CVS Pathophysiology PDF

CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury CARDIOVASCULAR SYSTEM INTRODUCTION TO CVS The heart is muscular organ about the size of a closed fist. It is located in the chest between the lungs behind th...

CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury CARDIOVASCULAR SYSTEM INTRODUCTION TO CVS The heart is muscular organ about the size of a closed fist. It is located in the chest between the lungs behind the sternum and above the diaphragm. It is surrounded by the pericardium. The heart is attached to the aorta, pulmonary arteries and veins, and the vena cava. The inferior tip of the heart, known as the apex which is pointing toward the left side. Because the heart points to the left, about 2/3 of the heart’s mass is found on the left side of the body and the other 1/3 is on the right. Heart is the pump which is responsible for maintaining adequate circulation of oxygenated blood around the vascular network of the body. It takes in deoxygenated blood through the veins and delivers it to the lungs for oxygenation before pumping it into the various arteries. 1 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury ANATOMY OF THE HEART A) HEART WALL: it is composed of 3 layers 1) Pericardium: Pericardium is a fibro-serous sac surrounding the heart & the roots of the great vessels arising from or entering the heart. It consists of 2 sacs: 1) Fibrous Pericardium ❖ An outer fibrous sac which is made up of strong fibrous tissue. 2) Serous Pericardium ❖ An inner double – layered closed serous sac having: I. Parietal layer: lines the fibrous pericardium. II. Visceral layer: covers the heart & is called the epicardium. III. Pericardial cavity: which is a potential space between the visceral & parietal layers of the serous pericardium, it contains a thin film of serous fluid secreted by the cells of the serous pericardium. 2) Myocardium: Myocardium is the thick middle layer of heart wall and consists of numerous layers of cardiac muscle fibers that wrap around the heart. 3) Endocardium: Endocardium is the endothelial layer that lines inside the heart. 2 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury B) HEART CHAMBERS: 1) The 2 atria (RT & LT): Smaller, thinner & weaker than the ventricles. They are the receiving chambers, so they are connected to the veins that carry blood to the heart. 2) The 2 ventricles (RT & LT): larger, stronger & thicker than the atria. They are the pumping chambers, so they are connected to the arteries that carry blood away from the heart. C) HEART VALVES: 1) Atrioventricular Valves (AV): The AV valves are located between the atria and ventricles and only allow blood to flow from the atria into the ventricles. The AV valve on the right side of the heart is called the tricuspid valve, which is made of three cusps. The AV valve on the left side of the heart is called the mitral valve or the bicuspid valve, which is made of two cusps. 2) Semilunar Valves: The semilunar valves, so named for the crescent moon shape of their cusps. They are located between the ventricles and the arteries that carry blood away from the heart. The semilunar valve on the right side of the heart is the pulmonary valve. The semilunar valve on the left side of the heart is the aortic valve. 3 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury Anatomy Function The 2 atria Chambers that receive blood returning from body through veins. The 2 ventricles Chambers where blood is pumped to body through arteries. Mitral valve The mitral valve controls the flow of oxygen-rich blood from the left atrium to the left ventricle. Tricuspid valve The tricuspid valve controls the flow of oxygen-poor blood from the right atrium to the right ventricle. Aortic valve The aortic valve controls flow of oxygen-rich blood from the left ventricle to the body. Pulmonary valve The pulmonary valve controls flow of oxygen-poor blood from the right ventricle to the lungs. 4 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury D) CONDUCTION SYSTEM OF THE HEART The heart is able to set its own rhythm and also to conduct the signals necessary to maintain and co-ordinate this rhythm throughout its structures. The conduction system starts with the pacemaker of the heart known as the sinoatrial (SA) node. The SA node is located in the wall of the right atrium. The signal from the SA node is picked up by another node known as the atrioventricular (AV) node. The AV node picks up the signal sent by the SA node and transmits it to the AV bundle (bundle of His). The AV bundle runs through the interventricular septum. The AV bundle splits into left and right bundle branches in the interventricular septum and continues running through the septum until they reach the apex of the heart. From the left and right bundle branches there are many Purkinje fibers that carry the signal to the walls of the ventricles, stimulate the cardiac muscle cells to contract. 5 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury PHYSIOLOGY OF THE HEART At any given time, the chambers of the heart may be found in one of two states: A) SYSTOLE: During systole, cardiac muscle is contracting to push blood out of the chamber. B) DIASTOLE: During diastole, the cardiac muscle cells relax to allow the chamber to fill with blood. Blood pressure increases in the major arteries during ventricular systole and decreases during ventricular diastole. This leads to the two values associated with blood pressure: 1) Systolic blood pressure is the higher value. 2) Diastolic blood pressure is the lower value. For example, a blood pressure of 120/80 describes the systolic pressure (120) and the diastolic pressure (80). 6 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury THE CARDIAC CYCLE The cardiac cycle includes all of the events that take place during one heartbeat. There are three phases to the cardiac cycle: atrial systole, ventricular systole and relaxation. 1) Atrial systole: During the atrial systole the atria contract and push blood into the ventricles. To facilitate this filling, the AV valves stay open and the semilunar valves stay closed to keep arterial blood from re-entering the heart. They only fill about 25% of the ventricles during this phase. The ventricles remain in diastole during this phase. 2) Ventricular systole: During ventricular systole, the ventricles contract to push blood into the aorta and pulmonary trunk. Durin this phase, the semilunar valves are open and the AV valves are closed, to allow the blood to flow from the ventricles to the great arteries. 3) Relaxation phase: During the relaxation phase, all four chambers of the heart are in diastole as blood pours into the heart from the veins. The ventricles fill to about 75% capacity during this phase and will be completely filled only after the atria enter systole. During this phase, the AV valves open to allow blood to flow freely into the ventricles while the semilunar valves close to prevent the regurgitation of blood from the great arteries into the ventricles. 7 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury BLOOD CIRCULATION Deoxygenated blood returning from the body first enters the heart from the superior and inferior vena cava. The blood enters the right atrium and is pumped through the tricuspid valve into the right ventricle. From the right ventricle, the blood is pumped through the pulmonary semilunar valve into the pulmonary arteries. The pulmonary artery carries blood to the lungs where it releases carbon dioxide and absorbs oxygen. The blood in the lungs returns to the heart through the pulmonary veins. From the pulmonary veins, blood enters the heart again in the left atrium. The left atrium contracts to pump blood through the bicuspid (mitral) valve into the left ventricle. The left ventricle pumps blood through the aortic semilunar valve into the aorta. From the aorta, blood enters into systemic circulation throughout the body tissues until it returns to the heart via the vena cava and the cycle repeats. 8 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury CARDIAC OUTPUT Cardiac output (CO): is the volume of blood being pumped by the heart in one minute. The equation used to find cardiac output is: CO = Stroke Volume × Heart Rate Stroke volume (SV): is the amount of blood pumped into the aorta during each ventricular systole, usually measured in millilitres. Heart rate (HR): is the number of heart beats per minute. The average heart can push around 5 to 5.5 litres per minute at rest. 9 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury HYPERTENSION Hypertension is a chronic medical condition that arises when the blood pressure is abnormally high (≥ 140 mm of Hg systolic and 90 mm of Hg diastolic). Although the heart and blood vessels can tolerate increased blood pressure for months and even years, eventually the heart may enlarge (a condition called hypertrophy) and be weakened to the point of failure. TYPES OF HYPERTENSION A) PRIMARY (ESSENTIAL) HYPERTENSION: About 95% of people with high blood pressure have essential hypertension or primary hypertension. This condition has no identifiable medical cause. Elevated blood pressure usually begins to appear between age 30 and 50, but can begin at older ages. Usually, people with essential hypertension have no symptoms, but may experience frequent headaches, tiredness, dizziness, or nose bleeds. Although the cause is unknown, but several factors and conditions may play a role in its development, including: 1) Age 2) Genetics 3) Smoking 4) Obesity 5) Lack of physical activity 6) Too much salt in the diet 7) Heavy alcohol consumption 8) Stress 9) Family history 10 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury B) SECONDARY HYPERTENSION: About 5% of people with high blood pressure have secondary hypertension. This condition has definite cause; the most common cause of secondary hypertension is renal. Other causes include hormone abnormalities, pregnancy, coarctation of aorta & drugs. PATHOPHYSIOLOGY Hypertension has a number of structural changes on the cardiovascular system. These structural changes in the vasculature often increase peripheral vascular resistance and reduce renal blood flow, thereby activating the renin–angiotensin–aldosterone axis. SYMPTOMS People who have high blood pressure typically do not know it until their blood pressure is measured. Sometimes people with markedly elevated blood pressure may develop: 1) Headache, Dizziness & Tinnitus. 2) Blurred vision. 3) Nausea and vomiting. 4) Chest pain and shortness of breath. People often do not seek medical care until they have symptoms arising from the organ damage caused by chronic high blood pressure. The following types of organ damage are commonly seen in chronic high blood pressure: 1) Heart attack or Heart failure. 2) Stroke or transient ischemic attack (TIA). 3) Kidney failure. 4) Eye damage with progressive vision loss. 5) Peripheral arterial disease-causing leg pain with walking (claudication). 11 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury DIAGNOSIS High blood pressure is diagnosed based on the results of a blood pressure test. The test yields two numbers: systolic and diastolic. Blood Pressure Categories in Adults: Following points are also taken into consideration in diagnosis: 1) Blood and urine tests 2) Chest-X-ray 3) Echo 4) Electrocardiograph 5) Ophthalmoscopy 12 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury TREATMENT There is no cure for primary hypertension but blood pressure can almost always be lowered with the correct treatment. The goal of treatment is to lower blood pressure to levels that will prevent heart disease and other complications of hypertension. In secondary hypertension, the disease that is responsible for the hypertension is treated in addition to the hypertension itself. Antihypertensive medicines fall into several classes of drugs. Classification Examples Central acting Clonidine and Methyldopa. agents Calcium Amlodipine & Nifedipine. Channel Diltiazem & Verapamil. Blockers Drugs acts on Captopril, Enalapril. RAA system Losartan. Antiadrenergic Atenolol, Metoprolol. drugs Carvedilol, Labetalol. Aldosterone Spironolactone. Receptor Antagonists Diuretics Furosemide & Hydrochlorothiazide. 13 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury CONGESTIVE HEART FAILURE Congestive Cardiac failure is a condition associated with heart disorders leading to impairment of the heart to supply sufficient blood to meet the body requirements. As a result, the heart is unable to pump enough oxygen and nutrients to meet the body's requirements. The heart chambers thus respond by enlargement (dilatation or hypertrophy) in order to hold more blood to pump through the body. The heart muscle walls tend to weaken with time and then are unable to pump with enough strength (↓contractility). The direct result of the reduced contractility causes a decrease in the cardiac output and systemic blood pressure. This causes the kidneys to often respond by causing the body to retain fluid (water) and sodium, as the systemic blood pressure and the renal blood flow both are reduced. This results into building up of fluid (edema) in the legs, ankles, feet, lungs or other organs causing oedema which makes the body congested, hence the name congestive cardiac failure. The term congestive heart failure is used for the chronic form of heart failure in which the patient has evidence of congestion of peripheral circulation and of lungs. ETIOLOGY 1) Coronary artery disease. 2) Cardiomyopathy 3) Hypertension 4) Heart valve disease 5) Myocarditis (an inflammation of the heart muscle). 6) Pericardial diseases 7) Alcohol abuse. 8) Arrhythmias. 14 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury PATHOGENESIS Heart failure may be caused by one of the following factors either singly or in combination. A) Intrinsic Pump Failure: The most common and most important cause of heart failure is weakening of the ventricular muscle that the heart fails to act as an efficient pump. The various diseases which may culminate in pump failure by these mechanisms are: ❖ Ischemic heart disease. ❖ Myocarditis. ❖ Cardiomyopathies. ❖ Arrhythmias. B) Increased workload (pressure or volume) on the heart: I. Increased pressure load: may occur in the following states: ❖ Systemic and pulmonary arterial hypertension. ❖ Valvular disease (stenosis) II. Increased volume load: occurs when a ventricle is required to eject more than normal volume of the blood resulting in cardiac failure. This is seen in the following conditions: ❖ Valvular insufficiency ❖ Severe anemia ❖ Hypoxia due to lung diseases. C) Impaired filling of cardiac chambers: ❖ As in pericardial diseases. 15 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury TYPES OF HEART FAILURE Systolic heart failure: This condition occurs when the pumping action of the heart is reduced or weakened. A common clinical measurement is ejection fraction (EF). The ejection fraction is calculated by SV/EDV A normal ejection fraction is greater than 55%. Systolic heart failure is diagnosed when the ejection fraction has significantly decreased below the threshold of 55%. Diastolic heart failure: This condition occurs when the heart can contract normally but is stiff, or less compliant, when it is relaxing and filling with blood. The heart is unable to fill with blood properly, which produces backup into the lungs. In diastolic heart failure, the ejection fraction is normal or increased. Acute heart failure: It is sudden and rapid development of failure. The sudden reduction in cardiac output, hypotension without edema is prominent features. Chronic heart failure: It develops slowly with gradual reduction in cardiac output. Blood pressure is well maintained but is associated with peripheral edema. 16 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury CLINICAL MANIFESTATIONS The most common manifestation of left ventricular failure is dyspnea. Dyspnea is most noticeable during periods of physical activity. It is also prominent when the person is lying down (orthopnea). Paroxysmal nocturnal dyspnea (PND) is an especially dramatic form of dyspnea that awakens the patients with sudden severe shortness of breath, accompanied by coughing, a chocking sensation, and wheezing. The most common manifestations of right ventricular failure are: Congested neck veins Fluid Retention and Swelling: Bilateral pitting lower limb edema. TREATMENT A) lifestyle improvement: 1) Regulation of the salt and fluid intake: 2) Regular exercise, according to the patient's tolerance level. B) Pharmacological Treatment 1) Inotropic Drugs: ❖ Cardiac glycosides: e.g. Digoxin, digitoxin etc. ❖ Sympathomimetic amines: e.g. Dopamine dobutamine. ❖ Phosphodiesterase enzyme inhibiters: Amrinone and milrinone 2) ACE inhibitors: Candesartan. 3) Diuretics: ❖ Loop diuretics: Furosemide ❖ Potassium sparing diuretics: Amiloride ❖ Thiazide diuretics: Chlorothiazide & Hydrochlorothiazide C) Surgical treatment: Heart transplantation. 17 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury ATHEROSCLEROSIS DEFINITION A chronic inflammatory response to lipid accumulation in the intimal layer of the arterial walls leads to plaque formation (atheroma) RISK FACTORS A) Non-modifiable Risk Factors Age Gender Family history B) Modifiable Risk Factors Lifestyle Obesity Physical inactivity Smoking C) Diseases that Increase Risk for Atherosclerosis DM Hyperlipidemia Hypertension 18 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury ATHEROSCLEROSIS PATHOPHYSIOLOGY a) Endothelial damage Multiple causes for endothelial cell damage (e.g. smoking, HTN, diabetes, high LDL, etc.) Damaged endothelium evokes inflammation with attraction of inflammatory cells including macrophages. Macrophages engulf oxidized LDL to form foam cells b) Fatty streaks/plaque Lots of foam cells creates what’s known as a fatty streak c) Fibrous plaque Collagen grows over the streak to make a fibrous cap fibrous plaque Can calcify and then protrude into the lumen to obstruct blood flow Complicated plaque and thrombus formation A plaque that ruptures is a ‘complicated plaque’ Exposure of the underlying tissue. Results in platelet adhesion, initiation of the clotting cascade, and thrombus formation. Thrombus can occlude a vessel. Partial occlusion leads to ischemia. Complete occlusion leads to infarction. 19 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury CORONARY ARTERY DISEASE (CAD) DEFINITIONS Coronary Artery Disease (CAD) = ischemic heart disease (IHD). Ischemia in general: Is defined as an inadequate tissue perfusion leads to → tissue hypoxia due to → imbalance between oxygen supply and tissue demand. Ischemic heart disease (IHD): Is a condition in which there is an imbalance between oxygen supply and demand to a portion of the myocardium. Narrowing or blocking of coronary arteries → decreased blood flow → low O2 supply to the heart → low tissue perfusion→ myocardial ischemia. CLASSIFICATION A) Chronic coronary artery disease: - stable angina B) Acute coronary syndrome (ACS): - unstable angina & MI (STEMI & Non-STEMI) 20 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury ANGINA Sudden onset of chest pain due to myocardial ischemia. Chest pain is a symptom of lactic acidosis (or the build-up of lactic acid as a by-product of anerobic metabolism in the absence of oxygen). No myocardial necrosis → so no elevated cardiac enzymes. The factors affecting angina pain are complex and multifactorial A) Precipitating factors: 1) Exertion 2) Stress 3) Heavy meals 4) Cold weather B) Relieving factors: 1) Rest 2) Nitrates TYPES OF ANGINA A) Typical (exertional) Chest pain with exertion Due to coronary obstruction 2 patterns 1) Stable Short duration. Predictable (does not occur at rest). Easily relieved by medications. 2) Unstable Prolonged pain May happen at rest (unpredictable) More dangerous (can be progressed to MI) B) Variant (Prinzmetal’s) Chest pain at rest (unpredictable). Due to coronary vasospasms 21 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury MYOCARDIAL INFARCTION MI: is an ischemic necrosis of part of the heart muscle due to total occlusion of a branch of coronary artery. Left ventricle (left main coronary artery) is more commonly affected. There is the leakage of enzymes and other proteins. These are cardiac markers that can be measured in the blood to diagnose as well as guide and evaluate treatment. Cardiac markers include: 1) CK-MB (specific to the heart muscle). 2) Troponin: Specific to the heart and essential for diagnosis of MI. 3) Myoglobin: Earliest marker visible in the blood, however less specific. Healing creates a fibrous scar that can weaken and rupture MANIFESTATIONS OF (MI): 1) Pain Similar to angina but more severe, prolonged, and does not respond to rest and vasodilators 2) Pallor & sweating. 3) Dyspnea 4) Hypotension 5) Fever (low grade) N.B. Whenever a person presents pale with sweating, chest pain (or left arm, shoulder, jaw, back pain), and hypotension (verified with blood pressure) always suspect heart attack COMPLICATIONS OF MI 1) Cardiac arrest. 2) Myocardial rupture. 3) Left ventricle dysfunction (left side heart failure). 4) May be a precursor to future heart failure and long-term need for nitrates to manage angina 22 CVS Pathophysiology Dr/ Abdelkhaleq Al-Mansoury INVESTIGATIONS OF ALL TYPES OF (CAD) ECG: ST segment elevation or depression. Cardiac enzymes: normal in angina but elevated in MI. ECHO CXR Leukocytosis, ↑ ESR & ↑ CRP: in MI Oher investigation for risk factors: e.g. FBS & lipid profile. MANAGEMENT OF ALL TYPES OF (CAD) Management of stable angina Purposes 1) Prevent the-progression of CAD. 2) Optimize life expectancy. 3) Relieve symptoms. Prevention of the progression of CAD: This is done by reducing the risk factors. 1) Weight reduction and exercise 30 minutes 4d/week. 2) Stop smoking. 3) Aspirin. 4) ACEI. 5) Statins for hyperlipidemia target to keep the (LDL35). 6) In hypertensive control BP to