the "load" that stretches the ventricle immediately before contraction

ventricular end diastolic volume

forces opposing ventricular ejection

tension in the ventricle that develops during systole to open semilunar valves

force of myofibril contractions

(over stretch-->can't Fx properly)

first line for volume overload

dec. preload and afterload

promote moderate diuresis

Prototype: hydrochlorothiazide(HCTZ)

common SE: hyponatremia

promote profound diuresis

prototype: Furosemide(lasix)

remember to check foley bag

prototype: spironolactone(aldactone)

prolongs survival by blocking aldosterone receptors

RALES study?

the "PRIL" family

weak action

blocks production of angiotensin II, this:

1. inc. vasodilation, dec. pre/afterload

2. dec. formation of aldosterone

3. inhibits cardiac remodeling in HF (inc. Kinins)

Prototypes: Captopril and analapril

improve morbidity, mortality, excercise tol., and LV ejection fraction (prolongs life)

check if dose is sufficient to lower mortality

check K⁺ before you give

Heart Rate?: Dry cough(kinins), angioedema(lips, tongue, airway), fetal toxic

dec. preload: may cause hyperkalemia (blocks aldosterone)

dec. afterload: causes hypotension. Take BP before dose. hold if SBP <110

the "sartan" family

Action: blocks vasoconstrictor effects of A2 at receptor sites

1. inc. vasodilation to dec. afterload

2. decreases formation of aldosterone to dec. preload

Prototypes: losartan (Cozaar), valsartan (diovan)

don't inc. level of Kinins (less cardiac remodeling than ACEI and no dry cough)

not very good for heart failure

sympatholytic - the "LOL" family

Actions: Blocks stim. of beta adrenergic receptors which blocks cardiac remodeling in heart failure. overall dec. in stroke volume leads to dec blood pressure.

prototype: propanolol (inderal)

decreases

used for dysrhythmias(supraventricular)

AE/NSG implications: bradycardia, check AP pulse, hold PRN

Hold <50?

decreases (reduces workload)

uses: mild to moderate HF, post MI to prevent recurrent MI

AE/NSG implications: watch for worsening HF, lethargy, depression

decreases

use: angina

AE: fluid retention

decreases

use: HTN

AE/NSG implications: dizziness, OH (hold PRN for SBP <110

dec. HDL, dec. libido, impotence

can cause withdrawl: rapid inc. HR and inc. BP, so wean off meds

minimize peripheral and pulmonary effects

metoprolol

carvedilol(coreg): also blocks alpha 1 receptors. used for mild/mod. systolic HF along with diuretics and ACE inhibitors. doesn't take effect for a while. SE? Afib(most common with HF)

report nocturia and daytime oliguria (first sign of renal impairment sec. to dec. CO)

don't abruptly stop drug - withdrawl grad. (1/2 to 2 wks) to prevent rebound tachycardia

report Sx of CHF immediately: weight gain >3 lb in 2 days, >5 lb in a week, dyspnea

give lowest dose effective

BB's may mask hypoglycemia and prolong (dec. gluconeogenesis)

prototype: digoxin(lanoxin)

action: alters electrolyte composition in myocardial cells (inhibits Na-K ATpase pump-->inc. intracellular Na and calcium)

inc. contractile force

results in a slower, stronger heart rate

dec. SA node automaticity(good for rapid A-fib)

only for systolic failure (inotrope)

decreases HR

use: rapid Afib

AE/NSG implications: dec. HR by dec. conduction speed through AV node. causes bradycardia. take AP for full min before dose. hold if <60, notify MD

increases

use: systolic HF

AE/NSG considerations: pos. inotrope. leads to increase urine output, decreases rennin release by the kidneys

decreases

NSG implications: increases CO leads to inc. urine output

decreased

NSG implications: decreases rennin release?

N/V/D

anorexia

visual dist. (yellow halo's in vision)

slow, irregular HR

draw digoxin blood level to confirm (norm. 0.5 - 0.8 mg/ml

Tx with digoxin antibody (digibind)

monitor K⁺ and Ca⁺ levels ( dec. K or Ca potentiates toxicity)

teach Pt to take pulse. report  rates <60 or >100 to MD

amidiarone and verapamil inhibit excretion so inc. dig levels

T¹/₂ 1.5 days. Pt may require IV loading dose followed by oral dose (digitalization)

stim. B₁ receptors to improve contractility and cardiac output. used to treat acute HF. IV only.

SE: HTN, PVC's, arrhythmias, angina, tachycardia

1. higer doses stimulate dopaminergic and B₁ and alpha receptors to inc. contractility and peripheral vasoconstriction. used in Tx of shock. given in ICU

2. SE: arrhythmias, hypotension, tissue necrosis at IV if infiltrated.

monitor BP and P: Q15min x 4, Q30min x 2, Q1hr x 4. check IV site Q1hr for tissue sloughing

Two RN's must verify set up and rate change

synthetic form of brain naturetic peptide(BNP) - released in response to inc. preload and stretch

used: short term support of Pt's in acute decompensated HF

Actions: 1. suppresses RAAS

2. suppresses sympathetic outflow from CNS (blocks the SNS)

3. binds with receptors on arterioles/veins--> direct vasodilation
rescusitation drug?

dec. conduction velocity and automaticity of myocardial tissue

prolong refractoriness of myocardial tissue to delay repolarization

inc. myocardial electrical stability

alter conduction path/dec. speed

use: dysrhythmias

AE/NSG implications: check VS, ases EKG for heart block

decreases (class II and IV)

AE/NSG implications: hypotension, watch for CHF

sodium channel blockers used for ventricular and supraventricular dysrhythmias

prototype: Pocainamide (pronestyl)

IA: Quinidine, disopyramide. SE: wide QRS, diarrhea, cardiac Tox, ringing in ears, dec. pulse

IB: lidocaine, mexilitine. SE: CNS depression, weakness, bradycardia

IC: profafenone, flecainide (if you see these it means they tried everything else). SE: worsening HF, bradycardia, proarrhythmias

beta adrenergic blockers

used for vent. rate control in Pt's with supraventricular tachydysrhythmias

prototype: propanolol

esmolol (IV), acebutolol. SE: bradycardia, hypotension, impotence, HF

Sotolol (also has class III properties). SE: same

potassium channel blockers

used for highly symptomatic atrial and life threatening ventricular arrhythmias

(delays repolarization of action potential)

prototype: amiodorone

sotolol, dofetilide, ibutilide fumarate, bretylium (given IV in ICU for vent. tachycardia/fibrilation)

SE: hypotension, inc. digoxin levels, lung damage/pulmonary fibrosis, bradycardia, cardiotoxicity

calcium channel blockers

used for vent. rate control for supraventricular arrhythmias

prototype: diltiazem

verapamil

SE: hypotension, flushing, edema, HA, bradycardia, HF, inc. digoxin levels

naturally occuring nucleotide hormone that inhibits cardiac pacemaker cells (dec. automaticity in the SA node) and slows conduction through AV node

IV bolus used for SVT. similar effect as verapamil. used in cardiac stress testing

can cause transient (<1 min) dyspnea, flushing, chest discomfort and bradycardia

T1/2: 1.5 - 10 sec. 6mg IV push given rapidly repeat 12 mg after 1 - 2 minutes. used to mimic excercise

blocks parasympathetic receptors (muscarinic)

used to treat symptomatic bradycardia (<40)

0.5 - 1mg IVP. max dose .04mg/kg (about 2-3mg)

use caution with myocardial ischemia-->tachycardia and myocardial O2 consumption

No S/S of HF but structural heart disease has become evident. goal is to prevent development of symptoms

Drugs: ACE inhibitor or ARB

Structural heart disease evident. S/S of HF have developed and are evident with moderate exertion, then with minimal exertion.

Goals: relieve pulmonary and peripheral congestive symptoms, improve Fx capacity and quality of life, slow cardiac remodeling and prog. of LV dysfuntion, prolong life

Drug Tx: diuretics, ACE inhibitor/ARB, spironolactone, BB's, Digoxin, isosorbide dinitrate

marked S/S of HF at rest despite medical therapy with advanced structural heart disease. repeated hospitalizations for exacerbations of HF. Heart transplant is only hope for reversal.

Goals: conrol of fluid retention with IV diuretics, symptom stabilization using IV inotropic agents