Random Learning Issues

Question 1

Diltiazem: Oral vs IV-what is it good for?

Answer 1

Oral-to treat HTN and exercise tolerance in patients with chronic stable angina
IV:Indicated for the short-term management of atrial fibrillation or atrial flutter for temporary control of rapid ventricular rate.9

Indicated for the rapid conversion of paroxysmal supraventricular tachycardias (PSVT) to sinus rhythm. This includes AV nodal reentrant tachycardias and reciprocating tachycardias associated with an extranodal accessory pathway such as the WPW syndrome or short PR syndrome.

Question 2

Dilt: MOA:

Answer 2

antihypertensive and vasodilating agent
L Type calcium channel blocker Diltiazem inhibits the influx of extracellular calcium ions across the myocardial and vascular smooth muscle cell membranes during depolarization. Diltiazem is classified as a negative inotrope (decreased force) and negative chronotrope (decreased rate).8 It is also considered a rate-control drug as it reduces heart rate.

Question 3

Don’t use Dilt if EF is less than:

Dilt dosing:

Answer 3

40% 0.25mg/kg (Max dose: 25mg) IV bolus x1. Start drip at 5mg/hr. Consider addition 30mg PO IR Diltiazem q6 hours or home dose to reduce need for drip. Drip can be titrated to 15mg/hr,

Question 4

T/F, Reduce Roc in liver failure:

Answer 4

True

Question 5

Depolarizing muscular block:

Answer 5

Ach agonists that create an action potential

Question 6

NDMB:

Answer 6

Nondepolarizing muscle relaxants act as competitive antagonists. They bind to the ACh receptors but unable to induce ion channel openings. They prevent ACh from binding and thus end plate potentials do not develop.

Question 7

Ketamine: what does it do to the heart? What does it do to SVR and LVEDP? How is ketamine different in critically ill patients?

Answer 7

It has a direct negative cardiac inotropic effect, ketamine causes dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow. Consequently, ketamine produces cardiovascular effects that resemble sympathetic nervous system stimulation. Ketamine is associated with increases in systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements. Systemic vascular resistance and left ventricular end diastolic pressure are normally unchanged. It is important to recognize that critically ill patients may occasionally respond to ketamine with unexpected decreases in blood pressure and cardiac output. This represents depletion of endogenous catecholamines and exhaustion of sympathetic compensatory mechanisms, unmasking ketamine’s direct negative inotropic effects

Question 8

Ketamine and the lungs:

Answer 8

Ketamine does not produce any significant depression of ventilation when used alone. In addition, upper airway skeletal muscle tone is maintained airway reflexes remain intact. Ketamine also possesses bronchodilatory activity but has been shown to increases salivary and tracheobronchial mucous gland secretions.

Question 9

If a patient has HTN, whats one of your anesthetic concerns? OSA-what’s one of your concerns?

Answer 9

Lability throughout the anesthetic
OsA:obstructive sleep apnea (mask ventilation, postoperative apnea, and
inadequate pain control),

Question 10

Patients on lithium: 
Which fluids to give?  
EKG? 
Anesthetic requirements with lithium? 
Lithium can cause what with electrolytes?

Answer 10

Give NS (or sodium containing fluids) to prevent excessive renal absorption of lithium. Sodium and lithium fight each other for absorption
EKG block for dysrhythmias
Lithium can reduce anesthetic requirements and prolong effects of depolarizing and non-depolarizing NM blockade
Can cause nephrogenic DI