Review of Cardiac Mechanics & Pharmacology 10/23/2016 Brent Dunworth, CRNA, MSN, MBA 1 Brent Dunworth, CRNA, MSN, MBA Associate Director of Advanced Practice Division Chief, Nurse Anesthesia Vanderbilt University Medical Center Nashville, Tennessee Learning Objectives 2 Review the principles of the cardiovascular system as they relate to the effects of anesthetic drugs. Describe the cardiovascular anatomy, physiology, and pathophysiology. Describe the impact of selection of pharmacologic agents on patient comorbidity. Continuous Professional Recertification Crosswalk to Examination Preparation Domain II: Applied Clinical Pharmacology (24%) ▪ II.A. Pharmacokinetics/pharmacodynamics/Pharmacogenetics of anesthetics and adjunct medications ▪ II.B. Factors influencing medication selection ▪ II. B.1. Physiological ▪ II. B.2. Pathophysiological ▪ II. B.3. Laboratory & diagnostic studies ▪ II. B.4. Utilization, actions, interactions, benefits, adverse effects, abnormal responses, alternatives, and antagonists ▪ II. B.5. Comorbidity ▪ II.C. Intraoperative monitoring techniques ▪ II.D. Infection prevention principles ▪ II.E. Adverse Pharmacological Reactions Domain III: Human Physiology and Pathophysiology (24%) ▪ III.A. Cardiovascular ▪ III. A.1. Normal anatomical structures and function ▪ III. A.2. Physiologic processes and anesthetic considerations ▪ III. A.3. Pathophysiologic disease processes and associated disorders 3
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Review of Cardiac Mechanics & Pharmacology · Describe the cardiovascular anatomy, physiology, and pathophysiology. ... (Rheumatic Heart Disease) 2% Unicommissural aortic valve 1%
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Review of Cardiac Mechanics & Pharmacology
10/23/2016
Brent Dunworth, CRNA, MSN, MBA 1
Brent Dunworth, CRNA, MSN, MBAAssociate Director of Advanced PracticeDivision Chief, Nurse AnesthesiaVanderbilt University Medical CenterNashville, Tennessee
Learning Objectives
2
Review the principles of the cardiovascular system as they relate to the effects of anesthetic drugs.
Describe the cardiovascular anatomy, physiology, and pathophysiology.
Describe the impact of selection of pharmacologic agents on patient comorbidity.
Continuous Professional RecertificationCrosswalk to Examination Preparation
Domain II: Applied Clinical Pharmacology (24%) ▪ II.A. Pharmacokinetics/pharmacodynamics/Pharmacogenetics of anesthetics and adjunct medications ▪ II.B. Factors influencing medication selection
▪ II. B.1. Physiological ▪ II. B.2. Pathophysiological ▪ II. B.3. Laboratory & diagnostic studies ▪ II. B.4. Utilization, actions, interactions, benefits, adverse effects, abnormal responses, alternatives, and
Domain III: Human Physiology and Pathophysiology (24%) ▪ III.A. Cardiovascular
▪ III. A.1. Normal anatomical structures and function ▪ III. A.2. Physiologic processes and anesthetic considerations ▪ III. A.3. Pathophysiologic disease processes and associated disorders
62About same LV volume; much greater pressureAbout same LV volume; much greater pressure
Management of AS
Parameter Goal
Preload Increase to distend the stiff ventricle
Afterload Decrease is hazardous
Rate Normal to Slow (increase in rate can produce ischemia)
Contractility Decreased to normal
Oxygen balance Increased demand as a result of increase in LV mass
Rhythm Sinus
63
Review of Cardiac Mechanics & Pharmacology
10/23/2016
Brent Dunworth, CRNA, MSN, MBA 22
Mitral Regurgitation
64
Mitral Regurgitation
▪ Etiologies▪ Alterations of the Leaflets, Commissures, Annulus▪ Rheumatic▪ MVP▪ Endocarditis
▪ Alterations of LV or LA size and Function▪ Papillary Muscle (Ischemic, MI, Myocarditis, DCM)▪ HOCM▪ LV Enlargement – Cardiomyopathies▪ LA Enlargement from MR▪ MR begets MR
65
Mitral Regurgitation
66Decreased ventricular volume during isovolumetric contractionDecreased ventricular volume during isovolumetric contraction
Review of Cardiac Mechanics & Pharmacology
10/23/2016
Brent Dunworth, CRNA, MSN, MBA 23
Mitral Regurgitation
67Increased LV emptying; retrograde flow into LAIncreased LV emptying; retrograde flow into LA
Management of MR
68
Parameter Goal
Preload Normal to increased
Afterload Decreased, vasodilator beneficial
Rate Prevent slow rate (<80 bpm)
Contractility Decreased from rheumatic or coronary artery disease
Oxygen balance increased demand as a result of increased mass
Rhythm Sinus• Atrial fibrillation tolerated if rate is
Low doses produce cardiac stimulation and vasodilation, which turns to vasoconstriction at high doses.
Norepinephrineβ1 = α1 >β2 = α2
Severe hypotension; septic shock
Reflex bradycardia masks direct stimulatory effects on sinoatrial node.
Dopamine
β1 = β2 > α1**At low doses, it stimulates the heart and decreases systemic vascular resistance; at high doses, vasodilation becomes vasoconstriction as lower affinity α-receptors bind to the dopamine; also binds to D1 receptors in kidney, producing vasodilation.
Acute heart failure, cardiogenic shock and acute renal failure
Biosynthetic precursor of norepinephrine; stimulates norepinephrine release.