Page 427 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 37: Myocardial Ischemia 297

may be present in acute ventricular septal rupture as well. Equalization decreasing venous return. A reduction in myocardial oxygen demand
of diastolic filling pressures may suggest pericardial tamponade. The and consumption results from the reduction of LV volume and arterial
hemodynamic profile of RV infarction includes high right-sided filling pressure primarily due to reduced preload. At higher doses, in some
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pressures in the presence of normal or low occlusion pressures. 18 patients, nitroglycerin relaxes arterial smooth muscle as well, causing
Right heart catheterization is most useful, however, to optimize ther- a modest decrease in afterload, which also contributes to wall stress.
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apy in unstable patients. Infusions of vasoactive agents need to be titrated In addition, nitroglycerin can dilate epicardial coronary arteries, and
carefully in patients with myocardial ischemia to maximize coronary nitroglycerin redistributes coronary blood flow to ischemic regions by
perfusion pressure with the least possible increase in myocardial oxygen dilating collateral vessels. Nitroglycerin has antithrombotic and anti-
demand. Invasive hemodynamic monitoring can be extremely useful in platelet effects as well.
allowing optimization of therapy in these unstable patients, because clini- The quickest route of administration of nitroglycerin is sublingual.
cal estimates of filling pressure can be unreliable ; in addition, changes Sublingual doses of 0.4 mg may be administered every 5 to 10 minutes to
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in myocardial performance and compliance and therapeutic interven- a total of three doses, if required to control pain. Topical or oral nitrates
tions can change cardiac output and filling pressures precipitously. may be used for chronic therapy.
Optimization of filling pressures and serial measurements of cardiac In patients with unstable angina, if sublingual nitroglycerin does not
output (and other parameters, such as mixed venous oxygen saturation) cause chest pain to resolve completely, intravenous nitroglycerin should
allow for titration of the dosage of inotropic agents and vasopressors be administered, starting at a dose of 10 to 20 µg/min. This dose may
to the minimum dosage required to achieve the chosen therapeutic be titrated upward as tolerated in increments of 10 to 20 µg/min every
goals. This minimizes the increases in myocardial oxygen demand and 5 to 10 minutes. An upper limit of 400 µg/min is usually accepted as
arrhythmogenic potential. Although PAC is useful to obtain indices of maximal; above this dose there is usually no further clinical response.
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cardiac output to guide the use of inotropic agents and to obtain filling Because of its hemodynamic actions, systemic blood pressure may fall
pressures on a serial basis to guide the use of both vasopressors and after nitroglycerin administration, so frequent blood pressure checks
vasodilators, other methods of obtaining these indices are reasonable are required; untoward decreases in blood pressure can compromise
as well. coronary perfusion. Hypotension usually resolves with Trendelenburg
position and/or intravenous saline boluses.
As previously noted, myocardial ischemia results from an imbalance of ■ β-BLOCKERS
MANAGEMENT OF ANGINA
myocardial oxygen supply and demand. Patients with a history of stable The rationale for administration of β-blockers during ischemic episodes
angina who develop chest pain while in the critical care setting are derives from their negative chronotropic and negative inotropic proper-
best treated by removal of provocative stimuli that increase myocardial ties. Heart rate and contractility are two of the three major determinants of
oxygen consumption or lead to compromised coronary blood flow, if myocardial oxygen consumption. By altering these variables, myocardial
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these factors can be identified. For example, correction of hypoxia, ane- ischemia can be attenuated significantly. These agents are particularly
mia, hypovolemia, tachycardia, or labile hypertension may be sufficient effective in patients with angina who remain tachycardic or hypertensive
to control anginal episodes. Often overlooked are fever, infection, anxi- (or both) and in patients with supraventricular tachycardia complicat-
ety, stress, activity, and the work of breathing. Antianginal medications ing myocardial ischemia. Rapid control can be achieved by intravenous
the patient was receiving before hospitalization should be continued, administration of metoprolol, a β -selective blocker, in 5 mg increments
1
and the doses possibly increased. every 5 minutes up to 15 mg. Thereafter, 25 to 50 mg every 6 hours can
In instances of refractory angina or where provocative stimuli cannot be given orally.
be ameliorated, it may be necessary to perform coronary angiography β-Blockers should be used with caution in patients with marginal
and revascularization of the culprit vessels (preferably percutane- blood pressure, preexisting bradycardia, AV nodal conduction distur-
ously), especially if the myocardial ischemia is complicating patient bances, and evidence for left ventricular failure, as well as those with
management. bronchospastic disease. A short-acting intravenous β-blocker, such as
■ ASPIRIN esmolol, may be the preferred agent in patients who have the potential
for hemodynamic instability or who have relative contraindications.
Aspirin is the best known and the most widely used of all the antiplatelet
agents because of its low cost and relatively low toxicity. Use of salicylates ■ CALCIUM CHANNEL BLOCKERS
to treat coronary artery disease in the United States was first reported in Non-dihydropyridine calcium channel blockers (verapamil and diltiazem)
1953. Aspirin inhibits the production of thromboxane A by irreversibly also have negative chronotropic and inotropic effects, and can be used to
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2
acetylating the serine residue of the enzyme prostaglandin H synthetase. control myocardial oxygen demand in patients with ischemia. Both can be
2
Aspirin has also been shown to be beneficial in preventing cardiovas- given as intravenous boluses, starting with low doses (diltiazem 10-20 mg,
cular events when administered as secondary prevention in patients after verapamil 2.5 mg), and can then be infused continuously.
acute myocardial infarction and as primary prevention in subjects with no Calcium channel blockers are particularly useful in the setting of
prior history of vascular disease. Doses of aspirin used in cardiovascular coronary vasospasm, because they cause direct dilation of coronary vas-
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disease range between 81 mg and 325 mg daily. Despite the fact aspirin cular smooth muscle. Vasospasm can produce variant angina in patients
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blocks thromboxane preferentially to prostacyclin at low doses and thus with mild or no coronary artery disease (Prinzmetal’s angina), or aggra-
has a more profound antiplatelet effect, high-dose aspirin has been found vate ischemia in patients with atherosclerotic coronary stenoses that are
to be as effective as low-dose aspirin in cardiovascular prevention, which subcritical but serve as sites of vasospasm, possibly as a consequence
may suggest that besides its antiplatelet effects, anti-inflammatory effects of abnormalities of the underlying smooth muscle or derangements in
of aspirin play a role as well. Once begun, aspirin should probably be endothelial physiology. The illicit use of cocaine is increasingly being
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continued indefinitely. Toxicity with aspirin is mostly gastrointestinal; recognized as a cause of coronary vasospasm leading to angina and
enteric-coated preparations may minimize these side effects. myocardial ischemia. Coronary vasospasm usually presents with ST
■ NITRATES elevation associated with chest pain, and can be difficult to differentiate
from vessel closure due to coronary thrombosis. Consideration of the
Nitroglycerin is a mainstay of therapy for angina because of its effi- clinical setting, rapid fluctuation of ST segments, and prompt resolu-
cacy and rapid onset of action. The most important antianginal effect tion with nitrates can provide useful clues. Variant angina attributable
of nitroglycerin is preferential dilation of venous capacitance vessels, to vasospasm responds well to treatment with calcium channel blockers.

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