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Post-Operative Hypertension

Christine Lee
January 6, 2010

An acute transient increase in blood pressure that develops within 30-90 min following surgical procedure
and lasts 4-8 hours. SBP > 160 mmHg or DBP > 90 mm Hg or an increase of 40-50 mm Hg in systolic
blood pressure or post-operative BP greater than 15-20% above baseline.

Factors Contributing to development of hypertension:

Pain, excitement on emergence, hypercarbia, hypoxia, hypervolemia, bladder distension.
Poor pre-op BP control, acute alcohol or cocaine intoxication, malignant hypertension, severe,
head trauma, pheochromocytoma, encephalopathy, thyroid storm, abrupt beta blocker
Types of surgery can also influence the likelihood of post-op hypertension: vascular, cardiac,
neck, endocrine.

Uncontrolled Post-op hypertension is an independent predictor of morbidity and mortality, more
unplanned ICU admissions and greater mortality. Left untreated, will depress LV performance, increased
myocardial O2 demand, CVA, acute MI, arrhythmias, suture line disruption and bleeding.

Unknown in 20% pts may be result of sympathetic stimulation and elevated catecholamines. In
cardiac surgery the cause is multifactoral and is characterized by an increase in total peripheral
resistance with normal cardiac output. An increase BP secondary to increase systemic vascular
resistance by reflex changes in humoral factors including catecholamines, renin, and serotonin
levels and well as alteration in baroreceptor function and cardiac reflexes. Occurs in pts with
preserved function and history of pre-op HTN.

Stimulation of carotid sinus receptors during surgery and activation of carotid sinus reflex.
Carotid sinus stimulation due to increased carotid artery pressure inhibits sympathetic activity to
decrease BP and HR. However, denervation of the receptors or dampening of the pulse pressure
produces increased BP and increase HR.

Patients who have chronic hypertension should resume their medications as soon as able. However in
the immediate post-op phase parental medications are appropriate.
Nitrovasodilators (Nitroglycerin, Nitroprusside, Hydralazine): mediators derived from Nitric Oxide
generating cGMP in vascular smooth muscle
o Nitroprusside arterial and venous vasodilator, rapid and short duration; vasodilation in
cerebral resistance vessels can cause increase cerebral blood volume and ICP, can
reduce coronary perfusion pressure resulting in shunting from ischemic areas further
exacerbating ischemia and can result in hypotension especially those with hypovolemia.
Toxicities include cyanide and thiocyanate accumulation.

o Nitroglycerine: venous vasodilator more than arterial vasodilator; dilates coronary

arteries. Onset 2-5 minutes, duration 3-5 min. Patients can develop tolerance, reflex
tachycardia with volume depletion. Toxicities: methemoglobinemia and inhibition of
platelet activation

Limitations of nitroprusside and nitroglycerin include a decrease in PaO2 and increase in venous
admixture by inhibiting hypoxic pulmonary vasoconstriction can worsen arterial oxygenation.
o Hydralazine: direct arteriolar vasodilator that produces rapid blood pressure affecting
DBP more than SBP. Reduction in peripheral vascular resistance leads to reflex
tachycardia and increased myocardial O2 consumption. 10-15 min onset. Duration 3-8
hours. Potent vasodilation of cerebral vessels which can cause increased ICP

Beta blockers:
o Labatelol: Reduces BP and only slightly reduces HR. Decreases SVR. Onset action 5
min, duration 6 hrs. Caution with patients with heart failure and avoid in pts with SSS,
heart block, asthma
o Esmolol: beta selective, short acting 1/2 life is 2 min, elimination 1/2 life is 9 min.
Exclusion criteria include cardiac index less than 2.2 L/min/m2. Caution in pts with heart
failure, avoid in patients with SSS or those with greater than 1 st degree heart block

Calcium channel blockers (phenylalkylamines (verapamil), benzothiazepines (diltiazem),

Dihydroperidines (nicardipine, nifedipine): bind with high affinity to the L-type calcium channels to
modulate voltage dependent calcium conductivity. Produce vasodilation by decreasing calcium
entry into vascular smooth muscle. Diltiazem and Verapamil have negative inotropic and
conducting effects.
o Dihydroperidines are arterial specific vasodilators of peripheral arteries resulting in
general vasodilation of renal, cerebral, intestinal and coronary vascular beds. Nifedipine
least vasoselective, isradipine and clevidipine are the most selective, nicardipine and
nimodipine are intermediately selective. Used in vasospasm treatment after cardiac

ACE-Inhibitors (Enalaprit): Angiotensin II is a potent vasoconstrictor, acts directly on vascular

smooth muscles interacts with the sympathetic nervous system both peripherally and centrally.
ACE also catalyzes the degradation of bradykinin. Bradykinin promotes vasodilation by
stimulating the production of arachidonic acid metabolites and nitric oxide in the vascular
endothelium. Adverse effects include renal insufficiency. Side effects include cough.

Lewis, Kelly S. Pharmacological Review of Postoperative Hypertension. Journal of Pharmacy Practice.
2002; 15;135-146.

Rose, D. Keith et al. Cardiovascular Events in the Postanesthesia Care Unit: Contribution of Risk Factors.
Anesthesiology.1996; 84:772-781.