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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