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Patho > Topic 5.2 - Cardiovascular Disorder II > Flashcards

Topic 5.2 - Cardiovascular Disorder II Flashcards

1
Q

What is stable, classic, or typical angina? What causes it?

A

Predictable onset: usually exertion, physical or emotional; with no change in duration or cause over time
–> Caused by fixed coronary obstruction (usually stenotic atherosclerotic vessel), so the vessel cannot respond to increase O2 demand

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2
Q

What is the most common cause of stable angina?

A

Stenotic atherosclerotic coronary vessel

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3
Q

How is stable angina pain releived?

A

Rest and nitrates
(Nitroglycerine causes vessel dilation & reduced preload)

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4
Q

What is Prinzmetal variant angina?

A

Unpredictable attacks of pain - unrelated to exertion, heart rate, or other obvious causes of increased myocardial oxygen demand.
May intensify or worsen but does not carry the same concern as unstable angina.

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5
Q

What is a proposed mechanism of Prinzmetal variant angina?

A

Vasospasm, abnormal calcium influx

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6
Q

How can Prinzmetal variant angina pain be relieved?

A

Calcium channel blockers

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7
Q

What is unstable angina?

A

Partial occlusion of a blood vessel by a thrombus due to plaque rupture.
–> Chest pain that is more severe and longer lasting that typical angina
–> Life threatening

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8
Q

What is MI?

A

Complete occlusion of a coronary vessel by thrombus due to a plaque rupture
–> Chest pain that is severe and longer lasting that typical angina
–> Life threatening

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9
Q

How is STEMI diagnosed and treated?

A

Patient presents with ACS + ST-Elevation + Biomarkers.
Treated with acute reperfusion therapy + fibrinolytics

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10
Q

What are percutaneous coronary interventions (PCIs)?

A

Inserting a catheter into the coronary arteries to open the occluded artery - such as removal of the thrombus, disruption
of plaque, or placement of stents.

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11
Q

How is NSTEMI diagnosed and treated?

A

Patient presents with ACS, no ST elevation (might be depressed or inverted), and biomarkers.
Treated with Percutaneous Coronary Interventions (PCI)

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12
Q

How is unstable angina differentiated from an MI?

A

Patient will present with ACS, but no ST elevation of biomarkers.

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13
Q

What are the signs and symptoms of Acute Coronary Syndrome?

A

Pain accompanied by nausea, diaphoresis, and vomiting.
–> 15< mins
–> Atypical presentation includes back, arm, and abdominal pain - more common in women

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14
Q

What are silent MIs?

A

Asymptomatic myocardial infarcts

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15
Q

What does ST elevation indicate?

A

Acute cellular injury and ischemia/injury ongoing

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16
Q

What biomarkers indicate MI?

A

Troponin I and troponin T are part of the contractile apparatus of cardiac cells, however they remain elevated for a prolonged period

CK-MB remains elevated for 24-72 hours after cell death and are considered specifically diagnostic of recent incident.

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17
Q

What are the four main complications of myocardial infarction?

A

–> Impaired contractility
–> Tissue necrosis
–> Electrical instability
–> Pericardial inflammation (Pericardidits)

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18
Q

Impaired contractility is a complication of MI. What further issues can this cause?

A

Ventricular thrombus –> Stroke (embolism)

Hypotension and ischemia –> Cardiogenic shock

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19
Q

Tissue necrosis is a complication of MI. What further issues can this cause?

A

Papillary muscle infarction can lead to mitral regurgitation –> CHF

Ventricular wall rupture –> Cardiac tamponade

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20
Q

Electrical instability is a complication of MI. What further issues can this cause?

A

Arrythmias

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21
Q

What are the the treatment goals of MIs?

A
  1. Decrease myocardial workload
  2. Increase myocardial O2 supply
  3. Monitor and manage complications
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22
Q

How can we decrease myocardial workload?

A

–> Reduce preload and afterload
–> Control heart rate
–> Pain management
(SNS antagonists, nitrates, morphine)

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23
Q

How can we increase myocardial O2 supply?

A

O2 administration, antiplatelet therapy, anticoagulants, angioplasty, stents, coronary bypass.

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24
Q

Myocardial infarction leads to a decrease in stroke volume - how does the body respond to this?

A

Baroreceptors activate SNS –> Increase in HR + contractility –> Increase SV and CO

Decrease in renal perfusion leads to activation of RAAS –> Fluid retention, which increases preload –> Increased SV and CO

25
Q

How does the increase in SV and CO caused by the body’s compensatory mechanisms during MI impact the body long-term?

A

The increase in pressure causes increased pressure on ventricular walls.
This leads to tissue remodeling and hypertrophy that eventually exacerbates HF

26
Q

What is chronic ischemic cardiomyopathy and who does it affect most?

A

Heart failure that develops insidiously due to progressive ischemic myocardial damage.

Affects elderly individuals with a history of angina or MI.

27
Q

What is sudden cardiac death and who does it affect most?

A

Sudden cardiac arrest results in unexpected death within 1hr of onset.
In most cases, it is associated with coronary atherosclerosis and the primary cause is dysrhythmia (like v-fib).

28
Q

What kinds of things can lead to cardiac valvular damage?

A

–> Inflammation and scarring
–> Calcification
–> Congenital malformations

29
Q

What is valvular stenosis?

A

Failure to open completely leads to extra pressure and work for the heart

30
Q

How can the heart compensate for a stenotic valve?

A

Hypertrophy

31
Q

What is valvular insufficiency?

A

The inability of a valve to close completely, which leads to regurgitation and extra volume work for the heart.

32
Q

How does the heart compensate for sudden valve insufficiency?

A

It cannot.

33
Q

How does aortic stenosis affect the left ventricle?

A

Increases resistance to ejection –> Hypertrophy –> Remodeling (fibrosis) –> Gradual decrease in LV Contractility

34
Q

How does decreased LV contractility affect the systemic circulation?

A

Decreased LV contractility –> Decreased cardiac output –> Decreased perfusion to systemic and coronary arteries –> Tissue ischemia –> Angina, syncope, oliguria, stroke

35
Q

How does decreased LV contractility affect pulmonary circulation?

A

Decreased LV contractility –> Increased LV pressure –> Increased atrial + pulmonary pressure –> Pulmonary edema –> Dyspnea, orthopnea, cough

36
Q

How does aortic regurgitation affect the heart?

A

Blood leaks back from aorta during diastole –> Increase LV end-diastolic volume –> wide pulse pressure + LV dilation –> Gradual decrease in LV contractility.

37
Q

How does mitral stenosis affect the heart?

A

Increased resistance to LA diastolic ejection –> LA hypertrophy –> Remodeling (fibrosis) –> Gradual decrease in LA contractility –> Increased LA pressure.

38
Q

What kind of valve disorder can cause palpitations?

A

Mitral stenosis, which leads to LA dilation and can cause A-fib

39
Q

How does mitral regurgitation affect the heart?

A

Blood leaks back into LA during diastole –> LA + LV volume increase/dilate –> Gradual decrease in LV contractility

40
Q

What is pericarditis?

A

Acute or chronic inflammation of the pericardium - painful

41
Q

What is pericardial effusion?

A

Accumulation of fluid in the pericardial cavity due to inflammation or infection

Large enough volume impairs filling during diastole –> Decreased CO (Cardiac tamponade)

42
Q

How does pericardiac effusion affect SV and HR?

A

Decreased SV, increased HR to compensate

43
Q

What is Beck’s triad?

A

Three classic signs of pericardiac effusion
–> Hypotension
–> Distended neck veins
–> Muffled heart sounds

44
Q

What is myocarditis?

A

Inflammation of the heart muscle which can lead to necrosis and degeneration

Characterized by LV dysfunction and general dilation of all chambers

45
Q

What might cause myocarditis?

A

–> Hypersensitivities
–> Autoimmune
–> Toxins (Cocaine)
–> Lyme disease

46
Q

What are the clinical manifestations of myocarcarditis?

A

Pain/tightness in the chest, may radiate across body
Dyspnea and fatigue UE
Palpitations or irregular rhythm

47
Q

What is cardiomyopathy?

A

Non-inflammatory disease of the heart muscle

48
Q

What are the two kinds of cardiomyopathy?

A
  1. Primary
    –> idiopathic, may be genetic
  2. Secondary
    –> Known cause, inherited disorders, infectious disease, exposure to toxin, systemic connective tissue disease, nutritional deficiencies
49
Q

What is dilated cardiomyopathy? Is it classified as a systolic or diastolic issue?

A

Progressive dilation of one of both ventricular chambers
Classified as a systolic dysfunction.

50
Q

What might cause dilated cardiomyopathy?

A

Ischemic heart disease or valvular disease
diabetes, renal failure, alcohol or drug toxicity, peripartum complications, infection

51
Q

What kind of imaging would be best to confirm diagnosis of dilated cardiomyopathy?

A

An echo or ECG

52
Q

What are the clinical manifestations of dilated cardiomyopathy?

A

General heart failure symptoms:
Chest pain, fainting, swelling

53
Q

What is the leading indicator for heart transplant?

A

Dilated cardiomyopathy

54
Q

What is hypertrophic cardiomyopathy?

A

The most common kind of CM, characterized by thickened, hyperkinetic ventricular muscle. Characterized as diastolic dysfunction

Disproportionate thickening of septum in 25% of cases, may lead to obstruction of blood flow through aortic valve.

55
Q

What is the most common cause of sudden cardiac death in young athletes?

A

Hypertrophic cardiomyopathy

56
Q

What kind of cardiomyopathy is caused by an autosomal dominant disorder characterized by mutations in cardiac sarcomere proteins?

A

Hypertrophic cardiomyopathy

57
Q

What is Restrictive cardiomyopathy?

A

A rare and potentially idiopathic disease characterized by stiff, fibrotic ventricle filling with impaired diastolic filling due to excessive rigidity of ventricular walls.

Restricted filling –> Low SV + heart failure

58
Q

What kind of cardiomyopathy most commonly causes right heart failure?

A

Restrictive cardiomyopathy

Patho (14 decks)

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