Cardiac impulse, conduction

Ipratropium is used in bradycardia and AV-block, respectively, to raise heart rate and to facilitate cardiac impulse conduction. As a quaternary substance, it does not penetrate into the brain, which greatly reduces the risk of OIS disturbances (see below). Relatively high oral doses are required because of an inefficient intestinal absorptioa... 

Due to their cationic amphiphilic nature, the TCA exert membrane-stabilizing effects that can lead to disturbances of cardiac impulse conduction with arrhythmias as well as decreases in myocardial contractility. All TCA lower the seizure threshold. Weight gain may result from a stimulant effect on appetite. 

Overdose with TCAs causes tachycardia, hypotension, prolonged EKG intervals, and fatal arrhythmias, including ventricular tachycardias and bundle branch blocks (lack of conduction of the cardiac impulse). Conduction deficits alone and in combination with hypotension account for most of the morbidity and mortality associated with TCA overdose (Baldessarini, 1996). 

O Cardiac arrhythmias may be caused by abnormal impulse formation (automaticity), abnormal impulse conduction (reentry), or both. 

In general, cardiac arrhythmias are caused by (1) abnormal impulse formation (2) abnormal impulse conduction or (3) both. 

Bradycardia, A-V block Elimination of sympathetic drive can lead to a marked fall in cardiac rate as well as to disorders of impulse conduction from the atria to the ventricles. 

As cationic amphiphilic drugs, p-blockers can exert a membrane-stabilizing effect, as evidenced by the ability of the more lipophilic congeners to inhibit Na+-channel function and impulse conduction in cardiac tissues. At the usual therapeutic dosage, the high concentration required for these effects will not be reached. 

In the undamaged myocardium, cardiac impulses travel rapidly antegrade through the Purkinje hbers to deliver the excitatory electrical impulse to the ventricular myocardium. During the normal activation sequence, retrograde conduction from ventricular myocardium to the conducting hbers is prevented by the longer duration of the membrane action potential and thus the refractory period in the Purkinje hbers. 

In the presence of myocardial ischemia, propagation of cardiac impulses may be interfered with and a functional unidirectional block may occur. Impulses may fail to conduct longer in the anterograde direction to excite the more distal ventricular myocardium. Thus,... 

Mechanism of Action An electrolyte that is necessary for multiple cellular metabolic processes. Primary action is intracellular. Therapeutic Effect Needed for nerve impulse conduction and contraction of cardiac, skeletal, and smooth muscle maintains normal renal function and acid-base balance. 

Many factors can precipitate or exacerbate arrhythmias ischemia, hypoxia, acidosis or alkalosis, electrolyte abnormalities, excessive catecholamine exposure, autonomic influences, drug toxicity (eg, digitalis or antiarrhythmic drugs), overstretching of cardiac fibers, and the presence of scarred or otherwise diseased tissue. However, all arrhythmias result from (1) disturbances in impulse formation, (2) disturbances in impulse conduction, or (3) both. 

Rohr S, Kucera JP, Fast VG, Kleber AG Paradoxical improvement of impulse conduction in cardiac tissue by partial cellular uncoupling. Science 1997 275 841-844. 

In some types of rhythm disorders, antiar-rhythmics of the local anesthetic, Na+-channel blocking type are used for both prophylaxis and therapy. These substances block the Na+ channel responsible for the fast depolarization of nerve and muscle tissues. Therefore, the elicitation of action potentials is impeded and impulse conduction is delayed. This effect may exert a favorable influence in some forms of arrhythmia, but can itself act arrhythmogenically. Unfortunately, antiarrhythmics of the local anesthetic, Na+-channel blocking type lack suf -cient specificity in two respects (1) other ion channels of cardiomyocytes, such as K1 and Ca+ channels, are also affected (abnormal QT prolongation) and (2) their action is not restricted to cardiac muscle tissue but also impacts on neural tissues and brain cells. Adverse effects on the heart include production of arrhythmias and lowering of heart rate, AV conduction, and systolic force. CNS side effects are manifested by vertigo, giddiness, disorientation, confusion, motor disturbances, etc. 

Q4 Where does the cardiac impulse, which starts each heart beat, arise Describe the pathway followed by the cardiac impulse as it is conducted through the heart to excite the ventricles. 

Q4 The cardiac impulse arises in the pacemaker tissue of the heart, the SA node. The nodal tissues of the heart-the SA and AV nodes in the right atrium - are spontaneously rhythmic. The impulse generated by the SA node spreads, rather like ripples on a pond, over the atria and reaches the AV node to excite it. From the AV node the impulse travels via the bundle of His along the Purkinje fibres, which are enlarged muscle cells with a high conduction velocity, to the ventricles. The cardiac impulse reaches the apex of the heart first and then spreads over the muscle of the two ventricles. 

The first wave form of the standard ECG is the small rounded P wave associated with conduction of the cardiac impulse from the SA node over the atria it represents atrial depolarization. This is followed by the spiky QRS complex, which represents a depolarization of the ventricles. The last major wave form is the rounded T wave, which represents ventricular repolarization repolarization of the atria is hidden amongst the QRS complex. 

Q10 Backflow of blood into the atrium from the L ventricle through the defective mitral valve increases the volume and pressure of blood in the L atrium, leading to atrial hypertrophy. Since some of the ventricular output returns to the atrium and does not enter the aorta, the ventricle needs to pump an increased volume of blood at each beat. This increases the work of the L ventricle, causing ventricular hypertrophy. The cardiac impulse may be conducted abnormally through the hypertrophied ventricle, leading to the development of ventricular dysrhythmias and possibly to cardiac failure. 

The prolonged action of acetylcholine at the parasympathetic nerve ending would greatly slow the rate of the heart (bradycardia) and also slow conduction of the cardiac impulse over the atria and the atrioventricular (AV) node. 

Heart-muscle contraction increases cardiac output by raising heart rate (positive chronic tropic) and increasing impulse conduction and contraction, thus increasing the volume expelled with each beat (increased ejection fraction)... 

Calciiun is involved in the initiation of smooth muscle and cardiac cell contraction and in the propagation of the cardiac impulse. Actions on cardiac pacemaker cells and conducting tissue are described in Chapter 24. 

Cardiac arrhythmias ore caused by a disturbance in the con-duciion of the impulse through the myocardial tissue, bj disorders of impulse formation, or by a combination of ihete factors. The aniianhythmic agents used most commonly il-feet impulse conduction by altering conduction velocity aisl the duration of the refractory period of heart muscle lis iie They also depress spontaneous diastolic dcpolarizalim. causing a reduction of automaticity by ectopic foci. 

There are three distinct types of muscle tissue in vertebrates striated, smooth, and cardiac. Striated, or skeletal, muscle is attached, at least at one end, to the skeleton via tendons. This muscle type is often referred to as the voluntary muscle, as it can be consciously controlled. Smooth muscle is usually arranged in sheets or layers in tubular systems, such as arteries and veins (see Blood Vessels), the gastrointestinal and respiratory tracts, and the genitourinary tracts. The activities of the smooth muscles are not under conscious control rather they are coordinated by the autonomic (involuntary) nervous system. The cardiac muscle comprises the bulk of the heart wall proper and small amounts are found in the superior vena cava and pulmonary vein. The cardiac muscle is not under conscious control it has an automaticity center which responds to the autonomic nervous system when needed (see section Impulse Conduction). In the heart, cardiac muscle cells are joined in a network of fibers and are connected by gap junctions, which facilitate the conduction of electrical impulses through the cardiac muscle network. In addition to the typical cardiac myocytes, there are other cardiac muscle cells that are specialized to initiate, attenuate, or accelerate the electrical impulses for coordinated contraction of the cardiac network. 

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