Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Cocaine-induced hyperthermia is treated with rapid cooling. Patients who sustain elevated core temperatures above 106° F (41° C) for more than 20 minutes are likely to subsequently have fatal multisystem organ failure.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
After the acute effects of cocaine have subsided from a binging episode, patients with “cocaine washout” are profoundly sleepy but arousable and oriented, with normal vital signs or a mild sinus bradycardia.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
People who binge on repeated doses of cocaine for an extended time have a prolonged state of arousal, which causes catecholamine depletion, salt and water depletion, and poor nutrition.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Acute cocaine-induced hypertension can cause serious injury to the cardiovascular and central nervous systems. Reported sequelae include aortic dissection, pulmonary edema, myocardial ischemia, intracranial hemorrhage and stroke.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Cocaine toxicity end-organ damage is rare but may be manifested as an acute hypertensive emergency. Patients may present with focal acute pain syndromes, circulatory abnormalities, delirium or seizures.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Patients with moderate cocaine toxicity are alert and awake but may have diaphoresis, tachycardia, mydriasis and hypertension without organ damage. A more severely toxic patient may be agitated, combative and hyperthermic.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Acute cocaine use causes release of dopamine, epinephrine, norepinephrine and serotonin. These neurotransmitters act on subtypes to cause many effects, but the most important is adrenergic stimulation by norepinephrine and epinephrine.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Cocaine, amphetamines and derivatives of amphetamines are called sympathomimetics. These agents cause central nervous system (CNS) stimulation and a cascade of adrenergic physiologic effects.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Sildenafil and related drugs (vardenafil [Levitra] and tadalafil [Cialis]) inhibit type 5 phosphodiesterase, relaxing vascular smooth muscle. These agents can prolong and intensify the vasodilating effects of nitrates, resulting in severe hypotension.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Nitrates can cause hypotension, a common complication. Typically it is accompanied by reflex tachycardia unless the patient also has taken another agent such as a beta-blocker that slows chronotropy.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Nitrates (nitroglycerin, isosorbide mononitrate and dinitrate) are used as vasodilators in the treatment of heart failure and ischemic heart disease. They augment coronary blood flow, as well as reducing myocardial oxygen consumption.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Clonidine exerts its effects by binding to pre-synaptic α2-adrenergic receptors in the brain, inhibiting neurons causing decreased norepinephrine release. This can lead to bradycardia, hypotension, decreased mental status, miosis and hypothermia.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Methylene blue in calcium channel blocker poisoning results in decreased production of cyclic guanosine monophosphate and inhibition of endothelial smooth muscle relaxation, causing an increase in systemic vascular resistance.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Methylene blue is an emerging therapy for calcium channel blocker poisoning. Although traditionally used as a reducing agent for the treatment of methemoglobinemia, methylene blue is also a vasoconstrictor.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
In calcium channel blocker poisoning, the endocrine system is affected. As calcium influx triggers the release of insulin, patients poisoned with calcium channel blockers are often hyperglycemic.