Cardiac Pathophysiology

Cardiac Pathophysiology A Short Overview

1. The Pathophysiology of Congestive Heart Failure (CHF) Congestive heart failure is a syndrome that can be caused by a variety of abnormalities, including: • Pressure and volume overload, • loss of muscle, • primary muscle disease or • excessive peripheral demands such as high output failure.

The Pathophysiology of CHF The main causes of heart failure are: • atherosclerosis (calcification of the arteries), • hypertension or coronary artery disease (due to calcification of the arteries). Other diseases affecting the myocardium or heart valves can cause heart failure : • Myocardial inflammation, myocarditis • Valve disease, endocarditis • Heart rhythm disorders • Pneumonia • Pericardial effusion (pericarditis) or narrowing of the pericardium • Hyperfunction of the thyroid, hyperthyroidism • Heart disease, congenital or acquired • Family history

In the usual form of heart failure, the heart muscle has reduced contractility. This produces a reduction in cardiac output, which then becomes inadequate to meet the peripheral demands of the body.

Cardiac output = stroke volume X heart rate (beats per minute) Normal for male is about 5.5 liters of blood pumped by the heart to the body every minuteNormal for female is about 5.0 liters per minute

Left and Right-Sided CHF: • Left heart failure occurs when the left ventricle cannot pump blood to the body and fluid backs up and leaks into the lungs causing shortness of breath. • Right heart failure occurs when the right ventricle cannot adequately pump blood to the lungs. Blood and fluid may back up in the veins that deliver blood to the heart. This can cause fluid to leak into tissues and organs. .

. • Anything that may affect the heart rate, stroke volume, and ejection fraction, may lead to the heart pumping less efficiently. This can cause blood to back up into the veins leading to the heart, increasing pressure within the capillaries, the smallest of blood vessels in the body and in turn cause water (fluid) to leak into the interstitial space (the space between cells that make up the tissue and organs of the body). • Consequently, ↓cardiac output results in → ↑pressure in capillary blood vessels→ water leaking→ heart failure symptoms

Left Sided CHF: The 4 primary determinants of left ventricular (LV) performance are generally altered as follows: (1) There is an intrinsic decrease in muscle contractility. (2) Preload or left atrial filling pressure is increased, resulting in pulmonary congestion and dyspnea. .

Crackles on auscultation, hypoxia, shortness of breath on exertion and often at rest, cough, and paroxysmal nocturnal dyspnea. Important Tip regarding left sided CHF:

Right-Sided CHF: • May occur when the heart has to pump against increased resistance in the blood vessels leading to the lungs. As pressure rises in the pulmonary arteries and veins, the right ventricle has to pump harder and may not be able to overcome this higher pressure. Some causes of right heart failure include the following: • Pulmonary embolus (blood clot to the lung) • Pulmonary hypertension (increased blood pressure within the lung's blood vessels) • Chronic obstructive pulmonary disease (COPD) • Pulmonary valve stenosis or narrowing of the valve that connects the right ventricle to the pulmonary artery

2. The Pathophysiology of Deep Vein Thrombosis (DVT) Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in the body, usually in the legs. DVT can cause leg pain or swelling, but may occur without any symptoms.

The Pathophysiology of DVT • DVT can develop in the presence of certain medical conditions that affect how the blood clots. Deep vein thrombosis can also happen with reduced movement, such as after surgery, following an accident, or when the patient is confined to a hospital or nursing home bed. • DVT is serious, because these blood clots can break loose, travel through the bloodstream and lodge in the lungs, blocking blood flow (pulmonary embolism).

The warning signs of a pulmonary embolism include: • Unexplained sudden onset of shortness of breath • Chest pain or discomfort that worsens with a deep breath or when patient coughs • Patient complains of feeling lightheaded or dizzy, or fainting • Rapid pulse • Coughing up blood

Pulmonary Emboli .

3. The Pathophysiology of Myocardial Infarction (MI) Myocardial infarction (MI) (i.e., heart attack) is the irreversible necrosis of heart muscle secondary to prolonged ischemia.

The Pathophysiology of Myocardial Infarction (MI): This most commonly occurs when a coronary artery becomes occluded following the rupture of an atherosclerotic plaque, which then leads to the formation of a blood clot (coronary thrombosis). This event can also trigger coronary vasospasm. If a vessel becomes completely occluded, the myocardium normally supplied by that vessel will become ischemic and hypoxic. Without sufficient oxygen, the tissue dies.

The Pathophysiology of Myocardial Infarction (MI): • The damaged tissue is initially comprised of a necrotic core surrounded by a marginal (or border) zone that can either recover normal function or become irreversibly damaged. The hypoxic tissue within the border zone may become a site for generating arrhythmias. Collateral blood flowis an important determinant of infarct size and whether or not the border zone becomes irreversibly damaged. • Infarcted tissue does not contribute to tension generation during systole, and therefore can alter ventricular systolic and diastolic function and disrupt electrical activity within the heart.

Myocardial Infarction .

. Myocardial infarctions produce clinical symptoms that include: • intense chest pain that may radiate into the neck, jaw or arms (i.e., referred pain), • a sense of substernal heaviness, squeezing or pressure, • shortness of breath (dyspnea), • fatigue, • fainting (syncope), • nausea, • sweating (diaphoresis), • anxiety, • sleeplessness, • hypertension or hypotension (depending in part on the extent of cardiac damage), • tachycardia and arrhythmias.

The Pathophysiology of Myocardial Infarction (MI): Recent clinical research indicates that the symptoms may be very different between men and women. Chest pain is less common in women. Instead, their most common symptoms are weakness, fatigue and dyspnea.

, The pathophysiology of acute myocardial infarction is complex. • Loss of viable myocardium impairs global cardiac function, which can lead to reduced cardiac output, and if damage is severe, to cardiogenic shock. • Systolic and diastolic dysfunction are associated with ischemic myocardium. If left ventricular function is significantly impaired, pulmonary congestion and edema can occur. • Ischemia can also precipitate abnormal cardiac rhythms and conduction blocks that can further impair function and become life-threatening in some cases. • Reduced cardiac output and arterial pressure can elicit baroreceptor reflexes that lead to activation of neurohumoral compensatory mechanisms (e.g., activation of sympathetic nerves and the renin-angiotensin-aldosterone system) similar to what occurs during heart failure.

. • The pain and anxiety associated with myocardial infarction further activates the sympathetic nervous system, which causes systemic vasoconstriction and cardiac stimulation (this explains why some patients become hypertensive and have tachycardia). • While sympathetic activation helps to maintain arterial pressure, it also leads to a large increase in myocardial oxygen demand that can lead to greater myocardial hypoxia, enlarge the infarcted region, precipitate arrhythmias, and further impair cardiac function.

Cardiac Anatomy & Physiology Quiz

1. In the systemic circuit, the _____________ half of the heart pumps __________ blood to all body tissues and then _________ blood flows back to the heart. a. right; deoxygenated; oxygenated b. right; oxygenated; deoxygenated c. left; deoxygenated; oxygenated d. left; oxygenated; deoxygenated

2. In the pulmonary circuit, the __________ half of the heart pumps __________ blood to the alveoli of the lungs, and then _____________ blood flows back to the heart. a. right; deoxygenated; oxygenated b. right; oxygenated; deoxygenated c. left; deoxygenated; oxygenated d. left; oxygenated; deoxygenated

3. The predominant driving force that moves blood back to the heart in the veins is: a. active transport b. passive transport c. the closing of one-way valves d. the beating of the heart e. the skeletal muscle contractions

4. Which of the following procedures involves a segment of a leg vein being used to provide an alternate pathway for blood flow past a point of obstruction between the aorta and a coronary artery? a. angioplasty b. coronary angiography c. heart transplant d. coronary bypass

5. Which of the following valves directs blood flow from the left atrium to the left ventricle? • Mitral • Tricuspid • Aortic • Pulmonic

6. The layer of squamous cells that lines the cardiac chambers and valves is called the: a. myocardium b. endocardium c. epicardium d. pericardium

7. Which of the following statements is true? a. The AV node stimulates the atria. b. The vagus nerve supplies both the SA and AV nodes. c. Sympathetic nerve stimulation reduces the heart rate. d. Parasympathetic nerve stimulation reduces the heart rate.

8. The echocardiogram (ECG/EKG) is especially useful in the measurement of the: a. coronary blood flow and location of obstructions. b. Structures and motion of the heart within the chest. c. Structures and function of the lungs. d. All of the above.

9. What effect does stimulation of the sympathetic nervous system have on the arterioles? a. Dilation, which results in increased vascular resistance, and increased blood pressure. b. Constriction, which results in increased vascular resistance, and decreased blood pressure. c. Constriction, which results in increased vascular resistance, and increased blood pressure d. Dilation, which results in decreased vascular resistance, and decreased blood pressure.

10. Which of the following conditions impedes blood flow from the left atrium to the left ventricle, and can be heard as a lub dub whoosh: a. Aortic Stenosis b. Pulmonary Valvular Stenosis c. Mitral Stenosis d. Tricuspid Stenosis

11. What is the pathophysiologic phenomenon underlying disseminated intravascular coagulation (DIC)? • Clotting that leads to bleeding • Elevated platelet and fibrinogen levels • Inadequate cardiac output • Mast cell degranulation

12. A patient with heart failure complains of awakening intermittently during the night with shortness of breath. Which of the following terms is appropriate for this clinical manifestation? • Dyspnea • Orthopnea • Paroxysmal nocturnal dyspnea • Cyanosis

Cardiac Pathophysiology