Cardiology Chapter Quiz

Cardiac Pathophysiology: Coronary Artery Disease

• Coronary artery disease (CAD) is a condition where the coronary arteries become narrowed or blocked.
• CAD can cause insufficient oxygen to reach the heart muscle, leading to ischemia or infarction.
• Risk factors for CAD include smoking, hypertension (HTN), hypercholesterolemia, physical inactivity, diabetes, obesity, stress, heredity, male sex (until age 50 when women catch up due to menopause), and age.
• The Framingham Study identified 10 risk factors.
• The study began in 1949 and tracked over 5000 men and women.

Objectives

• Understand the term coronary artery disease.
• Identify risk factors for coronary artery disease.
• Recognize gender disparity in CAD.
• Describe the pathogenesis of coronary artery disease.
• Detect the clinical presentation of CAD.
• List tools used for diagnosing CAD.

Coronary Artery Disease (CAD)

• CAD is the most common cause of death in both genders and most racial groups in the US
• More than 1 in 3 adults in the US have cardiovascular disease.
• About 40% of American adults have a total cholesterol of 200 mg per deciliter or higher.
• An average of 36 seconds pass between each death due to CVD in the US (based on 2018 data).
• An average of 3 minutes and 33 seconds pass between each death due to stroke in the US (based on 2018 data).

Coronary Artery Disease (CAD): Pathogenesis

• When coronary arteries become narrowed or blocked, the heart muscle areas supplied by that artery don't receive enough oxygen.
• This leads to ischemia, injury, and potential infarction.
• Ischemic heart disease (CHD) is another term for coronary heart disease.

Coronary Artery Disease (CAD): Epidemiology

• Deaths attributable to heart disease in the US, 1900–2018.
• Coronary heart disease accounts for 43.2% of all deaths due to heart disease.

Coronary Artery Disease (CAD): Risk Factors

• Modifiable: Smoking, hypertension (HTN), high cholesterol, physical inactivity, diabetes, obesity, stress
• Non-modifiable: Heredity, male sex (until age 50 when women catch up), age

Coronary Artery Disease (CAD): Life's Simple 7

• Seven approaches to staying heart healthy: be active, keep a healthy weight, learn about cholesterol, do not smoke or use smokeless tobacco, eat a heart-healthy diet, keep blood pressure healthy, and learn about blood sugar and diabetes.

Physical Activity and Risk

• Each 1000-step-per-day increase in activity is associated with a 10% lower risk of MetS in US men.
• Physical activity, risk stratification, therapy, and decision-making process play a crucial role in providing exercise prescription for cardiovascular disease.

Overweight/Obesity

• Trends in age-adjusted obesity prevalence among US adults ≥ 20 years.
• Overweight and obesity prevalence trends show an increase over the years.

Hypertension as a Risk Factor for CAD

• 121.5 million, or 47%, of US adults, are estimated to have hypertension (based on 2015–2018 data).
• On average, 1 in 4 adults in the US reported adequate leisure-time aerobic and muscle-strengthening activities to meet the physical activity guidelines (based on 2018 data).

Gender and CAD: Risk Factors

• Sex-specific risk factors: premature menopause, gestational diabetes, hypertensive disorders of pregnancy, preterm delivery, polycystic ovary syndrome, systemic inflammatory and autoimmune disorders
• Under-recognized risk factors: psychosocial risk factors, abuse and intimate partner violence, socioeconomic deprivation, poor health literacy, and environmental risk factors

Gender and CAD: Mortality Rates

• Cardiovascular disease (CVD) mortality trends for US males and females 1980–2018.
• Mortality rates for both males and females have been declining over time.

Coronary Artery Disease: Pathogenesis: Atherogenesis

• Atherogenesis begins with injury to the endothelial lining of the artery.
• This makes the vessel permeable to circulating lipoproteins.
• Fatty streaks, intermediate lesions, rupture and thrombosis, and fibrous plaques are stages in atherosclerotic plaque formation.

Coronary Artery Disease: Pathogenesis

• Infectious agents can initiate the inflammatory cascade leading to CAD development in general.
• The precise mechanism of CAD development remains unknown but is thought to involve the following steps in plaque formation:
  • Damage to the arterial wall (e.g., by high blood pressure)
  • Infiltration of macromolecules (especially cholesterol) into the underlying smooth muscle cells
  • Platelet aggregation and release of chemicals altering the arterial wall structure
  • Proliferation of platelets, muscle cells, and fibrous clots (forming a plaque).

Coronary Artery Disease: How does an Infarct Occur?

• Thrombus
• Embolism
• Rupture
• Coronary Spasm

Collateral Circulation

• Collateral vessels grow from occluded arteries in CAD and help maintain circulation, delaying ischemia.
• Exercise enhances collateral circulation.

Coronary Artery Disease: Clinical Manifestations

• By itself, CAD usually has no symptoms.
• Symptoms may include angina pectoris (chest pain) and myocardial infarction (MI).
• Critical deficit in blood supply (at 70–75% blockage) is characteristic of clinical manifestations.

Coronary Artery Disease: Diagnosis

• Blood cholesterol
• Coronary angiography
• Echocardiography
• Heart rate recovery after submaximal exercise

Cardiac Pathophysiology: Hypertension

• Hypertension is defined as a persistent elevation of diastolic blood pressure higher than 90 mmHg, systolic blood pressure higher than 140 mmHg, or both measured in at least two separate occasions at least two weeks apart. (WHO definition).

Hypertension: Clinical Manifestations

• Hypertension is often asymptomatic, causing significant health risk.
• Common symptoms may include headache.

Cardiac Pathophysiology: Angina Pectoris

• Angina pectoris is a symptom of ischemia often caused by an imbalance between cardiac workload and oxygen supply to myocardial tissue (usually secondary to CAD).
• It occurs when O₂ demand exceeds O₂ supply.

Angina Pectoris: Clinical Presentation

• Chest pain, pressure, tightness, squeezing, or crushing sensations.
• Shortness of breath.
• Radiating pain (arms and/or jaw).
• Pain/numbness and tingling: Jaw, back, arms, left side (more common), neck.
• Symptoms may appear in a variety of body areas (or just the chest.)

Angina Pectoris: Causes

• The "3 E's": exercise, exertion, emotions, eating
• Cold weather
• Smoking

Angina Pectoris: Types

• Stable (predictable): angina associated with a set level of O₂ demand.
• Unstable: angina may occur without increase in workload, persists longer, and is more intense; indicates CAD progression.
• Prinzmetal/Variant: occurs at odd times, e.g., while sleeping, more common in women, and is not associated with exertion.

Angina Pectoris: Diagnosis

• History
• Use of nitroglycerin to alleviate symptoms
• Electrocardiogram (ECG)
• Pharmacologic stress testing
• Cardiac catheterization

Angina Diagnosis: Cardiac Catheterization

• Fine catheter is inserted via femoral or brachial artery into heart chambers.
• Measurements of pressures, valve function, and cardiac output.
• Contrast medium is injected to visualize blood vessel blockages.

Cardiac Pathophysiology: Myocardial Infarction (MI)

• MI, or heart attack, is ischemia that results in myocardial tissue necrosis.
• Eighty percent to 90% of MIs result from a coronary thrombus at a site of a preexisting atherosclerotic stenosis.

Myocardial Infarction (MI): Pathogenesis

• Plaque ruptures or sclerosed arteries fill with thrombus.
• Blood vessels get occluded by a clot.
• The most common site involved is the left ventricle.
• The processes of ischemia and infarction form zones.

Myocardial Infarction (MI): Timeline

• 1st 6 hours - Ischemia may be reversible with thrombolytic agents.
• 18–24 hours - Inflammatory response, intercellular enzyme release.
• 1st 48 hours - High vulnerability to arrhythmia. After stabilization, Phase I cardiac rehab can begin.
• 6–8 weeks - Necrotic tissue replaced by scar tissue. Phase II of cardiac rehab may begin at this point.
• 2–3 months - Scar tissue becomes less vascular and firm, and the risk of complications typically decreases.

Myocardial Infarction (MI): Classification

• Degree of wall involvement (transmural vs. subendocardial).
• Location of infarct (e.g., anterior, posterior, inferior).
• Size of infarct (uncomplicated or complicated).

Myocardial Infarction (MI): Clinical Manifestations

• Symptoms may not follow the classic pattern, and women may have atypical symptoms (e.g. shortness of breath, sometimes in the middle of the night, and chronic, unexplained fatigue).
• Other signs of poor prognosis may include severe left ventricular dysfunction, severe symptoms, and limitation of exercise capacity, secondary renal insufficiency, and elevated plasma catecholamine levels.

Diagnosis and Prognosis: MI

• ECG
• Echocardiography
• Myocardial isoenzymes
• Newer biochemical markers
• Exercise tolerance test
• Angiogram
• Serial enzymes (e.g., CPK-MB, myoglobin, LDH, and troponin)

Diagnosis TEE and Angiogram

• Transesophageal echocardiography (TEE) provides clearer images of the heart and helps identify structural heart diseases.
• Angiogram is used to visualize blood vessels, identify blockage, etc

Cardiac Pathophysiology: Congestive Heart Failure (CHF)

• CHF is a group of clinical manifestations caused by inadequate pump performance from either cardiac valves or myocardium.
• It’s characterized by the heart's inability to pump blood effectively.
• Fluid backs up in the pulmonary veins, resulting in pulmonary congestion and edema, and/or in systemic veins, resulting in peripheral edema (especially in the lower extremities).
• Different types of CHF exist (left, right, systolic, or diastolic).
• The processes affecting the heart may be due to acute or chronic conditions.

CHF: Clinical Manifestations (Left-sided)

• Decrease in cardiac output results in fluid overload in the lung.
• Symptoms include dyspnea (shortness of breath).
• The alveoli (air sacs) in the lungs fill with fluid instead of air.

CHF: Clinical Manifestations (right-sided)

• Decreased output to pulmonary circulation
• Back up in the right atrium
• Fluid fills up systems—typically observed in the lower extremities
• Often occurs with left-sided failure.

CHF: Clinical Manifestations (General)

• Progressive dyspnea (exertional first)
• Paroxysmal nocturnal dyspnea
• Orthopnea
• Productive spasmodic cough
• Pulmonary edema
• Extreme breathlessness
• Anxiety
• Frothy pink sputum
• Nasal flaring
• Accessory muscle use (e.g., crackles; formerly called rales)
• Confusion, impaired memory, sleep disturbance, fatigue, exercise intolerance, and muscular weakness
• Renal changes
• Dependent edema; often beginning in the ankles or pretibial area
• Jugular vein distention
• Abdominal pain/distention, weight gain
• Right upper quadrant pain; liver congestion, ascites, jaundice, anorexia, nausea, cyanosis (nail beds) and psychological disturbances.

CHF: Diagnosis

• Assess HR, BP and SpO2 response to activity
• Monitor for signs of right-sided heart failure—specifically with VSD and ASD.
• Use of supplemental oxygen
• Annual assessment for individuals with surgical repair.

CHF: Prognosis

• CHF treatment remains difficult, and the prognosis is poor.
• Clinical signs of poor prognosis include severe left ventricular dysfunction, severe symptoms and limitation of exercise capacity, secondary renal insufficiency, and elevated plasma catecholamine levels.

Cardiac Pathophysiology: Valvular Heart Disease

• Valvular heart disease is a condition affecting the heart valves (e.g., mitral, aortic, tricuspid, and pulmonary).
• Conditions include stenosis (narrowing of valve), insufficiency (valve doesn’t close tightly), or prolapse (valve bulges).
• Causes of the conditions might be rheumatic heart disease or congenital issues.

Valvular Heart Disease: Physiological Effects

• The heart works harder to compensate, increasing myocardial mass and O₂ demand.
• Decreased ejection fraction and stroke volume decrease cardiac output, leading to increased HR.

Valvular Heart Disease: Clinical Manifestations

• Symptoms can be moderate or severe; include dyspnea and fatigue, left atrial pressure may rise enough to cause pulmonary congestion and/or reduced cardiac output, and/or right ventricular failure.

Mitral Valve Prolapse (MVP)

• MVP is a variation in the shape/structure of the mitral/left atrioventricular valve (with unknown cause/possible genetic component).
• The condition typically does not cause symptoms or serious issues if mild.

Mitral Valve Prolapse (MVP): Clinical Manifestations

• Symptoms may include profound fatigue, palpitations, or dyspnea (shortness of breath).

Valvular Incompetence/Insufficiency

• Valves don't close completely, resulting in blood flow back into the heart.
• Chambers must accommodate this increased load.

Aortic Stenosis

• Aortic stenosis is narrowing of the aortic valve, typically caused by progressive valvular calcification or a congenitally bicuspid valve.
• The older population often has this problem, or it may happen because of rheumatic fever.

Aortic Stenosis: Clinical Manifestations

• Characteristic heart sounds, but cardiac output remains maintained initially, then may experience left ventricular failure, angina pectoris, and/or exertional syncope.
• Prophylactic antibiotics should be used to prevent infective endocarditis in asymptomatic individuals.
• Warning signs such as angina, exercise-induced syncope, or cardiac failure point to a less favorable prognostic outcome.

Aortic Regurgitation/Insufficiency

• Aortic insufficiency is valve leakage during diastole, causing blood to flow back into the left ventricle.
• The left ventricle must increase to compensate for chronic conditions of this type of insufficiency.

Cardiac Pathophysiology: Congenital Heart Disease (Part 1)

• Congenital heart disease (CHD) is the most common birth defect.
• One out of every 100 live births is affected by CHD, requiring intervention in early childhood.
• Causes may include genetics, medications taken by the mother, smoking by the mother, or arise from idiopathic issues.

Congenital Heart Disease: Classification of lesions (acyanotic/left-to-right shunts)

• Typical defects include atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), atrioventricular septal defect, and coarctation of the aorta.
• Blood is shunted from the left to the right side of the heart
• These shunt conditions commonly cause an increase in blood volume, a faster heart rate, and a higher force of cardiac contraction to compensate.

Congenital Heart Disease: Classification of Lesions (cyanotic/right-to-left shunts)

• Typical defects include tetralogy of Fallot, hypoplastic left heart syndrome, transposition of the great arteries, tricuspid atresia, pulmonary atresia, and truncus arteriosus, and total anomalous pulmonary venous return.
• These shunt conditions involve deoxygenated blood moving from the right side of the heart to the left side of the heart and bypass the pulmonary circulation.

Congenital Heart Disease: Etiology

• Factors include genetics, medications taken by the mother, maternal smoking.

Peripheral Arterial Disease (PAD)

• PAD is a type of peripheral vascular disease (PVD).
• PAD is predominantly an atherosclerotic occlusive disorder affecting arteries that supply the body's extremities.
• Risks factors for PAD include cigarette smoking, diabetes, impaired glucose tolerance, male gender, and high cholesterol.

Arterial Thrombosis and Embolism

• Arterial thrombosis and embolism are complications of occlusive vascular diseases.
• Chronic incomplete arterial obstruction often leads to collateral vessel development.
• Symptoms/signs of PAD include pain, numbness, coldness, tingling, and changes in sensation, skin color (pallor, mottling), weakness, and muscle spasm (distally to block).

PAD: Clinical Manifestations

• Claudication (painful walking) occurs as vessel diameter decreases by 50%.
• The further a person can walk before pain onset indicates the severity; less than one block of distance suggests severe disease.
• Pain, weakness, and fatigue in extremities distal to block(s) may be relieved by rest.

Ankle-Brachial Index (ABI)

• ABI is a measure of arterial perfusion, used for prescriptive exercise program benefit and needs documentation.

Angioplasty

• Angioplasty is a procedure for opening blocked arteries.
• A balloon catheter is placed, inflated, and expanded to the desired diameter.

Bypass Surgery

• Bypass surgery involves creating a new path for blood flow around blocked artery segments.
• A healthy vein is used to create the bypass graft.

Additional Notes

• Specific definitions for each type of heart condition are noted in the information above.