Chapter 4 CV + hematology - other heart failure drugs

Question 1

acute pulmonary edema

Answer 1

• accompanies left heart failure
• successful tx of pulmonary edema reduces risk of 2ndary right heartfailure

early interventions
1) sit pt upright to decrease venous return and ease breathing
2) administer humidified o2 to increase PaO2

drug therapy
1) furosemide or bumetanide (reudce vascular volume, l/t shift of fluid from lungs into vasculatore
2) morphine (venodilator, which decreases preload and reduces anxiety)
3) nitrates + bronchodilators can be added to reudce ischemic damage and improve ventilation

Question 2

mgmt of shock

Answer 2

• fatal d/t tissues are poorly perfused and become ischemic

tx
1) oxygenation
2) support BP
3) tx metabolic acidosis if severe

vasopressors (constrict blood vessels and improve cardiac fx by stimulating adrenergic receptors)
* employed when fluids alone fail to inc central venous pressure
* vasconstrictors shunt blood from peripiheral to heart + lungs (therefore, in order to improve central venous pressure is frequently at expense of ischemci damage to peripheral tissue)
* low dose dopamine preferred agent for shock (dilates renal vessels (dopamine receptor-mediated) while constricting vessels in other tissues
* while high dose dopamine and NE constrict all vessels including those of kidneys and brain
* both improve cardiac fx by stimulating b1 receptors (dopamine more potent in this regard)

• dobutamine (beta-1 agonist) and isoproterenol (beta-1 and beta-2 adrenergic receptor agonist indicated primarily for bradydysrhythmias) used in cardiogenic shock b/c improve myocardial contractility (contraindicated when shock d/t hypovolemia than cardiac insuffiiency d/t no direct vasoconstrictor effects [weak a1 agonists]
• dobutamine cautious with use d/t potential worsening hypotension

Question 3

digoxin (lanoxin)

cardiac glycoside

Answer 3

• inhibits Na+/K+ - atpase (sodium pump) and inc inward current of Ca++
• 3 sodiums OUT for every 2 potassiums IN the cell
• watch out for hyperkalemia b/c it is a side effect of digoxin use since K+ cannot enter (toxic level of digoxin) and monitor for hypokalemia since digoxin replaces potassium in the sodium pump causing further worsening of digoxin toxicity
• sodium does not leave cell at all causing Na+2/Ca++2 exchanger to compensate by becoming inhibited so it won’t increase Na+ concentration side cell
• RESULT — no more Ca++ exchanged for Na+ l/t increased Ca+ concentration

Causing:
1) enhanced contraction
2) inc cardiac output
3) dec heart size, venous return and blood volume
4) diuresis (d/t inc renal perfusion)
5) inc peripheral vascular resistance
6) slow ventricular rate in a fib or flutter by inc sensitivity

indication
* HF
* a fib
* paroxysmal tachycardia
* hypoventilation
* cardiogenic shock
* thyrotoxic shock (Patients with thyrotoxicosis most commonly present with signs and symptoms related to excess thyroid hormone including: weight loss with a normal or increased appetite, heat intolerance with increased sweating, palpitations, tremor, anxiety, proximal muscle weakness, alopecia and increased fatigability)
* loading dose is administered first

effects
* digitalis intoxication (headache, malaise, insomnia, altered mental status, abdominal pain, nausea, and vomiting) – hyperkalemia
* bradycardia
* AV/SA node block
* arrhythmias
* inc peripheral resistance may inc heart’s workload + worsening ishcemic damage

contraindication
* v fib
* severe bradycardia
* allergic rx nto cardiac glycosides

interactions
* inc risk of toxicity w/ drugs that alter serum electrolyes (K+ depleting diuretics, corticosteriods, thiazide, and loop diurectis, amphotericin B [antifungal], quinidine [antiarrhythmic + antiparasistic]
* INC risk of complete AV block (beta blcokers, CCBs, or acetylcholinesterase)
* Drugs that alter GI absosrption

T-wave dec in amplitude or inverted
PR interval longer
Q-T interval shortened

Question 4

milrinone (primacor)

bipyridine derivative

Answer 4

• inhibits phosphodiesterase (enzyme for cAMP breakdown)
• cAMP inc calcium uptake

Causing
* contractility
* stroke volume
* ejection fration
* sinus rate
* decrease peripheral resistance

indication
* added to digoxin therapy when HF persists depsite digoxin
* NOT EFFECTIVE with HF that last more than 48 hrs

effects
* ventricular arrhythmias
* requires constance ECG monitoring

if cAMP depleted then drug not effective
* capable of inc myocardial contraction even inf presence of b-adrenergi antagonists

Question 5

dobutamine (dobutrex)

other

Answer 5

• beta1 receptor preffered adrenergic agonist
• moderate dose inc contractility w/o inc HR or BP; minimal effects on blood vessels

indication
* CHF
* tx of shock

effects
* tachycardia
* hypotension
* nausea
* headache
* palpitations
* anginal sx
* dyspnea
* ventricular arrhythmias

continuous infusio need to maintain therapeutic effect

contraindications
* hypersensitivity
* idiopathic hypertrophic subaortic stenosis

short half life — used for short term therapy

Question 6

Terazosin (hytrin)

Answer 6

• beta1 receptor preffered adrenergic agonist
• moderate dose inc contractility w/o inc HR or BP; minimal effects on blood vessels

indication
HF

effect
* tachycardia
* edema
* lightheadness
* fatigue
* nasal congestion

all pt must start with 1 mg dose before bed then inc dose slowly if hypotension is not a problem

Question 7

Nesiritide (natrecor)

Answer 7

• brain natriuretic peptide analog (causes diuresis, vasodilatation, and decreased renin and aldosterone secretion)

indication
* HF

effects
* hypotension

contraindication
* cardiogenic shock

Question 8

ivabradine (corlanor)

Answer 8

• blocks hyperpolarization-activated cyclic nucleotide-gated channel

indication
* CHF in pts who are on mximum dose of betablockers

effects
* bradycardia
* hypertension
* atrial fib
* visual brightness

contra
* acute decompensating HF

goal to reduce risk of hospitalization