Setting: ICU
CC: His blood pressure is low.
VS: R: 26 breaths/minute; BP: 102/52 mm Hg; P:110 beats/minute; T: 100.4°F
HPI: It is 2 o’clock in the morning on July 2 during your postgraduate year 2 (PGY-2). The intern finished medical school about an hour ago and is looking to your expert leadership with a patient admitted to the hospital a week ago for an anterior wall myocardial infarction (AWMI). The patient developed hypotension and lightheadedness a few hours ago and was moved to the ICU. He is a 67-year-old man with recurrent episodes of chest pain during this hospital stay. He was treated with thrombolytics on admission. An echocardiogram on hospital day 3 showed EF at 34% and decreased anterior wall motion.
PMHX: hypertension, diabetes, and hyperlipidemia
Medications:
Aspirin
Prasugrel
Metoprolol
Ramipril
Cerivastatin
PE:
Cardiovascular: bilateral JVD, no murmurs
Chest: clear to auscultation
Extremities: small amount of edema
Skin: diaphoretic
What is the mechanism of response to this hypoperfusion?
a. Increased beta-1-stimulation of peripheral vessels
b. Increased beta-2-stimulation of peripheral vessels
c. Decreased vagal stimulation of arterioles
d. Increased alpha-1-stimulation of peripheral vessels
e. Central alpha-2-stimulation
Answer d. Increased alpha-1-stimulation of peripheral vessels
α1-Stimulation is a vasoconstrictor of peripheral vessels. This will shunt blood from the skin, which is approximately 5% of blood flow into the central circulation, such as the heart and brain. Alpha-1-stimulation also constricts muscle vessels resulting in more shunting of blood to central organs. Beta-2-stimulation dilates skeletal muscle, which is undesirable with cardiac pump dysfunction.
Acetylcholine and parasympathetic stimulation do not touch peripheral vessels. Alpha-2-stimulation prevents the release of norepinephrine from nerves. Alpha-2-stimulation will result in vasodilation and will lower BP.
Acetylcholine neither constricts nor dilates skin and muscle arterioles.
Norepinephrine is an alpha-1-agonist.
After moving the clock forward 10 to 15 minutes, repeat vital signs: R: 28 breaths/minute; BP: 96/58 mm Hg; P:118 beats/minute.
What is the right step?
a. Bolus dextrose 5% in water (D5W)
b. Bolus half normal saline (NS)
c. Bolus NS
d. NS and dopamine
e. Ringers lactate and levarterenol
Answer c. Bolus NS
It is inappropriate to try to increase BP with D5W. The best initial fluids to raise BP are either NS or Ringer lactate (RL). Do not start pressors such as dopamine or levarterenol without first trying fluids. This is particularly true of dopamine in a patient with myocardial ischemia. Dopamine can worsen myocardial ischemia and oxygen consumption.
Initial Orders:
Bolus NS
ABG
Chest x-ray, portable
CBC
CK-MB
Why does the mechanism of NS make it the best fluid for hypotensive patients?
a. Lactate is converted to bicarbonate by the liver.
b. NS has higher tonicity compared to other fluids.
c. D5W increases free water loss at the kidneys.
d. NS increases oncotic pressure of the capillaries.
Answer b. NS has higher tonicity compared to other fluids.
NS has considerably higher osmotic content compared with that of D5W or half NS. This increases its tonicity and is more likely to keep the fluid in the vascular space. The majority of D5W and half NS will leave the vascular space and enter the interstitial fluid space. Although this may increase the overall volume status of the patient, it will not increase the BP as much as either NS or RL. NS does not contain lactate; RL has the lactate that is converted to bicarbonate by the liver. Because NS has no protein, it will not increase the oncotic pressure of the vascular space.
If two to three fluid boluses with NS do not raise BP >90 mm Hg, then use levarterenol or pseudoephedrine.
Levarterenol and pseudoephedrine are pure alpha-1-agonists.
After each fluid bolus, move the clock forward 5 to 10 minutes, and recheck BP. This patient’s BP stays at 94/60 mm Hg and his pulse rate remains 120 beats/minute. His neck veins are increasingly distended. His lungs remain clear. ABG results show PO2 68 mm Hg on room air with respiratory alkalosis. A chest x-ray reveals a cardiac shadow slightly enlarged bilaterally. His CK-MB level is elevated.
Monitoring CK-MB level is better than monitoring troponin level at detecting reinfarction.
What can be done first to detect the etiology?
a. Cardiac catheterization
b. Coronary angiography
c. A >10 mm Hg decrease in BP on inhalation
d. Transesophageal echocardiogram
e. Holter monitoring
Answer c. A >10 mm Hg decrease in BP on inhalation
Hypotension + JVD + Tachycardia = Pericardial Tamponade
Pulsus paradoxus is a >10 mm Hg decrease in BP on inhalation. Pulsus paradoxus can be checked at the bedside and is a good way to tell if the heart is being compressed. On inhalation, venous return to the right side of the heart increases. Normally, the heart expands in external diameter. When compressed by tamponade fluid, the heart cannot enlarge in total size. What happens when there is right-sided heart enlargement when the total cardiac size cannot increase? The RV enlarges from venous return on inhalation and compresses the LV. The right side of the heart expands in size; the left side of the heart is “squished” smaller. This decreases BP.
Tamponade seen on ECG has “electrical alternans,” which is alternating large and small QRS complexes.
NS is continued and pulsus paradoxus is found on examination. It is far more important to perform pericardiocentesis to remove fluid than to wait for an echocardiogram or cardiac catheterization. Removing as little as 50 mL of fluid will allow the heart to expand and increase BP. On CCS, order the procedure you need. Because you do not know which procedures will need a consultation on the computer program, just order the procedure and the program will tell you when a consultation is needed first.
What will be found on echocardiogram as the first sign of cardiac tamponade?
a. LV compression in systole
b. LV compression in diastole
c. RV compression in diastole
d. Opening of ventricular septal defect
e. LA dilation
Answer c. RV compression in diastole
The right side of the heart collapses first because the walls are thinner and more easily compressed (Figure 1-11). All compressions from pericardial effusion happen in diastole when the heart is trying to fill (Figure 1-12).
Figure 1-11. Right atrial collapse (arrow) in a patient with a small pericardial effusion. LA, left atrium; LV, left ventricle; RA, right atrium. (Reproduced with permission from Fuster V, et al., ed. Hurst’s The Heart, 13th ed. New York: McGraw-Hill; 2011.)
Figure 1-12. Pericardial effusion on posteroanterior film radiography. Chest radiogram (anterior) of a patient with rapidly increasing pericardial effusion and hemodynamic evidence of cardiac tamponade. Note how the cardiac silhouette is rounded in its lower portion and tapers at the base of the heart, resembling a plastic bag filled with water sitting on a table. (Reproduced with permission from Belenkie I. Pericardial disease. In: Hall JB, et al: Principles of Critical Care, 3rd ed. New York, McGraw-Hill; 2005).
Cardiac catheterization shows equalization or pressures in all chambers in diastole.
With bedside needle pericardiocentesis, the BP immediately increases after withdrawing 100 mL of straw-colored, nonbloody fluid. As you move the clock forward, the BP drops again the following day.Management of a recurring pericardial effusion is with surgical placement of a “window” or hole through which the fluid can drain into the pleural space (Figures 1-13 and 1-14). Once the fluid drains into the pleural space, it can easily be reabsorbed there. The most likely cause of pericardial effusion in the patient is the recent series of myocardial infarctions. Dressler syndrome, or post-MI pericardial inflammation is a rare event because of the routine use of aspirin in all patients. Despite this, the most likely explanation is the inflammation created by the multiple MIs.
Figure 1-13. Subxiphoid pericardial ultrasound reveals a large pericardial fluid collection. (Reproduced with permission from Brunicardi FC, et al: Schwartz’s Principles of Surgery, 9th ed. New York: McGraw-Hill; 2010.)
Figure 1-14. Electrocardiogram of a patient with cardiac tamponade demonstrates low voltages in the limb leads and marked electrical alternans. (Reproduced with permission from Hall JB, et al. Principles of Critical Care, 3rd ed. New York: McGraw-Hill; 2005.)