Trivia Quiz: What Do You Know About Cardiac Dysrhythmia?

(B) is the correct answer here. Because there is no resemblance of a QRS complex, this is a ventricular abnormality. Also, because the "waves" are not uniform, this is polymorphic (many forms). An example of this is Torsades de Pointes, which is a well-known and highly fatal form of ventricular tachycardia.

This statement is true. With increased automaticity, a site other than the normal pacemaker may take over the electrical control of the heart for one or more beats. How can this happen? Cardiac muscle cells can spontaneously depolarize, which is great if the normal pacemaker can control the heart. Since the SA node controls the heart rate, its spontaneous depolarization is faster than that of regular cardiac muscle cells. But those cells can be altered to depolarize more rapidly and begin to control the heart rate. Norepinephrine acts on beta-1 receptors in the heart to increase the rate of depolarization of SA node cells. Norepinephrine can also speed up the depolarization of non-SA node cells. Ischemia and damage can make cells more sensitive to the effects of norepinephrine and reach threshold faster. Beta-blockers can help prevent the effects of norepinephrine. Reentry circuits occur when there is some physical damage or ischemia in a region of the heart. This will alter conduction pathways and slow conduction keeps an impulse alive in damaged tissue. The impulse can then reenter into an area that has recovered from its refractory period.

(C) is the correct answer. This describes ventricular tachycardia. Since there is not a normal QRS complex, that means there is something wrong with the ventricles. In ventricular tachycardia, there is an ectopic site that is faster than the pacemaker. Thus, it is controlling the heart. This is a major problem because cardiac output is completely compromised and it is life-threatening. Treatment for this will be discussed later.

(D) is the correct answer. This EKG represents ventricular fibrillation. Since the QRS complex is not intact, this must be a ventricular issue. Unlike ventricular tachycardia, where there is some coordination (although fatally incorrect), ventricular fibrillation has no coordination of ventricular contraction. This also is a major problem. No coordination means that cardiac output drops all the way down to zero. Doing nothing means death. This requires defibrillation immediately.

(B) is the correct answer. This describes atrial fibrillation. Because the QRS complex is unaffected, it must be an issue with the atria, that is indeed the case. Because there is no well-defined P wave, this differentiates it from atrial flutter, which would have P waves. The atria are fibrillating in an uncontrolled manner, giving rise to no coordination of impulses.

This is the correct match-up. In first-degree heart block, there is a slowed conduction through the AV node. Although every P wave is followed by a QRS complex, there is a lengthening of the PR interval. In second-degree heart block, as what occurs in atrial flutter and atrial fibrillation, some of the P waves fail to conduct through the AV node. This means that the EKG would show more representations of P waves than QRS complexes. That is, not every P wave is followed by a QRS complex. In third-degree heart block, there is a complete block of conduction through the AV node. Pacemaker cells in the AV node take over control, but they are slower than the SA node. QRS complexes will still look normal since conduction beyond the AV node will be normal.

(B) is false. Once again, this is a condition where the QRS complex will look normal. This is because as the impulse reaches the AV node, the conduction pathway will be normal. Everything up to the AV node will be abnormal. In fact, there will be no regular P waves since depolarization won't be coordinated in the atria. (A) is a true statement. Atria will not be contracting in a coordinated manner and impulses will be random, striking the AV node. (C) is true. When these impulses strike the AV node at random, not all of the impulses will conduct through. That is, not all of the P waves will conduct through the AV node, resulting in second-degree block. (D) is very true. Since blood won't normally be ejected from the atria, there may be areas where blood is "still". The problem with this is that clotting may occur, which could lead to an embolic event, such as pulmonary embolism. This is a major problem and anticoagulation therapy may be necessary to prevent the formation of clots. Interestingly, the ventricular rate may be too rapid and/or irregular. This is because the ventricular rate is determined by how many impulses are transmitted through the AV node. The atria are fibrillating and thus will depolarize in a random manner, affecting the AV node. This ultimately may reduce cardiac output, causing heart failure. Thus, you can see that the goals are to prevent the thromboembolic events, control the ventricular rate, and maintain normal sinus rhythm (NSR).

(C) is the false statement. Recall that the action potential is the length for one beat of the heart. In the long-QT syndrome, the QT interval is prolongated, meaning that the time of the heartbeat is longer since the depolarization is slower. (A) is a true statement because there are indeed drugs that cause this syndrome. Because it is so fatal, drug testing must show the impact the drug will have on the QT interval. There is actually a website called www.AZCert.org that maintains a list of drugs that are associated with the prolongation of the QT interval. (B) is true. Normally, as the ventricle repolarizes, the number of sodium channels going to the resting state increases. If the prolongation takes too long, as is the case here, there is a chance that an ectopic site in the ventricle might take over and control the heart. That is absolutely a problem. (D) is true. Severe hypokalemia would indicate that there is not enough potassium in the blood. This means that when repolarization must occur, it will take longer for potassium to come back into the cell and bring the cell back to the resting membrane potential. This longer duration will be reflected in the longer QT-interval. Torsades de Pointes is a type of ventricular tachycardia that is specifically associated with a long-QT interval. This is fatal and unfortunately, many drugs have the potential (not guaranteed) to cause this syndrome.

(A) is the correct answer. This EKG represents atrial flutter. Since the QRS complex is intact, it must be a problem with the atria. That is indeed the case. Because P waves are well-defined, this differentiates atrial flutter from atrial fibrillation. Atrial flutter has this "sawtooth" appearance.

(C) is the false statement. The QRS complex will actually look normal. This is because as the impulse arrives at the AV node, the normal conduction pathway ensues. So, the P waves will look incorrect ("saw-tooth") but the QRS will look normal. (A) is a correct statement. This ectopic site is bombarding the AV node with impulses. This is why you see many P waves to still only 1 QRS complex. (B) is true. This reentry circuit can be due to damaged cells, but the ectopic site will control the beats. (D) is true. The second-degree block is when SOME P waves fail to conduct through the AV node. There is not a complete block nor is the conduction itself slowed.

(A) is the correct answer. This is a monomorphic ventricular tachycardia EKG. First, it is a ventricular abnormality because there is no resemblance of a QRS complex. You can see that the pattern is consistent, making it monomorphic (one form).

(C) is the true statement here. Although calcium channel blockers (CCBs) can affect these channels, the non-dihydropyridines have that effect, NOT the dihydropyridines. So verapamil and diltiazem are useful, but nifedipine and amlodipine are not. (A) is not true because both the sinoatrial node and the atrioventricular (AV) node act as pacemakers. The SA node is the main pacemaker of the heart. It will determine the heart rate. If for some reason the SA node malfunctions, the AV node can act as the pacemaker. The problem arises when a cell other than these two nodes acts as the pacemaker. That is called an ectopic site. (B) is also not correct. Calcium (not sodium) comes in via the activation of the voltage-gated calcium (not sodium) channels, accounting for the upstroke of the action potential of a slow response cardiac cell, such as the SA and AV nodes. (D) is incorrect because NON-dihydropyridines have this effect. Recall that calcium moves into the cell slower once the channels are unable to be activated from the CCBs. This makes sense intuitively. Fewer channels can be activated and thus the slope of the action potential will be less vertical. This all means that the speed of conduction is slowed.

This is the correct match-up. Phase 0 is when sodium channels are activated. When this happens, sodium ions move into the intracellular fluid and thus depolarize the cell. Two forces act to ensure this: the sodium concentration gradient and the attraction of the negativity of the intracellular side to bring in the positive sodium ions. This is called the fast current and the action potential is conducted extremely rapidly. This is also why you see a vertical slope. Drugs can actually be used to block this channel to stop conduction. Phase 1 is rapid repolarization. Sodium channels are inactivated, meaning that they cannot be used again for another action potential. Phase 2 is when voltage-gated calcium channels are activated. Calcium ions move down their concentration gradient into the cell. The movement is slower and thus you see a more shallow line for repolarization. Phase 3 is repolarization itself. Calcium channels close and cells repolarize. The key here is that voltage-gated potassium channels open, accelerating the repolarization. As the membrane potential becomes more negative, sodium channels gradually move from the inactivated state to the resting state. When enough reach the resting state, another action potential can occur. Phase 4 is the resting potential. Only passive potassium channels are open to maintain the negative membrane potential.