Setting: ICU
CC: Confusion
VS: R: 24 breaths/minute; BP: 70/40 mm Hg; P: 40 beats/minute; T: 97.4°F
HPI: You are called to see a 64-year-old woman admitted last night with an acute MI. She underwent angioplasty and was started on aspirin, ticagrelor, atorvastatin, metoprolol, enalapril, and nitroglycerin, and placed in the ICU. You are now called because the nurse found the patient to be suddenly confused.
PMHX:
Hypertension
Tobacco use
MR
Outpatient Medications:
Nifedipine
Hydrochlorothiazide
PE:
General: pale, uncomfortable
Cardiovascular: cannon A waves in neck
Cardiovascular: 2/6 pansystolic murmur found
Neurological: confusion, examination incomplete secondary to confusion
Chest: clear to auscultation
Which is most important?
a. Atropine
b. Transcutaneous pacemaker
c. Transvenous pacemaker
d. Epinephrine
e. Levarterenol
Answer a. Atropine
Bradycardia with symptoms needs atropine to speed up the heart rate and raise BP. All of the treatments listed will raise BP, but atropine is most appropriate. Atropine works faster than either form of pacemaker and is considerably more comfortable than the transcutaneous pacemaker. Epinephrine will both speed the heart rate and raise BP, but it is a disaster to use in acute MI. Epinephrine will provoke ischemia that can be fatal. It is wrong to use the alpha-1-agonist levarterenol without first using atropine, fluids, and a pacemaker. Alpha-agonists are used to raise BP when you cannot correct or control the underlying cause.
Initial Orders:
Atropine IV
NS bolus
ECG
CK-MB, troponin
CHEM-7 (electrolytes), calcium, magnesium
Atropine and NS are given. Remember that on CCS, treatments are considered “administered” the instant you confirm them. However, unless you move the clock forward, you cannot detect an effect of the treatment. As you move the clock forward 5 minutes, recheck the vital signs. If atropine is going to be effective, it will work instantly, but this cannot be detected on CCS unless there is a movement forward in time.
In symptomatic bradycardia, atropine is more important than etiology.
Atropine blocks the effect of acetylcholine at the SA and AV nodes. Acetylcholine slows heart rate.
How does atropine increase heart rate in bradycardia?
a. Decreases potassium efflux
b. Increases the rate of IF or “Funny” sodium channels
c. Prolongs phase-2 calcium entry
d. Increases the velocity in Purkinje fibers
e. Increases the conduction speed at the Bachmann bundle in the atria
Answer b. Increases the rate of IF or “Funny” sodium channels
Phase 4 in nodal tissue is flattened or slowed by acetylcholine. Atropine makes it rise faster. Phase 4 is created by “Funny” sodium channels or IF. Faster IF channels equate to faster depolarization in nodal tissue. Atropine speeds the rate at which both the SA and AV nodes depolarize. This is identical to the effect norepinephrine has.
On Nodal Tissue:
Atropine = Decreased Acetylcholine = Increased Norepinephrine Effect
Decreased Acetylcholine = Faster Phase 4 = Faster IF = Faster Heart Rate
Phase 4 depolarization in nodal tissue is the site of the vagal effect on heart rate.
As you move the clock forward, the pulse rate increases from 40 to 50 beats/minute; BP rises from 70/40 to 84/50 mm Hg. You give an addition stat dose of atropine and another bolus of NS and move the clock forward 5 minutes. Repeat the vital signs, which takes 2 minutes of “simulated time” on CCS. The pulse rate is now 55 beats/minute and BP is 106/60 mm Hg. If the BP had not risen to a systolic above 90 mm Hg, the answer would have been, “transcutaneous pacemaker.” The stat ECG report returns 10 minutes after ordering it indicating third-degree (complete) heart block at a rate of 40 beats/minute.
How can the ECG report show the heart rate at 40 beats/minute, when the heart rate has increased at the time of the report?
a. Any test ordered on CCS is done instantly. It was ordered when the rate was 40 beats/minute.
b. CCS is not based on time.
c. ECG cannot be done stat on CCS.
Answer a. Any test ordered on CCS is done instantly. It was ordered when the rate was 40 beats/minute.
When writing original orders, the heart rate was 40 beats/minute. All test are considered “done” at the instant you confirm the order. The report comes up later as you pass the time on the clock with the notice “report available.” You can cancel any order you do not want by double clicking on the order before the report comes back. You will always be asked to confirm everything on CCS two to three times before it is implemented. It is critical that you understand that tests are done instantly, otherwise you will give extra treatment the patient does not need, thinking “Hey, why is the heart rate still low? I should give more atropine!” No. The ECG report is delayed, and the patient has improved since the test was done.
Test reports on CCS always list the exact time they were ordered.
You ask for an “Interval History” at the physical examination tab. The patient reports feeling much better and the confusion has resolved. BP is 106/60 mm Hg. Cannon A waves are still present. Lungs are clear. You order a temporary transcutaneous pacemaker to be placed on the patient’s chest wall. It will not fire if you set the low limit of the heart rate to 50 beats/minute and the patient’s heart rate continues higher than that.
What is the mechanism of the cannon A wave?
a. Atrial systole against a closed tricuspid valve
b. Shunt through a patent foramen ovale
c. Ventricular systole
d. Back pressure from the ventricle when the mitral valve opens
Answer a. Atrial systole against a closed tricuspid valve
The A wave is a sign of atrial systole in the jugular vein. It is normal to have an A wave. It is abnormally large in complete heart block because the atrium is often contracting when the tricuspid valve is closed. Complete or third-degree heart block means that the atria and ventricles are contracting with no relationship to each other (Figure 1-15). Normally, the tricuspid valve is always open when the atrium is contracting. Now it will sometimes be closed, and the blood will rush backward into the neck veins like a person bouncing up on a trampoline. “Boing” and the blood moves backward into the neck veins.
Figure 1-15. Third-degree atrioventricular block. (Reproduced with permission from Tintinalli JE, et al. Tintinalli’s Emergency Medicine, A Comprehensive Study Guide, 7th ed. New York: McGraw-Hill; 2011.)
Bradycardia + Hypotension + Cannon A Waves = Complete Heart Block
Cannon A waves indicate third-degree AV block.
When BP normalizes (systolic > 100 mm Hg) in an ICU patient, you can move the clock forward at greater intervals such as 2 to 4 hours. On CCS, you can never tell in advance precisely when the case will end in “simulated” time. You have 10 to 25 minutes of “real” time, which is your time for each case. It can be disconcerting when you suddenly see a screen that says, “This case will end in 5 minutes of real time.” Test takers often become anxious because there is no objective way to verify whether the case is ending. It could be because you achieved the objectives and the test has run its course, or because you made a mistake. Make liberal use of the “interval history” button, which is the only means of obtaining a status report on your patient. In a patient such as one with complete heart block, the emphasis will be on initial management.
You move the clock forward 2 hours and BP remains at 108/70 mm Hg. A repeat ECG shows persistent complete heart block. Order a transvenous pacemaker. Make sure you have discontinued the beta-blockers. CCS will not send you a message saying, “Hey, you idiot! Stop giving drugs that slow the heart rate in symptomatic bradycardia.”
Which wall of the heart is most likely to have infarcted in this patient?
a. Anterior
b. Inferior
c. Lateral
d. Posterior
Answer b. Inferior
An inferior wall infarction is most frequently associated with AV nodal block and bradycardia. When it is accompanied by nausea and vomiting, it is from direct inflammation of the diaphragm related to the infarction. When associated with bradycardia, it is from increased vagal tone inhibiting the SA node. This is sometimes called the Bezold-Jarisch reflex.
Inferior MI stimulates vagal tone.
What coronary vessel led to AV block in this patient?
a. Left main
b. Left circumflex
c. Right coronary
d. Left anterior descending
e. Septal perforators
Answer c. Right coronary
The right coronary artery is the most frequent source of the blood supply to the AV node. If there was just a vagal reflex, it would produce sinus bradycardia. This is why a permanent pacemaker is so frequently necessary in patients with ischemia-induced complete heart block. The damage is often permanent.
Later the same day, a transvenous pacemaker is placed. An ECG is obtained, showing functioning pacer spikes and a wide QRS complex. The heart rate is 70 beats/minute and BP is 118/70 mm Hg. Mentation is normal, and there is no chest pain.
What is the mechanism of wide QRS complex in this case?
a. Pacer impulses travel slowly from myocyte to myocyte instead of down the normal His-Purkinje system.
b. The pacer lead is in the atrium.
c. Smooth muscle junctions are not functioning in paced rhythm.
d. The pacer lead is overly fibrosed, blocking impulse propagation.
e. Intercalated discs do not function between myocytes with pacemakers.
Answer a. Pacer impulses travel slowly from myocyte to myocyte instead of down the normal His-Purkinje system
All pacemakers placed in ventricles produce a wide complex. You cannot put the lead in the atrium because in this case, the AV node is injured, and the impulse would not conduct to the ventricle.
An echocardiogram confirms an inferior wall MI. The pacemaker is functioning normally. Metoprolol and enalapril are restarted. Chemistry is normal including calcium and magnesium levels. CK-MB level is elevated. Several hours later, BP suddenly drops to 80/40 mm Hg. Pulse rate is 70 beats/minute, which is the set rate of the pacemaker, and pacemaker spikes are seen. Chest is clear to auscultation. Neck vein distention is visible.
What is the most likely cause of the hypotension?
a. Free wall rupture
b. Valve rupture
c. Septal rupture
d. Right ventricular infarction
Answer d. Right ventricular infarction
Right ventricular infarction accompanies inferior wall MI in 30% to 40% of patients. This is because they both have the same arterial supply, which is the right coronary artery. The test is to flip the ECG leads to the right side of the chest and get a right ventricular ECG. There is no specific therapy except to load fluids.
After a bolus of NS, BP rises and symptoms resolve.