Ch 37 Flashcards
heart failure
myocardium weakens and enlarges> loss of ability to pump blood through the heart, and into the systemic circulation.
Compensatory mechanisms fail>peripheral and lung tissues become congested.
Increased preload> excess blood volume in ventricle at end of diastole > thickening of ventricular walls > greater filling pressure > weakened heart.
Classified in stages based on severity.
Two types: left or right sided
left sided HF
- Ventricle does not contract sufficiently to pump blood returned from the lungs and left atrium out through the aorta into the peripheral circulation> blood backs up into lungs
- SOB, dyspnea
right sided HF
- Heart doesn’t sufficiently pump blood returned into the right atrium from the systemic circulation
- Blood backs up into peripheral tissues > peripheral edema, JVD
nonpharm tx for HF
a. Dietary changes: Water restriction > reduce circulating volume, Sodium restriction <2,000 mg/day ( 1 tsp).
b. No smoking: deprivation of oxygen to myocardial cells
c. Mild exercise
lab testing for HF
BNP
- Desired value is < 100
- Gold standard for heart failure/fluid overload
- Secreted from atrial cardiac cells
- Considered more sensitive than ANP in diagnosing heart failure
digoxin class, PT, PD, CI, adv, labs, NI
cardiac glycoside.
tx HF and A FIB by inhibiting Na/K ATPase, promoting ^ force of heart contraction, CO, and tissue perfusion. Also decreases ventricular rate.
CI ventricular dysrhythmia/2nd or 3rd degree heart block.
adv: bradycardia. life thrt: AV block, dysrhythm.
causes hypokalemia, hypomagnesemia, hypercalcemia –> increased risk of dig toxicit.
-monitor dig tox/serum dig.
-apical pulse 1 min. hold <60BPM
-teach s/s of dig tox
-consume high K foods to prevent hypokalemia which would potentiate dig tox
foods high in K
- fresh/dried fruits
- fruit juice
- sweet potatoes
- kidney beans
- spinach
- avocado
dig toxicity, s/s
accumulation of digoxin –> digitalis tox.
s/s: n/v/d/a, brady/PVC/dysrhythm, headache/malaise/blurry/confusion/delirium, yellow green halos.
severe adv rxn: cardio tox (3 cardiac altered fx)
3 cardiac altered fx that contribute to digoxin induced ventricular dysrhtyhm:
- Suppression of AV conduction
- Increased automaticity
- Decreased refractory period in ventricular muscle
antidote for dig tox
Digoxin immune Fab (ovine, Digibind)
-Binds with digoxin to form complex molecules> excreted in urine, making digoxin unable to bind at cellular site of action
antianginal drug types
nitrates, beta blockers, calcium channel blockers
antidysrhtyhm drugs
restore cardiac rhythm to normal. class I: sodium channel blockers (Class IA, IB, IC) class II: beta blockers class III: drugs prolonging repolarization class IV: calcium channel blockers
antianginal drugs tx what?
tx angina pectoris
angina pectoris description/causes/complications
condition of acute cardiac pain from inadequate blood flow to myocardium (decreased oxygen to tissues > pain) Causes: 1. Plaque occlusions 2. Spasms of coronary arteries *Anginal attacks may lead to a MI
angina pectoris tests
Tests need to be performed to determine severity of blockage
i. ECHO
ii. Stress test
iii. Cardiac enzymes
iv. Possible cardiac catheterization
nonpharm methods for angina
i. Combination of pharmacologic and nonpharmacologic to control/prevent recurrences
ii. Avoid heavy meals, smoking, extreme weather changes, strenuous exercise, emotional upset
iii. proper diet, moderate exercise, smoking cessation, stress reduction
nitrates
antianginal drug.
reduces venous tone>decreases workload of heart>vasodilation.
generalized vascular/coronary vasodilation>increased blood flow to myocardial cells
nitroglycerin(nitro-bid) Class, PD, route, PT, CI, SE, NI, DFL, ADV
nitrate antianginal drug
dec myocardial demand for o2, decreases preload by dilating (indirect decrease in afterload) to control angina pectoris.
-PO, IV, subling, transd, or aerosol spray.
CI: ^ICP, severe anemia, cardiomyopathy.
adv: hypotn, reflex tachy, paradox brady. life thrt: circulatory collapse.
SE: headache (discuss OTC pain relief for headache)
hold SBP<90 if not emergent. rotate sites if transd, and don’t place near defib (explosion or burns).
^eff with alc, B blockers, Ca blockers, antihypertensives, ASA, benzos, vasodilators.
dec eff of heparin.
nitrate doses
subling: 0.4mg every 5 mins x3. if still unrelieved, call 911.
patch/paste: must have off periods to prevent ___?
must be kept in sealed container, protected from light to prevent degradation
beta blockers
antianginal drug.
decrease conduction velocity, automaticity, recovery time.
examples: propranolol (Inderal), acebutolol (Sectral), sotalol (Betapace)
calcium channel blockers
antianginal.
- Block calcium influx > decreasing excitability and contractility (negative inotropic)
- Increases refractory period of AV node> decreases ventricular response
- Examples: verapamil (Calan), diltiazem (Cardizem)
cardiac dysrhythmia definition, types, dx test, frequently follow what?
Any deviation from normal rate or pattern of the heartbeat
- Too slow: bradycardia
- Too fast: tachycardia
- Irregular
- An ECG (electrocardiogram) identifies dysrhythmias
- Dysrhythmias frequently follow an MI, hypoxia, hypercapnia, thyroid disease, CAD, cardiac surgery, excess catecholamines, or electrolyte imbalances
sodium channel blockers
class I antidisrhythm drugs. decrease Na influx into cardiac cells > decrease conduction velocity in cardiac tissues > suppress automaticity > decrease ectopic foci. Class Ia: slow conduction, prolong repolarization Class 1b: slow conduction, shorten repolarization. Class 1c: prolong conduction, little to no effect on repolarization
beta blockers
Class II antidysrhtyhm.
decrease conduction velocity/recovery time.
ex: propoanolol(Inderal), sotalol(Betapace), acebutolol (Sectral)
