EPIDEMIOLOGY AND ETIOLOGY OF STROKE

            Stroke is the fourth leading cause of death and the leading cause of long-term disability among adults in the United States. An estimated 7,000,000 Americans older than 20 years of age have experienced a stroke. Each year approximately 795,000 individuals experience a stroke; approximately 610,000 are first attacks and 185,000 are recurrent strokes. 

             Women have a lower age-adjusted stroke incidence than men. However, this is reversed in older ages; women over 85 years of age have an elevated risk compared to men. Compared to whites, African Americans have twice the risk of first-ever stroke; rates are also higher in Mexican Americans, American Indians, and Alaska Natives. he incidence of stroke increases dramatically with age, doubling in the decade after 65 years of age. Twenty-eight percent of strokes occur in individuals younger than 65 years of age. Between 5% and 14% of persons who survive an initial stroke will experience another one within 1 year; within 5 years stroke will recur in 24% of women and 42% of men. Current data reveal that stroke incidence has been declining in recent years in a largely white adult cohort. he incidence of stroke deaths is greater than 143,000 annually, and strokes account for 1 of every 18 deaths in the United States. he type of stroke is significant in determining survival. Of patients with stroke, hemorrhagic stroke accounts for the largest number of deaths, with mortality rates of 37% to 38% at 1 month, whereas ischemic strokes have a mortality rate of only 8% to 12% at 1 month. Survival rates are dramatically lessened by increased age, hypertension, heart disease, and diabetes. Loss of consciousness at stroke onset, lesion size, persistent severe hemiplegia, multiple neurological deficits, and history of previous stroke are also important predictors of mortality.1,2 Stroke is the leading cause of long-term disability in the United States. Of ischemic stroke survivors 65 or older, incidences of disabilities observed at 6 months include hemiparesis (50%), unable to walk without assistance (30%), dependent in activities of daily living (ADL) (26%), aphasia (19%), and depression (35%). Stroke survivors represent the largest group admitted to rehabilitation hospitals and about a third of patients receive outpatient rehabilitation services. Another indicator of disability is the fact that approximately 26% of patients with stroke are institutionalized in a long-term care facility. Direct and indirect costs of stroke are in the billions. Atherosclerosis is a major contributory factor in cerebrovascular disease. It is characterized by plaque formation with an accumulation of lipids, fibrin, complex carbohydrates, and calcium deposits on arterial walls that leads to progressive narrowing of blood vessels. Interruption of blood flow by atherosclerotic plaques occurs at certain sites of predilection. hese generally include bifurcations, constrictions, dilations, or angulations of arteries. he most common sites for lesions to occur are at the origin of the common carotid artery or at its transition into the middle cerebral artery, at the main bifurcation of the middle cerebral artery, and at the junction of the vertebral arteries with the basilar artery

          Ischemic strokes are the result of a thrombus, embolism, or conditions that produce low systemic

perfusion pressures. The resulting lack of cerebral blood flow (CBF) deprives the brain of needed oxygen and glucose, disrupts cellular metabolism, and leads to injury and death of tissues. A thrombus

results from platelet adhesion and aggregation on plaques. Cerebral thrombosis refers to the formation

or development of a blood clot within the cerebral arteries or their branches. It should be noted that

lesions of extracranial vessels (carotid or vertebral arteries) can also produce symptoms of stroke. Thrombi lead to ischemia, or occlusion of an artery with resulting cerebral infarction or tissue death (atherothrombotic brain infarction [ABI]). Thrombi can also become dislodged and travel to a more distal site in the form of an intra-artery embolus. Cerebral embolus (CE) is composed of bits of matter (blood clot, plaque) formed elsewhere and released into the bloodstream, traveling to the cerebral arteries where they lodge in a vessel, producing occlusion and infarction. The most common source of CE is disease of the cardiovascular system. Occasionally systemic disorders may produce septic, fat, or air emboli that affect the cerebral circulation. Ischemic strokes may also result from low systemic perfusion, the result of cardiac failure or significant blood loss with resulting systemic hypotension. The neurological deficits produced with systemic failure are global in nature with bilateral neurological deficits. Hemorrhagic strokes, with abnormal bleeding into the extravascular areas of the brain, are the result of rupture of a cerebral vessel or trauma. Hemorrhage results in increased intracranial pressures with injury to brain tissues and restriction of distal blood flow. Intracerebral hemorrhage (IH) is caused by rupture of a cerebral vessel with subsequent bleeding into the brain. Primary cerebral hemorrhage (nontraumatic spontaneous hemorrhage) typically occurs in small blood vessels weakened by atherosclerosis producing an aneurysm. Subarachnoid hemorrhage (SH) occurs from bleeding into the subarachnoid space typically from a saccular or berry aneurysm affecting primarily large blood vessels. Congenital defects that produce weakness in the blood vessel wall are major contributing factors to the formation of an aneurysm. Hemorrhage is closely linked to chronic hypertension. Arteriovenous malformation (AVM) is another congenital defect that can result in stroke. AVM is characterized by a tortuous tangle of arteries and veins with agenesis of an interposing capillary system. he abnormal vessels undergo progressive dilation with age and eventually bleed in about 50% of cases. Sudden and severe cerebral bleeding can result in death within hours, because intracranial pressures rise rapidly and adjacent cortical tissues are compressed or displaced as in brainstem herniation.

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WHAT IS STROKE ?

  Stroke (cerebrovascular accident [CVA]) is the sudden loss of neurological function caused by an interruption of the blood flow to the brain. Ischemic stroke is the most common type, affecting about 80% of individuals with stroke, and results when a clot blocks or impairs blood flow, depriving the brain of essential oxygen and nutrients. 

Hemorrhagic stroke occurs when blood vessels rupture, causing leakage of blood in or around the brain. Clinically, a variety of focal deficits are possible, including changes in the level of consciousness and impairments of sensory, motor, cognitive, perceptual, and language functions. To be classified as stroke, neurological deficits must persist for at least 24 hours. Motor deficits are characterized by paralysis (hemiplegia) or weakness (hemiparesis), typically on the side of the body opposite the side of the lesion. he term hemiplegia is often used generically to refer to the wide variety of motor problems that result from stroke. he location and extent of brain injury, the amount of collateral blood flow, and early acute care management determine the severity of neurological deficits in an individual patient. Impairments may resolve spontaneously as brain swelling subsides (reversible ischemic neurological deficit), generally within 3 weeks. Residual neurological impairments are those that persist longer than 3 weeks and may lead to lasting disability. Strokes are classified by etiological categories (thrombosis, embolus, or hemorrhage), specific vascular territory (anterior cerebral artery syndrome, middle cerebral artery syndrome, and so forth), and management categories (transient ischemic attack, minor stroke, major stroke, deteriorating stroke, young stroke)

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Heart Valves

HEART DISEASE

      CARDIAC ANATOMY AND PHYSIOLOGY OF HEART 

     HEART TISSUE

      CORONARY ARTERIES 

Heart Valves ;    

            Four heart valves ensure one-way blood flow through the heart. Two atrioventricular valves are located between the atria and ventricle. The atrioventricular valve, positioned between the RA and RV, is termed the tricuspid valve; the left atrioventricular valve is the mitral valve (also known as the bicuspid valve), located between the left atrium and ventricle. he semilunar valves lie between the ventricles and arteries and are named based on their corresponding vessels (i.e., pulmonic valve on the right in association with the pulmonary artery, and aortic valve on the left relating to the aorta).

           Flaps of tissue called leaflets or cusps guard the heart valve openings. he right atrioventricular valve has three cusps and is therefore termed tricuspid, whereas the left atrioventricular valve has only two cusps and hence is termed bicuspid. These leaflets are attached to the papillary muscles of the myocardium by chordae tendineae. the primary function of the atrioventricular valves is to prevent backflow of blood into the atria during ventricular contraction or systole, while the semilunar valves prevent backflow of blood from the aorta and pulmonary artery into the ventricles during diastole. Opening and closing of each valve depends on pressure gradient changes within the heart created during each cardiac cycle.

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CORONARY ARTERIES

HEART DISEASE

        CARDIAC ANATOMY AND PHYSIOLOGY OF HEART 

      HEART TISSUE

 

Coronary Arteries ;

                The coronary arteries originate in the sinus of Valsalva located in the wall of the aorta near the aortic valve.The right coronary originates from the area near the right aortic leaflet, the left coronary from the area near the left aortic leaflet. When the aortic valve is open during systole, the origins of the coronary arteries are located behind the aortic leaflets within the wall; when the aortic valve is closed during diastole, the openings of the coronaries are clearly exposed, allowing them to be easily perfused.5 he coronary arteries therefore receive the majority of their blood flow during diastole, unlike the other arteries of the body that are perfused during systole.

                    The left coronary artery begins as the left main (LM) and then branches into the left anterior descending (LAD) and the circumflex (CX) (Fig. 13.3). he LAD may have further divisions, known as diagonal branches, that come off of the primary LAD. he LAD and its diagonal branches primarily supply the anterior and apical surfaces of the LV, as well as portions of the interventricular septum. he circumflex may also have branches, known as marginal branches. he circumflex and its marginal branches supply the lateral and part of the inferior surfaces of the LV and portions of the left atrium (LA). he right coronary artery (RCA) supplies the RA, most of the RV, part of the inferior wall of the LV, portions of the interventricular septum, and the conduction system. he posterior descending artery (PDA) is most commonly a branch of the RCA and perfuses the posterior heart. If the RCA does not perfuse the posterior heart, the CX will supply this area. When the PDA comes from the RCA, the anatomy is referred to as being right dominant; if the PDA comes from the circumflex, the anatomy is referred to as being left dominant. For physical therapists, there is no clinical importance to whether the anatomy of the myocardium is either left or right dominant.

                     The inner diameter (i.e., the opening) of the arteries through which the blood flows is the lumen. he size of the lumen is critical for adequate blood flow. A significant narrowing of the lumen, such as that which occurs with a fixed atherosclerotic lesion of CAD, will decrease the available blood supply to the myocardium. Lumen size may also be altered by the smooth muscle within the walls of the arteries, because smooth muscle regulates vasomotor tone of the coronary arteries. Vasodilation will increase lumen diameter as a result of relaxation of smooth muscle, and vasoconstriction will decrease lumenal diameter as a result of smooth muscle contraction. he responsiveness of arterial smooth muscle is also influenced by the integrity of the endothelium, the lining of the coronary artery that is in direct contact with the lumen. The endothelium has a number of normal functions and “plays the central role in controlling the biology of the vessel wall.”10, p. 1,265 Some of these important functions are anti-inflammatory actions, antithrombotic activity, and its influence on vasodilation. Endothelial cells release endothelial-derived relaxing factor (EDRF), which facilitates vascular smooth muscle relaxation. Nitric oxide (NO) is the most prevalent EDRF. An injury to endothelium can result in impaired NO release and a decrease in vasodilation.11 NO release is influenced by many factors, including acetylcholine, norepinephrine, serotonin, adenosine diphosphate, bradykinin, and histamine.The etiology of the clinical condition known as coronary spasm, in which smooth muscle contraction within the walls of the artery results in narrowing of the coronary artery, is not clearly understood. Coronary spasm occurs in arteries that have endothelial injury (e.g., atherosclerosis), as well as in those arteries that appear to be normal but exhibit hyperreactivity to a variety of vasoconstrictor stimuli, such as serotonin and ergonovine, and loss of EDRF.

Heart Valves

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HEART TISSUE

HEART DISEASE

CARDIAC ANATOMY AND PHYSIOLOGY OF HEART

       HEART TISSUE ;

    The heart wall is made up of three tissue layers.The outermost layer of the heart is a doublewalled sac termed the pericardium. he two layers of the pericardium include an outer tough fibrous layer of dense irregular connective tissue termed the parietal pericardium and an inner thin visceral pericardium.5 Between these two layers is a closed space filled with pericardial fluid, which serves as a lubricant allowing the two surfaces to slide past one another. Clinically, patients may develop an infection with resultant inflammation of the pericardium termed pericarditis. he clinical signs that accompany this pathology and used to differentially diagnose pericarditis include a pericardial friction rub (an audible grating sound suggesting irritation of the pericardium) that can be auscultated with each heartbeat accompanied by constant chest pain.In some patients excessive fluid accumulation within the closed pericardial space may lead to a secondary condition known as cardiac tamponade. Tamponade involves compression of the heart caused by fluid buildup in the space between the myocardium and pericardium. In this state, patients will demonstrate compromised cardiac function and contractility due to the excess fluid within the closed space pushing against the heart.7,8 he muscular middle layer of the heart is termed the myocardium. It is the layer that facilitates the pumping action of the heart to move blood to the entire body.

             Alterations in the muscular wall of the heart are termed cardiomyopathies. here are three common classifications of cardiomyopathies: dilated, hypertrophic, and restrictive. Dilated cardiomyopathy is evidenced by ventricular dilation and altered cardiac muscle contractile function. CAD is the prime cause of dilated cardiomyopathy, causing mitochondrial dysfunction and resultant myocardial damage. Myocarditis (inflammation of the heart muscle) and alcohol abuse are additional causes of dilated cardiomyopathy. Hypertrophic cardiomyopathy presents as diastolic dysfunction with an increased ventricular mass. Chronic HTN and aortic stenosis are examples of hypertrophic cardiomyopathy. Restrictive cardiomyopathy also presents as diastolic dysfunction owing to the presence of excessively rigid ventricular walls, resulting in a decrease in compliance. he connective tissue changes of the heart associated with diabetes are an example of a restrictive cardiomyopathy. Damage to myocardial cells from cardiomyopathies and various other etiologies lead to cardiac muscle dysfunction and resultant heart failure, which will be comprehensively discussed later in this chapter. he innermost layer of the heart is termed the endocardium.

                The tissue of the endocardium forms the inner lining of the chambers of the heart and is continuous with the tissue of the valves and the endothelium of the blood vessel. Because the endocardium and valves share similar tissue, patients with infections of the endocardium are at risk for developing valvular dysfunction. Endocardial infections can spread into valvular tissue developing vegetations (a mixture of bacteria and blood clots) on the valve.9 In patients with newly developed vegetations, bronchopulmonary hygiene procedures including percussions and vibrations are contraindicated because they may dislodge, move as emboli, and cause an embolic stroke.

CORONARY ARTERIES

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CARDIAC ANATOMY AND PHYSIOLOGY OF HEART

HEART DISEASE

 Surface Anatomy ;

The heart lies within the left thoracic cavity. The base of the heart is located superiorly, approximately between the second and third rib; the apex is located inferiorly, approximately at the level of the fifth rib. In this position, the heart is rotated in the sagittal plane so that the right ventricle (RV) is positioned anterior to the left ventricle (LV) and tipped anteriorly, bringing the apex closer to the chest wall. In the posterior–anterior view of a chest x-ray, the RV occupies a significant portion of the frontal plane. he right atrium (RA) is generally located in the area of the second intercostal spaces and the angle of Louis. When one palpates the sternum, the angle of Louis is the “bump” that demarcates the manubrium from the body of the sternum. 

The second intercostal spaces are lateral and slightly below the angle of Louis. The second intercostal spaces are an important auscultatory landmark; the right space is known as the aortic area, the left as the pulmonic area. he apex of the normal heart is in the fifth intercostal space at the midclavicular line. In a healthy heart, this area, known as the point of maximal impulse (PMI), is where the contraction of the LV is most pronounced.

HEART TISSUE

CORONARY ARTERIES

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HEART DISEASE

INTRODUCTION;

                    Cardiovascular disease (CVD) is a term referring to the pathological process of atherosclerosis affecting the entire arterial circulation. Coronary artery disease (CAD), also called coronary heart disease (CHD), refers to the pathological process of atherosclerosis, specifically affecting the coronary arteries.

                     CAD includes the diagnoses of angina pectoris, myocardial infarction (MI), silent myocardial ischemia, and sudden cardiac death. he pathophysiological conditions that underlie CVD are atherosclerosis, altered myocardial muscle mechanics, valvular dysfunction, arrhythmias, and hypertension (HTN). Atherosclerosis is a disease in which lipid-laden plaque (lesions) is formed within the intimal layer of the blood vessel wall of moderate and large size arteries; over time the plaque may extend into the lumen causing a decreased lumenal diameter. Atherosclerosis is also a primary contributor to cerebrovascular disease (cerebrovascular accident [CVA]) and peripheral vascular disease (PVD). Alteration in myocardial muscle mechanics involving the systolic and/or diastolic properties of the myocardium results in an impairment of left ventricular (LV) function. Heart failure is a clinical diagnosis caused by impaired LV functioning and is referred to as congestive heart failure (CHF) when it is accompanied by signs and symptoms of edema (i.e., congestion). here are many causes of heart failure, including myocardial scarring and remodeling as a result of an MI, cardiomyopathy (involving an enlarged, thickened, and/or hardened heart muscle) from various causes, or impaired valvular function, especially within the mitral and aortic valves. Arrhythmias are caused by a disturbance in the electrical activity of the heart, resulting in impaired electrical impulse formation or conduction. Arrhythmias may present as benign or malignant (i.e., life threatening). Examples of malignant arrhythmias are sustained ventricular tachycardia (V-tach) and ventricular fibrillation (V-fib). An example of a common benign arrhythmia in the elderly is atrial fibrillation (A-fib) with a controlled ventricular response involving a ventricular rate between 60 and 100 beats per minute (bpm). HTN is the most prevalent CVD in the United States and one of the most powerful contributors to cardiovascular morbidity and mortality. HTN occurs when the systolic blood pressure is consistently greater than 140 mm Hg or the DBP is equal to or greater than 90 mm Hg. CVD remains the leading cause of death and disability in the United States. According to the American Heart Association’s Heart Disease and Stroke Statistics 2011 Update, an estimated 82,600,000 American adults (more than 1 in 3) have one or more types of CVD.1 Currently, HTN occurs in 76,400,000 individuals, CHD affects 16,300,000, and heart failure is seen in 5,700,000 patients.1 he average annual rates of first cardiovascular events rise from 3 per 1,000 men at age 35 to 44 years to 74 per 1,000 at age 85 to 94. For women, comparable rates occur 10 years later in life with a narrowing gap with advancing age.1 On average, 2,200 Americans die of CVD each day with an average of 1 death every 39 seconds.2 In every year since 1900 except 1918, CVD accounted for more deaths than any other major cause in the United States.3It is also important to note that the United States is in the midst of a demographic shift with a remarkable increase in the diversity of the American population. By 2050, there will be a decrease in the white non- Hispanic population to 52.5% from 75.7% in 1990. Hispanic population will increase to 22.5%, a change in African Americans to 15.7%, and Asian and Pacific Islanders will account for 10.3% of the population.4 hese statistics will have a major impact on the epidemiology, pathophysiology, and treatment of CVD in the forthcoming years. within the United States and worldwide, we are faced with major challenges as CVD dominates as a major cause of death and disease. his chapter provides a review of normal anatomy and physiology of the cardiovascular system and its relevance to physical therapist practice followed by a discussion of various pathologies and pertinent physical therapy implications.

CARDIAC ANATOMY AND PHYSIOLOGY OF HEART 

HEART TISSUE

     CORONARY ARTERIES

 

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