperglycemia, increased LDL cholesterol, and plasma TG

Electrolytes: hyponatremia, hypoK, HyperCa

Front 45

mechanism responsible for pain relief in pts with anginal pain tx with nitroglycerin

Back 45

dilation of veins and decrease in ventricular preload

Front 46

pathophysiologic mechanism responsible for vfib patients?

Back 46

reentrant ventricular arrythmia (ventricular fibrillation) -> most common cause of death in pts with acute MI

Front 47

HOCM murmur gets louder with what? autosomal dominant disorder

Back 47

located at hte left lower sternal border and is worsened by maneuvers that decrease preload (eg valsalva, standing)

Contrary to most murmurs, the murmur of HOCM increases as preload decreases since this lessens the size of the ventricular cavity and causes increased outflow obstruction

Front 48

maneuvers that decrease/increase venous return

Back 48

Increase: Squatting, Recumbency, Leg raising

Decrease: Valsalva

what about sustained handgrip?

Hint 48

leads to increase in SVR and increased afterload!! -> leads to larger ventricular volume nad thus a decrease in outflow obstruction and quieter murmur

usually used to differentiate btw murmurs of aortic stenosis and mitral regurg where it causes a decrease and increase, respectively, in the severity of the murmur.

Front 49

pharmacologic cardioversion for atrial fibrillation

Back 49

amiodarone and quinidine

Front 50

lidocains used for what?

Back 50

ventricular arrhythmias

Front 51

MR caused by what?

Back 51

myxomatous degeneration of the mitral valve leaflets and chordae and causes a mid-systolic click followed by a mid-to-late systolic murmur.

chronic severe MR causes what?

Hint 51

left atrial and ventricular enlargement leading to Afib, LV dysfunction, and CHF

Front 52

tx for acute desponsated heart failure

Back 52

acute pulmonary edema, supplemental O2, assisted ventilation as needed, aggressive IV diuresis, and possible vasodilator therapy (nitroglycerine, nitroprusside)

Front 53

Chagas dz caused by what and characterized by what?

Back 53

chronic dz that can cause megaesophagus, megacolon, and/or cardiac dysfunction. Protozoan trypanosoma cruzi, endemic to Latin America, is responsible

Front 54

Afib -> what should be used pharmacologically?

Back 54

rate control better -> initially with beta blockers or Ca channel blockers.

immediate synchronized electrical cardioversion is indicated in hemodynamically unstable pts with rapid Afib

Front 55

How to prevent ventricular remodeling in the weeks-months following MI?

Back 55

ventricular remodeling may lead to dilatation of the ventricle -> lessened by ACE inhibitors!

Front 56

how does arteriovenous fistula cause high-output cardiac failure?

Back 56

shunt blood from arterial to venous side, thereby increasing cardiac preload.

pt develops heart failure despite maintaining a nl or high CO bc the circulation is unable to meet the O2 demand of the peripheral tissues

Front 57

describe reinin-angiotensin-aldosterone system in understanding HTN

Back 57

renin produced by JGA cells of kidney in response to hypoperfusion.

renin cleaves angiotensinogen into angiotensin I.

angiotensin I is converted to angiotensin II by ACE in lung

angiotensin II is a potent vasoconstrictor. also promotes vasopressin (ADH) release from pituitary and aldosterone production in the adrenal cortex.

Front 58

three major mechanical rupture due to MI

Back 58

mitral regurg due to papillary muscle rupture

left ventricle wall rupture

interventricular septum rupture

(all 3 can result in hTN)

Front 59

medications that improve mortality in CHF pts

Back 59

ACEi, beta blocker, ARB, spironolactone

Front 60

digoxin in CHF

Back 60

improves symptoms but no mortality benefit (is that true? also reduces hospitalizations

Front 61

cardiac stress testing: which meds should be withheld for at least 48 hrs

Back 61

beta blockers, ca channel blockers, and nitrates (antianginal agents)

however, should be continued in pts with known CAD undergoing stress testing to assess efficacy of antianginal therapy

Front 62

strongest predictors of AAA expansion and rupture

Back 62

strongest predictors: large aneurysm diameter, rapid rate of expansion, and current cig smoking

What are current indications for operative/endovascular repair?

Hint 62

large aneurysm diameter (>5.5cm), rapid rate of expansion (>1cm/yr), and presence of sx (abdominal, back or flank pain; limb ischemia) regardless of aneurysm size

Front 63

Aortic dissection with sx of lower extremity weakness. Mechanism?

Back 63

dissection extending into the spinal arteries causing spinal cord ischemia

Front 64

most useful lab test for assessment of re-occlusion after MI

Back 64

CK-MB because it typically returns to nl levels within 1-2 days. Troponin takes 10 days to return to nl

Front 65

most common causes of AR

Back 65

bicuspid aortic valve in young adults in developed countries

rheumatic heart dz in developing countries

Front 66

First line medical therapy for HOCM?

Back 66

either beta blockers or cardiac acting Ca channel blockers (dilt) since they promote DIASTOLIC RELAXATION (ie beta blockers increase time to refill ventricle during diastole)

differentiate murmur of HOCM vs aortic stenosis

Hint 66

HOCM: left sternal border
aortic stenosis: R sternal border

Front 67

symptomatic bradycardia treated with what?

Back 67

IV atropine, followed by transcutaneous pacing. Meds that slow the HR should be replaced with alternative therapeutic regimens. If bradycardia doesn't resolve, permanent pacemaker may be necessary

Front 68

role of IV adenosine

Back 68

causes temporary AV block, which is useful in identifying, and sometimes terminating, SVT.

Front 69

common cause of endocarditis a/w nosocomial UTI

Back 69

Enterococcus

what about healthcare-associated and community-acquired?

Hint 69

healthcare-associated: staphylococcal

community acquired: streptococcal

Front 70

Mitral stenosis - how is it connected with Afib and hemoptytis?

Back 70

Mitral stenosis results in LA dilation and a risk of Afib and cardiac emboli. The pressure is also transmitted to the pulmonary vasculature, which can result in dyspnea, cough, and hemoptysis

Front 71

niacin causing flushing and pruritis. mechanism?

Back 71

side effect explained by prostaglandin-induced peripheral vasodilatation that can be reduced with low dose ASA

Front 72

CHADS2 score

Back 72

0 - no anticoagulation (preferred) or ASA
1 - anticoagulation (preferred) or ASA
2-6 - anticoagulation

CHF
HTN
Age>75
DM
Prior stroke or TIA

Front 73

Most frequent origin for ectopic foci causing Afib?

Back 73

pulmonary veins

Front 74

chostochondritis

Back 74

chest pain that is reproducible with palpation suggest MSK etiology -> sharp, focal, lasts for hours, worsens with inspiration and movement all suggests musculoskeletal etiology

Front 75

primary hyperaldosteronism (conn's syndrome) causes what findings?

Back 75

HTN, mild hypernatremia, hypoK, and metabolic alkalosis

dx suggested by low renin and elevated aldosterone levels

Front 76

Constrictive pericarditis can cause what?

Back 76

CO compromised and venous pressures become chronically elevated -> increased JVP, severe ascites and hepatic congestion, dyspnea and weakness.

how is dx made and tx?

Hint 76

calcified pericardium on CXR, thickened pericardium on CT or MRI,, pressures during cardiac cath; sharp x and y descents are characteristically seen on central venous tracing

tx: diuretics or pericardiectomy

Front 77

Most common causes of pericarditis?

Back 77

US: idiopathic or viral pericarditis (>40%, rads therapy, cardiac surgery, and connective tissue disorders (less than 10%)

In developing countries, TB!

Front 78

distinguishing tricuspid regurg on exam

Back 78

augmentation of intensity of holosystolic murmur with inspiration (100% sensitivity and 88% specificity in differentiating R sided systolic murmurs from all others

Front 79

How to treat stable vs unstable SVT

Back 79

stable: initially with vagal maneuvers followed by adenosine and AV nodal blockers.

unstable: DC cardioversion

Front 80

tx for third degree heart block

Back 80

characterized by complete independence of P waves and QRS complexes, both of which contract at completely separate rates.

tx is expeditious pacemaker placement, as the rhythm can degenerate into Vtach or Vfib

Front 81

causes of restrictive cardiomyopathy

Back 81

sarcoid, amyloid, postradiation fibrosis, endocardial fibroelastosis, loffler's syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate) and hemochromatosis (dilated cardiomyopathy can also occur)

common causes of amyloidosis?

Hint 81

multiple myeloma and chronic inflammatory dz such as RA

Front 82

S4 causes

Back 82

a-stiff-heart

restrictive cardiomyopathy or LV hypertrophy from prolonged HTN

S4 corresponds with atrial contraction and is believed to result from the sound of blood striking a stiffened LV

Front 83

tx of first degree AV nodal block

Back 83

nl QRS: due to delayed AV nodal conduction and require no further evaluation

widened QRS: likely conduction delay below the AV node and should have electrophysiology testing to determine its nature

Front 84

ICU patient requiring aggressive vasopressors to maintain BP develops cool, dusky fingertips.

What happened?

Back 84

pressors such as NE can cause ischemia of the distal fingers and toes 2/2 vasospasm. dx suggested by symmetric duskiness and coolness of all fingertips.

Front 85

nl JVP

Back 85

3cm above sternum when bed at 45 degrees

Front 86

hypoK + HTN

Back 86

look up!

Front 87

adverse effects of digoxin

Back 87

N/V, diarrhea, vision changes, arrhythmias

Front 88

Prinzmetal's angina characteristics

Back 88

vasospastic disorder that typically occurs in young female smokers. Chest pain usually occurs in the middle of the night, and episodes are a/w transient ST elevations on EKG

most a/w what condition?

Hint 88

Raynaud phenomenon

Front 89

patient with MI who develops cold leg and no distant pulses. Next step?

Back 89

ECHO to r/o thrombus in LV

Front 90

Physical exam finding a/w aortic dissection

Back 90

tearing CP radiating to the back and neck.

AORTIC REGURG is complication and p/w early diastolic murmur

Front 91

premature atrial complexes tx

Back 91

asymptomatic: tobacco and alcohol are reversible risk factors for PACs (also caffeine and stress)

symptomatic: beta blockade

Front 92

ARDS criteria

Back 92

bilateral lung opacities on imaging c/w pulm edema, no signs of cardiac failure or fluid overload (PCWP < 18), PaO2/FiO2 < 300 mmHg and PEEP > 5cm H20

Front 93

characteristics of second degree heart block

Back 93

prolongation of PR interval with occasional dropped beats

Mobitz I: PR interval gradually lengthens until beat is dropped --> due to AV NODE CONDUCTION IMPAIRMENT

tx =

Mobitz II: PR intervals are of constant length before dropped beat, below level of AV node block

Prognosis better for type I

Front 94

approach to wide complex tachy

Back 94

pic

Front 95

EKG findings with pericardial effusion

Back 95

electrical alternans: amplitudes of QRS complexes vary from beat to beat. Fairly specific for pericardial effusion.

Enlargement of cardiac silhoutte can be seen on CXR. Echo for definitive dx

Front 96

orthostatic hypotension

Back 96

drop in 20mmHg systolic or 10mmHg diastolic when moving from lying down to standing.

Front 97

reasons for increased susceptibility to orthostatic hTN in elderly

Back 97

progressively decreasing baroreceptor sensitivity, arterial stiffness, decreased NE content of sympathetic nerve endings, and reduced sensitivity of the myocardium to sympathetic stimulation

Front 98

objective findings of cardiogenic shock?

Back 98

reduced cardiac index and elevated pulm capillary wedge pressures (>12) d/t ventricular pump failure.

SVR is typically increased to maintain adequate tissue perfusion pressure.

Front 99

Aortic regurgitation causes what realizations in the patient?

Back 99

widening of pulse pressure can be felt as a "water hammer" pulse

lying down and turning to the left brings the heart closer to the chest wall and can make the pt more aware of the forceful heartbeat

Front 100

peripheral edema in someone taking BP meds

Back 100

dihydropyridine Ca channel antagonists such as AMLODIPINE should always be considered in differential dx, along with other causes of peripheral edema such as heart failure, renal dz and venous insufficiency

Front 101

what can occur as a complication of aortic dissection?

Back 101

cardiac tamponade with rupture of the aorta and rapid accumulation of blood in the pericardial space.

-> increased pericardial pressure causes compression of cardiac chambers and limits diastolic filling of the R sided chambers.

Front 102

s/e of amiodarone

Back 102

indicated for ventricular arrhythmias. also used for rhythm control in pts with atrial fib and underlying left ventricular systolic dysfunction

a/w broad range of adverse effects, including hypo and hyperthyroidism, hepatotoxicity, pneumonitis, corneal deposits, and skin changes (blue gray skin discoloration)

Front 103

vasovagal syncope workup

Back 103

usually a clinical dx and needs no further testing. if hx and physical exam point strongly toward diagnosis and resting ECG is nl.

upright tilt table test may be used to establish dx! patient passively moves pt from different positions and if there are signs of unconsciousness, the test is positive > limited sensitivity/specificity

Front 104

PVCs following MI

Back 104

3829

common in pts post MI and can be recognized by their widened QRS (>120msec), bizarre morphology, and compensatory pause. even though they may indicate a worse prognosis, tx NOT INDICATED unless pt is symptomatic.

if symptomatic, beta blockers

Front 105

which murmurs should always be investigated using echo?

Back 105

diastolic and continuous murmurs as well as loud systolic murmurs.

midsystolic soft murmurs (grade 1-II/VI) in an asymptomatic young pt are usually benign and need no further workup

Front 106

WPW mgmt

Back 106

those who develop afib with RVR should be treated with cardioversion or antiarrhythmics like procacinamide

AV nodal blockers like beta blockers, ca channel blockers, digoxin, and adenosine should be avoided bc they can increase conductance through the accessory pathway.

Front 107

young pt with severe symptomatic HTN with HA, epistaxis, and e/o L ventricular hypertrophy on ECG


dx?

Back 107

probably coarctationo f hte aorta -> simultaneous palpation of hte brachial and femoral pulses to assess for brachial-femoral delay.

also have supine bilateral brachial and popliteal blood pressures measured to assess for differential pressures

Front 108

flecainide

Back 108

typically used to treat ventricular arrhythmias or SVT such as Afib. class 1c antiarrhythmic med that blocks sodium channels.

Front 109

when should renovascular htn be suspected

Back 109

all pts with resistant HTN and diffuse atherosclerosis, asymmetric kidney size, recurrent flash pulm edema, or elevation in serum creatinine > 30% from baselineafter starting ACEi or ARB.

prsence of continuous abdominal bruit has a high specificity for hte presence of renovascular HTN

Front 110

beck's triad

Back 110

hypotension, distended neck veins, and muffled heart sounds -> indicative of cardiac tamponade.

reduction of LV preload, stroke volume and CO!

Front 111

necessary adjunct to tx of MI if pulmonary edema is present

Back 111

diuretics such as furosemide

aka flash pulmonary edema

Front 112

OCP use and hypertension

Back 112

OCP can be a potential cause of elevated BP and hypertension, and discontinuing its use can correct the problem in most pts

Front 113

pulsus paradoxus

pulsus parvus et tardus

Back 113

fall in systemic arterial pressure by more than 10mmHg during inspiration, and is often a/w cardiac tamponade
- may also occur in conditions w/o pericardial effusion such as severe asthma or COPD

pulsus parvus et tardus: decreased pulse amplitude and delayed pulse upstroke: a/w aortic stenosis

Front 114

procainimide, lidocaine, quinidine

Back 114

procainimide: treats atrial and ventricular arrhythmias

lidocaine: used to treat ventricular arrhythmias

quinidine: used to treat atrial arrhythmias

Front 115

what do pericardial effusions appear as on cxr?

Back 115

enlarged, watter bottle shaped cardiac silhouttes on cxr

PE of pericardial effusions without cardiac tamponade include diminished heart sounds on auscultation and a difficult to palpate PMI.

4445

Front 116

young person with heart failure. suspect what? and what do you expct on echo

Back 116

dilated cardiomyopathy, particularly after coxsackievirus B infxn. dx made by echo, which typically shows dilated ventricles and diffuse hypokinesia resulting in systolic dysfunction (low EF).

tx largely supportive, involving mainly the mgmt of CHF sx

Front 117

cardiac index, TPR, and LVEDV in heart failure?

Back 117

decreased CI (decreased cardiac output), increased TPR, and increased LVEDV

Front 118

three clinical findings characteristic of aortic dissection

Back 118

abrupt onset "tearing" pain in the chest or back, variation in the blood pressure between right and left arms, and widened mediastinum on CXR.

when two or more of these findings are present, the incidence of dissection exceeds 80%

Front 119

pt with wide complex Vtach following IV furosemide (h/o heart failure)

next step?

Back 119

measure serum electrolytes --> loop diuretics cause hypoK and hypoMg -> can cause ventricular tachy, adn also potentiates the side effects of digoxin

Front 120

property of dipyrimidole in the use of myocardial perfusion scanning

Back 120

reveals areas of restricted myocardial perfusion

the redistribution of coronary blood flow to nondiseased segments induced by this drug is called coronary steal phenomenon

dipyridamole and adenosine are coronary vasodilators

Front 121

differentiating between cardiac adn liver related causes of lower extremity edema?

Back 121

hepatojugular reflux

pts with peripheral edema d/t heart failure have elevated JVP and positive hepatojugular reflux.

those with peripheral edema from primary hepatic dz and cirrhosis have reduced or nl JVP and negative hepatojugular reflux

Front 122

acute aortic dissection: when to do surgery vs medical mgmt

Back 122

type A (ascending aorta): medical therapy and surgery

type B (descending aorta): medical therapy alone -> beta blockers!

Front 123

electrical alternans and sinus tachycardia

Back 123

identify on 4390

highly specific sign for large pericardial effusion.

due to swinging motion of the heart in the pericardial cavity causing a beat to beat variation in QRS axis and amplictude.

emergency pericardiocentesis!

Front 124

acute limb ischemia

Back 124

angio typically shows an abrupt cutoff of arterial blood flow. IV heparin should be started immediatley upon suspicion.

definitive treatment is surgical embolectomy or intra-arterial fibrinolysis/mechanical embolectomy via interventional radiology

Front 125

middle or older age male with prostatic hypertrophy who loses consciousness after awakening to void at night

Back 125

situtional syncope

Front 126

paroxysmal supraventricular tachycardia (PSVT)

Back 126

most commonly results from accessory conduction pathways through the AV node.

vagal maneuvers and meds that decrease conduction through the AV node often resolve the PSVT

Front 127

hemodynamic monitoring in septic shock, cardiogenic shock

Back 127

septic: low pulmonary capillary wedge pressure, low SVR, increased CO, and high mixed venous oxygen saturation

cardiogenic: low CO, elevated PCWP!, increased SVR. decreased CO decreases tissue perfusion which signals tissue to extract more O2 from the blood and decrease MVO2

Front 128

important cause of hypertension in elderly patients

Back 128

isolated systolic hypertension. caused by decreased elasticity of the arterial wall.

should always be treated due to increased risk for cardiovascular events.

initial therapy involves monotherapy with low dose thiazide, ACEi, or long acting ca channel blocker

Front 129

when are nitrates contraindicated?

Back 129

aortic stenosis, recent PDEi use, or RV infarction!!!!

When right ventricular SV decreases, CO is impaired. Therefore, any medication that reduces preload (nitrates or diuretics) will exacerbate rather than improve sx.

First step in tx of RV MI is generally IV fluid resuscitation to increase the RV stroke volume and enhance LV filling.

Front 130

hyperthyroidism related tachysystolic afib -> next step in mgmt?

Back 130

beta blocker!

Front 131

first line therapies for improving exercise tolerance in pts with stable angina pectoris

Back 131

beta blockers! (in addition to ASA and sublingual nitroglycerin prn)

ca channel or long acting nitrates if beta blockers contraindicated or can be used in combination

Front 132

sudden onset of syncope without warning signs, presence of structural heart disease, and frequent ectopic beats

likely cause of syncope?

Back 132

arrythmia

Front 133

edema in CHF

Back 133

multifactorial

most important contributor is increased renal sodium retention, resulting from activation of the RAAS system.

activation of this system is a reuslt of renal hypoperfusion 2/2 decreased cardiac output

Front 134

vascular and immunologic manifestations of infective endocarditis

Back 134

4668

Front 135

new conduction abnormality in pt with infective endocarditis

Back 135

perivalvular abscess with extension in the adjacent cardiac conduction tissue!

aortic valve endocarditis and IVDU are both independently a/w increased risk of periannular extension of native valve endocarditis

Hint 135

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