Cardiovascular Disorders PDF

Pathophysiology (2) (MBS 214) Cardiovascular disorders Textbook ;Pathophysiology for the Health Professions, 4th edition, 2011 Chapter 18, P.271-320 Path of erythrocyte in the circulation  Cardiovascular disorders lecture outline:...

Pathophysiology (2) (MBS 214) Cardiovascular disorders Textbook ;Pathophysiology for the Health Professions, 4th edition, 2011 Chapter 18, P.271-320 Path of erythrocyte in the circulation  Cardiovascular disorders lecture outline:  Review of the normal cardiovascular system  Heart disorders  Vascular disorders  Shock Learning objectives: After studying this lecture,the student is expected to:  Describe the Common diagnostic tests for cardiovascular function  Describe the pathophysiology of the following disorders;  Heart disorders  Vascular disorders  Shock  REVIEW OF THE NORMAL CARDIOVASCULAR SYSTEM HEART: The heart functions as the pump for circulating blood in both the pulmonary and systemic circulations The heart is located in the mediastinum between the lungs and is enclosed in the double-walled pericardial sac 4 chambers(2 upper &2 lower)separated by septum, the left and right sides of the heart. the four heart valves that separate the chambers of the heart and ensure one-way flow of blood. The atrioventricular (AV) valves, The semilunar valves Heart layers:The outer fibrous pericardium, consisting of parietal and visceral pericardium with pericardial cavity in between. The middle layer is the myocardium The inner layer is the endocardium,  REVIEW OF THE NORMAL CARDIOVASCULAR SYSTEM Heart :Conduction System Impulses to initiate cardiac contractions are conducted along specialized myocardial (cardiac muscle) fibers. No nerves are present within the cardiac muscle – These specialized structures ensure that all muscle fibers of the two atria normally contract together, followed shortly by the two ventricles. This coordinated effort results in a rhythmic contraction The conduction pathway originates at the sinoatrial (SA) node, often called the pacemaker, located in the wall of the right atrium. The SA node automatically generates impulses at the basic rate, called the sinus rhythm (approximately 70 beats per minute), but this can be altered by autonomic nervous e hikimamines bundle system fibers that innervate the SA node and by Av circulating hormones such as epinephrine. bundle of From thecSA node, impulses then spread through the atrial his Or conduction pathways, resulting in contraction of both atria……..arrive at the AV node, located in the floor of the right atrium near the septum, continue into the ventricle through the AV bundle (Bundle of His) the right and left bundle branches, and the terminal Purkinje network of fibers, stimulating the simultaneous contraction of the two ventricles. FIGURE 18-18 Conduction system in the heart  REVIEW OF THE NORMAL CARDIOVASCULAR SYSTEM Conduction of impulses produces a change in electrical activity that can be picked up R by electrodes attached to the skin at various points on the body surface, producing the electrocardiogram (ECG) The atrial contraction is represented by the depolarization in the P wave, and the ventricular contraction is shown by the large wave of depolarization in the ventricles (QRS). This wave masks the effect of atrial repolarization, but the third wave (T wave) represents the repolarization Intrigues of the ventricles, or recovery phase. Abnormal variations in the ECG known as arrhythmias or dysrhythmias may indicate acute problems, such as an infarction, or systemic problems, such as electrolyte imbalances (for example, potassium FIGURE 18-18 Conduction system in the deficiency) heart and its relationship to the electrocardiogram  Control of the Heart rate and contractions Two main receptors found in the wall of aorta and carotid arteries are involved. _ The baroreceptors detect changes in blood pressure. If blood pressure increases, heart rate decreases. – The chemoreceptors detect changes in CO2. If CO2 concentration is high, heart rate increases. When stimulated, these receptors send a signal to the Cardiovascular center in the medulla oblongata. – The cardiovascular center has 2 regions: Cardio-inhibitory center Cardio-accelerating center _ Nervous impulses are sent from these centers along the autonomic nervous system to the sinoatrial node (SAN). – Sympathetic innervation increases heart rate (tachycardia) and contractility, – Parasympathetic stimulation by the vagus nerve slows the heart rate (bradycardia).  Cardiac Cycle The pulse indicates the heart rate(rhythm). The pulse can be felt by the fingers (not the thumb) placed over an artery that passes over bone or firm tissue (peripheral pulse), most commonly at the wrist (the radial pulse). During ventricular systole, the surge of blood expands the arteries. The characteristics of the pulse, such as weakness or irregularity often indicate a problem The apical pulse refers to the rate measured at the heart itself. A pulse deficit is a difference in rate between the apical pulse and the radial pulse.  Cardiac Cycle Refers to the alternating sequence of diastole, the relaxation phase of cardiac activity, and systole, or cardiac contraction, which is coordinated by the conduction system for maximum efficiency The heart sounds, “lubb-dupp,” which can be heard with a stethoscope, result from vibrations due to closure of the valves. Closure of the AV valves at the beginning of ventricular systole causes a long, low “lubb” sound, followed by a “dupp” sound as the semilunar valves close with ventricular diastole. Defective valves that leak or do not open completely cause unusual turbulence in the blood flow, resulting in abnormal sounds, or murmurs. A hole in the heart septum resulting in abnormal blood flow would also cause a heart murmur..  Diagnostic tests for cardiovascular function 1- Electrocardiogram(ECG) : This test records the electrical activity of the heart, shows abnormal rhythms (arrhythmias), and can sometimes detect heart muscle damage. ( useful in the initial diagnosis and monitoring of arrhythmias, myocardial infarction). A portable Holter monitor , battery-powered ECG machine, may be worn by an individual to record heartbeats over a period of 24 to 48 hours during normal activities. (While do daily activities) Exercise Stress test (also called treadmill or exercise ECG). This test is done to monitor the heart while you walk on a treadmill or pedal a stationary bike. A positive" stress test means that an artery may have one or more fatty plaques large enough to interfere with blood supply  Diagnostic tests for cardiovascular function 2-Valvular abnormalities or abnormal shunts of blood cause murmurs detected by: Auscultation of heart sounds by means of a stethoscope Echocardiography (echo) a noninvasive test using ultrasound, or reflected sound waves to record a live image on the monitor of the heart and valve movements. 3-Chest x-ray films: Cardiac CT scan. Where size & shape can determine, uses an X-ray machine and a computer to create a 3- dimensional pictures of the heart.  Diagnostic tests for cardiovascular function 4- SPECT: is a specialized CAT scan accurately assesses cardiac ischemia at rest gives information about the flow of blood through the coronary arteries to the heart muscle 5- Cardiac catheterization (also called coronary angiogram). A small catheter (hollow tube) through the large artery in your upper leg, or sometimes your wrist or arm, into your heart. Dye is given through the catheter, and moving X-ray pictures are made as the dye travels through your heart. It shows: narrowing in the arteries, heart chamber size, how well your heart pumps, and how well the valves open and close, as well as a measurement of the pressures within the heart chambers and arteries. Coronary angiography shows stenosis (arrow) of left anterior descending coronary artery. 6-Doppler studies: assess blood flow in the peripheral vessels 7-Arterial blood gas determination(ABG) 8-Enzymes (isoenzymes):CK = creatine kinase/LDH = lactate dehydrogenase /C-reactive protein  Cardiovascular disorders  Heart disorders  Vascular disorders  Shock  Heart disorders 1) CORONARY ARTERY DISEASE (CAD) 1) Arteriosclerosis and Atherosclerosis 2) Angina Pectoris 3) Myocardial Infarction 2) CARDIAC DYSRHYTHMIAS (ARRHYTHMIAS) 1) Sinus Node Abnormalities 2) Atrial Conduction Abnormalities 3) Atrioventricular Node Abnormalities—Heart Blocks 4) Ventricular Conduction Abnormalities 5) Cardiac Arrest or Standstill (Asystole) 3) CONGESTIVE HEART FAILURE 4) CONGENITAL HEART DEFECTS 1) Ventricular Septal Defect 2) Valvular Defects 3) Tetralogy of Fallot 5) INFLAMMATION AND INFECTION IN THE HEART; 1) Rheumatic Fever and Rheumatic Heart Disease 2) Infective Endocarditis / Pericarditis 1) Coronary artery diseases (CAD) 1) Arteriosclerosis and Atherosclerosis 2) Angina Pectoris 3) Myocardial Infarction (heart attack)  Arteriosclerosis and Atherosclerosis Arteriosclerosis: Degenerative changes of small arteries and arterioles, Elasticity is lost, the walls become thick and hard, and the lumen narrows and may become obstructed. This leads to diffuse ischemia and necrosis in various tissues, such as the kidneys, brain, or heart. Atherosclerosis is differentiated by the presence of atheromas – Plaques consisting of lipids, cells, fibrin, and cell debris, often with attached thrombi, – Formed inside the walls of large arteries , such as the aorta , the iliac arteries, the coronary arteries, and the carotid arteries.  Atherosclerosis Etiology: multifactorial, two groups of risk factors – Factors that cannot be changed (non-modifiable) include: Age, with atherosclerosis more common after age 40 years, particularly in men Gender, that is, women are protected by higher HDL levels until after menopause, when estrogen levels decrease Genetic or familial factors – Predisposing modifiable factors such as: Obesity or diets high in cholesterol and animal fat, which elevate serum lipid levels, especially LDL Cigarette smoking(decreases HDL, increases LDL, promotes platelet adhesion, and increases fibrinogen) Sedentary lifestyle, which predisposes to sluggish blood flow and obesity Diabetes mellitus, especially those whose disease is not well controlled, Poorly controlled hypertension or combination of high blood cholesterol and high blood pressure Combination of some oral contraceptives and smoking  Diagnostic tests Serum lipid levels, including those of LDL and HDL? Serum levels of high-sensitivity C-reactive protein (CRP) indicate the presence of inflammation, indicating increased risk. Exercise stress testing can be used for screening or to assess the degree of obstruction in arteries. Nuclear medicine studies can be used to determine the degree of tissue perfusion, the presence of collateral circulation , and the degree of local cell metabolism FIGURE 18-11 Composition of lipoproteins and transport of lipoproteins in blood  stroke Possible consequences of atherosclerosis  Summary Arteriosclerosis refers to degeneration of small arteries with – loss of elasticity; – development of thick, hard walls and narrow lumens – causing ischemia and possibly local necrosis. In atherosclerosis, large arteries such as the aorta and the coronary and carotid arteries are obstructed by cholesterol plaques and thrombi. » Obstructions may be partial or complete, and emboli are common. » Factors predispose patients to development of atheromas: such as genetic conditions, high cholesterol diet, elevated serum LDL levels, and elevated blood pressure  Angina Pectoris  The medical term for chest pain or discomfort  The discomfort also can occur in your shoulders, arms, neck, jaw, or back.  It is a symptom of an underlying heart problem, usually coronary heart disease  It may feel like :  pressure or squeezing in your chest.  Angina pain may even feel like gas or indigestion.  Angina Pectoris Etiology: an imbalance between oxygen supply and demand of the heart. heart muscle doesn't get enough oxygen-rich blood because one or more of the coronary arteries is narrowed or blocked, also called ischemia. supply 1-Insufficient myocardial blood supply as in cases of : bad atherosclerosis, arteriosclerosis, vasospasm (a localized contraction of arteriolar smooth muscle), and myocardial hypertrophy, in which the heart has outgrown its blood supply. 2-Severe anemias and respiratory disease can also cause an oxygen deficit. 3-Increased demands for oxygen can arise in circumstances such as: – tachycardia associated with hyperthyroidism or – the increased force of contractions associated with hypertension.  Angina Pectoris Angina pectoris attacks are precipitated when the demand for oxygen by the myocardium exceeds the supply. activities that increase the demands on the heart, such as ; – running upstairs, – Emotional Stress (getting angry) – respiratory infection with fever, – Exposure to very hot or cold temperatures or pollution , – eating a large meal or heavy meals – Smoking.  Types of angina  There are many types of angina, including : Stable angina (classic or exertional angina); Occurs when the heart must work harder, usually during physical exertion Unstable angina, a serious form Often occurs while you may be resting, sleeping, or with little physical exertion the most common cause is blood clots from a break in an atheroma that block an artery partially or totally Variant angina (Prinzmetal angina /Angina inversa) – Usually severe pain occurs when a person is at rest, between midnight and early morning. – Causes : a spasm in the coronary arteries (which supply blood to the heart muscle).  Myocardial Infarction(MI, or heart attack) Occurs when a coronary artery is totally obstructed, leading to: – prolonged ischemia and cell death, or infarction, of the heart wall(The majority involve the critical left ventricle) The most common cause is atherosclerosis, usually with thrombus attached Signs and symptoms Pain: Sudden persisting substernal chest pain that radiates to the left arm, shoulder, jaw, or neck is the hallmark of MI. The pain is usually described as severe, steady, and crushing, and no relief occurs with rest or vasodilators. Pallor and diaphoresis, nausea, dizziness and weakness, and dyspnea Marked anxiety and fear Hypotension: Hypotension is common, and the pulse is rapid and weak as cardiac output decreases and shock develops. Low-grade fever  Diagnostic tests 1. Typical changes occur in the ECG confirm the diagnosis and assist in monitoring progress. 2. Serum enzymes with elevations of lactic dehydrogenase (LDH-1), aspartate aminotransferase (AST), and creatine phosphokinase with M and B subunits (CK-MB or CPK-2) 3. Serum levels of myosin and cardiac troponin are elevated a few hours after MI, providing for an earlier confirmation. A rise in cardiac troponin levels is considered most specific for myocardial tissue damage. 4. Serum electrolyte levels, particularly potassium and sodium, may be abnormal. 5. Leukocytosis and an elevated CRP and erythrocyte sedimentation rate are common, signifying inflammation 6. Arterial blood gas measurements 7. Pulmonary artery pressure measurements are also helpful in determining ventricular function.  Myocardial Infarction Complications Ventricular arrhythmias and fibrillation – This is the major cause of death in the first hour after an MI. Cardiogenic shock , Congestive heart failure (CHF) Rupture of the necrotic heart tissue Thromboembolism Treatment Rest, oxygen therapy, and analgesics Anticoagulants medication to reduce dysrhythmias, defibrillation, or a pacemaker Specific measures may be required if shock or congestive heart failure develops  Summary MI results from total obstruction in a coronary artery, resulting in : Tissue necrosis and loss of function. Continuing chest pain, hypotension, and Typical changes in the ECG are diagnostic. Arrhythmias are a common cause of death shortly after infarction occurs  2- Congestive heart failure fattyhypertenison owned state Definition = the heart is unable to pump sufficient blood to meet the metabolic needs of the body (w/o extraordinary effort) It occurs as a complication of another condition things that leadto A problem in the heart itself, such as an infarction or aothcond.tn valve defect Iink easengffy Increased demands on the heart, such as hypertension or lung disease It may involve a combination of factors more than one problem – Types A-Left sided heart failure Most timebeouseofthelungs B- Right Sided Failure of the C- Combined right & left sided failure is the most common presentation 0  Congestive heart failure inotquitsureonthis one If f d FETED 50 watchin b off e f faffidhne 19 49am ethos  note 0 0 dTt FN hypertension Iii iiif 0 E in Cor pulmonale is defined as an alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system.  we Summary Depending on the cause, congestive heart failure may develop first in either the right or the left0 side of the nee backup and congestion or heart, causing systemic pulmonary congestion, respectively. In either case, cardiac output to the body is reduced, causing general fatigue and weakness, and stimulating the renin angiotensin mechanism. keeping water F  3- CARDIAC DYSRHYTHMIAS (ARRHYTHMIAS) III__ Deviations from normal cardiac rate or rhythm – Etiology is usually damage to the heart’s conduction system e IIIIffathffedonduction – Or systemic causes such as electrolyte abnormalities (potassium imbalance), e It fever , hypoxia, stress, infection, inflammation or scar tissue associated with e e rheumatic fever or myocardial infarction or drug toxicity. Is f Diagnosis : Ctf Arrhythmias – The ECG provides a method of monitoring the conduction system and detecting abnormalities. – Holter monitors record the ECG over a prolonged period as a patient follows normal daily activities. Effects : Reduce the efficiency of the heart’s pumping cycle.  Types of cardiac arrhythmias May be related to origin, pathway and speed Sinus node abnormalities Partoftheconductingsystem IItis – Bradycardia: regular slow heart bother rate below 60 beats/min. to e rate100 to160 beat/min out – Tachycardia; regular rapid heart abnormalities northeast manductingwhen Atrial conduction abnormalities g a Atrioventricular node masquerade IS abnormalities (Heart block) Ventricular conduction mandated ventreculalabnormhdshearab.bg abnormalities Cardiac Arrest or Standstill e to (Asystole): no cardiac output, flat ECG Arrhythmias on electrocardiogram. i Normal sinus rhythm c tachycardia themers Sinus tachycardia e Regular fast rate =100-160/min DO nothing closetonormal Ventricular fibrillation Irregular Rate >300/min that  larruthmia mid r e e we e IILITY h pthet  g ffoodterested 4-CONGENITAL HEART DEFECTS Structural defects in the heart that develop during the first 8 weeks of embryonic life 0_ may include: sidesadd – Valvular defects (stenosis, With e the normal flow of blood incompetence, or prolapse), that interfere with thesis – Septal defects( ventricular septal defect), that allow mixing of oxygenated _I_ blood from the pulmonary circulation with unoxygenated blood from the systemic circulation shape ofthebig_vessels abnormal – Shunts or abnormalities in position or shape of the large vessels (aorta and e pulmonary artery), or combinations of these. F The primary outcomes is decreased oxygen to all cells in the body Most defects can be detected by the presence of heart murmurs as to Congenital heart disease is divided into 2 categories: Acyanotic & e e cyanotic a  Acyanotic :disorders in TIE which systemic flow consists of blood oxygenated blood, F although the amount may be reduced. dayanotic 1-Causes due to increase pulmonary blood flow sides betwaenthe.li e the I Ventricular Septal Defect (VSD)most common (1/3 of all congenital heart problems) Icftu Atrial Septal Defect (ASD) Patent Ductus Arteriosus (PDA) 2- Causes due to obstructive lesions Coarctation of the Aorta Aortic stenosis Pulmonary stenosis FIGURE 18-25 Effects of heart valve defects.  Cyanotic disorders, where significant FIFE amounts of unoxygenated blood bypass the lungs and enter the systemic circulation, produces a bluish color in the skin and mucous membranes, a particularly the lips and nails. Tetralogy of Fallot Ifr The most common cyanotic congenital heart condition. (infants are sometimes called “blue babies”). Includes four abnormalities:  I Pulmonary valve stenosis e  Ventricular septal defect (VSD)  Dextroposition of the aorta (to the right over the VSD) Which is the most  Right ventricular hypertrophy. NH This combination alters pressures within the common congenital 71 cause of early cyanosis? at heart and therefore alters blood flow  Summary to 00 Congenital heart defects consist of a variety of single or multiple developmental abnormalities in the heart. These structural abnormalities may involve the heart valves, such e as mitral stenosis; the septae, such as ventricular septal defect; or F the proximal great vessels. too The primary outcome is decreased oxygen to all cells in the body. Cyanotic defects such as the tetralogy of Fallot refer to congenital defects where blood a fo leaving the left ventricle consists of mixed oxygenated and unoxygenated blood, thereby delivering only ekt bdf.gg__ small amounts of oxygen to all parts of the body. 5-Inflammation and infection in the heart  Rheumatic E fever and rheumatic heart disease Iter  Infective endocarditis TIFF  Pericarditis Wh mostof these case fibrosis  Rheumatic Fever and Rheumatic Heart Disease E If e likeattacking itself F Is 1 0 f FIGURE 18-29 Development of rheumatic fever and rheumatic heart disease.  Rheumatic Fever and Rheumatic Heart Disease Rheumatic fever ; 0 An acute systemic inflammatory condition – appears to result from an abnormal immune reaction occurring a few 8 weeks after an untreated infection,fusually caused by certain strains of group A beta-hemolytic Streptococcus. we e o Antibody formed and react with connective tissue (collagen ) ooo in heart, joints, skin and brain causing inflammation (collagen disease) o The heart is the only site where scar tissue e f occurs causing e rheumatic heart disease III baseof the scartissue It usually occurs in children 5-15 years of age Rheumatic fever & heart disease: 1. Inflammation of the heart includes; Endocarditis------valve damage Myocarditis------arrhythmias Pericarditis--------effusion (an abnormal accumulation of fluid in the pericardial cavity) Scar tissue with loss of valve functions and arrhythmias characteristic of rheumatic heart disease fo ce 2. Polyarthritis of large joint, Particularly of the legs knee 3. Subcutaneous nodules on extensor surfaces of wrists, elbows, knees or ankles 4. Rash on trunk (erythema marginatum) non pruritic, never on face or hands (usually on the trunk and limbs) 5. Involuntary jerky movementse 000 of the face, arms, &legs (Chorea ) -- from effect on basal nuclei in the brain  a Rheumatic fever & heart disease Signs and symptoms; – General signs of inflammation; __ – Low grade fever/Leukocytosis/Malaise/anorexia, fatigue/Tachycardia – Heart murmurs indicate the site of inflammation – A normal heartbeat makes two th (sometimes o sounds like "lubb-dupp" described as "lub-DUP"), which are the sounds of your heart valves closing. – A heart murmur is an abnormal heart sound that can only be detected by a doctor with a stethoscope, it's so low and soft – Acute heart 0 failure may develop Diagnostic tests; – Elevated serum antibody levels (antistreptolysin O titer ) F – Leukocytosis and anemia – Characteristic ECG changes; increase PR & QT intervals, AV block  Summary Rheumatic fever is acute systemic inflammatory condition caused by an abnormal immune response to certain strains of hemolytic IF streptococcus. Inflammation causes scar tissue on heart valves and in the myocardium, leading to rheumatic heart disease.  5- Inflammation and infection in the heart Infectious endocarditis causes destruction and so permanent damage to heart valves and chordae tendineae. Individuals with heart defects or damage should take prophylactic antibacterial drugs before invasive E_ procedures in which bacteremia is a threat. When pericarditis leads to a large volume of fluid accumulating in the pericardial cavity, filling of the heart is restricted, and cardiac output is reduced.  BLOOD VESSELS The arteries, capillaries, and veins constitute a closed system for the distribution of blood throughout the body. Major blood vessels, most of which are paired left and right, There are two separate circulations— the pulmonary circulation allows the exchange of oxygen and carbon dioxide in the lungs, and the systemic circulation  6- VASCULAR DISORDERS ARTERIAL DISEASES: –Hypertension –Peripheral Vascular Disease and Atherosclerosis –Aortic Aneurysms VENOUS DISORDERS: –Varicose Veins –Thrombophlebitis and Phlebothrombosis  BLOOD PRESSURE Blood pressure refers to the pressure of blood against the systemic arterial walls. In adults a normal pressure is commonly in the range of 120/70 mmHg at rest. d f 120170 mm Hg – Systolic pressure, the higher number, is the pressure exerted by the blood when ejected from the left ventricle. – Diastolic pressure, the loweravalue, is the pressure that is sustained when the ventricles are relaxed. The brachial artery in the arm is used to measure blood pressure with a sphygmomanometer and an inflatable blood pressure cuff. e Pulse pressure is the difference between the systolic and diastolic pressures. SP DP 12870  Cardiac Cycle Is Cardiac function can be measured in a number of ways; 1.Cardiac output (CO) is the volume of blood ejected by a ventricle in one minute and depends on heart rate (HR) and stroke volume (SV, the volume pumped from one ventricle in one contraction) o 2.Cardiac reserve refers to the ability of the heart to increase output in response to increased demand. 3.Preload refers to the amount of blood delivered to the heart by venous return. 4.Afterload is the force required to eject blood from the ventricles and is determined by the peripheral resistance to the opening of the semilunar valves. FIGURE 18-5 Cardiac output.  Arterial diseases; Hypertension – Called “silent killer” Because of the insidious onset , mild signs, and undiagnosed until complications arise – 3 types: Primary or essential hypertension is idiopathic, develops when the blood pressure is consistently above 140/90 Secondary hypertension results from renal (e.g., nephrosclerosis) or endocrine (e.g., hyperaldosteronism) disease, or pheochromocytoma, a benign tumor of the adrenal medulla or SNS chain of ganglia Malignant or resistant hypertension: persistent elevation of BP with vascular necrosis : bad prognosis severe, and rapidly progressive form with many complications.  Hypertension Sometimes hypertension is classified as systolic or diastolic, depending on the measurement that is elevated. For example, elderly persons with loss of elasticity in the arteries frequently have a high systolic pressure and low diastolic value Toumani  Hypertension Etiology; – Genetic factors, African Americans have a higher incidence than do Caucasians and experience a more severe form of hypertension. – lifestyle characteristics – high sodium intake, – excessive alcohol intake (small amounts of alcohol appear to decrease blood pressure), – obesity, and prolonged or recurrent stress. Signs and symptoms Hypertension is frequently asymptomatic in the early stages The Initial signs are often vague and nonspecific. They include fatigue, malaise, and sometimes morning headache. Consistently elevated blood pressure under various conditions is the key sign of hypertension. The complications are also asymptomatic until they are well here advanced.  Primary or essential hypertension Essential hypertension develops when the blood pressure is consistently above 140/90. 1489900 This figure may be adjusted for the individual’s age. takethecasestudyas anexample The diastolic pressure is important because it indicates the degree of peripheral resistance and the increased workload of the left ventricle. The condition may be mild, moderate, or severe.  Primary or essential hypertension The areas most frequently damaged by elevated pressure are the kidneys, brain, and retina Effects of uncontrolled hypertension: – Chronic renal failure, – Brain: stroke due to hemorrhage, – Eye : loss of vision, – Congestive heart failure.  2 keeps everything in o CHF nosuffient pumpfor metabolicneeds To FIGURE 18-32 Development of hypertension  Summary unknownreasonofcourse Essential or primary hypertension is idiopathic and marked by a persistent elevation of blood pressure above 140/90, related to increased systemic vasoconstriction. normal 120170 140190 Leadsto renalfaluir ritralfakirt problems n It is frequently asymptomatic, but if not monitored and controlled may cause permanent damage to the kidneys, brain, and retinas as well as possible congestive heart failure. CHF one of thecauses hypertension heart can not Pump enugonbloodfor meta needs  Peripheral Vascular Disease and Atherosclerosis Peripheral Vascular Disease: refers to any abnormality in the arteries or veins outside the heart. Atherosclerosis : – The most common sites of atheromas in the peripheral circulation are the abdominal aorta and the femoral and iliac arteries Where partial occlusions may impair both muscle activity and sensory function in the legs. Of 1 Total occlusions may result from a thrombus obstructing the lumen or 1 breaking off (an embolus) and eventually obstructing a smaller artery. Loss of blood supply in a limb leads to necrosis, ulcers, and gangrene, which is a bacterial infection of necrotic tissue. Peripheral Vascular Disease and Atherosclerosis Signs and symptoms Increasing fatigue and weakness in the legs develop as blood flow decreases. Intermittent claudication, or leg pain associated with exercise due to muscle ischemia, is a key indicator. Sensory impairment may also be noted as paresthesias,or tingling, burning, and numbness. e feelpulsforfromobstrefs.to If Peripheral pulses distal to the occlusion (e.g., the popliteal and pedal pulses) become weak or absent The appearance of the skin of the feet and legs changes, with I or cyanosis bluishcolor marked pallor The skin is dry and hairless, the toe nails are thick and hard, and poorly perfused areas in the legs or feet feel cold. Diagnostic tests  Blood flow can be assessed by Doppler studies (ultrasonography) and arteriography.  Aneurysms An aneurysm is a localized dilatation and weakening of an arterial wall. The most common location is either the abdominal or thoracic aorta, also occur in the cerebral circulation Etiology : Common causes are atherosclerosis, trauma, infections , congenital defects and Hypertension Signs and symptoms : frequently asymptomatic for a long period of time until they become very large or rupture Diagnostic tests : Radiography, ultrasound, CT scans, or MRI confirm the problem. IS  Summary Atherosclerosis in the abdominal aorta or iliac arteries – may cause ischemia in the feet and legs, EEE – Resulting in fatigue, intermittent claudication, sensory impairment, ulcers, and possibly gangrene and amputation. Aortic aneurysms are frequently asymptomatic until e they are very large or rupture e occurs. c  Venous Disorders Varicose Veins Varicosities are irregular dilated and tortuous areas of the superficial or deep veins. 8800 The most common location is the legs, but varicosities are also found in the esophagus (esophageal varices) and the rectum (hemorrhoids) I varicosities Signs and Symptoms : O Superficial varicosities on the legs appear as Irregular, purplish, bulging structures. Edema in the feet as the venous return is OO reduced. Fatigue 00 o and aching are common as the increased interstitial fluid interferes with arterial flow and nutrient supply Varicose ulcers may develop as arterial blood flow continues to diminish leading to skin break down The superficial leg veins are frequently involved because there is less muscle support for these veins. formed 1 backflow abnormal normal abnormal  Thrombophlebitis and Phlebothrombosis Thrombophlebitis 0 refers to the development of a thrombus in a vein in which inflammation is present. thrombusinvein inflimation Phlebothrombosis, a thrombus forms spontaneously in a vein ON without prior inflammation. thrombus in vein  Several factors usually predispose to thrombus he inflammation development: stasis of blood or sluggish blood flow, endothelial injury, (trauma, chemical injury, intravenous injection, or inflammation). increased blood coagulability (dehydration, cancer, pregnancy , or increased platelet adhesion).  Thrombophlebitis and Phlebothrombosis  The critical problem is that venous thrombosis may lead to pulmonary embolism venousthrombosis Pulmonary embolism  Sudden chest pain and shock are indicators of pulmonary embolus. Signs and symptoms: Aching pain, tenderness, and edema in the affected leg A positive Homans’ sign (calf pain on dorsiflexion of foot ) is common, but not always reliable. Pale leg & cool with diminished arterial pulse Systemic signs such as: o fever, malaise, o leukocytosis may be present  Summary Varicose veins in the legs tend to be progressive. They cause fatigue, swelling, and possible ulcers in the skin. e Pulmonary emboli are a greater risk with phlebothrombosis Phlebothrombosis is usually a silent problem, than with thrombophlebitis, in which inflammation is more apparent.  Shock or Hypotension  Shock is a major medical emergency (circulatory failure)  results from a decreased circulating blood volume, leading to decreased tissue perfusion and general hypoxia  PathophysiologyShockcirculatoryLaliure bloodvolume tissueprofusion general hypoxia Blood pressure is determined by blood volume, heart contraction, and peripheral resistance. When one of these factors fails, blood pressure drops – When blood volume is decreased, it is difficult to maintain pressure within the distribution system. VR – If the force of the pump declines, blood flow slows, and venous return is reduced. – The third factor, peripheral resistance, is altered by general vasodilation, which increases the capacity of the vascular system, leading to a lower pressure within the system and sluggish flow. cuzofdialation  Shock Types (causes ): 1. Hypovolemic shock 2. Cardiogenic shock 3. Vascular shock : O O because of vasodilation may be classified in a variety of ways:  Vasogenic(Neurogenic) shock  Anaphylactic shock hearseoftherealseoftoomuchhistamin 4. Septic shock FIGURE 18-36 A-D, Causes of shock.  Problemin theheartitself Mduetoharonstimuli r histamine  as Compensation mechanisms: are initiated as soon as blood SHR pressure decreases:  The SNS andwetter sampa adrenal medulla are Bloodvolu stimulated to increase the heart rate, the force of contractions, and systemic volume Blood vasoconstriction.  Renin is secreted to activate angiotensin, a vasoconstrictor, and aldosterone to increase blood volume.  Increased secretion of antidiuretic hormone (ADH) also promotes reabsorption of water from the kidneys to increase blood volume and acts as a vasoconstrictor. I  Glucocorticoids are secretedethat help stabilize the vascular system.  Acidosis stimulates respirations, increasing oxygen supplies and reducing carbon dioxide levels Note: Organs which are the source of the problem cannot compensate for the problem. Thus cardiogenic shock cannot be compensated for by increased cardiac output. FIGURE 18-37 Progress of shock.  Shock The signs and symptoms of shock include low blood pressure (hypotension); over breathing (hyperventilation); a weak, rapid pulse; cold, clammy, grayish-bluish (cyanotic) skin; decreased urine flow (oliguria); and a sense of great anxiety and confusion,  Shock Signs and symptoms: Often missed, the first signs of shock are thirst and agitation or restlessness because the SNS is quickly stimulated by hypotension, weak rapid pulse and hyperventilation. This is followed by the characteristic signs of compensation: cool, moist, pale skin; tachycardia; and oliguria Vasoconstriction; shunts blood from the viscera and skin to the vital areas. FIGURE 18-38 General effects of circulatory shock.  Summary Circulatory shock may result from decreased blood volume, impaired cardiac function with reduced output, or generalized vasodilation, any of which reduce blood flow and available oxygen in the microcirculation. Compensation mechanisms include: – The sympathetic nervous system; – renin mechanism; – increased secretion of ADH, – aldosterone, and cortisol; – and increased respirations. Decompensated shock develops with complications such as organ failure or infection.