Usmle Cardiology

Front 1

What are the structures inside the carotid sheath?

Back 1

1. Internal jugular vein (lateral)
2. Common carotid Artery (medial)
3. Vagus Nerve (posterior)

Front 2

What factors (4) cause increase of contractility (and stroke volume) ?

Back 2

1. Catecholamines - increase activity of Ca2+ pump in sarcoplasmic reticulum.
2. Increase in intracellular calcium
3. Decrease in extracellular sodium
4. Digitalis - increase intracellular Na, resulting in inc of Ca)

Front 3

What 5 factors decrease contractility and stroke volume?

Back 3

1. Beta blockade
2. Heart failure
3. Acidosis
4. Hypoxia/hypercapnea
5. Non-dihydropyridine Ca2+ blockers

Front 4

The 4 factors that increase myocardial O2 demand are

Back 4

1. Inc afterload (proportional to increase in arterial pressure)
2. inc contractility
3. Inc heart rate
4. Inc heart size (inc wall tension)

Front 5

Name the three differences between cardiac and skeletal muscle

Back 5

1. Cardiac muscle action potential has a plateau, due to Ca2+ influx
2. Cardiac nodal cells spontaneously depolarize, resulting in automaticity
3. Cardiac myocytes are electrically coupled via gap junctions

Front 6

Congenital Heart Disease
5 Causes of Right to Left Shunt
Early cyanosis

Back 6

1. Tetrology of Fallot - most common
2. Transposition of great vessels
3. Truncus arteriosus
4. Tricuspid atresia
5. Total anomalous pulmonary venous return TAPVR

Front 7

Congenital Heart Disease
3 Causes of Left to Right Shunt

Back 7

1. VSD - most common congenital cardiac anomaly
2. ASD - loud S1; wide, fixed split S2
3. PDA close with indomethacin.

Frequency VSD > ASD > PDA

causes increase in pulm resistance because of arteriolar thickening, leading to progressive right-to-left shunt (Eisenmenger's)

Front 8

Tetrology of Fallot

Back 8

1. Pulmonary stenosis (imp prognostic factor)
2. RVH
3. Overriding aorta
4. VSD

boot-shaped heart
caused by anterosuperior displacement of the infundibular septum

squatting relieves symptoms

Front 9

What's the deal with transposition of the great vessels? hmm?

Back 9

Aorta leaves RV and pulm trunk leaves LV = separation of systemic and pulm circulations. Not compatible with life unless a shunt is present to allwo adequate mixing (VSD, PDA or PFO)

Due to failure of the articopulmonary septum to spiral.

Die w/in a few months unless surgery.

Front 10

Coarctation of the aorta

Back 10

Infantile type - aortic stenosis proximal to insertion of ductus arteriosis (preductal)

Adult type - stenosis is distal to ductus arteriosus (postductal). associated with notching of ribs due to collateral circulation, hypertension in upper extremities, weak pulses in lower extremities

Assoc w/ Turner's syndrome

Male 3 : Female 1

Check Femoral pulses

Front 11

Patent Ductus Arteriosus

Back 11

In fetal period, shunt is right to left (normal). In neonatal period, lung resistance decreases and shunt becomes left to right with subsequent RVH and failure (abnormal).

Associated with a continuous, "machine-like" murmur. Patency is maintained by PGE synthesis and low O2 tension

Front 12

cardiac defects w/ 22q11 syndromes

Back 12

truncus arteriosus,
tetrology of fallot

Front 13

cardiac defects in down's syndrom

Back 13

ASD, VSD, AV septal defect (endocardial cushion defect)

incomplete atria/ventricular septum and abnormal tricuspid valve

Front 14

cardiac defects assoc w/ congenital rubella

Back 14

Septal defects, PDA, pulm artery stenosis

Front 15

cardiac defects w/ Turner's syndrome

Back 15

coarctation of the aorta

Front 16

cardiac defects w/ Marfans

Back 16

aortic insufficiency (late complication)

aka aortic regurg

Front 17

cardiac defects in offspring w/ diabetic mother

Back 17

transposition of great vessels

Front 18

Monckeberg arteriosclerosis

Back 18

calcification in the media of the arteries, esp radial or ulnar. usually benign, pipestem arteries

Front 19

First day after MI

Back 19

Infarct for dark mottling; pale w/ tetrazolium stain

No visible change by light microscopy in first 2-4 hours

Coagulative necrosis; contraction bands visible after 4 hours. Release of contents of necrotic cells into bloodstream and the beginning of neutrophil emigration.

Front 20

What does an MI look like after 2-4 days?

Back 20

RISK FOR ARRHYTHMIA

Tissue surrounding infarct shows acute inflammation.

Dilated vessels (hyperemia)

Neutrophil emigration

Muscle shows extensive coagulative necrosis

Front 21

What does an MI look like after 5-10 days?

Back 21

RISK FOR FREE WALL RUPTURE

hyperemic border; central yellow-brown softening, maximally yellow and soft by 10 days.

Outerzone with ingrowth of granulation tissues.

Macrophages

Neutrophils

Front 22

What does an MI look like after 7 weeks?

Back 22

Risk for ventricular aneurysm

Recanalized artery
Gray-white infarcted area
Contracted scar complete

Front 23

Dilated (congestive) cardiomyopathy

Back 23

Most common cardiomyopathy 90%

Etiologies: Alcohol abuse, Beriberi, Coxsackie B viral myocarditis, Cocaine use, Chagas disease, Doxorubicin toxicity, peripartum cardiomyopathy

Heart dilates and looks like a ballon on CXR

Systolic dysfunction ensues

Front 24

Hypertrophic cardiomyopathy

Back 24

Hypertrophy often asymmetric and involving interventricular septum. Near normal heart size.

50% cases are familial, autosomal dominant.

Sudden death in young athletes.

Loud S4, apical impulses, systolic murmur.

Rx - beta-blocker or non-dihydropyridine Ca channel blocker (verapamil)

Diastolic dysfunction ensues

Front 25

Restrictive/obliterative cardiomyopathy

Back 25

Major causes: sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler's syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate) and hemochromatosis (dilated cardiomyopathy may also occur)

Diastolic dysfunction.

Front 26

Libman-Sacks endocarditis

Back 26

Verrucous vegetations on both sides of the valve. Can be associated with mitral regurg and less commonly, mitral stenosis. Seen in lupus.

Front 27

Rheumatic heart disease

Back 27

consequence of group A strep. Early deaths due to myocarditis. Late sequelae include rheumatic heart disease that affects heart valves - mitral > aortic >> tricuspid. (high pressure areas affected most)

Associated with Aschoff bodies (granuloma w/ giant cells), Anitschkow's cells (activated histiocytes), migratory polyarthritis, erythema marginatum, elevated ASO titers.

Immune mediated (type II hypersensitivity), not direct effect of bacteria.

Front 28

Cardiac tamponade

Back 28

Compression of heart by fluid in pericardium, leading to decrease CO. equilibriation of diastolic pressures in all 4 chambers.

Hypotension, inc venous pressure JVD, distant heart sounds, inc HR, pulsus paradoxus, ECG shows electrical alternans (beat to beat alterations of QRS complex height)

Pulsus paradoxus Kussmaul's pulse - decrease in amplitude of pulse during inspiration. also seen in asthma, obstructive sleep apnea, pericarditis and croup.

Front 29

Pericarditis

Back 29

Serous - caused by SLE, RA, viral infxn, uremia

Fibrinous - caused by uremia, MI (Dressler's), rheumatic fever

Hemorrhagic - TB or malignancy

Sx - pericardial pain, friction rub, pulsus paradoxus, distant heart sounds. ECG changes w/ diffuse ST elevation.

resolves w/o scarring, chronic adhesives or chronic constrictive pericarditis

Front 30

Syphilitic heart disease

Back 30

Tertiary syphilis disrupts vaso vasorum of the aorta resulting in dilation od the aorta and valve ring.

May lead to calcification of aortic root and ascending arch. Leads to tree bark appearance of the aorta.

Front 31

What abnormalities can be heard at the left sternal border?

Back 31

Diastolic murmur
Aortic regurgitation
Pulmonic regurgitation

Front 32

The many equations for Cardiac output

Back 32

CO = SV x HR

CO = (rate of O2 consumption) / (arterial O2 - venous O2 content)

MAP = CO x TPR

CO = (135 x BSA) / ( 13 x Hb x SaO2 - SvO2)

SV = EDV - ESV

Front 33

Ejection fraction

Back 33

EF = SV/ EDV = (EDV - ESV) / EDV

EF is an index of ventricular contractility

EF is normally >= 55%

Front 34

Resistance, pressure, flow

Back 34

delta P = Q x R

Resistance = (viscosity x length) / (radius^4)

Viscosity mostly depends on hemotocrit.
Increased in polycythemia, hyperproteinemic states, hereditary spherocytosis

Front 35

S3 Heart Sound occurs when?

Back 35

Early in diastole during rapid ventricular filling phase

Associated wiht increased filling pressures and more common in dilated ventricles

Normal in children

Front 36

S4 Heart Sound occurs when?

Back 36

Atrial kick - high atrial pressure.

Associated with ventricular hypertrophy

Front 37

When do you get S2 splitting?

Back 37

Normally, the aortic valve closes before the pulmonic,
This difference is exaggerated w/ inspiration

Wide splitting - associated w/ pulmonic stenosis

Fixed splitting - associated w/ ASD

Paradoxical splitting - (pulm before aortic) - aortic stenosis

Front 38

Mitral/tricuspid regurgitation sounds like...

Back 38

Holosystolic, high-pitched blowing murmur

Mitral - loudest at apex and radiates toward axilla

Tricuspid - loudest at tricuspid and radiates to right sternal border

Front 39

Aortic stenosis sounds like...

Back 39

crescendo-decrescendo systolic ejection murmur following ejection click (maximal aortic opening)

LV >> aortic pressure during systole

Radiates to carotids/apex

Pulsus parvus et tardus - pulses weak compared to heart sounds

If severe - Syncope, Angina, Dyspnea

Front 40

VSD sounds like...

Back 40

Holosystolic, harsh-sounding murmur.

Loudest at tricuspid area

Front 41

Mitral prolapse sounds like...

Back 41

Late systolic murmur with midsystolic click (being held down by chordae, papillary muscle).

Most frequent valvular lesion.

Loudest at S2

Front 42

Aortic regurgitation sounds like...

Back 42

Immediate high-pitched blowing diastoic murmur

Wide pulse pressure when chronic

Front 43

Mitral stenosis sounds like..

Back 43

Follows opening snap
Delayed rumbling late diastolic murmur.

LA >> LV pressure during diastole

Tricuspid stenosis differs because it gets louder with inspiration
(more blood flows into RA w/ inspiration)

elevates LAEDP and PCWP > LVEDP - should be equal

shorter A2 to opening snap interval = more severe

Front 44

PDA sounds like...

Back 44

Continuous machine-like murmur

Loudest at time of S2

Front 45

Wolff-Parkinson-White Syndrome

Back 45

Accessory conduction pathway from atria to ventricle (bundle of Kent)
Bypasses the AV node

Ventricles begin to partially depolarize earlier, giving rise ot delta wave on ECG

May result in reentry current leading to supraventricular tachycardia

WPW triad:
1. Delta wave
2. Shortened PR interval
3. Widened QRS

Front 46

First degree AV block

Back 46

PR interval is prolonged > 200 ms

Asymptomatic

Front 47

2nd degree AV block
Mobitz type I
Wenckeback

Back 47

Progressive lengthening of PR interval until a beat is dropped (P wave not followed by QRS complex)

Usually asymptomatic

Front 48

2nd Degree AV block
Mobitz type II

Back 48

Dropped beats that are not preceded by a change of length in PR interval

Abrupt, nonconducted P waves result in pathologic condition.

Often found as 2:1 block, where there are 2 P waves to 1 QRS response.

May progress to 3rd degree block

Front 49

3rd degree AV block
complete

Back 49

The atria and ventricles beat independently of each other

Both P waves and QRS complexes are present, although P waves bear no relation to QRS complexes.

The atrial rate is faster than the ventricular rate

Usually treat with pacemaker

Front 50

What factors do the peripheral chemoreceptors respond to?

Back 50

pO2 less than 60
Inc pCO2
Dec pH of blood

Front 51

What factors do Central chemoreceptors respond to?

Back 51

changes in pH and pCO2 of brain interstitial fluid, which are influenzed by arterial pCO2

Does not directly respond to pO2

Cushing rxn - Inc intracranial pressure constricts arterioles, leads to cerebral ischemia, hypertension (sympathetics), reflex bradycardia

Cushing's triad - hypertension, bradycardia, respiratory depression

Front 52

Factors causing edema

Back 52

1. Inc capillary pressure - heart failure

2. Dec plasma proteins - nephrotic syndrome, liver failure

3. Inc capillary permeability - toxins, infections, burns

4. Inc interstitial fluid colloid osmotic pressure - lymphatic blockage

Front 53

Ebstein's anomaly

Back 53

Apical displacement of tricuspid valve leaflets increased volume of right atrium, atrialization of RV

linked to in utero lithium for bipolar disorder

Front 54

Osler-Weber-Rendu syndrome

Back 54

Hereditary hemorrhagic telangectasia

autosomal dominant

nosebleeds and skin discolorations

Front 55

Cardiac tumors

Back 55

Myxomas are most common in adults
Occur in mostly LA, "ball-valve" obstruction associated w/ multiple syncopal episodes

Rhabdomyomas are most frequent cardiac tumor in children - assoc w/ tuberous sclerosis

Mets to heart from melanoma, lymphoma

Front 56

Churg-Strauss

Back 56

Granulomatous vasculitis w/ eosinophilia

Involves lung, heart, skin, kidneys, nerves

Often seen in atopic patients

p-ANCA

Front 57

Wegener's polyangitis

Back 57

Triad :
Focal necrotizing vasculitis
Necrotizing granulomas in lung and upper airway
Necrotizing glomerulonephritis

Sx - perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea, hemoptysis, hematuria

cANCA

CXR w/ nodular densities; hematuria and red cell casts

Cyclophosphamide and corticosteroids

small vessels

Front 58

Sturge-Webber

Back 58

Congenital vascular disorder that affects capillary sized blood vessels

port-wine stain of face and leptomeningeal angiomatosis (intracerebral AVM)

Front 59

Henoch-Schonlein purpura

Back 59

Most common form of childhood systemic vasculitis

Skin rash (palpable purpura), arthralgia, intestinal hemorrhage, abd pain, melena

Follows URIs, multiple lesions of same age

IgA immune complexes deposit on BV's and vessel mesangium

Skin, joints, GI

Front 60

Buerger's disease

Back 60

Aka thromboangiitis obliterans.
idiopathic, segmental, thrombosing vasculitis of small and medium peripheral arteries and veins.

Seen in heavy smokers.

Sx - intermittent claudication, superficial nodular phlebitis, cold sensitivity (Raynaud's), severe pain, maybe gangrene

Front 61

Kawasaki's disease

Back 61

Acute, self-limiting disease of infants/kids

necrotizing vasculitis of small/medium-sized vessels.

Fever, congested conjuctiva, changes in lips/oral mucosa "strawberry tongue", lymphadenitis

May develop coronary aneurysms

Front 62

Polyarteritis nodosa

Back 62

Characterized by necrotizing immune complex inflammation of medium-sized muscular arteries

Sx - fever, weight loss, malaise, abd pain, melena, HA, myalgia, HTN, neurologic dysfunction, cutaneous eruptions

Medium arteries - usually renal and visceral

HBV in 30%
Multiple anuerysms and constrictions on arteriograms

typically not associated w/ ANCA

Corticosteroids, cyclophosphamide

Front 63

Takayasu's arteritis

Back 63

Pulseless disease

granulomatous thickening of aortic arch and/or proximal vessels.

Elevated ESR

Asian females < 40.

Fever, Arthritis, Night sweats, Myalgia, Skin nodueles, Weak pulses in extremities

Front 64

Temporal giant cell arteritis

Back 64

Common vasculitis that affects medium and large arteries, branches of the carotid

Focal, granulomatous inflammation

Elderly females

Unilateral HA, jaw claudication, impaired vision (occlusion of ophthalmic artery)

Elevated ESR
Polymyalgia rheumatica
Medium and large vessels

Front 65

Treatment for malignant hypertension

Back 65

Nitroprusside - short acting
Fenoldopam - D1 agonist - relaxes renal smooth muscle
Diazoxide - K channel opener - hyperpolarizes and relaxes vascular smooth muscle

Front 66

HMG-CoA reductase

Back 66

Decrease LDL a lot
Inc HDL
Dec TG

Inhibit cholesterol precursor, mevalonate

Expensive, reversible LFTs, myositis

Front 67

Niacin

Back 67

Dec LDL
Inc HDL a lot
Dec TG

Inhibits lipolysis in adipose tissue
reduces hepatic VLDL secretion into circulation

Red flushed face, dec by aspirin use

Front 68

Bile acid resins
cholestyramine, colestipol

Back 68

Dec LDL
Inc HDL slightly
Inc TG slightly

Prevents intestinal reabsorption of bile acids
Liver must use cholesterol to make more

Gi discomfort, decreased vit ADEK

Front 69

Cholesterol absorption blockers
Ezetimibe

Back 69

Dec LDL
No effect on HDL/TG

Preven cholesterol reabsorption at small intestine brush border

Rare LFTs

Front 70

Fibrates
gemfibrozil, clofibrate, bezafibrate, fenofibrate

Back 70

Dec LDL
Inc HDL
Dec TG a lot!

Upregulate LPL, inc TG clearance

Myositis, LFT inc

Front 71

Class IA antiarrhythimcs

Back 71

quinidine, amiodarone, procainamide, dysopyrimide

Inc AP, Inc refractory period, Inc QT

Na channel blockers

Front 72

Class IB

Back 72

lidocaine, mexilitien, tocainide

Dec AP duration

CNS/cardiovascular depression

Front 73

Class IC

Back 73

Flecainide, encainide, propafenone

no effect on AP duration

proarrhythmic, esp post MI

Front 74

Class III

Back 74

Sotalol, ibutilide, bretylium, amiodarone

Inc AP duration, Inc refractory, Inc QT interval

pulm fibrosis, hepatotoxicity, hypothyroidism, hyperthyroidism