Cardiovascular System PDF

Physiology Cardiovascular System Cardiovascular System :Structure of the heart :The heart consists of four c...

Physiology Cardiovascular System Cardiovascular System :Structure of the heart :The heart consists of four chambers.Two upper chambers (atria) -.Two lower chambers (ventricles) - The heart also has four valves that open and close to let blood flow in only one.direction when the heart beats :The four heart valves are.Tricuspid valve: located between the right atrium and right ventricle.Pulmonary or pulmonic valve: between the right ventricle and the pulmonary artery.Mitral valve: between the left atrium and left ventricle Aortic valve: between the left ventricle and the aorta Blood flow occurs only when there's a difference in pressure across the valves, which causes them to open. Under normal conditions, the valves permit blood to flow in.only one direction :Important definitions.Preload: The load on the cardiac muscle at the end of diastole-.Afterload: The load on the cardiac muscle at the end of systole-.Cardiac output: The amount of blood pumped from the heart per unit time-.Stroke volume: The volume of blood ejected from the heart in each beat-.Heart rate: The number of heart beats per unit time-.Positive inotropy: Increased heart force of contraction-.Positive chronotropy: Increased heart rate- Positive dromotropy: Increased conduction velocity between the auricle and-.ventricle A-Hypertension Hypertension means elevated blood pressure to a degree high enough to perfuse tissues and organs. Blood pressure is considered high when its systolic.reading exceeds 140 mmHg and diastolic reading exceeds 90 mmHg Normal blood pressure is that blood pressure which is not exceeding 120/80 mmHg. Pre-hypertension is considered in patients with blood pressure not exceeding 140/90 mmHg. Stage 1 hypertension is that not exceeding 160/100 mmHg. Stage 2.hypertension is that exceeding 160/100 mmHg Hypertension is the most common cardiovascular disorder. Incidence of hypertension is highly associated with age. It was found that about 60-70% of persons exceeding 60 years of age have hypertensions. The usual incidence of.hypertension is between 30 and 50 years of age Elevated untreated hypertension is associated with higher incidence of myocardial infarction, stroke, heart failure, retinal damage, cerebrovascular bleeding, headache, neurological symptoms and kidney disease. Cardiovascular findings include angina pain (due to insufficient blood supply to the constricted coronary vasculature), left ventricular hypertrophy and dyspnea (due to incrased preload and afterload causing heart failure) as well as peripheral edema (due to increased aldosterone secretion). Neurological findings include severe occipital headache with nausea, vomiting, drowsiness, anxiety, mental impairment and stroke. These are caused by vessel damage within the brain (due to weakened blood vessel wall) causing transient ischemic attacks. Renal findings include polyuria, nocturia, proteinuria, red blood cells in urine and elevated serum creatinine. These are mostly related to arteriolar nephrosclerosis (hardening of renal arterioles). Ocular findings include retinal hemorrhage and exudates. These are due to damage of arterioles that.supply the retina : Regarding causative factor, hypertension is classified into two main types :Primary (essential) hypertension-1 This type has no specific cause. It constitutes more than 95% of all cases of.systemic hypertension :Secondary hypertension-2 This results from an identifiable cause such as renal disease or adrenal hyper-.function. It constitutes about 2-5% of all cases of systemic hypertension : Blood pressure can be expressed in the following equation Blood pressure = cardiac output (heart rate x stroke volume) x peripheral resistance Therefore, elevation of any of these values increases blood pressure. For :example Increased sympathetic nervous system activity: Baroreceptors (pressure-1 receptors) in carotid and aortic arch respond to changes in blood pressure by inducing reflex changes in cardiac output (through cardiac accelerator centre and cardiac inhibitory centre) and peripheral resistance (through vasomotor centre). In case of sustained untreated hypertension, resetting of baroreceptors to a higher level takes.place, making blood pressure sustained at a higher value Increased renin-angiotensin system activity: Renin is produced in the kidneys in-2 response to both decreased intra-renal blood pressure at the juxtaglomerular cells, or decreased delivery of Na+ and Cl- to the macula densa. It is also secreted in response to sympathetic stimulation. Angiotensin I (a weak vasoconstrictor) is formed by the action of renin on angiotensinogen (a peptide produced constitutively by the liver and released into circulaton). Angiotensin I is converted to angiotensin II by the enzyme angiotensin-converting enzyme (ACE, or kinase), which is found predominantly in the capillaries of the lung. Angiotensin II actions are mediated by binding to what is known as angiotensin AT1 receptors. Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Increased activity of rennin-angiotensin system is therefore.associated with elevated blood pressure ================== B-Congestive Heart Failure Heart failure (HF) is generally defined as inability of the heart to supply sufficient blood flow to meet the body's needs. It is a common, costly, disabling and.potentially deadly condition. Heart failure may be left-sided or right-sided Failure of the left ventricle causes congestion of the pulmonary vasculature, and so the symptoms are predominantly respiratory in nature. The patient will have dyspnea (shortness of breath) on exertion and, in severe cases, dyspnea at rest..Increasing breathlessness on lying flat, called orthopnea, occurs Failure of the right ventricle leads to congestion of systemic capillaries. This generates excess fluid accumulation in the body. This causes swelling under the skin (termed peripheral edema) and usually affects the dependent parts of the body first (causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down). Nocturia (frequent nighttime urination) may occur when fluid from the legs is returned to the bloodstream while lying down at night. In progressively severe cases, ascites (fluid accumulation in the abdominal.cavity causing swelling) and hepatomegaly (enlargement of the liver) may develop :Causes of heart failure include Ischaemic heart disease (62%).1 Cigarette smoking (16%).2 Hypertension (10%).3 Obesity (8%).4 Diabetes (3%).5 Valvular heart disease (2%).6 :Heart failure progresses as follows Reduced contractility, or force of contraction, due to overloading of the.1 ventricle. In health, increased filling of the ventricle results in increased contractility (by the Frank-Starling law of the heart) and thus a rise in cardiac output. In heart failure this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-.stretched heart muscle A reduced stroke volume, as a result of a failure of systole, diastole or both..2 Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling - as.occurs when the compliance of the ventricle falls (i.e. when the walls stiffen) Reduced spare capacity. As the heart works harder to meet normal metabolic.3 demands, the amount cardiac output can increase in times of increased oxygen demand (e.g. exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart failure. This translates to the loss of one's cardiac reserve. The cardiac reserve refers to the ability of the heart to work harder during exercise or strenuous activity. Since the heart has to work harder to meet the normal metabolic demands, it is incapable of meeting the metabolic.demands of the body during exercise Increased heart rate, stimulated by increased sympathetic activity in order to.4 maintain cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause.potentially fatal arrhythmias Hypertrophy (an increase in physical size) of the myocardium, caused by the.5 terminally differentiated heart muscle fibres increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and.decreased ability to relax during diastole Enlargement of the ventricles, contributing to the enlargement and spherical.6  shape of the failing heart. The increase in ventricular volume also causes a.reduction in stroke volume due to mechanical and contractile inefficiency Heart failure is associated with increased preload (load on cardiac muscle at the.7 end of the diastole) and afterload (load on cardiac muscle while ejecting blood.during systole) Heart failure is also associated with increased activation of renin-angiotensin.8.system (due to decreased renal blood flow) ====================== C-Angina Pectoris Angina pectoris, commonly known as angina, is severe chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Angina may feel like pressure or squeezing in chest. The pain also extends to.shoulders, arms, neck, jaw or back. Angina pain may even feel like indigestion Anginal attacks take place when oxygen demand exceeds oxygen supply. This results in failure of oxidation of cardiac muscle metaboloic products during exercise,.e.g. lactic acid The types of angina are stable, unstable, variant (Prinzmetal's), and microvascular. Knowing how the types differ is important. This is because they have.different symptoms and require different treatments Stable (effort) angina: It is the most common type of angina. It occurs if the heart-1 is working harder than usual. It increases with effort and is relieved by rest. The most.common cause is atherosclerosis. Stable angina has a regular pattern Unstable angina: This doesn't follow a pattern. It can occur with or without-2 physical exertion, and it may not be relieved by rest or medicine. Unstable angina is very dangerous and requires emergency treatment. It may be caused by hypertension.and fever. This type of angina is a sign that a heart attack may happen soon Variant (Prinzmetal's) angina: Variant angina is rare. It occurs mainly due to-3 coronary vasospasm. It usually occurs while at rest, and the pain can be severe. Variant angina usually happens between midnight and early morning. Medicine can.relieve this type of angina Microvascular angina: Microvascular angina can be more severe and may last-4 longer than other types of angina; medicine may not relieve it. This type of angina.may be a symptom of coronary microvascular disease ================== D-Arrhythmia The heart beats when an electrical impulse from the sinoatrial node (SA node, natural pacemaker) moves through it. The normal electrical sequence begins in the right atrium and spreads throughout the atria to the atrioventricular (AV) node. From the AV node, electrical impulses travel down a group of specialized fibers called the His- Purkinje system to all parts of the ventricles. As long as the electrical impulse is transmitted normally, the heart pumps and beats at a regular pace. In an adult, a normal heart beats 60 to 100 times a minute. Electrocardiography (ECG or EKG) is a painless, non-invasive procedure that records the heart’s electrical activity and can help diagnose arrhythmias. It is the net sum of depolarisation and repolarisation potentials of all myocardial cells.It is P-QRS-T pattern.P means atrial depolarisation-.QRS maens ventricular depolarisation-.T means ventricular repolarisation-  Cardiac Cell Phases + Phase 0 slope: Rapid depolarisation (inflow of Na ).It is related to the conduction velocity in that the more rapid the rate of depolarization the greater the rate of impulse.propagation + +.Phase 1: Partial repolarisation (inward Na , current deactivated, outflow of K ) 2+ + Phase 2: Is the combination of slow inward Ca current balanced by an outward, K.current (plateau) + Phase 3: Phase 3 is repolarizing because the outward (repolarizing) K current increases 2+.while the inward (depolarizing) Ca current is decreasing Phase 4 in normal His-Purkinje and ventricular muscle cells is characterized by a + +.balance between outward Na current and inward K current ?What is arrhythmia The term "arrhythmia" refers to any change from the normal sequence of electrical impulses. The electrical impulses may happen too fast, too slowly, or erratically causing the heart to beat too fast, too slowly, or erratically (unpredictable manner). When the heart doesn't pump blood effectively, the lungs, brain and all other.organs can't work properly and may shut down or be damaged ;Usually the names of specific arrhythmias are generally composed of two words First word indicates the location of the electrophysiologic abnormality resulting in the ,arrhythmia (sinus, AV node, atrial, or ventricular) Second word describes the arrhythmia in terms of whether it is abnormally slow (bradycardia) or fast (tachycardia), or the type of arrhythmia (block, fibrillation, or.flutter) :Main causes of arrhythmia :A- Abnormal impulse formation Sinus pulse: either increased or decreased activity of the SA or AV or the ventricular -1.pulse Ectopic pulse: This may occur in nonpacemaker cells immediately following an -2.action potential, mainly as a result of increased intracellular calcium concentration B- Abnormal impulse conduction :Re- entry-1 Normally a conducted impulse in a ring of heart tissue is propagated in both directions around the ring but dies down when two impulses meet again. When there is a defect in conduction in one side of the ring (unidirectional block).this will allow the impulse to go through in the non damaged ring side and to proceed round through the damaged area resulting in a continuous circulation of the impulse (circus movement). Re entry is the usual cause of paroxysmal atrial tachycardia and atrial and ventricular.arrhythmia.Conduct block: This may be due to damage of nodal or conducting tissue -2 Types of arrhythmia :Bradycardia (bradyarrhythmia)-1 A heart rate of less than 60 beats per minute (BPM) in adults is called bradycardia. Elderly people are more prone to problems with a slow heart rate. This may be caused :by.Problems with the sinoatrial (SA) node - Problems in the conduction pathways of the heart (electrical impulses are not -.conducted from the atria to the ventricles) Tachycardia-2 There are three types of :tachycardia :A- Atrial or Supraventricular Tachycardia (SVT) Atrial or Supraventricular tachycardia (SVT) is a fast heart rate that starts in the upper chambers of the heart. Some forms are called paroxysmal atrial tachycardia (PAT) or paroxysmal supraventricular tachycardia (PSVT). Electrical signals in the heart's upper chambers fire abnormally, which interferes with electrical signals coming from the sinoatrial (SA) node. A series of early beats in the atria speeds up the heart rate. The rapid heartbeat does not allow enough time for the heart to fill before it contracts so.blood flow to the rest of the body is compromised B- Sinus Tachycardia (fast but steady): The SA node sends out electrical signals faster.than usual. The heart rate is fast, but the heart beats properly A rapid heart beat may be a response to common conditions such as: fever, anxiety, fright, severe emotional distress, anemia, increased thyroid activity, heart muscle.damage and hemorrhage :C- Ventricular Tachycardia Ventricular tachycardia is a fast heart rate that starts in the heart's lower chambers (ventricles). It often occurs in life-threatening situations that need rapid diagnosis and treatment. Electrical signals in the ventricles fire abnormally, which interferes with.electrical signals coming from the SA node  :Atrial Fibrillation-3 The fibrillating heart is like shaking a bowl of gelatin it just quivers (shake, tremble) but doesn't produce the coordinated pumping action needed to force blood through the heart and out into the body. In atrial fibrillation, many parts of the atria start emitting uncoordinated electrical signals. The atria pump too fast, unevenly (irregularly) and won't fully contract. Some electrical signals go to the ventricles, which still pump.out blood. No stable ratio exists between number of atraial beats and ventricular beats :Atrial Flutter-4 Atrial flutter is similar to atrial fibrillation, but instead of the electrical signals spreading through the atria in a fast and irregular rhythm, they travel in a fast and regular rhythm. For example, each 3 beats of the auricle are translated into one beat of the.ventricle (3:1 block) Bundle Branch Block -5 Normally, the electrical impulse travels down both the right and left branches at the same speed. Thus, both ventricles contract at the same time. Occasionally there is a block in one of the branches, so impulses must travel to the affected side by a detour that slows them down. That means one ventricle contracts a fraction of a second slower than.the other Premature Atrial Contraction (PAC) and Premature Ventricular Contraction-6 :(PVC) Premature beats or extra beats most often cause irregular heart rhythms. Those that start in the atria are called premature atrial contractions or PACs. Premature ventricular contractions or PVCs start in the ventricles. If the patient had the feeling that his heart "skipped a beat," it was probably from this type of arrhythmia. The heart really.doesn't skip a beat. Instead, an extra beat comes sooner than normal Wolff-Parkinson-White Syndrome -7 If an abnormal conduction pathway runs between the atria and ventricles, the electrical signal may arrive at the ventricles sooner than normal. This condition is called Wolff-Parkinson-White syndrome (WPW syndrome). WPW syndrome is recognized by certain changes on the ECG. Many people with WPW syndrome don't have symptoms.but are at risk of sudden cardiac arrest :Sick Sinus Syndrome-8 Sometimes the sinus node does not fire its signals properly, so that the heart rate slows down. Sometimes the rate changes back and forth between a slow (bradycardia) and fast (tachycardia) rate. This most often occurs in the elderly as a result of.degenerative changes to the conduction pathways of the heart :Complete Heart Block -9 Heart block means that the heart's electrical signal can't pass normally from the upper to the lower chambers. The electrical signal within the heart is blocked, not the blood flow. When this occurs, another "natural" pacemaker in the lower chambers takes over, but at a slower rate. Heart block may be present at or even before birth. (Congenital heart block.) Disease or an injury to the electrical conduction system during.heart surgery can also cause it :Torsade de Pointes-10 It is defined as a polymorphous ventricular tachycardia. Ventricular rate ranges.from 150-250 bpm ====================== 73.Dr. Amira Morad, Dr. Basim Anwar, PhD