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Term autorhymthmicity pacemaker activity autorhythmic cell channels autorhythmic cell AP

Description
the heart contracts rythmically as a result of action potentials that it generates by itself autorhythmic cells don't have a resting potential, their membrane slowly depolarizes between action potentials until threshold is reached at which time AP is reached Leaky Na+, Vsensitive K+, Ca2+ T and Ca2+ L Na+ enters the cell through leak channels faster than K+ leakage --> MP reaches -50, Ca2+ T channels open, MP reaches -40 Ca2+ L channels open, MP reaches 5-10 and activate Vsensitive K channels that let K+ efflux bring the MP back to resting

What causes the long AP slow calcium channels which are slower to open and remain open for serveral tenths of a second maintaing a prolonged state of depolarization and plateau? In cardiac muscle, exra calcium comes from T tubules themselves because its sarcoplasimic reticulium is less How do skeletal and developed and doesn't store enough calcium to provide full sontraction. The T-tubules have 5x the volume as cardiac contractions Skeletal. Mucopolysaccharides are also in the T tubules that bind calcium keeping them available to the interior differ? stroke work output minute work output volume-pressure work kinetic energy of blood flow normal right ventricular pressure normal left ventricular pressure preload afterload effiency of cardiac contraction heart pumping intrinsic heart pumping Frank Starling Mechanism
of the cardiac fiber during APs. The contraction of Cardiac also depends heavily on the [Ca] in the ECF. amount of energy the heart converts to work during each heartbeat while pumping blood into the arteries total amount of energy converted to work in 1 minute; equal to the stroke work output times heart rate per minute aka external work, left ventricle has 6x more because of the 6x difference between systolic pressures that the two ventricles pump proportional to the mass of blood ejected times the wquare of velocity of ejection (normally neglegable except for in aortic stenosis in which blood flows with great velocity through the stonsed valve and more than 50% of the total work may be required to create kinetic energy of blood flow 60-80 mmHg 250-300 mmHg degree of tension on the muscle when it begins to contract. In cardiac muscle, considered to be end-diastolic pressure load against which the muscle exerts its contractile force. In cardiac muscle, considered to be the pressure in the artery leading from the ventricle. ratio of work output to chemical energy. Maximum for a healthy heart is 20-25% and with heart failure 5-10% 4-6L/min at rest; exersize 4x-7x this ammount --- regulation is by intristic and by autonomic nervous system called the Frank Starling Mechanism: the greater the heart is stretched during filling, the greater is the force of contraction and greater the quanity of blood pumped into the aorta: "The heart pumps all the blood that returns to it by the way of the veins" Extra blood flows into the ventricles stretching the cardiac muscle closer to optimal overlap --> automatic pumping of extra blood into the arteries; Stretch of the right atrial wall also directly increases the heart rate by 10-20% (different than FS)

Sympathetic stimulation of heart Paratympatietic stimulation of heart Potassium's effect on heart function

For given atrial input, blood pumped per minute (cardiac output) can be increased 2-3x in addition to the Frank Starling mechanism; depressing sympathetic stimulation will depress cardiac pumping as much as 30% below normal. *Mostly to the ventricles, but widely distributed. Most fibers are to the atria. Decreases heart rate but not really the strength of contraction, but can indirectly by more than 50%.

Excess K+ in the ECF dialates the heart flacid and slows heart rate. Large amts can block conduction of cardiac impules from the A-V bundle. Elevation 3x normal can cause weakness of the heart and abnormal rhythm that can cuase death. It decreases the MP of the cardiac fibers. As MP decreases, intensity of AP decreases making heart contraction progressively weaker. Calcium's effect on heart An excess of Ca2+ ions causes the opposite effects than K+. Makes it spastically contract. This is caused by direct effect of Ca+2 ions to initiate contractile processes. Deficiency of Ca2+ ions causes flaccidity, similar to function the effect of high K+. Blood Ca2+ is normally regulated within a narrow range (seldom a clinical concern). Increased temperature (fever) can increase heart rate to as much as 2x normal. Decreased temperature can Temperature effect on cause it to beat only a few times per minute as with hypothermia. Heat increases the permeability of the cardiac heart function muscle membrane to ions that control heart rate resulting in acceleration of the self-excitation process. Contractile strength is also temporarily by a moderate increase in temperature as with exercise. Prolonged elevation will exhaust the metabolic systems of the heart and eventually cause weakness. Doesn't decrease the Cardiac Output during normal function (150mmHg). Cardiac Output is determined almost Increasing Aterial entirely by the resistence of the tissues (and thus control of venous return) Pressure Load

Rythmical and conductive Can be damaged by heart disease, especially by ischemia of the heart tissue from poor coronary blood flow. The result is often bizarre heart rhythm or abmormal sequence of contraction of the heart chaimbers. The pumping system of the heart
effectiveness is reduced and can cause death.

Delay between contraction of Atria and Ventricae Purkinje System

Caused mostly by the nature of the A-V node. The delay from the AV node to the bundle system is .16 seconds. This slow conduction is caused by diminished numbers of gap junctions between successive cells in the conducting pathways so there si a greater resistance to conduction between fibers. Lead from the AV node through the AV bundle into the ventricles. Very lerge fibers (larger than even ventricle muscle) and transmit with 6x velocity (4m/s) of ventricle muscle and 150x the AV fibers. Rapid transmission of AP believed to be caused by high levels of permeability of gap junctions at the intercalated discs that make up these fibers. Have very few myofibrils which means they contract little or none during transmission. One way conduction. AP unable to travel backward from ventricles to atria. Everywhere except the AV bundle the atrial muscle is separated from the ventricle muscle by a fibrous barrier. Wraps around the heart in a double spiral with fibrous septa between the spiraling layers. The electrical impulse doesn't necessarily travel outward toward the surface of the heart, but angulates toward the surface along the directions of the spirals. Time for transmission of cardiac impulse from initial bundle branches to last of ventricular muscle fibers is 0.06s. In absence of SA node, AV and purkinjes can also generate rhythm. Has a fast discharge rate relatevly speaking. A pacemaker elsewhere than the sinus node. Causes abnormal contraction sequence and debility of heart pumping. Can be caused by interruption of the SA signal and AV may take over. When the cardiac impulse fails to pass from atria to ventricle through AV and bundle system. Atria continue to beat at normal rhythm while a new pacemaker usually develops in the Purkinje system of the ventricles and drives the new rate.

AV Bundle Cardiac muscle arrangement The SA Node Ectopic pacemaker AV Block

Stokes-Adama syndrome Delayed pickup of the heartbeat caused by an AV block. The Rapid SA impulses override the Purkinje fibers at Ventricular escape Mechanism of Vagal effects Mechanism of Sympathetic Effect Why no repolarization wave of atria in ECG? ECG time axis Normal Voltages in ECG P-Q or P-R Interval Q-T Interval Heart Rate from ECG

first and can fail for 5-20 seconds with the ventricles failing to pump blood. The person faints the first 4-5 seconds because of lack of blood to the brain. Can lead to death if the delay is too long. Stimulation of Parasympathetic nerves to the heart caused the release of Ach at the vagal endings. Decreases the rhthm of the SA node and decreases excitability of the AV bundle --> slows impulse to the ventricles, Purkinje fibers develop a rhythm of their own. (rate of 15-40 beats a min) ACh increases permeability to K+ ions, they flow out of the fibers leaving it hyperpolarized. As a result, the leakage of Na+ into the cell takes much longer to get it to reach threshold Norepi is believed to increase the permeability of the fiber membrane to Na+ and Ca2+ ions. This causes a more positive resting potential thus accelerating self-excitation and increasing heart rate. The increase in Ca2+ ions is at least partially responsible for increased contractility. It is obscured by the QRS complex and is seldom observed. Each inch in the horozontal direction is 1 second, smaller divisions are .2 and smallest .04 Depend on placement of leads. Usually 1-1.5 when placed on one arm and one leg or two arms. Time between the beginning of the P wave and and beginning of QRS complex. Normally .16 seconds. (Contraction of the atria) Lasts from beginning of R/Q wave to the end of T wave. Usually .35 seconds. (Contraction of Ventricle) The heart rate is the reciprocal of the time interval between two successive heartbeats. If the interval between two beats as determined from the time calibration lines is 1 seconds, the heart rate is 60 beats per minute. The normal interval between two successive QRS complexes in the adult person is about .83 seconds. This is a heart rate of 60/.83 times per minute, or 72 beats per minute. Which leads are recorded aren't important for detecting arrhythmias because time relations are important there, if trying to diagnose defects with different conducting portions, placement is a big deal. Lead 1 + 3 = 2; Positive terminal of electrocardiograph placed directly over heart, negative (indifferent) electrode is connected to the right arm, left arm, and left leg all at the same time. Usually six standard chest leads are recorded one at a time, V1-6. Ventricular abnormalities will cause marked changes between individual chest leads. In leads V1-2 the QRS recordings will be mainly negative because these electrodes are closer to the base of the heart. In V3-6 the QRS complex will read mainly positive because they are placed nearer the apex. Two of the limbs are connected to the negative terminal and the third is connected to the positive. When the positive terminal is on the right arm, the lead is known as the aVR lead. When on the left arm, the aVL lead; when on the left leg, the aVF lead. The recording from the aVR lead is inverted. Placed directly on the two arms (- on R arm). Because the electrodes lie exactly in the horizontal direction, with the positive electrode to the left, the axis of lead I is 0 degrees. *Left Chest Placed on the right arm and left leg (- on R arm). The right arm connects to the torso in the upper right-hand corner and the left leg connects in the lower left-hand corner. Therefore, the direction of this lead is about 60 degrees. *Left Upper Quadrant Placed on the left leg and right arm (- on L arm). Has an axis of about 120 degrees *Right Upper Quadrant Faces the heart from the right shoulder and is oriented to the cavity of the heart. *Right lateral arm Faces the heart from the left shoulder and is oriente to the Left Ventricle. *Left lateral arm

Standard Bipolar Limb Leads Einthoven's Law Chest leads

Augmented Unipolar Limb Leads Lead I Lead II Lead III aVR aVL

aVF QRS Complex - Q QRS Complex - R QRS Complex - S T Wave Atrial P Wave Atrial T Wave Zero Reference Point Mean electrical axis of the Ventricles Normal Ventricular Axis Range Deviations from Normal Range - Left Shift Deviations from Normal Range - Right Shift

Faces the heart from the left hip and is oriented to the inferior surface of the Left Ventricle. *Right lateral lower leg When the ventricle is first depolarized, it travels to the left side of the septum initially The major positive deflection in the QRS complex. The final negative wave on lead 3. the greatest portion of ventricular muscle mass to repolarize first is the entire outer surface of the ventricles, especially near the apex of the heart. The endocardial areas, conversely, normally repolarize last. Caused by BP inside ventricles during contraction reducing BF to endocardium. Depolarization of the atria. Begins in the SA node and spreads inall directions over atria. All leads are positive because the depolarization spreads in the same direciton. Repolarization of the Atria. The T wave appears at the same time as the QRS complex therefore its almost always obscured. At this point is the negative end of all successive vectors. The preponderant direction o fthe potential during depolarization (60 degrees) From 20-100 because of the normal variations of Purkinje distribution or in muscle itself. Change in position of the heart in the chest. If the heart is angled to the left, the mean axis will shift left. This occurs: at the end of deep expiration, when a person lies down, fat epople

This occurs (1) at the end of deep inspiration, (2) when a person stands up, and (3) normally in tall, lanky people whose hearts hang downward. When one ventricle greatly hypertrophies, the axis of the heart shifts toward that ventricle. Caused by more Hypertrophy of One muscle and excess generation of electrical potential on that side. Also more time is requred for the Ventricle depolarization wave to travel through the hypertrophied ventricle. The normal ventricle becomes depolarized considerably faster than the hypertrophied ventricle (axis deviates toward hypertrophied ventricle) Ex: mean vector points -15. This is typical of increased muscle mass of left ventricle. The axis deviation was Vector analysis of Left caused by hypertension which caused the left ventricle to hypertrophy so it could pump against elevated Axis Deviation systemic arterial pressure. Other conditions: aortic valve stenosis, aortic valve regurgitation, or congenital heart conditions where the left ventricle is enlarged. Ex: mean vector points 170. (Hypertrophy of the Right Ventricle) as a result of congenital pulmonary valve Vector analysis of Right stenosis. Can also occur with: congenital heart conditions that cause hypertrophy of the right ventricle such as Axis Deviation tetralogy of Fallot and interventricular septal defect. Causes axis deviation. Ordinarily the lateral wallf of the two ventricles depolarize at almost the same instant Bundle Branch Block because both the left and right bundle branches of the Purkinje system fire at the same time and the 2 sides of the heart neutralize eachother. If one of the major bundle branches is blocked, the cardiac impulse spreads through teh normal ventricle long before the other. When the left branch is blocked, depolarization spreads through the R ventricle 2-3x faster than the L. Much of Left axis deviation in Left Bundle Branch Block the L ventricle remains depolarized after the R ventricle has become totally depolarized: thus the R ventricle becomes electronegative and the L remains electropositive. A strong vector projects from teh R ventricle toward the L ventricle. QRS complex is greatly prolonged

Right axis deviation in Right Bundle Branch Block High QRS Complex Voltages

When the right bundle is blocked, the L ventricle depolarizes faster than the R ventricle, so the left side of the ventricles becomes electronegative sooner than the right. A strong vector develops with its negative end toward the L ventricle and its positive end toward the R ventricle. QRS complex is greatly prolonged. Normally, the voltages of the 3 leads are measured from the peak of the R wave to the bottom of the S wave and = 0.5-2.0 mV. They vary even in the normal heart and 4 mV indicates high voltage. Most common cause is increased muscle mass of the heart which results from hypertrophy in response to excess load. Ex: Right ventricle hypertrophies when it pumps blood through a stenotic pulmonary valve; Left ventricle hypertrophies when it pumps against high blodo pressure. The increased muscle causes generation of increased quantities of electricity around the heart. Caused by Cardiac Myopathies. Ex: Old myocardial artery infarctions with diminished muscle mass. This causes the depolarization wave to move through the ventricles slowly and prevents the heart from being massively depolarized all at once. QRS complex is prolonged. Also caused by fluid in the pericardium. Short circuits the electrical potentials generated by the heart decreasing the voltages. The QRS complex lasts as long as depolarization continues to spread through the ventricles (as long as part is polarized and part depolarized). Prolonged conduction of the impulse always causes prolonged QRS complexes. When one or more ventricles are hypertrophied or dialated it can go from normal (0.08s) to long (0.12) When the Purkinje system is blocked, the impulse must be conducted by the ventricular muscle itself. This lowers velocity of impulse to 1/3 normal. With complete blockage of one of the bundle branches, the duration of the QRS complex is increased to 0.14 or more. (0.09 is abnormally long) Most frequently caused by 2 conditions: 1: destruction of cardiac muscle in cvarious areas throughout the ventricle and replacement of this muscle by scar tissue. 2: multiple small local blocks in the conduction of implulses at many points in the Purkinje system.... As a result cardiac impule conduction becomes irregular causing rapid shifts in voltages and axis deviations. Often causes double or triple peaks in some leads. Cardiac damage will cause part of the heart to remain partially or totally depolarized all the time. When this occurs, current flows between the pathologically depolarized and normally polarized areas even between heartbeats (current of injury). Caused by 1: mechanical trauma. 2: Infectious processes that damage muscle membranes. 3: Ischemia of local areas of heart muscle caused by coronary occlusions (by far the most common) During the T-P interval (when the normal ventricular muscle is totally polarized) abnormally negative current still flows from the infarcted area at th ebase of the left ventricle and spreads toward the rest of the ventricles. The vector is of about 125 degrees with the base of the vector (-) toward the injured muscle. This vector causes an initial record in lead I below the zero potential line. In lead II the record is above the line. In lead III the projected vector points in the same direction as teh positive terminal of lead III (+). BECAUSE THE VECTOR LIES ALMOST EXACTLY IN THE SAME DIRECTION AS THE AXIS OF LEAD III, THE VOLTAGE OF THE CURRENT OF INJURY IN LEAD III IS MUCH GREATER THAN IN I AND II. Repolarization causes a return of the current of injury in each lead. The exact zero reference level in the ECG. 1: One notes the exact point which the wave of depolarization just completes its passage through the heart (end of the QRS complex). 2: At this point all the ventricle is depolarized, in cluding both the damaged and normal parts (no current is flowing around the heart at this time). 3: The horizontal line is then the zero potential level in the ECG from which all potentials caused by currents of injury must be measured.

Low QRS Complex Voltages Bizarre patterns of QRS Complex Prolonged QRS resulting from Purkinje System Blocks Conditions That Cause Bizarre QRS Complexes Current of Injury

Effect of Current of Injury on QRS Complex

The J Point

Insufficient blood flow to the cardiac muscle depresses the metabolism of the muscle for 3 reasons: 1: Lack of Coronary Ischemia as a Cause of Injury Potential oxygen. 2: Excess accumulation of carbon dioxide. 3: Lack of sufficient food nutrients. Consequently,

Acute Anterior Wall Infarction

Posterior Wall Infarction

Infarction in Other Part of the Heart

Recovery from Acute Coronary Thrombosis

Abnormalities in the T Wave

repolarization of the muscle membrane can't occur in areas of severe myocardial ischemia. As long as this persists, the anastomoses will keep it alive, and an injury potential continues to flow during the diastolic portion (T-P portion) of each heart cycle. In infaction, a strong current of injury flows from the infacted area of the ventricles during the T-P interval. Therefore: one of the most important diagnostic features of ECGs recorded after acute coronary thrombosis is the current of injury. The most important diagnostic feature of this ECG is the intense injury potential in chest lead V2. If one draws a zero horizontal potential line through the J point of this ECG a strong negative injury potential during the T-P interval is found which means the chest electrode over the front of the heart is in an area of strongly negative potential. The negative end of the injury potential vector in this heart is against the anterior chest wall. This means the current of injury is emanating from the anterior wall of the ventricles which diagnoses this condition as "anterior wall infarction". Lead I: (-) Lead III (+). So the resultant vector of the injury potential in the heart is about 150 degrees!!!. One would conclude that this anterior wall infacrtion almost certainly is caused by thrombosis of the anterior descing branch of the left coronary artery. The major diagnostic feature of the ECG is also in the chest lead. If the zero horozintal potential line through the J point of this ECG is a strong positive during the T-P interval. The current of the injury is positive. The positive end of the vector is in the direction of the anterior chest wall and the negative end (injured end) points away from the chest wall. In other words: the current of injury is coming from teh back of the heart opposite to the anterior chest wall. Lead II and III show injury potentials that are negative in both leads. The resultant vector of the injury potential is about -95 degrees. Thus the chest lead shows the infarct is on the posterior wall of the heart and is in the apical portion of the heart. One would suspect this infarct is near the apex on the posterior wall of the left ventricle. By the same procedures demonstrated in the anterior and posterior wall infarctions, it is possible to determine the locus of any infarcted area emitting a current of injury, regardless of which part of the heart is involved. THE POSITIVE END OF THE INJURY POTENTIAL VECTOR POINTS TOWARD THE NORMAL CARDIAC MUSCLE, AND THE NEGATIVE END POINTS TOWARD THE INJURED PORTION OF THE HEART THAT IS EMITTING THE CURRENT OF INJURY. the injury potential is strong immediately after the acute attack (T-P segment displaced positively from the S-T segment). However, after about 1 week, the injury potential has diminished considerably, and after 3 weeks, it is gone. After that, the electrocardiogram does not change greatly during the next year. This is the usual recovery pattern after acute cardiac infarction of moderate degree, showing that the new collateral coronary blood flow develops enough to re-establish appropriate nutrition to most of the infarcted area. Normally positive in all standard bipolar limb leads because repolarization of the apex and outer surfaces of the ventricles ahead of the intraventricular surfaces. That is, the T wave becomes abnormal when the normal sequence of repolarization doesn't occur.

wave is developing. In othe rwords: the mean axis of the T wave is now deviated to the right, which is opposite to the mean axis of the QRS complex. Thus: when conduction of depolarization is greatly delayed, the T wave is of opposite polarity to that of the QRS complex. (below 0) Shortened Depolarization If th base of the ventricles should exhibit an abnormally short period of depolarization, a short ended action potential, repolarization of the ventricles, wouldn't begin at the apex as it normally does. Instead the base would in Portions of the repolarize ahead of the apex. The T wave in all 3 leads would be negative rather than the usual positive. Ventricular Muscle as a CAUSES: Mild ischemia ex: progressive coronary occlusion, acute coronary occlusion, or relative coronary Cause of T Wave insufficiency during exercise. DETECT: any change in the T wave (inversion, biphasic wave) would indicate some abnormalities. portion of the ventricle has a period of depolarization out of proportion to the rest of the heart.

Effect of Slow Conduction When the QRS complex is very long, it is because of delayed conduction in the left ventricle resulting from left of Depolarization on the bundle branch block. This causes the left ventricle to depolarize after the right. The R ventricle begins to repolarize first also.This causes strong positivity in the R ventricle and negativity in the Left at the time the T T-Wave.

Effect of Digitalis on the T Wave

digitalis is a drug that can be used during coronary insufficiency to increase the strength of cardiac muscle contraction. But when overdosages of digitalis are given, depolarization duration in one part of the ventricles may be increased out of proportion to that of other parts. As a result, nonspecific changes, such as T wave inversion or biphasic T waves, may occur in one or more of the electrocardiographic leads. A biphasic T wave caused by excessive administration of digitalis is shown in Figure 1224. Therefore, changes in the T wave during digitalis administration are often the earliest signs of digitalis toxicity 1. Abnormal rhthmicity of the pacemaker 2. Shift of the pacemaker from the SA node to another place 3. Blocks at different points in the spread of the impulse through the heart 4. Abnormal pathways of impulse transmission through the heart 5. Spontaneous generation of spurious impulses in almost any part of the heart >100 beats per minute. Less time intervals between QRS complex. CAUSES: increased body temp, sympathetic stimulation, toxic conditions of the heart For 1 degree ferenheit increase, 10 beats/min; At about 105, the heart rate may decrease because of debility of the heart muscle as a result of fever. Fever causes tachycardia because it increases the rate of metabolism of the SA node which increases its excitability and rate. Increases heart rate because the weakened heart doesn't pump blood in to the arterial tree to a normal extent, and it elicits sympathetic reflexes to increase heart rate. <60 beats/min Larger and stronger heart than a normal person (large stroke volume). When at rest this large stroke volume fills the arteries, feedback circulatory reflexes cause bradycaria. Any circulatory reflex that stimulates the Vegas nerves causes release of ACh at the vagal endings. See Carotid Sinus Syndrome. Most striking example of parasympathetic bradycaria. The pressure receptors in these patients (baroreceptors) in the carotid sinus are excessively sensitive. Therefore, even mild pressure elicits a strong vagal ACh effect on the heart. Can actually stop the heart 5-10 seconds. During deep respiration the heart rate increases and decreases by as much as 30%. There is a small change during resting respiration. Can result from any one of many circulatory conditions that alter strengths of the sympathetic and parasympathetic nerve signals to the SA node.

Causes of Cardiac Arrhythmias Tachycardia Temp and Tachycardia Weakening of the Myocardium Bradycaria Bradycaria in Athletes Vagal stimulation as a Cause of Bradycaria Carotid Sinus Syndrome Sinus Arrhythmia

Respiratory type of Sinus Results mainly from "spillover" of signals from the medullary respiratory center into adjacent vasomotor center during inspiratory and expiratory cycles of respiration. The spillover signals cause alternate increase and Arrhythmia SA Block AV Block First Degree AV Heart Block Second Degree AV Heart Block Complete/Third Degree AV Heart Block

decrease in the number of impulses transmitted through the sympathetic and vagus nerves to the heart. Rarely, the impulse from the SA node is blocked before it enters the atrial muscle. Results in cecessation of P waves, with resultant standstill of the atria. However the ventricles pick up a new rhythm, usually from the AV node. (QRS-T complex slowed) Caused by: 1. Ischemia of the AV node or bundle fibers 2. Compression of the AV bundle by scar tissue 3. Inflammation of the AV bundle 4. Extreme vagal stimulation Prolonged P-R (or P-Q) interval. Measuring the P-R interval could determine the severity of Acute Rheumatic Heart Disease Will see atrial P wave but no QRS-T wave, and there are "dropped beats" of the ventricles. The atria beat twice for every single beat of the ventricles.

Complete block of the AV impulse from atria to ventricles. The ventricles spontaneously establish their own signal usually from the AV node. P wave becomes dissociated from the QRS-T complexes. Atria beat much faster than ventricles which beat at their own rate. When the AV conduction ceases and the ventricles take 5-30 seconds to start their own beating. Overdrive Supression Some part of the Purkinje system beyond the AV block begins discharging rhythmically acting as the pacemaker Ventricular Escape of the ventricles. Stokes-Adams Syndrome Fainting spells. The brain can't be active for 4-7 seconds without blood supply, most patients faint a few seconds after complete block occurs. The slowly beeting ventricles after escape usually pump enough to allow rapid recovery from the faint and then sustain the person. Condition which results from partial intraventricular block every other heartbeat. Can be caused by rapid Electrical Alternans heartbeat. Purkinje system trying to recover from the previous refractory period quickly enough to respond during every succeeding heartbeat. CAUSES: ischemia, myocarditis, digitalis toxicity. Premature Contractions Most result from ectopic foci in the heart which emit abnormal impulses at odd times during the cardiac rhythm. CAUSES OF ECTOPIC FOCI: 1. Local areas of ischemia 2. Small calcified plaques that press against the adjacent cardiac muscle and irritate the fibers 3. Toxic irritation of the AV node, Purkinje system, or myocardium caused by drugs, nicotine, or caffeine. Frequent during catheterization of R Ventricle where it pushes against the endocardium. P wave occurres too soon; P-R interval is shortened (indicating the ectopic origin of the beat is in the atria near Premature Atrial the AV node). Prolonged interval between premature and regular contraction. Occur frequently in otherwise Contractions healthy people. Often occur in athletes. Other causes: SMOKING, LACK OF SLEEP, COFFEE, ALCOHOLISM, DRUGS When the heart contracts ahead of schedule, the ventricles will not have filled with blood normally, and the Pulse Deficit stroke volume during that contraction is depressed or almost absent. Thus, a deficit in the radial pulses occurs when compared with the actual # of heartbeats. A-V Nodal or A-V Bundle Missing P wave. It's instead superimposed onto the QRS-T complex because the cardiac impulse traveled Premature Contractions backward into the atria at the same time it traveled foreward to the ventricles. Slightly distorts the QRS Comlex. P wave itself can't be discerned.

Premature Ventricular Contractions (PVCs)

Paroxysmal Tachycardia Atrial Paroxysmal Tachycardia AV Nodal Paroxysmal Tachycardia Ventricular Paroxysomal Tachycardia Quinidine Ventricular Fibrillation

1. QRS Complex considerable prolonged (impulse conducted through slow muscle of venticle rather than Purkinje system). 2. QRS has high voltage (no neutralization effect, one side of ventricle depolarized before the other) 3. T wave has an electrical potential polarity exactly opposite to that of teh QRS complex (slow conduction of the impulse through the cardiac muscle causes the muscle fibers that depolarize first also to repolarize first) :::::: Some PVCs are benign: coffee, sleep, cigarettes, emotional irritability. Some are serious and can result in ventricular fibrillation. MOST VULNERABLE DURING END OF T WAVE Form of tachycardia which begins and ends in an acute (or paroxysmal) manner. Can often be stopped by eliciting a vagal reflex. DRUGS USED: QUINIDINE AND LIDOCAINE (depress the sodium permeability of the cardiac muscle membrane during generation of AP) Inverted P wave seen before each QRS-T complex Often results from aberrant rhythm that involves the AV node. Usually causes almost normal QRS-T complexes but totally missing or obscured P waves. Usually occur in young healthy people (both AV and atrial aka Supraventricular Tachycardias). Seldomly does harm occur. On ECG, appears as a series of ventricular premature beats occuring one after another without any normal beats interspersed. SERIOUS BECAUSE: 1. Doesn't occur unless considerable ischemic damage is present in the ventricles 2. Frequently initiates ventricular fibrillation because of rapid stimulation of ventricle 3. Digitalis can cause irritable foci that lead to ventricular tachycardia Increases the refractory period and threshold for excitation of cardiac muscle. Used to block irritable foci causing ventricular tachycardia. Most serious of all cardiac arrhythmis. If not stopped within 1-3 minutes DEATH. Results from cardiac impulses that have gone berserk within the ventricular muscle mass, stimulating different portions of ventricular muscle feeding back onto itself to re-excite over and over - never stopping. Never a coordinated contraction. Unconsciousness occurs within 4-5 seconds. Death of tissues occurs within a few minutes. 1. Sudden electrical shock of the heart 2. Ischemia of the heart muscle, of its specialized conducting system, or both

What sparks Ventricular Fibrillation Circus Movements as the If a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred Basis for Ventricular with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely Fibrillation
over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar tissue. 1: If the pathway around the circle is too long, by the time the impulse returns to the 12 oclock position, the originally stimulated muscle will no longer be refractory and the impulse will continue around the circle again and again. 2: If the length of the pathway remains constant but the velocity of conduction becomes decreased enough, an increased interval of time will elapse before the impulse returns to the 12 oclock position. By this time, the originally stimulated muscle might be out of the refractory state, and the impulse can continue around the circle again and again. 3: The refractory period of the muscle might become greatly shortened. In this case, the impulse could also continue around and around the circle.

Necessary for Circus Movements

Necessary for Circus Movements - With the Heart

All these conditions occur in different pathological states of the human heart, as follows: (1) A long pathway typically occurs in dilated hearts. (2) Decreased rate of conduction frequently results from (a) blockage of the Purkinje system, (b) ischemia of the muscle, (c) high blood potassium levels, or (d) many other factors. (3) A shortened refractory period commonly occurs in response to various drugs, such as epinephrine, or after repetitive electrical stimulation. Thus, in many cardiac disturbances, re-entry can cause abnormal patterns of cardiac contraction or abnormal cardiac rhythms that ignore the pace-setting effects of the sinus node. Caused by 60-Cycle Alternating Current. (1) The velocity of conduction through the heart muscle decreases, Chain Reaction Mechanism of Fibrillation which allows a longer time interval for the impulses to travel around the heart. (2) The refractory period of the muscle is shortened, allowing re-entry of the impulse into previously excited heart muscle within a much shorter time than normally. Third, one of the most important features of fibrillation is the division of impulses. When a depolarization wave reaches a refractory area in the heart, it travels to both sides around the refractory area. Thus, a single impulse becomes two impulses. Then, when each of these reaches another refractory area, it, too, divides to form two more impulses. In this way, many new wave fronts are continually being formed in the heart by progressive chain reactions until, finally, there are many small depolarization waves traveling in many directions at the same time. Bizarre, shows no regular rhythm of any type. First coarse irregular waves, then low voltage irregular waves. No repetitive ECG pattern can be ascribed. A strong high-voltage alternating current passed through the ventricles for a fraction of a second can stop fibrillation by throwing all the ventricular muscle into refractoriness simultaneously. Has to hit both sides of the heart at the same time. Heart is still 3-5 seconds and starts up. Fibrillation can be stopped using 110 volts of 60 cycle AC applied for .1 seconds or 1000 V for a few thousandth of a second. Unless defibrillated within 1 minute the heart is usually too weak to be revived by defibrillation because of lack of nutrition from coronary blood flow. It is still possible to squeeze the heart by hand and defibrillating the heart later. Lack of blood flow to the brain for more than 5-8 minutes usually causes permanent mental impairment Fibrillation often occurs in the atria w/o ventricular fibrillation and vice versa. Identical mechanism. FREQUENT CAUSE: atrial enlargement resulting from heart valve lesions that prevent atria emptying or ventricular failure with damming of blood in the atria. The dilated atrial walls provide ideal conditions of a long conductive pathway as well as slow conduction, both prime for atrial fibrillation. A person can live for months or years with atrial Fibrillation* Waves almost completely neutralize one another, therefore there are no P waves or a fine wavy record. The ventricle however, shows just an irregular rate of heartbeat. Same as Ventricle Caused by circus movement in the atria. Different than Fibrillation as the electrical signal travels as a single large wave always in one direction around the atrial muscle mass. Causes rapid rate of contraction of atria. The signals passed into the ventricles, because the refractory periods of the AV node and AV bundle are too long to pass more than a fraction of the signals. Usually just 2-3 beats of atria for every single beat of the ventricles. STRONG P WAVE, QRS ONCE FOR EVERY 2 OR 3 BEATS OF ATRIA.

ECG in Ventricular Fibrillation Electroshock Defibrillation of the Ventricles Hand Pumping of the Heart (Cardiopulmonary Resuscitation) as an Aid to Defibrillation CPR Atrial Fibrillation

ECG in Atrial Fibrillation Electroshock Treatment of Atrial Fibrillation Atrial Flutter

Cardiac Arrest

Results from cessation of all electrical control signals in the heart. No spontaneous rhythm remains. Likely to occur during deep anesthesia, when many patients develop severe hypoxia because of inadequate respiration. Prolonged CPR is quite successful in reestablishing a normal heart rhythm. In some patients, severe myocardial disease can cause permanent cardiac arrest which can cause death. TREATMENT: rhythmical electrical impulses from a PACEMAKER (keeps patient alive months to years). Renal output of salt and water & Intake of salt and water ::: It is impossible to change one of these long term without changing the other

Two Determinants of the Long-Term Arterial Pressure Level (100mmHg) Arterial Pressure Hypertension Increased Fluid Volume

Cardiac output x total peripheral resistence It is renal resistence that is the culprit, not the increased total peripheral resistance. Can elevate Arterial Pressure by Increasing Cardiac Output or Total Peripheral Resistence.

Term A-V Block Stokes-Adams Syndrome Change in Heart Position (Left Shift) Change of Heart Position (Right Shift) Hypertrophy of One Ventricle Bundle Branch Block High-Voltage Electrocardiogram Decreased Voltage ECG Causes of Bizarre QRS Complexes Current of Injury Acute Anterior Wall Infarction Posterior Wall Infarction T Wave Abnormalities (Slow Conduction) T Wave Abnormalities (Shortened Depolarization) T Wave Abnormalities (Effect of Digitalis) Tachycardia Bradycardia Carotid Sinus Syndrome

Description
When cardiac impulse fails to pass from the atria into the ventricles. Atria beat at normal rhythm, while the Purkinje system stimulates the ventricles to beat at 15-40 BPM. (119) After acute AV Block, there is a delay before the Purkinje system establishes rhythm (Ventricular Escape). During these 5-20 seconds, the ventricles fail to beat. Results in periodic fainting spells which can be fatal. (119) 1) End of deep expiration 2) Supine position 3) Fat fucks (135) 1) End of deep inspiration 2) Standing up 3) Tall, lanky folks (135) When one ventricle greatly hypertrophies, the axis of the heart shifts toward the hypertrophied ventricle. Also produces a high-voltage ECG. (IE: RV->Right Shift; LV->Left Shift) (135) Causes deviation in the same direction as the branch that is blocked. (Left Branch Blocked->Shift Left; Right Branch Blocked->Shift Right. If compete block of a branch occurs, QRS complex can be extended to 0.14s (136) When the sum of the voltages of all the QRS complexes of the three standard leads is >4mV. Commonly caused by hypertrophy; more muscle/more electricity. (137) 1) Caused by myocardial infarctions due to decreased muscle mass. Also causes prolonged QRS. 2) Fluid in the pericardium 3)Pleural Effusion 4)Pulmonary Emphysema (lungs act as insulator) (137) 1) Destruction of Cardiac muscle and replacement with scar tissue. 2) Multiple small local blocks of impulses at many points in the Purkinje system. (The latter causes double/triple peaks) (138) Abnormalities causing damage to the heart muscle itself which cause part of the heart to remain partially or completely depolarized all the time, even between heartbeats. The injured part of the heart is negative. Result of: 1) Mechanical Trauma 2) Infect Focus lead V2. 1)Strong negative injury potential during T-P. 2) (-) Potential in lead 1; (+) Potential in lead 3. After 1 year, indicated by strong Q wave in Lead I (140-1) Focus lead V2. 1)Strong positive injury potential during T-P. 2) (-) Potential in leads 2&3. After 1 year, indicated by strong Q wave in Lead III. (140-1) When conduction of the depolarization impulse through the ventricles is greatly delayed, the T Wave is almost always opposite polarity of the QRS complex. (142) If repolarization begins at the base, instead of the apex, the vector of repolarization would point from the apex towards the base of the heart. The T Wave in all three leads would be negative. Most commonly caused by Mild Ischemia. (142) Increases strength of cardiac muscle contraction. During overdose, depolarization duration in one part of the heart may be increased out of proportion to that of other parts. Causes T Wave inversion or Biphasic T Waves. (142) Abnormally increased HR (>100BPM). Caused by: 1) Increase body temperature (10 BPM for every 1F up to 105) 2)Sympathetic Stimulation. 3) Weakening of myocardium. (143) Abnormally slow HR (<60BPM) Causes: 1) Drugs 2) Training (Normal) 3) Vagal (parasympathetic) Stimulation. (144) Baroreceptors in the carotid sinus region are over-sensitive. Mild external pressure can cause extreme bradycardia. (144)

Cardiotachometer Sinoatrial Block Atrioventricular Block First-Degree AV Block Second-Degree AV Block Third-Degree AV Block Over-Drive Supression Electrical Alternans Premature Contractions Ectopic Foci Premature Atrial Contraction Compensatory Pause Pulse Deficit Premature Ventricular Contractions (PVC) Long QT Syndrome (LQTS) Torsades de pointes Paroxysmal Tachycardia Atrial Paroxysmal Tachycardia

An instrumen that records by the height of successive spikes the duration of the interval between the successive QRS complexes. (144) Impulse from the SA node is blocked before it enters the atrial muscle. Results in sudden cessation of P Waves and slightly prolonged QRS-T complex. (144) Caused by: 1) Ischemia of the AV Node or AV Bundle Fibers. (Coronary Insufficiency) 2)Compression of the AV Bundle (Scar tissue or calcified portions) 3) Inflammation of the AV Node/Bundle (Myocarditis) 4) Extreme Vagal Stimulation (Carotid Sinus Syndrome Prolonged P-R Interval. Normal P-R Interval (beginning of P to beginning of QRS) is 0.16s. If prolonged to >0.20>First Degree Block. Helpful in determining the severity of some heart diseases (IE: Acute Rhumatic Heart Disease) (145) P-R slowed to >0.25-0.45s. Impulse is not always strong enough to pass into the ventricles resulting in occasional absence of QRS-T complex "Dropped Beats" (145) Complete block of the impulse from the atria to the ventricles. Atria maintain rhythm, while the ventricles establish their own rhythm resulting in dissociation of P Wave from the QRS-T complex due to ventricular escape. (145) When AV conduction ceases, the ventricles do not start beating on their own until a delay of 5-30 seconds. (145) Most of the same factors that can cause AV block can also block impulse conduction in the peripheral ventricular purkinje system causing partial intraventricular block every other heartbeat. (145) AKA: Extrasystole, premature beat, or ectopic beat. Most caused by ectopic foci. Regions of the heart that emit abnormal impulses out of rhythm. Cause by 1)Ischemia 2)Calcification 3)Toxic or Mechanical irritation. (146) The P wave occurs too soon in the heart cycle; the P-R interval is shortened indicating the ectopic origin of the beat is in the atria, near the AV node. A compensatory pause preceeding the next contraction is also seen. (146) Occurs because the premature contraction originiated in the atrium some distance from the SA Node, and the impulse had to travel through a considerable amount of atrial muscle before it discharged the SA node. Consequently, the SA node discharges late in When the heart contracts ahead of schedule, the ventricles will not have filled with blood, and the stroke volume output can be depressed or absent. Therefore, there is a deficit in the number of radial pulses when compared to the actual number of contrac On ECG: 1)QRS Complex is considerably prolonged because the impulse is conducted mainly through muscle. 2)QRS has high voltage 3)After the PVC, the T wave has an electrical polarity exactly opposite of the QRS (1467). Disorders that delay repolarization of ventricular muscle following the action potential cause prolonged ventricular AP, and therefore excessively long Q-T intervals. Congenital Forms: Genetic defect in Sodium or Potassium channels. Acquired Forms:Plasma Ventricular arrhythmia characterized by changes in the shape of the QRS complex over time usually following a premature beat, a pause and then another beat with a prolonged Q-T interval. (147) Rapid rhythmical discharge of impulses that spread in all directions throughout the heart caused most frequently by re-entrant circus movement feedback pathways that set up local repeated self-re-excitation. Because of the rapid rhythm, the irritation bec ECG characterized by an inverted P Wave before each QRS-T complex. Abnormal P wave shape indicates that origin is not near the sinus node. (148)

AV Nodal Paroxysmal Tachycardia Ventricular Paroxysmal Tachycardia Circus Movements "One-Kidney" Goldblatt Hypertension "Two-Kidney" Goldblatt Hypertension Coarctation of the Aorta Hypertension in Preeclampsia (Toxemia of Pregnancy)

Results from an aberrant rhythm that involves the AV node. Usually causes normal QRS-T complexes but missing or obscured P-Waves. Typically not a problem. Often seen in pre-adolescents. (148) On ECG has the appearance of a series of ventricular premature beats occurring one after another without any normal beats interspersed. Usually a very serious condition: 1)Doesn't present without significant ischemic damage. 2)Frequently initiates ventric Re-entry of impulses leading to self-re-excitation and VFib. Caused by three things: 1)Pathway around the "circle" is too long (DCM) 2)Length of pathway remains the same but the velocity of conduction becomes decreased (Blockage of fibers, ischemia of mus When one kidney is removed, and the renal artery of the remaining kidney is partially occluded, the immediate effect is significantly reduced pressure in the renal artery beyond the constrictor. Within seconds to minutes, systemic arterial pressure raises Occurs when a pt with both kidneys has unilateral stenosis of one renal artery, while the other kidney is normal. The impared kidney increases RAAS, leading to increased arterial pressure due to bilateral retention of salt and water. (224) Pathological constriction of the aorta beyond the point of the upper aortic arterial branches, but proximal to the renal arteries. As a result, blood flow to the lower body is carried by multiple collateral arteries with significant vascular resistance, r Believed to be caused by ischemia of the placenta, and release of toxic factors. These factors cause dysfunction of vascular endothelial cells, including the blood vessels of the Kidneys. This endothelial dysfunction decreases the release of NO and other

Neurogenic Hypertension Acute hypertension caused by strong stimulation of the sympathetic nervous system. (224) Monogenic Hypertension water reabsorption in the renal tubules. (225) Primary (Essential) Hypertension Hypereffective Heart Hypoeffective Heart BeriBeri AV Fistula (Shunt) Hyperthyroidism Anemia
Group of genetic hypertensive disorders resulting from a single gene. In all cases, there is excessive salt and Idiopathic, but associated with fat fucks and sitting on your ass too much. When you're fat as shit, the characteristics of this disorder are: 1) Cardiac Output is increased because it takes more blood to perfuse your man boobs, and your GI tract when it Heart that is beating better than normal. Seen in any condition which causes non-pathological hypertrophy (IE: Conditioning). Can also occur in response to a combination of: 1)Sympathetic Stimulation 2)Parasympathetic Inhibition. (231) Heart that is pumpling at levels below normal. Caused by any factor that decreases the heart's ability to pump blood. Causes include: Increased arterial pressure (hypertension), inhibition of nervous excitation to the heart, pathological abnormal heart rh Disease caused by Thiamine (B1) deficiency. Causes inability for some tissues to utilize cellular nutrients, local mechanisms cause significant compensatory vasodilation. Peripheral resistance can decrease by as much as half, and therefore CO can increase Fistula between a major artery and vein, decreasing peripheral resistance, increasing venous return and increasing CO. (232) Metabolism of most tissue in body increases. Oxygen useage increases, and vasodilator products are released. Decreased peripheral resistance, increased venous return, and substantially increased CO. (233) Reduced viscosity of the blood and diminished Oxygen delivery elicit peripheral vasodilation, increased venous return and increased CO. (233)

Decreased Cardiac Output Caused by Cardiac Factors Cardiac Shock Decreased Cardiac Output caused by Peripheral Factors

1) Severe coronary blood vessel blockage and consequent infarction. 2)Severe valvular disease 3)Myocarditis 4)Cardiac Tamponade 5)Cardiac Metabolic Derangements. Can lead to cardiac shock. (233) When the CO falls so low that the tissues throughout the body begin to suffer nutritional defficiency. (233) 1)Decreased Blood Volume (most common) 2)Acute Venous Dilation (IE: Fainting; blood "pools" in vessels and doesn't return to the heart) 3)Obstruction of the Large Veins 4)Decreased Tissue/Muscle Mass (IE: Aging) 5)Decreased Metabolic Activity of Tissues ( 1)Cyclical Changes of IPP during respiration (Right shift) 2)Breathing against Negative Pressure (Left shift)

Effect of External 3)Positive Pressure Breathing (Right Shift) 4)Opening the Thoracic Cage (Right Shift) 5)Cardiac Tamponade Pressure on the CO Curve (Right Shift) (234) Cardiac Tamponade Three Principal Factors That Affect Venous Return Compensated Heart Failure Decompensated Heart Failure
Accumulation of a large quantity of fluid in the pericardial cavity around the heart with resultant increase in external cardiac pressure. (234) 1)Right Atrial Pressure (back-pressure) 2)Degree of filling of systemic circulation (Mean Systemic Filling Pressure) 3)Resistance to Blood flow between the peripheral vessels and RA. (235) Final stage of recovery following acute heart failure. Cardiac output is normal, but only because atrial pressure has increased to 6mmHg. At this point, no further edema occurs, but existing edema is likely to persist. Note: At this stage, there is no Car You are totally fucked. It's main cause is the failure of the heart to pump sufficient blood to make the kidneys excrete daily the necessary amounts of fluid. (257)