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Module 9 - Cardiovascular disorders > Coronary Artery Disease > Flashcards

Coronary Artery Disease Flashcards

1
Q

What is CAD?

A

Heart disease d/t impaired delivery of blood to the myocardium.

Results from atherosclerosis of coronary arteries.

AKA = ischemic heart disease

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2
Q

What happens to intramyocardial arteries during systole?

A

During systole, these arteries are compressed = most coronary perfusion occurs during diastole.

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3
Q

What factors influence coronary perfusion (3)?

A
  1. Perfusion pressure
  2. Coronary artery diameter/patency
  3. duration of diastole.
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4
Q

What is collateral circulation?

A

Collateral circulation is new vasculature (angiogenisis) that forms around a slow atheroma growth in order to preserve blood flow.

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5
Q

What factors contribute to collateral circulation?

A
  • possible genetic predisposition for angiogenisis
  • regular cardiovascular exercise stimulates collateral growth

NOTE: b/c of collateral growth, a patient may be unaware of a developing problem.

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6
Q

Presentation of CAD is dependent on…?

A

Extent of occlusion (partial or complete)

Speed of ischemic development (acute or chronic)

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7
Q

What is cardiogenic shock?

A

Heart is unable to pump enough blood and oxygen to the body’s vital organs. Can result from an MI.

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8
Q

CAD presents in what 3 different ways?

A
  1. Angina (stable (stable plaque) or unstable (transient thrombus on a plaque))
  2. Acute MI
  3. Heart failure (ischemic cardiomyopathy or cardiogenic shock))
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9
Q

Define Angina Pectoris.

A

Chest pain or discomfort caused by insufficient O2 supply to meet myocardial O2 demands.

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10
Q

What is the most common cause of Angina Pectoris?

A

Myocardial ischemia d/t CAD

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11
Q

What are some reasons, other than CAD for decreased myocardial infusion (4)?

A
  1. hypovolemia
  2. coronary vasospasm (e.g. cocaine overdose)
  3. coronary embolism
  4. heart failure
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12
Q

What are some reasons for decreased oxygen in the blood?

A

-anemia
- hypoxemia d/t to chronic respiratory disease (e.g. COPD)
- acute gas exchange impairments (pneumonia)

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13
Q

What are some causes of increased myocardial oxygen demand (5)?

A
  • ventricular hypertrophy (d/t HTN, aortic stenosis)
  • large pulmonary embolism
  • tachycardia
  • hyperthyroidism
  • hyperthermia, physical exertion, stress/anxiety
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14
Q

How would someone experiencing angina describe their pain?

A
  • substernal, sometimes epigrastic
  • may be referred to inner arm, shoulder, neck, jaw or back
  • described as pressure, tightness, heaviness, constricting, squeezing
  • may come with associated symptoms: dyspnea, nausea or dizziness
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15
Q

Provide a description, the pathophysiology, duration and outcome of stable angina.

A

Description - exertion or emotional stress. Chronic stable angina is predicable.

Patho - narrowing of the atherosclerotic coronary arteries means then cannot dilate to meet increased oxygen demands = myocardial ishcemia

Duration = 2-5 mins. Pain stops with rest or nitro.

Outcome = no significant permanent damage to myocardium.

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16
Q

What are some aggravating factors for angina?

A

Any activity that increases myocardial demands or impedes O2 supply

  • Eating a large meal (diverts blood flow)
  • Cold temperatures (vasoconstriction increases BP and myocardial workload)
  • cigarette smoke (vasoconstriction and increased HR = increased myocardial workload)
  • lying down (increases venous return = increased myocardial workload)
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17
Q

Describe unstable angina including pathophysiology, duration and outcome.

A

Pain is more easily induced (occurs at rest) unpredictable

Transient, reversible complication with an unstable plaque (e.g. plaque rupture causes a thrombus which partially or completely obstructs blood flow)

Pain is prolonged but < 20 mins (body’s own fibrinolytic system breaks down clot)

No significant permanent damage to myocardium but precedes an MI and requires observation and treatment.

18
Q

What is vasospastic angina?

A

AKA = prinzmetal or varient angina

Cause often unknown but cigarette smoke is a known trigger

Occurs at rest - often at night or early morning.

Lasts 5-15 mins and responds to nitro

Calcium channel blockers prevents episodes.

19
Q

What is coronary microvascular dysfunction (CMD)?

A

Chest pain caused by abnormalities of the coronary microcirculation.

Endothelial dysfunction impairs dilation in response to exercise or stress and/or causes vasospasm

Primarily affects females (approx 75%)

20
Q

Define acute myocardial infarction.

A

Acute MI is myocardial cell death caused by prolonged (>20 min) ischemia.

21
Q

What is the primary cause of an acute MI?

A

Sustained coronary artery occlusion d/t thrombus formation on an atherosclerotic plaque.

Plaque erosion or rupture exposes the subendothelium or lipid core to stimulate thrombus formation.

22
Q

What factors influence severity of infarction and myocardial damage (5)?

A
  • degree of obstruction (partial or complete)
  • artery affected
  • site of occlusion along the artery (proximal vs distal)
  • duration of ischemia before reperfusion occurs
  • extent of collateral circulation
23
Q

What is a transmural infarction (cause and outcome)?

A

= ST elevated MI (STEMI)
1. full thickness
2. complete obstruction
3. necroses endocardium to epicardium

Involves full thickness damage of the myocardium in 3-6 hours (without intervention)

Caused by the complete obstruction of a major coronary artery

Necrosis begins in the subendocardium (furthest from the blood supply) and spreads to the epicardium.

24
Q

Reperfusion (Percutaneous Coronary Intervention - PCI or thrombolytics) needs to occur within… to prevent progression of damage to the full wall.

A

90-120 mins

25
Q

What is a subendocardial infarcation?

A

NSTEMI = non ST elevated MI

Infarcted area is in the inner third or half of the myocardium

Partial occlusion that impairs blood supply to the most distal subendocardium.

Occlusion of smaller coronary branches

CAD + O2 supply/demand imbalance

26
Q

Which wall of the heart is most often affected with an MI?

A

Left ventricle as it receives blood from all major epicardial arteries.

27
Q

What is located in the interventricular septum that will be damaged by a septal MI?

A

Bundle branches of the conduction system of the heart

Can cause a partial or complete heart block.

28
Q

What are the cellular effects of ischemia on the myocardium?

A
  • shift to anaerobic metabolism = immediate decrease in contractility (within 60 secs)
  • ATP depletion = cell swelling and increased intracellular Ca2+
  • irreversible cell injury = when ischemia persists > 20-40 mins
  • cell destruction results in the release of intracellular proteins and K+
  • necrotic tissue fills the affected area (affected region is pale and firm)
29
Q

How does the body respond post MI?

A
  • infarction causes a severe inflammatory response (within 1-3) days which activates healing process
  • necrotic tissue is removed by macrophages
  • cardiac muscle cannot regenerate = replaced with fibrous scar tissue
30
Q

Describe complications of an acute MI within 24 hours, 3 days, 14 days and more than 2 weeks.

A

0-24 hours = dysrhthmias, cardiogenic shock

1-3 = pericarditis

3-14 = mural thrombosis, myocardial rupture

> 2 weeks = ventricular aneurysm, heart failure

31
Q

What is the reason for 25% of individuals dying shortly after the onset of an acute MI?

A

A majory dysrhythmia = ventricular fibrillation = uncoordinated ventricular contractions (quivering) which impairs relaxation and filling (risk greatest in the 1st hour)

32
Q

What are the 2 mechanisms and 4 common types of dysrhythmias?

A

Mechanism:
- injury to the conduction system
- conditions that alter myocardial sensitivity to nerve impulses (e.g. electrolyte imbalances, SNS stimulation)

Common types:
- sinus dysrhythmias (tachycardia or bradycardia)
- atrial or ventricular fibrillation
- AV (heart) block
- premature ventricular contractions (PVCs)

33
Q

What is acute pericarditis?

A

Inflammation extends to the epicardial surface and pericardium (occurs in the first 1-3 days)

Manifests as pericardial friction rub and chest pain = worse with deep inhalation (sharp, stabbing).

34
Q

How many weeks does healing take post MI?

A

Recommended to engage in physical activity after 6 weeks.

At 4 weeks the heart is still healing. Necrotic tissue is being replaced by scar tissue, but damaged area is still weak and prone to rupture.

35
Q

What are the types of myocardial ruptures that can occur (3)?

A
  1. Heart wall rupture (cardiac tamponade)
  2. Papillary muscle rupture (valvular regurgitation)
  3. rupture of the interventricular septum (L-R shunt)
36
Q

Why are patients prescribed both anti-platelets and anticoagulants?

A

Antiplatelet medication:
- reduces the risk of recurrent coronary artery thrombosis or stent thrombosis
- dual antiplatelet therapy post PCI is standard (clopidogrel or ticagrelor PLUS ASA 81 mg)

Anticoagulants:
- prevent ventricular thrombosis or thrombosis d/t to atrial fibrillation (additional complications r/t MI)

37
Q

What is a mural thrombosis and how can it be prevented?

A

Forms in the heart over the site of injury d/t inflammation, blood pooling (decreased contractility), and hypercoagulability.

Most develop within the first 2 weeks after an MI and increase the risk of a stroke (left ventricle) or PE (right ventricle).

38
Q

What is ventricular aneurysm?

A

Gradual stretching of heart wall d/t weakening and inelastic scar tissue. The wall bulges outwards.

Prone to thrombus formation d/t the pooling of blood (rupture is rare).

39
Q

How does scar tissue formation following an acute MI cause a decrease in CO and Heart failure (systolic and diastolic dysfunction)?

A
  • systolic dysfunction = replacement of functional tissue with scar tissue decreases contractility
  • diastolic dysfunction = scar tissue is inelastic and decreases ventricular compliance (and thus filling)
40
Q

What is the mechanism of action for nitroglycerin?

A
  • vasodilator with greater effect on veins compared to arterioles
  • relieves pain by reducing workload of the heart. Venodilation reduces venous return, which decreases preload which decreases workload of the heart
  • corrects the O2 supply and demand balance (reduced supply in angina) by reducing demand
  • arteriolar dilation reduces systemic BP (resistance), which reduces cardiac workload by reducing afterload
  • Nitro does not have an effect on athersclerotic veins as they can’t dilate, but can dilate collateral vessels if they are present

Module 9 - Cardiovascular disorders (6 decks)

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