CARDIOVASCULAR PHYSIOLOGY DURING PREGNANCY - ELECTROPHYSIOLOGY
If a microelectrode is introduced into a single myocardial cell, an action potential (Fig. 1-9) can be recorded by measuring the potential difference between the inside and the outside of the cell (inside negative). The resting membrane potential of a normal Purkinje cell is approximately - 90 millivolts (mv) with respect to the outside of the cell. When the membrane potential is depolarized to a certain threshold level, an action potential occurs with a rapid upstroke (phase 0); a return toward zero from the initial overshoot or early rapid repolarization (phase 1); a plateau (phase 2); final rapid repolarization (phase 3); and resting membrane potential and ” diastolic depolarization (phase 4). The normal resting potential is maintained by the active (i.e., energy-requiring) exclusion of sodium and the accumulation of potassium inside the cell. Phase 0 or rapid depolarization is due chiefly to the opening of the sarcolemmal channels to sodium entrance in atrial and ventricular muscle and cells in the His-Purkinje system. Calcium is important in the maintenance of the action potential plateau of fast
Action potentials recorded from different tissues in the heart remounted with a His bundle recording and scalar ECG from a patient to illustrate the timing during a single cardiac cycle. SN = Sinus nodal potential; A = atrial muscle potential; AVN = atrioventricular nodal potential; PF = Purkinje fiber potential; V = ventricular muscle potential; HB = His bundle recording; II = lead II. The A-H interval measured in the His bundle recording approximates AV nodal conduction time, and the H-V interval approximates His-Purkinje system conduction time.
sodium channeldependent cells and in the generation of the action potential upstroke in slow calcium channeldependent cells such as the sinus and AV nodes. Phase 3 is mediated chiefly by an outward potassium current, and the membrane returns to its negative resting potential during electrical diastole. Automaticity is a property of some cardiac tissues to undergo gradual phase 4 depolarization spontaneously until threshold potential is reached and the cell initiates an action potential that is propagated from one cell to another. Normal automaticity is present in sinus nodal tissue, some atrial and junctional tissues, the bundle branches, and Purkinje fibers. The sinus node discharges more rapidly than the other cells and is the normal pacemaker of the heart. Conduction is the propagation of a cardiac impulse and is most closely influenced by the amplitude and upstroke velocity of phase 0 of the action potential. Refractoriness is a property of cardiac tissue during which a stimulus occurring soon after a previous action potential fails to elicit another normal action potential; it is most closely related to the duration of phase 3 of the cardiac action potential in most tissues.
The genesis of the normal electrocardiogram is from electrical activity recorded by skin electrodes that is the sum of all the cardiaC action potentials of its component cells. The P wave represents atrial depolarization. The PR interval is a measure of the time necessary to travel from the sinus node through the atrium, AV node, and His-Purkinje system to activate ventricular myocardial cells. The QRS complex represents the sum of all ventricular muscle cell depolarizations (phase 0), the ST segment represents the plateau phase, and the T wave represents the rapid repolarization (phase 3) of the heart as a whole.
Although the autonomic nervous system may affect atrial and ventricular tissue to a small extent, the most prominent autonomic effects are observed on the sinus and the AV nodes. Sympathetic stimulation increases the rate of automaticity and increases conduction velocity, whereas parasympathetic (vagal) activation does the opposite. Baroreceptors in the carotid sinus, located at the bifurcation of the internal and external carotid arteries, activate the vagus nerve when blood pressure increases and reflexively decrease heart rate and AV nodal conduction velocity.
- Phenytoin
- PERFUSION
- NONATHEROSCLEROTIC CAUSES OF CORONARY ARTERY OBSTRUCTION
- Miscellaneous
- TREATMENT OF MALABSORPTION
- APPROACH TO THE PATIENT WITH RENAL DISEASE
- NORMAL INTESTINAL PHYSIOLOGY
- Progressive Crescentic Glomerulonephritis
- MOTOR DISORDERS OF THE ESOPHAGUS
- GENERAL MANAGEMENT OF MYOCARDIAL INFARCTION
- DEFINITION
- Treatment and Prognosis
- OTHER ESOPHAGEAL DISORDERS
- RESPIRATORY SENSORS
- EFFECTS OF PULMONARY HYPERTENSION ON PULMONARY FUNCTION
- EMPHYSEMA
- BROliCHIECTASIS
- CLINICAL ASSESSMENT OF THE REGULATION OF VENTILATION
- CLASSIFICATION OF THE MALABSORPTION SYNDROMES
- DEFINITION
- OBLITERATIVE OR OBSTRUCTIVE PULMONARY HYPERTENSION
- Screening and Prevention
- BILIRUBIN METABOLISM
- Genitourinary System
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- Treatment
- ADAPTATION TO NEPHRON LOSS
- Peutz-Jeghers Syndrome
- Pathology
- Tocainide
- Pneumonia in the Immunocompromised Host
- GENERAL PRINCIPLES OF CARDIAC SURGERY
- Cardiovascular
- Anatomical Imaging of the Urinary
- ACID-PEPTIC DISEASE