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N552 Patho > Cardiac > Flashcards

Cardiac Flashcards

0
Q

How many Americans have myocardial ischemia? How many have myocardial infarction?

A

Ischemia: 10 million
Infarction: 1.5 million, mortality is 1/3

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1
Q

Causes of myocardial ischemia

A

Decreased supply due to narrowing of coronaries due to atherosclerosis (most common cause), coronary artery vasospasm, hypotension
Increased demand due to hypertension, tachycardia
Other: hypoxia, anemia, aortic insufficiency or stenosis

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2
Q

Major/other risk factors for myocardial ischemia?

A

Major: Age, male, hypercholestremia, diabetes, hypertension, smoker, family history
Other: Obesity, CV disease, PVD, menopause, high-estrogen contraceptives, sedentary, type A personality

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3
Q

Characteristics of an atherosclerotic plaque at high risk of rupturing?

A
  1. T cells recruited to shoulder
  2. macrophages clustered around T cells
  3. thin fibrous cap
  4. lipid-rich core
  5. newly formed intrawall capillaries
  6. lymphocyte and mast cell infiltration to adventitia
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4
Q

Stable vs. unstable angina

A

Stable: associated with narrowing (over 75%), O2 demand can be normal, relieved by rest or nitroglycerine
Unstable: increases in frequency and duration, can cause infarction or thrombosis

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5
Q

What is Prinzmetal Angina?

A

Coronary spasm at rest in a plaque area or normal vessel. This can be associated with vasospastic disease such as Raynaud’s.

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6
Q

What is infarction, how quickly does it occur?

A

Necrosis caused by ischemia, occurs within 20-30 min of ischemia typically in the subendocardial regions
Full size of infarction reached in 3-6 hours
Size depends on proximity of lesion and collateral circulation

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7
Q

Complications of an MI

A

Papillary muscle dysfunction, valvular disease
day 4-7 rupture of infarct, tamponade, death
Mural throbi can lead to stroke
Acute pericarditis day 2-4
Ventricular aneurysm (most common in anteroapical region)
Arrythmias, thromboembolism
LVF, pulmonary edema
Cardiogenic shock (rare)
Rubture of wall, septum, papillary muscle

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8
Q

What type of MI is associated with occlusion of..

RCA LCA, LAD, LCX?

A

RCA: posterior/inferior MI
LCA: anterolateral MI
LAD: anteroseptal MI
LCX: lateral MI

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9
Q

How is hypertension defined? What is the incidence?

A

Systolic over 140, diastolic over 90, sustained, 3 readings to diagnose
25% of general public
*90% of hypertension is idiopathic/primary
*10% of hypertension is secondary to renal disease, also can be secondary due to endocrine, CV, or neurologic diseases

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10
Q

What does BP depend on? (hint: it’s an equation)

A

BP = CO x PVR

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11
Q

What are risk factors for primary hypertension?

A

Genetic: polygenic and heterogenous, polymorphisms in several genes
Environmental: stress, obesity, smoking, salt, sedentary

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12
Q

What are two theories of the mechanism of hypertension?

A

1- renal retention of excess sodium due to genetics leads to decreased sodium excretion, increased fluid volume/ CO, increased BP
2- Vasoconstriction and vascular hypertrophy, increased PVR caused by neurogenic factors, release of vasoconstrictor agents, or genetic defect in Na/Ca transport. This can be added to stimulus that induces structural. changes in vessel walls

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13
Q

What are some pathogenesis of secondary hypertension?

A 
Oral contraceptives
Renal parenchymal disease
Renin-secreting tumors
Primary aldosteronism
Cushing's
Pheochromocytoma
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14
Q

What is a hypertensive crisis and what is the treatment?

A

DBP: over 130
Treatment: decrease DBP to 100 over several min to hours, controlled, use artline and foley

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15
Q

Mitral stenosis: explanation and causes

A

Mitral stenosis impairs blood flow from LA to LV. Autoimmunity to antigens leads to inflammation and scarring of the valvular leaflets. Scarring causes leaflets to become fibrous and fused and the chordae tendinae become shortened. Enlargement of LA increases risk of A fib. Stasis of blood in the LA predisposes to formation of thrombi.
Most commonly caused by rheumatic fever.

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16
Q

Increase vs. Decrease

Mitral stenosis: ____ LA emptying, ____ LA preload, ___ oxygen supply, ___ force of LA contraction

A

DECREASE LA emptying
INCREASE LA preload
DECREASE oxygen supply leading to RV failure
DECREASE force of LA contraction leading to decreased LV output and LV failure

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17
Q

Untreated, severe mitral stenosis leads to what?

A

Pulmonary hypertension, edema, RV failure, CHF

Also these pts are at higher risk of systemic thromboembolism and venous thrombosis

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18
Q

S/S of mitral stenosis? (from book)

A

Diastolic murmur over cardiac apex, “opening snap” which is a loud/delayed S1 due to increased LA pressure
Other s/s of pulmonary congestion and R heart failure

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19
Q

Aortic stenosis causes?

A

Congenital
Calcific degeneration from aging
Rheumatic heart disease
Note: Aortic stenosis is the most common valve disorder

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20
Q

Aortic stenosis pathophysiology?

A

Aortic semilunar valve narrows causing diminished blood flow from LV to aorta. LV hypertrophy develops, increasing myocardial oxygen demand which can lead to ischemia, MI, dysrhythmias, and heart failure

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21
Q

Aortic stenosis s/s

A

Triad: Syncope, Angina (in absence of ischemic heart disease), Dyspnea on exertion
Also in the book: dec SBP, narrow pulse pressure, slow HR, faint pulses, murmur (2nd intercostal space)

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22
Q

Aortic stenosis early : ___ LV mass, ___ LV compliance, ___ contractility, ____ preload, ____ stroke volume
Aortic stenosis late: ___ contractility, LV dilation, ___ stroke volume

A

Early: inc LV mass (these people have MASSIVE hearts), dec LV compliance, no change contractility, inc preload, no change stroke volume yet
Late: dec contractility, dec stroke volume

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23
Q

Mitral stenosis and aortic stenosis treatment?

A

Valve replacement or repair surgery

This is also the treatment for mitral and aortic regurgitation.

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24
Q

Mitral regurgitation causes?

A

Most commonly rheumatic fever, also caused by (from book) mitral valve prolapse, infective endocarditis, CAD, connective tissue disease, congestive cardiomyopathy.
Note: almost always associated with mitral stenosis

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25
Q

Mitral regurgitation pathophysiology?

A

Allows back flow of blood from LV to LA during systole, leads to atrial dilation which can cause A fib. LV function can become impaired and LV failure can occur. Increased atrial pressure can cause pulmonary hypertension and RV failure.

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26
Q

Regurgitant flow is responsible for ___ wave on PAOP.

A

V wave

Note: the size of the V wave correlates with the magnitude of the regurgitant flow.

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27
Q

What murmur would you hear on a patient with mitral regurgitation? (from the book)

A

Loud pansystolic murmur at apex

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28
Q

Aortic regurgitation causes?

A

Acute: infective endocarditis, trauma, dissection of thoracic aneurysm
Chronic: rheumatic fever, persistant systemic hypertension

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29
Q

Aortic regurgitation pathophysiology?

A

Inability for aortic valve leaflets to close properly during diastole. Some of the ejected blood flows back into the LV during diastole leading to volume overload in the ventricle. Then ventricular hypertrophy and heart failure.

30
Q

Aortic regurgitation s/s? (from the book)

A

Wide pulse pressure, diastolic murmur heard from 2nd to 4th intercostal space, carotid pulsation, bounding pulse. Dysrhythmias and endocarditis are common complications.

31
Q

Aortic insufficiency leads to ___ LV volume, ___ wall tension early on. Later, ___ wall tension, ___ mass, ___ contractility, ___ stroke volume, ___ LA pressure

A 
Inc LV volume
Dec wall tension early 
Inc wall tension late, inc mass
Dec contractility, dec stroke volume (dec CO)
Inc LA pressure
32
Q

Risk factors for infective endocarditis? (from book)

A

Acquired valvular heart disease , prosthetic heart valve, congenital lesions (vent septal defect), IV drug use, pacemaker, heart transplant

33
Q

Endocarditis (infective) pathophysiology? (from book)

A
  1. Endocardial damage causes inflammatory reaction
  2. Bacteria adhere to damaged surface and enter bloodstream
  3. Bacteria activate clotting cascade and form infective endocardial vegetations
34
Q

Infective endocarditis s/s? (from book)

A

Fever
New murmur
Petechial lesions of skin, conjunctiva, or oral mucosa

35
Q

What EKG changes are associated with mitral valve disease? (from book)

A

Broad, notched P waves (“P mitrale”) suggests LA enlargement, typical in mitral valve disease

36
Q

Anesthesia considerations for a patient with mitral stenosis? (from book)

A

Prevent or treat decreased CO and pulmonary edema

37
Q

What is mitral valve prolapse? (from book)

A

Prolapse of mitral leaflets into the LA during systole, with or without mitral regurgitation. Associated with mid systolic click and late systolic murmur
Associated with connective tissue disorders (Marfan)

38
Q

Anesthesia considerations for a patient with aortic stenosis? (from book)

A

Prevent decreased CO and hypotension

39
Q

Anesthetic management of aortic regurgitation? (from book)

A

Keep HR up, bradycardia will produce LV volume overload

40
Q

Mitral valve regurgitation anesthetic considerations? (from book)

A

Keep CO from decreasing, keep HR normal or slightly increased. Bradycardia will result in LV volume overload

41
Q

Why would valve disease produce angina (without ischemia)?

A

Due to increased myocardial oxygen demand from ventricular hypertrophy

42
Q

Aortic and mitral stenosis require ___ (slow/fast) HR

Aortic and mitral regurgitation require ___ (slow/fast) HR

A

M/A stenosis require slow HR to prolong diastole and improve LV filling and coronary blood flow
M/A regurgitation require faster HR to shorten the time of regurgitation

43
Q

What is cardiomyopathy?

A

A group of diseases of the myocardium associated with mechanical/electrical dysfunction that usually exhibit ventricular hypertrophy/dilation due to a variety of causes that are usually genetic

44
Q

What is dilated cardiomyopathy?

A

LV/biventricular chamber is large/overstretched but with normal wall thickness, systolic dysfunction, diminished contractility
Most common cardiomyopathy, common cause of HF

45
Q

Dilated cardiomyopathy symptoms?

A

Inflammatory early symptoms are fatigue, dyspnea, and palpitation, progress to CHF, pulses alternates, tachycardia, pulmonary edema. Treat with ABX
Non-inflammatory manifests as CHF

46
Q

Dilated cardiomyopathy is characterized by ___ (inc/dec) filling pressures, ____ (inc/dec) contractile strength, ____ (direct/inverse) relationship between arterial impedance and stroke volume

A

INC filling pressures
DEC/ FAILURE of contractile strength
INVERSE relationship between impedance and stroke volume

47
Q

What causes non-Inflammatory dilated cardiomyopathy?

A 
Toxicity (ethanol)
Idiopathic
Degenerative process
Infiltrative process
Post MI
48
Q

What are three symptoms of CHF associated with dilated cardiomyopathy due to forward failure?

A

Fatigue
Hypotension
Oliguria

49
Q

What are signs of CHF associated with dilated cardiomyopathy due to backward failure?

A

Elevated filling pressures required by the failing heart

Secondary mitral regurgitation caused by the dilation of the ventricle

51
Q

What are signs of CHF associated with dilated cardiomyopathy due to left sided failure?

A 
High LVEDP leads to pulm congestion
Orthopnea
Pulmonary edema
Paroxysmal nocturnal dyspnea
S3 gallop
51
Q

How does a person get hypertrophic cardiomyopathy? How is it characterized?

A

Genetic, autosomal dominant trait

Characterized by LV hypertrophy in the absence of other causes (like hypertension)

52
Q

What are signs of CHF associated with dilated cardiomyopathy due to right sided failure?

A

Hepatomegaly
JVD
Peripheral edema
(systemic venous congestion)

53
Q

Pathophysiology of hypertrophic cardiomyopathy (aka. IHSS)?

A

Contraction is a problem with hypertrophied septum, rapid LV ejection, leads to mitral regurgitation and diastolic dysfunction

54
Q

S/S of hypertrophic cardiomyopathy?

A

Most patients are asymptomatic. Symptoms are angina, syncope, dyspnea, HF, abnormal EKG, tachydysrhythmias, murmurs. Half the cases present with sudden death or cardiac arrest.

55
Q

With hypertrophic cardiomyopathy, patients have ___ (inc/dec) preload, _____ afterload, and ____ contractility. So what is treatment?

A

DEC preload, DEC afterload, INC contractility

Tx is fluid, unlike the other cardiomyopathies. B-blockers, and Ca channel blockers are used too.

56
Q

What would be found on an Echo with hypertrophic cardiomyopathy? What would EKG show?

A

Echo shows thickened septum, myocardial hypertrophy, poor septal motion, anterior displacement of mitral valve, diastolic dysfunction
EKG shows ST and T wave abnormalities, Q waves, LA enlargement

57
Q

Why are nitroprusside and dopamine a good treatment for heart failure or cardiomyopathy patients (not IHSS)?

A

Improve frank starling curve, improve CO and decrease pulmonary congestion
We want to reduce preload and afterload, and increase inotrophy

58
Q

Which congenital heart diseases are acyanotic? Which way is the shunt?

A

Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Left to right shunts

59
Q

What is the result of a L to R shunt? (acyanotic)

A

Increased pulmonary blood flow with pulmonary hypertension, RV hypertrophy, and eventually R heart failure

60
Q

What is atrial septal defect (ASD)?

A

Most common malformation diagnosed in adulthood, septum forms 4-6 weeks of embryonic age, defect due to foramen ovale not closing properly/completely. Blood flows from L atrium to R atrium.

61
Q

Clinical features of ASD?

A

Can lead to pulm htn
Can be associated with mitral insufficiency
Can reverse to R to L shunt causing cyanosis and CHF, fatal.

62
Q

What is ventricular septum defect (VSD)?

A

Most common heart defect at birth
Septum forms 4-6 weeks of embryonic age, defect due to foramen ovale not closing properly/completely in childhood
Blood flows from L ventricle to R ventricle
Can cause pulm htn, CHF, and endocarditis

63
Q

Which congenital heart diseases are cyanotic? Which way is the shunt?

A

Tetralogy of fallot
Transposition of great vessels
R to L shunt

64
Q

What factors contribute to constricting and closing the PDA at birth?

A

Increased O2 level
Decreased pulmonary resistance
Decrease in PGE2
Indomethacin (COX inhibitor) is first line therapy before surgery

65
Q

What are the 4 components of tetralogy of fallot?

A

VSD
Dextraposed aortic root that overrides the VSD (misaligned aorta)
RV outflow obstruction (narrow PA)
RV hypertrophy
This is the most common cyanotic congenital heart disease

66
Q

Tetralogy of fallot leads to ___ (inc/dec) blood flow to the lungs and ____ blood flow to the aorta

A

DEC blood flow to lungs

INC blood flow to aorta

67
Q

List some manifestations of tetralogy of fallot (these are avoided with surgery)

A

Hypoxemia, Erythrocytosis
Inc blood viscosity, inc hct
Clubbing, cyanosis between 2-6 months old
Infective endocarditis, Squatting
Systemic emboli
Brain accesses
Systolic ejection murmur at L sternal border

68
Q

What is transposition of great vessels?

A 
Aorta rises from RV
PA rises from LV
Associated with ASD, VSD, or PDA
Cyanotic congenital heart disease
RV hypertrophy, CHF are common
Give PGE1 and surgery to switch the vessels
69
Q

What is coarctation of the aorta?

A

Abnormal narrowing/stenosis of the aorta
More common in males
Can be preductal or postductal (named in relation to ductus arteriosus)

70
Q

When is preductal vs. postductal diagnosed?

A

Preductal infantile

Postductal more common, in older children or young adults

71
Q

What symptoms are noted with preductal coarctation of aorta?

A

Weak femoral pulses
Cyanosis of lower extremities
CHF
Need surgery to survive

72
Q

What symptoms are noted with postductal coarctation of aorta?

A

Collaterals develop
Decreased perfusion to kidneys and decreased SV, activation of RAS
High SBP in upper extremities, lower SBP in lower extremities
Intermittent claudication

73
Q

Why should you avoid trendelenburg and high airway pressures in patients with cyanotic heart disease?

A

High airway pressures will increase pulmonary vascular resistance and worsen R-L shunt
Trendelenburg will increase central venous pressure and can cause cerebral hypoperfusion

N552 Patho (13 decks)

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