Cardiovascular Physiology Lecture Notes PDF

Physiology Second stage Cardiovascular Physiology (part 2) lecture :4  The Electrocardiogram (ECG) When the cardiac impulse passes through the heart, electrical current also spreads from the heart into the adjacent tissues surrounding the heart. A small portion of the current spreads...

Physiology Second stage Cardiovascular Physiology (part 2) lecture :4  The Electrocardiogram (ECG) When the cardiac impulse passes through the heart, electrical current also spreads from the heart into the adjacent tissues surrounding the heart. A small portion of the current spreads all the way to the surface of the body. Because the body fluids are good conductors, fluctuations in potential of myocardial fibers can be recorded extracellularly. The record of these potential fluctuations during the cardiac cycle is the electrocardiogram (ECG). Most electrocardiograph machines record these fluctuations on a moving strip of paper.  Depolarization produces a positive deflection, where as repolarization produces a negative deflection. -The P wave is produced by atrial depolarization - the QRS complex by ventricular depolarization, and the ST segment and T wave by ventricular repolarization. - The U wave is an inconstant finding, believed to be due to slow repolarization of the papillary muscles.  ECG Leads The standard limb leads, leads I, II, and III, each record the differences in potential between two limbs. An additional nine leads are commonly used in clinical electrocardiography. There are six chest leads (precordial leads) designated V1–V6 and three limb leads: VR (right arm), VL (left arm), and VF (left foot). Augmented limb leads, designated by the letter a (aVR, aVL, aVF), are generally used. Normal ECG The ECG of a normal individual is shown in Figure below. The sequence in which the parts of the heart are depolarized and the position of the heart relative to the electrodes are the important considerations in interpreting the configurations of the waves in each lead.  Elements of ECG Waves are parts of ECG, which are located above or below the isoline. Segments are parts of ECG, which are located on the isoline. Intervals include waves and segments.  Cardiac Arrythmia An arrhythmia (also called dysrhythmia) is an irregular or abnormal heart beat. Heart rhythm problems (heart arrhythmias) occur when the electrical impulses that coordinate heartbeats don't work properly, causing the heart to beat too fast, too slow or irregularly. Heart arrhythmias may feel like a fluttering or racing heart and may be harmless. However, some heart arrhythmias may cause bothersome — sometimes even life- threatening — signs and symptoms. Tachycardia (tak-ih-KAHR-dee-uh). This refers to a fast heartbeat — a resting heart rate greater than 100 beats a minute. Bradycardia (brad-e-KAHR-dee-uh). This refers to a slow heartbeat — a resting heart rate less than 60 beats a minute. ECG ECG strip showing a normal heartbeat ECG strip showing bradycardia ECG strip showing tachycardia  Atrial fibrillation (AF) Atrial flutter Supraventricular tachycardia (SVT) Bradycardia Heart Block ventricular fibrillation (VF) Atrial fibrillation. Atrial fibrillation is a rapid heart rate caused by chaotic electrical impulses in the atria (rate ~ 110 – 160.). These signals result in rapid, irregular, weak contractions of the atria. Atrial fibrillation is associated with serious complications such as stroke. Atrial flutter. Atrial flutter is similar to atrial fibrillation. The heartbeats in atrial flutter are more-organized and more-rhythmic electrical impulses than in atrial fibrillation. Atrial rates are typically above 250 bpm and up to 320 bpm Atrial flutter may also lead to serious complications such as stroke. Supraventricular tachycardia. Supraventricular tachycardia is a broad term that includes many forms of arrhythmia originating above the ventricles (supraventricular) in the atria or AV node. These types of arrhythmia seem to cause sudden episodes of palpitations that begin and end abruptly. Bradycardias, including: Sick sinus syndrome. If sinus node, which is responsible for setting the pace of the heart, isn't sending impulses properly, the heart rate may alternate between too slow (bradycardia) and too fast (tachycardia). Sick sinus syndrome can also be caused by scarring near the sinus node that's slowing, disrupting or blocking the travel of impulses. Sick sinus syndrome is most common among older adults. Conduction block. A block of heart electrical pathways can occur in or near the AV node, which lies on the pathway between atria and ventricles. A block can also occur along other pathways to each ventricle.  ETIOLOGICAL FACTORS Heart disease Myocardial infarction(MI) Systemic hypertension Hyperkalemia/hypokalemia Chronic obstructive pulmonary disease(COPD) Thyroid disorders Drug therapy Toxic doses of cardioactive drugs Increased sympathetic tone Vagal stimulation  ETIOPATHOGENESIS 1) Abnormal impulse formation may stem from Decreased automaticity, as in escape beats and bradycardia Increased automaticity, as in premature beats, tachycardia. 2)Abnormal impulse conduction results from. A conduction block or delay Reentry occurs when an impulse is rerouted through certain regions in which it has already travelled. The impulse depolarizes the same tissue more than once, producing an additional impulse. Reentry sites include the SA and AV nodes as well as various accessory conditions. Electrocardiographic findings in other cardiac & systemic diseases Myocardial Infarction When the blood supply to part of the myocardium is interrupted, profound changes take place in the myocardium that lead to irreversible changes and death of muscle cells (myocardial infarction). The ECG is very useful for diagnosing ischemia and locating areas of infarction. The hallmark of acute myocardial infarction is elevation of the ST segments in the leads overlying the area of infarction. Effects of Changes in the Ionic Composition of the Blood Changes in ECF Na+ and K+ concentration would be expected to affect the potentials of the myocardial fibers, because the electrical activity of the heart depends upon the distribution of these ions across the muscle cell membranes. Increases in extracellular Ca2+ concentration enhance myocardial contractility. Hypocalcemia causes prolongation of the QT interval, a change that is also produced by phenothiazines and tricyclic antidepressant drugs. Mechanical Events of the Cardiac Cycle The Heart as a Pump The contraction produces sequential changes in pressures and flows in the heart chambers and blood vessels. It should be noted that the term systolic pressure in the vascular system refers to the peak pressure reached during systole; similarly, the diastolic pressure refers to the lowest pressure during diastole. Events in Late Diastole Late in diastole, the mitral and tricuspid valves between the atria and ventricles are open and the aortic and pulmonary valves are closed. Blood flows into the heart throughout diastole, filling the atria and ventricles. The rate of filling declines as the ventricles become distended, and—especially when the heart rate is low—the cusps of the atrioventricular (AV) valves drift toward the closed position. The pressure in the ventricles remains low. Arterial Pulse The blood forced into the aorta during systole not only moves the blood in the vessels forward but also sets up a pressure wave that travels along the arteries. The pressure wave expands the arterial walls as it travels, and the expansion is palpable as the pulse. Heart Sounds Two sounds are normally heard through a stethoscope during each cardiac cycle. The first is a low, slightly prolonged "lub" (first sound), caused by vibrations set up by the sudden closure of the mitral and tricuspid valves at the start of ventricular systole. The second is a shorter, high-pitched "dup" (second sound), caused by vibrations associated with closure of the aortic and pulmonary valves just after the end of ventricular systole. Concepts of Preload and Afterload In assessing the contractile properties of muscle, it is important to specify the degree of tension on the muscle when it begins to contract, which is called the preload, and to specify the load against which the muscle exerts its contractile force, which is called the afterload. For cardiac contraction, the preload is usually considered to be the end- diastolic pressure when the ventricle has become filled. The afterload of the ventricle is the pressure in the artery leading from the ventricle. The force of contraction of cardiac muscle depends on its preloading and its after loading. Cardiac Output Cardiac output (liters of blood pumped by the ventricles per minute) is an extremely important cardiovascular variable that is continuously adjusted so that the cardiovascular system operates to meet the body's moment-to-moment transport needs. Methods of Measurement In experimental animals, cardiac output can be measured with an electromagnetic flow meter placed on the ascending aorta. Two methods of measuring output that are applicable to humans. Doppler combined with echocardiography. Echocardiography Wall movement and other aspects of cardiac function can be evaluated by echocardiography, a noninvasive technique that does not involve injections or insertion of a catheter. It's a type of ultrasound scan, which means a small probe is used to send out high-frequency sound waves that create echoes Cardiac Output in Various Conditions The amount of blood pumped out of ventricle per beat, the stroke volume, is about 70 mL in a resting man of average size in the supine. The output of the heart per unit time is the cardiac output. In a resting, supine man, it averages about 5.0 L/min (70 mL x 72 beats/min). There is a correlation between resting cardiac output and body surface area. The output per minute per square meter of body surface (the cardiac index) averages 3.2 L. Factors Controlling Cardiac Output Variations in cardiac output can be produced by changes in cardiac rate or stroke volume. ( CO = HR * SV ) The cardiac rate is controlled primarily by the cardiac innervation, sympathetic stimulation increasing the rate and parasympathetic stimulation decreasing it. The stroke volume is also determined in part by neural input, sympathetic stimuli making the myocardial muscle fibers contract with greater strength and parasympathetic stimuli having the opposite effect. When the strength of contraction increases, more of the blood that normally remains in the ventricles is expelled; ie, the ejection fraction increases and the end systolic ventricular blood volume falls. The (cardiac accelerator action?) of the catecholamines liberated by sympathetic stimulation is referred to as their chronotropic action, whereas their effect on the strength of cardiac contraction is called their inotropic action. Factors that increase the strength of cardiac contraction are said to be positively inotropic; those that decrease it are said to be negatively inotropic. Relation of Tension to Length in Cardiac Muscle The length–tension relationship in cardiac muscle is similar to that in skeletal muscle; as the muscle is stretched, the developed tension increases to a maximum and then declines as stretch becomes more extreme. Starling pointed this out when he stated that the "energy of contraction is proportional to the initial length of the cardiac muscle fiber." This has come to be known as Starling's law of the heart or the Frank–Starling law. For the heart, the length of the muscle fibers (ie, the extent of the preload) is proportionate to the end-diastolic volume. The relation between ventricular stroke volume and end-diastolic volume is called the Frank–Starling curve.  Myocardial Contractility The contractility of the myocardium exerts a major influence on stroke volume. When the sympathetic nerves to the heart are stimulated, the whole length–tension curve shifts upward and to the left (as in the next figure ). The positively inotropic effect of the norepinephrine liberated at the nerve endings is augmented by circulating norepinephrine, and epinephrine has a similar effect. There is a negatively inotropic effect of vagal stimulation on the atrial muscle and a small negatively inotropic effect on the ventricular muscle. The catecholamines exert their inotropic effect via an action on cardiac adrenergic receptors, with resultant activation of adenylyl cyclase and increased intracellular cAMP. Xanthines such as caffeine and theophylline that inhibit the breakdown of cAMP are positively inotropic. Glucagon, which increases the formation of cAMP, is positively inotropic, and it has been recommended for use in the treatment of some heart diseases. are due to their inhibitory effect on the Na+–K+ ATPase in the myocardium. Hypercapnia, hypoxia, acidosis, and drugs such as quinidine, procainamide, and barbiturates depress myocardial contractility. The contractility of the myocardium is also reduced in heart failure. The positively inotropic effect of digitalis and related drugs