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1
Q

MI Scare Type

A
  • 0-7 days: granulation tissue/type 3 collagen

- replaced by type 1 collagen as infarct matures (type 1 collagen is also seen in tendons)

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2
Q

First phase of infective endocarditis?

A

-disruption of normal endocardial surface followed by fibrin deposition

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3
Q

Concentric Ventricular Hypertrophy

A
  • pressure overload
  • chronic hypertension
  • aortic stenosis
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4
Q

Eccentric Ventricular Hypertrophy

A
  • volume overlaod
  • aortic or mitral regurg
  • MI
  • dilated cardiomyopathy
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5
Q

Order of conduction velocity of cardiac tissue.

A

Fastest>purkinje>atrial muscle>ventricular muscle>AV node>slowest
Park at venture avenue.

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6
Q

Rate Control Drugs

A

AV nodal blocking drugs like beta blockers and Ca channel blockers to prevent rapid ventricular response.

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7
Q

Rhythm Control Drugs

A

Attempt to maintain sinus rhythm. Sotalol, flecanide, amiodarone. Inc. risk of torsades de pointes.

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8
Q

Brain Natriuretic Peptide

A

Released in response to high atrial and ventricular filling pressure. Induces diuretic, natriuretic, and vasodilatory effect. Antagonizes actions o RAAS.

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9
Q

Dresslers

A

-2-3 weeks after MI presents with friction rub

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10
Q

Midsystolic Click Followed by mid/late systolic murmur

A

-mitral valve prolapse

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11
Q

Systolic crescendo decrescendo

A

-aortic stenosis

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12
Q

S. gallolyticus

A
  • S. bovis

- causes endocarditis and is associated with colorectal tumors

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13
Q

Inotropy

A

-cardiac contractility

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14
Q

Lusitropy

A

-cardiac relaxation

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15
Q

Pulsus Paradoxus

A
  • dec. systolic pressure during inspiration >10 mmHg

- most commonly seen it pts with tamponade

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16
Q

Mitral Regurgitation

A

-high pitched blowing murmur. Radiates toward axilla. increase with maneuvers that increase TPR like squatting or expiration. S3 indicates severity due to increased ventricular filling (volume overload). Often due to mitral valve prolapse, LV dilation

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17
Q

Tricuspid Regurgitation

A

-high pitched blowing murmur radiates to right sternal border. Enhanced by maneuvers that increase right atrium blood return like inspiration. Endocarditis, Rheumatic fever

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18
Q

Aortic Stenosis

A

-crescendo-decrescendo systolic ejection murmur following click. Radiates to carotids/apex. Often from age related calcified aortic stenosis or bicuspid aortic valve.

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19
Q

VSD

A

-holosystolic, harsh sounding murmur. Loudest at lower left sternal border (tricuspid area)

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20
Q

Mitral Prolapse

A

Late systolic crescendo murmur with midsystolic click. Loudest at S2. Enhanced by maneuvers that increase TPR (squatting). Most frequent valvular lesion - rheumatic fever, myxomatous degeneration). Usually benign.

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21
Q

Aortic regurgitation

A
  • high pitched “blowing” diastolic murmur. Wide pulse pressure when chronic. Bounding pulses with head bobbing. Due to rheumatic fever, bicuspid valve, aortic root dilation.
  • best heard along left sternal border at third and fourth intercostal spaces while pt is sitting up and leaning forward with breath held at end expiraiton
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22
Q

Mitral stenosis

A

Opening snap with late diastolic rumbing. Secondary to rheumatic fever. S2 to opening snap time indicates severity. Shorter the interval the worse the stenosis. Enhanced by maneuvers that increase LA return (expiration).

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23
Q

PDA

A

Continuous machine like murmur. Loudest at S2 on left sternal border. Wide and fixed splitting of S2.

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24
Q

S2 wide splitting

A

-anything decreasing RV emptying - pulmonic stenosis, right bundle branch block.

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25
Q

S2 fixed splitting

A

ASD, shunting of blood from left to right increasing blood in RV and delays closing

  • does not change with respiration
  • may allow paradoxical embolism to travel to brain (even with L t R shunt due to transient reversals in elevated R sided pressure situations such as cough)
26
Q

S2 paradoxical splitting

A

-conditions that delay LV emptying (aortic stenosis, left bundle branch block). A2 after P2. Interval gets smaller on inspiration.

27
Q

Prolonged QT Syndrome Causes:

A

torsades de pointes

28
Q

Transthyretin

A
  • protein produced by liver, that acts as a carrier for thyroxine and retinol
  • mutations inc. TTR misfolding and produce an amyloid protein the infiltrates the myocardium and can cause diastolic dysfunction and CHF
29
Q

Cardiac Tamponade

A
  • heart sac fills with fluid
  • common after viral illness
  • becks triad: pulsus paradoxus, elevated JVD, and muffled heart sounds
30
Q

Pathogenesis of Abdominal Aortic Aneurism

A
  • transmural wall inflammation
  • abnormal collagen remodeling and cross-linking
  • loss of elastin and smooth muscle cells
31
Q

What drugs inc. survival in CHF by dec. cardiac remodeling?

A
  • ACEi

- ARB

32
Q

Libman Sacks Endocarditis

A
  • associated with SLE
  • has verrucous endocarditis (immune complex deposition)
  • results in fibrotic valve thickening and deformity
33
Q

How occluded do coronary arteries have to be to cause stable angina?

A

> seventy five percent

34
Q

Which drugs cause prolonged QT syndrome?

A

Class 1A antiarrhythmics and class 3. Only amiodarone does not cause inc. risk of torsades de pointes.

35
Q

A Fib

A

Irregularly irregular rhythm, absent P waves, narrow QRS

36
Q

Hypertrophic Obstructive Cardiomyopathy

A
  • dynamic L ventricular outflow obstruction that worsens with dec. L ventricular volume
  • genetic
  • avoid vasodilators and diuretics that will dec. blood volume returning to heart
37
Q

Jervell and Lange-Nielsen Syndrome

A
  • congenital QT prolongation syndrome
  • AR
  • accompanied by congenital neurosensory deafness
  • mutation in gene coding for potassium channels
  • risk of sudden death from torsades de pointes
38
Q

Romano Ward Syndrome

A
  • AD
  • congenital QT prolongation syndrome
  • no sensorineural deafness like in Jervell and Lange-Nielsen Syndrome
  • risk of sudden death from torsades de pointes
  • mutation in gene coding for potassium channels
39
Q

Location of SA Node

A
  • SA node acts as dominant pacemaker and site of earliest site of electrical activation
  • located at the junction of the right atrium and superior vena cava
40
Q

Location of the AV Node

A
  • located in R atrium near the septal cusp of the tricuspid valve
  • interatrial septum near the opening of the coronary sinus
41
Q

How long after total ischemia begins does it take for that area of the heart to step contracting?

A

-60 seconds

42
Q

Change 0-4 hours after MI?

A

-no visible change

43
Q

Change 4-12 hours after MI?

A

-wavy fibers with narrow, elongated myocytes

44
Q

Change 12-24 hours after MI?

A

-myocyte hypereosinophilia with pyknotic (shrunken) nuclei

45
Q

Change 1-3 days after MI?

A
  • coagulation necrosis (loss of nuclei & striations)

- prominent neutrophilic infiltrate

46
Q

Change 3-7 days after MI?

A
  • disintegration of dead neutrophils and myofibers

- macrophage infiltration at border areas

47
Q

Change 7-10 days after MI?

A
  • robust phagocytosis of dead cells by macrophages

- beginning formation of granulation tissue at margins

48
Q

Change 10-14 days after MI?

A

-well developed granulation tissue with neovascularization

49
Q

Change 2 weeks-2 months after MI?

A

-progressive collagen deposition and scar formation

50
Q

Electrical Alterans

A
  • sign of big pericardial effusion

- inc. HR, dec. BP, inc. JVD, inc. pulsus paradoxis

51
Q

Holosystolic

A

-sound begins at first heart sound and continues to second heart sound

52
Q

Leading cause of death in US?

A

-cardiovascular disease

53
Q

Ventricular Septal Defect

A
  • most common congenital defect

- holocystolic murmur at lower left sternal border

54
Q

Rheumatic Fever

A
  • type 2 hypersensitivity rxn (antibodies cross react with self antigens)
  • major risk factor of death during rheumatic fever is myocarditis (inflammation of heart muscle)
55
Q

Causes of Pericarditis

A
  • viruses
  • uremia
  • dresslers syndrome
56
Q

Kussmaul Sign

A
  • occurs during restrictive pericarditis
  • inc. JVP during inspiration
  • volume restricted right heart cannot accomodate the inspiratory inc. in venous return
57
Q

Myxoma

A
  • most common primary cardiac neoplasm
  • common in left atrium as large pendunculated mass
  • scattered cells within a mucopolysaccharide stroma
  • may have abnormal vessels and hemorrhaging
58
Q

What vessel is occluded if ST elevation in leads II, III, and aVF?

A
  • right coronary artery
  • leads to transmural ischemia of the inf. wall of L ventricle and possible sinus node involvement
  • expect low BP and low HR
59
Q

What vessel is occluded if ST segment elevation in leads V1-V4?

A
  • proximal left anterior descending artery

- anteroseptal transmural ischemia

60
Q

What vessel is occluded if ST segment elevation in leads V5 and V6?

A
  • left circumflex

- transmural ischemia of lateral wall of left ventricle

61
Q

EKG Leads I, II, III

A
  • lead I goes R hand to L hand
  • lead II goes R hand to foot
  • lead III goes L hand to foot

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