michigan hypertension core curriculum - State of Michigan

CARDIAC EMERGENCIES
Acute Coronary Events
Increased left ventricular afterload and wall tension increases myocardial oxygen consumption,
while LVH may reduce oxygen supply by compressing coronary artery lumina and increasing
microcirculatory and epicardial coronary wall thickness. Even in the absence of obstructing epidcardial
lesions, vascular remodeling in the micro-circulation leads to impaired endothelial vasodilatory
reserve which can significantly limit increases in myocardial blood flow and thus result in myocardial
ischemia when oxygen demands increase. Pressure related endothelial injury can also occur in the
coronary arteries. This can result in angina pectoris or myocardial infarction. While controlling BP
with any medication quickly reduces oxygen demand, nitroglycerin is the preferred agent because of
its preload reduction and coronary vasodilation. As in other situations of myocardial ischemia, betablockers
are also useful for their negative inotropic and chronotropic effects which further decrease
oxygen utilization. Beta- blocking agents commonly used in parenteral form are esmolol and labetolol.
The combination of decreased myocardial oxygen demand and increased afterload can lead to acute
congestive heart failure and pulmonary edema. In this case, intravenous furosemide, in addition to
intravenous nitroglycerine, is indicated while beta-blockers should be avoided.
Acute Aortic Dissection
A parenteral beta blocker (either labetolol or esmolol) should be used initially in this setting
to reduce heart rate and cardiac contractility, thereby reducing the shear mechanical forces imposed
on the aortic walls and limiting further dissection. This is combined with the use of intravenous
nitroprusside. The beta blocker reduces the reflex tachycardia that may otherwise occur with the use
of a potent vasodilator. An aggressive reduction in BP (< 100- 120 systolic) needs to occur within 30
minutes.
HYPERADRENERGIC STATES
Hypertensive emergencies can arise from states of catecholamine excess, such as
pheochromocytoma, interactions between monoamine oxidase inhibitors and sympathomimetic drugs,
or cocaine use. In this situation, beta blockers can worsen the hypertension because of unopposed alpha
adrenergic stimulation and peripheral vasoconstriction. Therefore, the use of a ganglion blocking agent
such as intravenous phentolamine (or in less urgent situations oral phenoxybenzamine) must precede
the use of a pure beta blocker. Alternatively, the combined alpha and beta adrenergic blocker labetalol
is safe and effective. Rebound hypertension following sudden discontinuation of high dose clonidine (>
1.2 mg/day) is also a state of catecholamine excess. Although it also responds quickly to combined alpha
and beta adrenergic blockade, resumption of clonidine is another simple alternative.
NKFM & MDCH 243