Nurs 2004- Medications for hypertension and heart failure

Cardiac preload

Amount of stretch blood puts on the heart

Cardiac after load

Resistance ventricles must pump against

Where do most pts with heart failures symptoms come from

Impaired left ventricular myocardial function

How patients with heart failure usually present?

1. Dyspnea

2. Decrease exercise tolerance

3. Fluid retention (pulmonary and peripheral edema)

Heart failure causes

1. Myocardial injury

2. Ischemic heart disease

3. Chronic hypertension or volume overload

4. Cardiomyopathy

What edema comes from left sided heart failure

Pulmonary edema

What edema comes from right sided heart failure

Systemic/ pedal edema

What does RAA regulate

1. Blood pressure

2. Blood volume

3. Fluid and electrolyte balance

Non pharmacological measures to prevent/treat heart failure

1. Moderate aerobic exercise

2. Sodium restriction

3. Flu and pneumonia vaccines

4. Close supervision and follow up

5. 1.5-2L of fluid/day

6. Daily weights

7. Patient education

What vaccines can help prevent heart failure?

Flu and pneumonia vaccines

ACE inhibitor uses

1. Hypertension

2. Heart failure

3. Diabetic nephropathy

4. Myocardial infarction

ACE inhibitors MOA

1. Block angiotensin converting enzyme in the lung

2. Decreases vasoconstriction

Common ACE drugs

1. Captopril (capoten)

2. Enalapril (Vasotec)

3. Lisinipril (zestril or prinivil)

4. Ramipril (altace)

Captopril absorption

Well absorbed, less when taken with food

When should you take Captopril?

Before breakfast because it absorbed better on an empty stomach

Captopril dose

12.5-50 mg TID

Long acting ACE inhibitors

1. Enalapril

2. Lisinopril

Enalapril dose

BID

Lisinopril dose

Daily

Why is elanapril and Lisinopril taken less than Captopril?

They are 10-20x more potent and have a longer effect

Why might someone prefer to take Enalapril or Lisinopril over Captopril?

1. Easier adherence (BID or daily instead of TID)

2. Reduced cost (less pills/day)

ACE inhibitors side effects

1. Cough (dry, hacking)

2. Angioedema

3. First dose hypotension

4. Hyperkalemia

5. Neutropenia

What adverse effect means you should discontinue ACE inhibitors immediately

Angioedema

Why should you take the first dose of an ACE inhibitors at night

Hypotension with the first dose

ACE inhibitors drug interactions that intensify the first dose hypotension

Diuretics

ACE inhibitors drug interactions that can cause hypotension

1. Beta blockers

2. Diuretics

ACE inhibitors drug interactions: drug that decreases ACE inhibitors effectiveness

NSAIDS (Get increased Na+ reabsorption)

What can cause serious hyperkalemia when taken with ACE inhibitors

Supplemental vitamin K

What can ACE inhibitors lead to

Lithium accumulation

Angiotensin 2 receptor blockers (ARBs) uses

1. Heart failure if intolerant to ACE 1 (cough)

2. Used with ACE 1 if persistent heart failure symptoms or if B-Blocker not tolerated or contraindicated

Common ARBs

1. Candesertan (atacand)

2. Valsartan (Diovan)

3. Losartan (Cozaar)

4. Irbesartann (Avapro)

ARBs MOA

1. Blocks angiotensin 2 receptors

2. Bradykinin can still be broken down

Diuretics indications

For HF patients with evidence of congestion symptoms (pulmonary/peripheral edema, use lowest dose once congestion clears)

Diuretics dose adjustment

Supervised self adjustment based on weight and symptoms

What to do if persistent volume overload occurs with diuretics

1. Add thiazide diueretic or low dose metolazone

2. Monitor weight, renal function and potassium

Loop/high ceiling diuretic

1. Furosemide

2. Thiazide

Potassium sparing aldosterone agonist diuretic

Spironolactone

Potassium sparing non aldosterone agonist diuretic (osmotic)

Mannitol

Most powerful diuretic, not for every day use

Mannitol

Mannitol decreases Na+ reabsorption by:

65%

Where in the nephron does mannitol act

Proximal convoluted

Where in the nephron does Furosemide act

Ascending limb of Henles loop

Furosemide decreases Na+ reabsorption by:

20%

Where in the nephron do Thiazides act:

The early distal convoluted tubule

Thiazides decrease Na+ reabsorption by:

10%

Where in the nephron does Spironolactone and triamterene work

Late distal convoluted tubule and collecting duct

Spironolactone and triamterene decrease Na+ reabsorption by:

1-5%

Diuretics typically used as an add on for lasix

Spironolactone and triamterene

What is the MOA of most diuretics

1. Block Na and Cl reabsorption

2. Creates osmotic pressure that prevents reabsorption of water

3. Leads to increased urine flow

How do diuretics help with heart failure

Decrease volume and FOC, therefore decreasing blood pressure

Furosemide MOA

1. Blocks passive Na and Cl reabsorption at different sites in the nephron

2. H2O follows Na+ out to maintain osmotic equilibrium

3. Excess water is excreted in urine Decreases volume, PVR, CO and therefore also decreasing BP, SOB and fatigue

How can furosemide have a rebound effect

1. If Na or Cl become depleted, blood volume will be decreased

2. Leading to decreased blood pressure

3. Decreased volume and renal perfusion (RAA is activated)

4. Beta 1 is stimulated

5. Cardiac O2 consumption is increased

Furosemide adverse effects

1. Hyperuricemia (kidney stones and gout)

2. Ototoxicity

3. Hyperlipidemia

4. Hyperglycemia

5. Hypokalemia

6. Hypotension

7. Hyponatremia

8. Dehydration

What drug can increase the risk of Ototoxicity when taken with furosemide

Gentamycin

Diuretic that can’t be given with kidney failure

Thiazide diuretics

Diuretic that can be given with kidney failure

Furosemide

Thiazide diuretic drugs

Hydrochlorothiazide (hydroDIURIL)

Hydrochlorothiazide uses

1. Hypertension

2. Edematous state

Hydrochlorothiazide potency

Less potent than loop diuretics (furosemide)

Hydrochlorothiazide adverse effects

Same as furosemide but not as ototoxic

Spironolactone (aldactone) MOA

1. Modest increase in urine production

2. Retains potassium (reduces excretion)

3. Binds to aldosterone receptors in late distal convoluted tubule

Spironolactone (aldactone) uses

1. Hypertension

2. Edematous state

3. Severe heart failure with hypokalemia

Spironolactone (aldactone) side effects

Hyperkalemia

Mannitol uses

1. Renal failure

2. Increased intracranial pressure

3. Increased intraocular pressure

Mannitol side effects

Very potent (not for home use, ICU/ER/OR only!!!!)

Inotropic agents

Cardiac glycosides:

1. Digoxin

2. Lanoxin

Digoxin uses

1. Symptomatic, moderate to severe heart failure (little effect when used alone)

2. Dysrhythmias

3. Chronic atrial fibrillation and rate control despite beta blocker

Digoxin positive ionotropic effects

Increases FOC by reversible inhibiting myocardial Na-K ATPase pump

Digoxin AV node inhibition

1. Stimulates parasympathetic nervous system

2. Slows electrical conduction in AV node

3. Decreasing heart rate

Why is digoxin considered a last effort for heart failure

It’s highly toxic and has little effect in its own

Digoxin half life

Long half life, easily retained in small people, elderly, women and those with renal impairment

Digoxin toxicity adverse effects

1. N/V

2. Visual changes

3. Dysrhythmias

4. Anorexia

5. Headache

6. Confusion

What can increase effects and risk of toxicity with digoxin

Hypokalemia

Digoxin therapeutic range

0.5-1.1 ng/ml (very narrow, requires close monitoring!)

When does digoxin toxicity increase

As the serum drug levels increase above 2.0 ng/ml

Digoxin drug interactions: drugs that decrease effects and absorption of digoxin

Antacids

Digoxin drug interactions: Drugs that increase levels of digoxin in the blood

Quinidine

What should you do if taking digoxin and quinidine together?

Reduce digoxin dose

Digoxin drug interactions: Drug that decreases digoxins therapeutic effects

Verapamil

Digoxin drug interactions: Drugs that increase digoxins risk of dysrhythmias

Diuretics

BAADDA

1. Beta blockers

2. Ace inhibitors

3. ARBs

4. Diuretics

5. Digoxin

6. Aldactone

When are beta blockers safe to use?

If stable and no fluid overload

How do beta blockers work

decrease O2 consumption of the heart muscle by reducing HR and BP through SNS

What do ACE inhibitors and ARBs counteract

RAAS

What do ACE inhibitors and ARBs both do

Vasodilate