CardioCH3 (Ischemic Heart Dz)

What are the outer and middle layers of the coronary arteries and their functions?

• The outer layer is the adventitia, which is the basic support structure.

• The middle layer is the media, which contains multiple layers of smooth muscle cells and makes adjustments to luminal diameter.

What is the name of the inner layer of the coronary arteries?

Intima

What makes up the intima and what substances are most likely to accumulate there?

• The intima consists of the endothelial layer, basement membrane, and smooth muscle cells.

• Arterial endothelium is selectively permeable to macromolecules of the size of low-density lipoprotein.

• Lipoproteins and fibrinogen are most likely to accumulate in the intima.

What are the basic rules of fluid dynamics?

Fluids flow from an area of high pressure to low pressure and follow the path of least resistance.

What are the major determinants of myocardial blood flow (F)?

• Diastolic blood pressure (DBP) is the primary driving force moving blood into myocardial tissue.

• Vasomotor tone (VMT) plays a role in determining the volume of blood passed along to tissue.

• Resistance (R) to flow is commonly caused by atherosclerosis.

• Left ventricular end-diastolic pressure (LVEDP) is the pressure within the ventricle at end diastole.

• F = DBP + VMT − R − LVEDP.

What are atherosclerosis, atherosis, and sclerosis?

• Atherosclerotic plaques are composed of lipid and thrombus.

• Atherosis is a fatty streak that consists of lipid-laden macrophages and smooth muscle cells.

• Sclerosis is responsible for reduction of blood vessel compliance and involves organization of a “fibrous cap” of thrombi over advanced plaques that have developed on the endothelial lining.

How does atherosclerosis progress?

It progresses from a fatty streak to plaque, formation of thrombus, and complications such as total occlusion of the artery by thrombus. A thrombus can also break off the plaque, flow along the artery as an embolus, and block a small artery.

What are the consequences of atherosclerosis in different areas of the body?

• In the heart, partial coronary artery occlusion can cause angina pectoris and total occlusion can cause myocardial infarction.

• In the brain, partial occlusion can cause a transient ischemic attack and total occlusion can cause a cerebrovascular accident.

• Atherosclerosis can also affect peripheral arteries, the aorta, and the legs, resulting in aneurysm, occlusion, rupture and hemorrhage, peripheral vascular disease, gangrene, and amputation.

What is vasospasm and how is it related to Prinzmetal angina?

• A vasospasm is a sudden, abnormal tightening of an artery's muscular wall.

• Hyperplasia of intimal smooth muscle cells is a hallmark of advanced atherosclerosis, creating a coronary artery that is prone to spasm.

• Prinzmetal angina is variant angina associated with ST-segment elevation, at rest, and not associated with any preceding increase in myocardial oxygen demand.

• Prinzmetal angina is thought to occur through vasospasm of the coronary arterial smooth muscle.

What did the Framingham Study examine regarding coronary atherosclerosis?

The Framingham Study tested the relationship between genetic and behavioral factors and their contribution to the development of coronary atherosclerosis. The greater the number of risk factors present, the greater the likelihood that CAD, and ultimately CHD, will exist.

What are the modifiable and nonmodifiable major risk factors for heart disease?

Modifiable risk factors include

• cigarette/tobacco smoking

• High blood pressure (over 140/90)

• High blood cholesterol levels—the best predictor is the ratio of total cholesterol to HDL

• Physical inactivity.

• Stress

Non-modifiable risk factors

• Heredity

• Male Sex

• Increased Age

What are contributing risk factors for myocardial perfusion/heart disease?

• Diabetes - nonenzymatic glycosylation, or the chemical attachment of glucose to proteins without enzymes affects fibrinogen, collagen, and antithrombin III, HDL, and LDL, thrombus formation enhanced

• obesity (BMI ≥30 kg/m²),

• Family history involving a parent or sibling,

• Increased age

• Gender- Before 55 years of age, men are 6× more likely than women to have an MI. CHD is the second leading cause of death in all women <45 years

What are the four ways myocardial perfusion disease typically presents or occurs?

• Sudden cardiac death

• Chronic stable angina,

• Acute coronary syndrome (ACS)

  • Unstable angina

  • ST- segment elevation myocardial infarction (STEMI)

  • Non-STEMI

• Cardiac muscle dysfunction.

What is the usual cause of sudden cardiac death and what immediate treatment is necessary?

Ventricular tachycardia and ventricular fibrillation, leading to cessation of cardiac output, are the usual cause of death. Prompt delivery of CPR with AED and entry into the emergency medical system are necessary.

What is angina and how is it typically described?

Angina is an Old English term meaning “strangling.” It is described as substernal pressure and can occur anywhere from the epigastric area to the jaw. It may feel like squeezing, tightness, or crushing and results from an imbalance in supply and demand of myocardial oxygen.

How do classic stable angina and unstable angina differ?

• Classic stable angina is described as tightness, pressure, or indigestion anywhere above the waist that develops with exertion and diminishes with rest or nitroglycerin (NTG). Women may complain of nausea, indigestion, discomfort between the scapulae, or excessive fatigue, while diabetics often complain of SOB (Autonomic neuropathy).

• Unstable angina is chest discomfort accelerating in frequency or severity that may occur at rest but does not result in necrosis. It may be more severe and prolonged or may be the first occurrence of anginal pain.

How do vasospastic angina and pericarditis differ?

• Vasospastic angina (Prinzmetal or variant) is chest discomfort associated with ST-segment elevation or depression. It occurs at rest, typically in the early AM, and is not associated with a preceding increase in myocardial O₂ demand.

• Pericarditis causes pain at rest that may worsen with activity, is not relieved with rest or NTG, is relieved with anti-inflammatory medications, and is common post-CABG.

How can chest wall, pulmonary/pleuritic, and bronchospasm pain be differentiated?

• Chest wall pain increases with palpation over the chest wall.

• Pulmonary/pleuritic pain is often sharp and changes with breathing; there may be a pleural friction rub, decreased breath sounds, other adventitious sounds, tracheal shift, or fever.

• Bronchospasm is induced by exertion or cold, causes extreme difficulty breathing, and is relieved with a bronchodilator or stopping activity.

How can vascular and gastrointestinal chest pain be differentiated?

• Vascular pain from pulmonary embolism or aortic dissection has a sudden (paroxysmal) onset and is constant. Pleuritic pain with SOB is often seen in pulmonary embolism, while pain is “unrelenting” in aortic dissection.

• Gastrointestinal pain from esophageal reflux, peptic ulcer, or gallbladder disease causes prolonged epigastric discomfort usually related to food intake and/or relieved by antacid.

What are chronic stable angina and acute coronary syndrome?

• Chronic stable angina has a well-established level of onset and results from not enough blood supply to meet metabolic demand. Symptoms can usually be controlled by reducing exercise intensity or taking sublingual nitroglycerin.

• Acute coronary syndrome includes unstable angina—chest discomfort accelerating in frequency or severity that may occur at rest—and acute myocardial infarction.

What factors contribute to unstable angina?

Circadian variations in catecholamine levels, increases in plasma viscosity, increases in platelet activation, and pathological changes in atherosclerotic

What is the difference between STEMI and Non-STEMI?

• STEMI develops a Q-wave on ECG in the subsequent 24 to 48 hours (Full thickness or transmural infarction). STEMI shows elevation of the baseline/ST segment. Compared with small Q-waves generated during normal depolarization, pathologic Q-waves are more prominent.

• Non-STEMI does not develop a Q-wave on ECG and is referred to as non-transmural or subendocardial region infarction. They are diagnosed through cardiac enzyme testing, etc. (Partial thickness infarction)

What is the medical management of acute coronary syndrome?

• The primary concern is to reperfuse the area of the heart not receiving enough blood and oxygen, control cardiac pain with nitrates, morphine, and beta-blockers, limit necrosis, and prevent complications.

• Fibrinolysis and PTCA may be used if within 3 hours of onset.

• Management also includes aspirin, improving oxygenation, limitation of infarct size, prophylaxis for arrhythmias, and control of other complications.

What abnormal contraction patterns can occur with STEMI and Non-STEMI? (Dysynchrony, Hypokinesis, Akinesis, Dyskinesis and Hyperkinesis)

• Dysynchrony is disassociation in the time course of contraction of adjacent segments.

• Hypokinesis is reduction in the extent of shortening.

• Akinesis is cessation of shortening.

• Dyskinesis is paradoxical expansion and systolic bulging.

• Hyperkinesis is compensation of normal myocardium that initially accompanies dysfunction of the infarcted segment.

• Persistent angina and arrhythmias may occur with STEMI.

What is ventricular remodeling after STEMI and what factors affect it?

• With STEMI, ventricular remodeling involves changes in the shape, size, and thickness of the myocardium, including areas of ventricular dilation and ventricular hypertrophy.

• Factors that affect remodeling include size of infarct, ventricular load, and patency of the artery that was infarcted.

What factors determine prognosis after an infarction?

1. Complications,

2. Infarction size

3. Presence of disease in other coronary arteries

4. Left ventricular function.

What are the criteria for a complicated post-MI course?

1. Ventricular Tachycardia and Fibrillation

2. Atrial Flutter or Fibrillation

3. Second- or Third-Degree Atrioventricular block

4. Persistent Sinus Tachycardia (>100 bpm)

5. Persistent Systolic Hypotension (<90 mmHg)

6. Pulmonary Edema

7. Cardiogenic Shock

8. Persistent Angina or Extension of Infarction

What are the blood pressure categories?

•Normal: Less than 120/80 mm Hg;

•Elevated: Systolic between 120-129 and diastolic less than 80;

•Stage 1: Systolic between 130-139 or diastolic between 80-89;

•Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg

•Hypertensive Crisis: Systolic greater than 180 and/or diastolic at greater than 120

What happens to the heart with hypertensive heart disease?

• Hypertensive heart disease produces a pressure overload on the left ventricle.

  • This leads to ventricular hypertrophy

• Diastolic dysfunction with impairment of LV relaxation develops early.

Note: in the presence of diastolic dysfunction the mitral valve is affected

What is systolic dysfunction?

• Systolic dysfunction is impairment in ventricular contraction.

• It results in decreased stroke volume, decreased ejection fraction (<40%), and increased end-systolic volume.

• It is now called heart failure with reduced ejection fraction (HFrEF).

What is diastolic dysfunction?

• Diastolic dysfunction involves changes in ventricular diastolic properties that lead to impairment in ventricular filling (reduction in ventricular compliance) and impairment in ventricular relaxation

• It results in increased end-diastolic pressure and is now called heart failure with preserved ejection fraction (HFpEF).

What are the treatment guidelines for elevated BP and Stage 1 and Stage 2 HTN?

• Elevated BP (120–129/<80): lifestyle modification with reassessment in 3–6 months.

• Stage 1 HTN (130–139/80–89): lifestyle modification if no CVD or high 10-year CVD risk; if CVD or higher 10-year risk, add medications such as thiazide diuretics, ACE inhibitors or angiotensin II receptor blockers, or calcium channel blockers.

• Stage 2 HTN (>140 systolic or >90 diastolic): lifestyle modification with a two-drug combination of the above BP medications.

How does hypertension affect exercise and how does exercise affect BP?

• Exercise capacity is reduced by 15% to 30%.

• Stroke volume increases sub-normally and peak heart rate is lower, reducing cardiac output.

• Exercise leads to reductions in both systolic and diastolic BP.

What BP guidelines should be followed for exercise testing and training with HTN?

• For exercise testing, resting BP >200 systolic or >100 diastolic requires physician clearance, and exercise should be discontinued if BP is >250 systolic or >115 diastolic.

• For exercise training, uncontrolled and severe resting BP >180 systolic or >110 diastolic requires medical clearance.

• Consider side effects of medications.

• A gradual cool-down is best.

• Use low weights and high repetitions in deconditioned/high-risk patients; 60%–80% 1RM for others.

• Endurance training should be at moderate intensity.

What are the implications of carotid or vertebral disease for physical therapy intervention?

Patients with a diagnosis of carotid or vertebral disease should have BP monitored at rest and with all new activities, be educated about primary and secondary prevention, and be taught symptoms of instability.

What is peripheral arterial disease (PAD), and how does it affect exercise?

• PAD is referred to as atherosclerotic occlusive disease (AOD) and involves atheromatous plaque obstruction of large or medium-sized arteries supplying blood to the extremities.

• Patients are unable to produce normal increases in peripheral blood flow, and intermittent claudication leads to moderate to severe impairment in walking ability.

What are the four grades of claudication discomfort?

I — Initial discomfort
II — Moderate discomfort but attention can be diverted
III — Intense pain (attention cannot be diverted)
IV — Excruciating and unbearable pain.

What are the signs and symptoms of arterial insufficiency?

Painful walking (intermittent claudication), increased pallor when the foot is elevated, delayed venous filling following foot elevation, redness of the distal limb (dependent rubor), and death of tissue (gangrene).

What are the exercise recommendations for PAD?

• Perform exercise in intervals of 1–5 minutes alternating with rest periods.

• Increase the length of exercise intervals and decrease rest time.

• Patients should exercise to levels of maximal tolerated pain—if possible, to grade III/IV discomfort.

• The ideal mode is walking at least 30 minutes, 3 or more times per week. NWB activities may allow longer duration and higher intensities, but progressive walking is more functional and convenient and should be encouraged.

• Educate the patient on the need for a longer warm-up time because of peripheral vasoconstriction.

• Perform a sensory examination and fall risk screen because of the possibility of peripheral neuropathy.

• Emphasize proper footwear and hygiene.

What are renal artery disease and aortic aneurysm?

• Renal artery stenosis results from atherosclerosis of the renal artery.

• An aortic aneurysm is a pathological permanent dilation of the aortic wall involving any number of segments of the aorta. It is described in terms of location, size, morphological appearance, and origin. Rupture is the major risk of abdominal aortic aneurysms.

What findings should a physical therapist look for with an aortic aneurysm?

Check for a pulsating tumor/mass in the abdominal area, bruit heard over the swollen area in the abdomen, pressure on surrounding parts such as the low back, leg pain/claudication pain, numbness in the lower extremities, excessive fatigue, poor distal pulses, and low back pain.