Week 1 Flashcards
Correlate the changes observed in the patient’s ECG to the underlying mechanism (sinus to PSVT) inducing this arrhythmia.
- changes observed in the patient’s ECG are a sudden increased rate in the setting of narrow (normal) QRS complexes indicative of paroxysmal supraventricular tachycardia (PSVT); P waves cannot be clearly detected in this case
- changes are a result of spontaneously occurring premature atrial (ectopic) beats. If these premature atrial beats occur while the fast conduction pathway is still in the refractory period, then the impulse will propagate down the slow pathway in the AV node. As it reaches the Bundle of His, the impulse will propagate distally down the ventricles AND in retrograde toward the atria through the recovered fast pathway. This impulse will then travel back down the slow conducting pathway, completing a reentry loop and initiating supraventricular tachycardia as shown in the patient’s ECG.
Explain the effects of the patient’s caffeine consumption on the action potentials in her nodal cells.
Caffeine stimulates catecholamine release which activates the beta1-adrenergic receptors on nodal cells increasing If and ICa currents. This results in an increase in the steepness of phase 4 depolarization, a reduction in the threshold to a more negative value, and an increase in cardiac nodal action potential frequency (the end result is a positive chronotropic effect resulting in increased heart rate).
Explain how the patient’s stress-induced catecholamine release alters the absolute refractory period of fast-wave action potentials.
Her stress-induced catecholamine release would activate the beta-1 adrenergic receptors on the cardiac myocytes. As a result, calcium channels are phosphorylated increasing the inward calcium current during the plateau phase 2. These elevated levels of intracellular calcium increase the permeability of potassium via activation of the potassium channels and the efflux of potassium out of the cell. This terminates the plateau phase of the action potential and contributes to early repolarization. As a result, the absolute refractory period is shortened
outline the structural examination findings that could be expected as a result of sympathetic autonomic reflexes
we could expect right-sided greater than left-sided tissue texture findings due to the involvement of the SA node (supplied by the right T1-T5 nerve roots). We can also expect tissue texture changes and muscle hypertonicity suggesting an acute viscerosomatic reflex at T1-T5. Chapman’s reflexes would be found at the T2 transverse process on the right and 2nd intercostal space on the right. Due to the changes associated with the viscerosomatic reflexes, if the somatic dysfunction is sustained for a prolonged period, it could also contribute to the development of a right pectoralis major Travell Myofascial triggerpoint at the fifth intercostal
A screening osteopathic structural exam is performed, which reveals an area of exquisite tenderness at the right 5th intercostal space, a reproducible pain radiation pattern to the right chest and right arm, and a limitation of right shoulder external rotation.
Name this finding, and justify treating this finding in this patient.
This finding is a pectoralis major Travell myofascial trigger point.
A somatovisceral reflex caused by a Travell myofascial trigger point at the right pectoralis muscle will contribute to increased sympathetic facilitation of the SA node, which may cause or exacerbate supraventricular tachycardias. Treating this trigger point would reduce the overall facilitation of the sympathetic supply to the SA node, and if the contribution to the facilitation is significant enough, treating this trigger point and underlying postural abnormalities may fully resolve the tachyarrhythmia and restore normal cardiac function.
Justify the atrial and ventricular rhythm. Indicate the foci of the arrhythmia in A fib
The atrial rhythm is chaotic and is a result of multiple wandering reentry circuits within the atria. The ventricular rhythm is an irregularly irregular rhythm because many of these spontaneous atrial impulses encounter refractory tissue at the AV node which only allows some depolarizations to be conducted to the ventricles. These rhythms are indicative of atrial fibrillation (A-Fib) with rapid ventricular response (RVR).
Because the patient’s atrial fibrillation is paroxysmal, the rapidly firing foci are likely in the sleeve of the atrial muscle and can extend to the pulmonary veins.
Explain how verapamil’s effects on nodal action potentials could treat this patient’s arrhythmia. Include the antiarrhythmic drug subclass and phases of the action potential affected.
Verapamil is a non-dihydropyridine calcium channel blocker/antagonist (CCB) that belongs to antiarrhythmic Class IV. CCBs bind to L-type calcium channels located in the SA and AV nodal tissue; this blocks calcium entry into the cell. As a result, there is a decrease in the rate of rise of depolarization (Phase 0) and a reduction in conduction velocity (negative dromotropy). CCBs also raise the threshold potential in the SA node and lengthen the refractory period (Phase 4) of the AV node. This slows the heart rate and decreases the transmission of rapid atrial impulses through the AV node to the ventricles, thereby slowing the rapid ventricular rate that results from this patient’s atrial fibrillation.
Describe the effects of metoprolol on cardiac chronotropy, conduction, and automaticity.
The antiarrhythmic effects of beta blockers such as metoprolol (Class II anti-arrhythmics) arise from sympathetic nervous system blockade, which depresses sinus node function and atrioventricular node conduction, and prolongs atrial refractory periods. Metoprolol selectively inhibits beta1-adrenergic receptors (competitive blockade), with little or no effect on beta2-receptors. Beta-blocker chronotropy is G alpha s protein dependent (and appears to be cAMP independent in cardiac nodal cells), which competitively blocks the activation of ion channels (HCN; Na+; L-type Ca++) by catecholamines (epinephrine; norepinephrine; dopamine). To summarize, beta-blockers have negative chronotropic effects and decrease cardiac conduction velocity and automaticity.
Justify the use of warfarin in the treatment of afib
Patients with atrial fibrillation are at increased risk of mural clot formation due to irregular blood flow (Virchow’s triad). Mural clots may dislodge and lead to embolic stroke. For this particular patient, anticoagulation is indicated due to a CHA₂DS₂-VASc Score of 2 (+1 point for age 65-74 and +1 point for history of hypertension).
Warfarin helps to prevent clot formation (and reduces major adverse cardiac and cerebrovascular events more effectively than aspirin) by blocking the vitamin K-dependent gamma-carboxylation of clotting factors (factors II, VII, IX, and X) via inhibition of vitamin K epoxide reductase, which keeps vitamin K in its inactive form.
describe two supplements that may be beneficial for a fib
Omega-3 fatty acids appear to influence several myocardial channels (specifically, calcium and potassium channels) that can affect arrhythmias, and numerous studies have demonstrated improved outcomes.
Coenzyme Q10 may decrease episodes of atrial fibrillation (and ventricular and atrial ectopy) via enhanced mitochondrial function in the sinoatrial (SA) node, although this mechanism is not fully known.
Magnesium has been associated with a decrease in arrhythmias; magnesium decreases triggered activity and can slow conduction in the AV node.
L-Carnitine can improve mitochondrial function and left ventricular function (although the mechanism is not clear) and may prevent some atrial and ventricular arrhythmias.
Correlate the patient’s use of erythromycin to long QT syndrome
Erythromycin is a macrolide antibiotic known to contribute to prolonged QT intervals through blockade of the potassium channels. This leads to an accumulation of intracellular potassium as well as activation of the recovered sodium channels leading to early after-depolarizations (EADs). Potassium channel blockade delays Phase 3 repolarization of the cardiac action potential, which prolongs the QT interval (Figure 1) and increases the patient’s risk of torsades de pointes (Figure 2).
The attending physician reads the patient’s ECG and identifies a 4:1 “Mobitz Type II” second-degree (2°) AV block. Indicate how the physician identifies this rhythm
The physician uses the rhythm strip (Lead II) to identify intermittent non-conducting P waves (not followed by a QRS complex) without progressive prolongation of the PR interval (unlike Mobitz Type I “Wenckebach”). In addition, there is a widened QRS complex, because the conduction block in a Mobitz Type II is usually distal to the AV node.
Explain how age-associated fibrosis in this patient could contribute to his “Mobitz Type II” second-degree (2°) AV block.
Aging is associated with increased cardiac fibrosis which can alter the structure of the nodal cells and conducting fibers resulting in a decrease in the diameter of the fibers. In addition, there is disruption of the intercalated disks increasing the resistive properties of the gap junctions. These changes can reduce the intensity of the local depolarizing currents resulting in a slower conduction velocity and causing a conduction block. Because these changes are occurring in the AV node and His-Purkinje system, they are preventing appropriate propagation into the ventricles
Describe a 3rd degree heart block? Justify use of atropine.
The patient’s cardiac rhythm has progressed to a third-degree (3°) atrioventricular (AV) block as demonstrated by complete discordance of his P waves and QRS complexes.
Therefore, atropine, a muscarinic acetylcholine receptor antagonist, would be indicated. This reduces the parasympathetic tone of the heart via competitive antagonism of acetylcholine at muscarinic acetylcholine receptors (M2) located in the SA and AV nodes. The vagolytic actions of atropine will allow for an unopposed sympathetic response to increase conduction.
Discuss how increased potassium contributes to altered cardiac conduction
A moderate increase in the extracellular concentration of K+ prevents the efflux of K+ which leads to a chronic moderate depolarization of the cell. This increases the resting membrane of all his cardiac cells. With moderate hyperkalemia, there is inactivation of the fast sodium channel by closing the h gate without inactivation of the slow L-type calcium channels (very high serum levels of K+ can also inactivate calcium channels). As a result of h gate inactivation, all of the cardiac action potentials become slow type, which impairs his cardiac conduction.
