Towards a Greater Understanding of Cardiac Medications



Towards a Greater Understanding of Cardiac Medications

But first a little cardiac patho…

Foundational Cardiac Concepts:

Cardiac Output (CO) …CO=SVxHR

• Stroke volume-amount of blood that returns to right atrium from venous circulation and left atrium from pulmonary veins

o Larger SV increases workload of the heart

o Faster HR increases cardiac O2 demands and workload

o Goal of medication therapy with any cardiac client is to DECREASE cardiac workload through influencing SV, HR, Preload, Afterload and Contractility

I. Preload

• Preload is the filling pressure of the RV-LV and is influenced by venous return…higher venous return or blood volume in atria-the higher the SV will be…opposite is also true

• Pressure/Stretch in ventricles end diastole just before contraction

• In a healthy heart, as you INCR Preload…You will increase stroke volume which will increase force of contraction

• Only up to a certain point-then further stretching may actually decrease contractility

• Drugs that cause venous dilation (nitrates)-DECREASE preload

• Diuretics that eliminate excess fluid volume DECREASE preload

Starling’s Law of the Heart:

• The greater the preload- greater quantity of blood that can be ejected during systole due ti INCR stretch of myocardium

• But only up to a maximal point. Greatest force of contraction is when the muscle fibers are stretched 2 ½ times their normal length

• Overstretch of cardiac muscle is like an overstretched rubber band-will DECREASE cardiac contractility and efficiency over time

2). Afterload

• Force of resistance that the LV must generate to open aortic valve

• Correlates w/SBP…How much pressure is needed to push blood out of the heart into the aorta and into entire systemic circulation

• Influenced by resistance of blood vessels in the body-are the arteries dilated or constricted

• Arterial vasodilators (Ca++ channel blockers (CCB), ACE inhibitors) DECREASE afterload

3) Contractility: Inotropic-influencing contractility independent of Starling mechanism

• Ability of heart to change force of inherent contraction strength

• Influenced by Ca++ in action potential…therefore CCB will do what to contractility?

• Decrease contractility (inotropic) DECREASE cardiac workload and O2 demands

• Negative inotropic meds: CCB, beta blockers

• Positive inotropic: Digoxin, Dopamine & Epinephrine gtts.

Ejection Fraction (EF) on echocardiogram

– 65-70% normal

– reflects that with each contraction 65-70% of the blood in the LV is ejected into circulation

– As this % goes down it is reflecting the loss of cardiac contractility and degree of CHF

– 35% EF is half the normal cardiac output with each contraction

– 10-15% EF end-stage heart failure-near death

I.Angiotensin Converting Enzyme (ACE) Inhibitors…(end in “pril”)

• Captopril (Capoten)

• Enalapril (Vasotec)

• Lisinopril (Prinivil)

Mechanism of Action: A normal plasma protein-renin is secreted by the kidneys when BP falls which converts inactive liver protein angiotensinogen to angiotensin I. The conversion to angiotensin II is enhanced by angiotensin-converting-enzymes (ACE) from the lungs to one of the most potent vasoconstrictors known. The effects of angiotensin II are:

• Vasoconstriction of arterioles and veins (incr. afterload)

• Stimulation of the sympathetic nervous system (incr. workload of heart)

• Retention of water by the kidneys due to aldosterone a hormone secreted by the adrenal glands (incr. preload)

ACE inhibitors block the conversion of angiotensin I to angiotensin II. This inhibition decreases angiotensin II concentrations and causes:

• Vasodilation which decreases BP (decr. Afterload) and decrease sodium and water retention (decr. Preload).

Uses: HTN, CHF, CAD

Side Effects-most common: hypotension, dry cough, dizziness

• Angioedema (life threatening) Laryngeal swelling that can cause asphyxia. Facial swelling also concerning precursor.

Nursing Considerations:

• Obtain BP before administering-hold typically if SBP ................
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