This document summarizes key aspects of cardiac function and disorders of cardiac rhythm and conduction. It describes the anatomy and function of the cardiac conduction system, including the sinoatrial node, atrioventricular node, and Purkinje fibers. It discusses the phases of the cardiac action potential and how disorders can disrupt normal rhythm. Treatment options covered include medications that affect sodium, calcium, potassium channels or conduction, as well as non-pharmacological approaches like cardioversion, defibrillation, and ablation.

1. Disorders of Cardiac Function NURS 315/501 Kathryn T. Von Rueden RN, MS, FCCM University of Maryland School of Nursing

3. Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen Consumption 100%

4. Coronary Circulation

6. Anatomy of the Conduction System SA Node AV Node Bundle of His Bundle branches Purkinje fibers Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 331.

11. SLOW SA & AV Nodes FAST Purkinje Fiber & Muscle

19. Cardiac Muscle Action Potential 5 Phases Phase 0 : Upstroke, rapid depolarization Phase 1: Early, short repolarization Seen only in ventricular mus cle Phase 2: Plateau phase; membrane potential remains depolarized Phase 3: Final rapid repolarization Phase 4: Resting, diastolic repolarization ** Unlike nerve cells, cardiac cells have 5 phases in their action potential.

22. Cardiac Conduction & Rhythm Disorders

24. Lehne 5 th ed Figure 47-3 Electrical event precedes mechanical event !!!

25. Porth 2007, Figure 16-12 P wave PR Interval QRS complex T wave: Repolarization

30. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class II Antidysrhythmic

34. Beta Blocker Administration (remember from last week) Drug Route ½ Life (hrs) Indication Esmolol IV ONLY! 0.15 Dysrh, angina Metoprolol IV, PO 3-7 Dysrh, angina, AMI, HF, HTN Atenolol IV, PO 6-9 Dysrh, angina, AMI Carvedilol PO 5-11 Angina, AMI, HF, HTN Propanolol IV, PO 3-5 Dysrh, angina, AMI, HTN

35. Atrial Dysrhythmias Atrial Fibrillation : Chaotic & disorganized current. Atria are depolarizing without contracting (just quivering). Ventricular rhythm irregular. Only irregularly irregular rhythm. No discernable P waves.

38. Lehne 6 th ed Figure 47-4

39. Digoxin: Pharmacokinetics Absorption 60 – 80% (tabs) 70 – 85% (elixir) 90 – 100% (caps) Metabolism Liver Half Life 5-7 DAYS to eliminate & T½ 1.5 days

43. Digoxin Contraindications & Precautions Contraindications Precautions 2 nd /3 rd degree heart block V. Fib/V. Tach Sick Sinus Syndrome Acute MI Renal insufficiency Hypokalemia Severe pulmonary disease

47. Digoxin: Nursing Implications Apical pulse for 1 min. & document Monitor ECG Monitor potassium & dig levels

49. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node

52. Disorders of Atrioventricular Conduction 1st degree AV block: Slightly prolonged PR interval; ALL atrial impulses are conducted to ventricles; asymptomatic. 2nd degree AV block: Not all atrial impulses are conducted to ventricles, see some P waves, not followed by QRS. Can be very symptomatic. 3rd degree AV block = complete AV block: Conduction link between atria & ventricles lost, each controlled by independent pacemakers. Atria continue at their rate, ventricles contract at their rate (30-40 bpm).

53. Case study: Digoxin toxicity Serum dig level = 1.7 ng.ml (0.5-1.1 desired) 3 rd degree AV Block Temporary pacemaker inserted, SR  100% paced

54. Complete A-V block with 100% atrio-ventricular pacing Atrial Pacing spike Ventricular Pacing spike P QRS

55. Ventricular Dysrhythmias: More Serious! PVC: Ventricles contract prematurely. W/ a PVC, diastolic volume is insufficient for ejection of blood into arterial system. Therefore, no or weak pulse palpated. Few/day = OK, More/minute, the worse (>6). Common post MI, SNS activity,  K+, hypoxia. V-Tachycardia: rhythm originates below Bundle of His, in ventricular muscle. Wide, tall QRS complexes. Stops spontaneously or continue. Dangerous rhythm,  diastolic filling time   CO. Can cause Cardiac Arrest V-Fib: ventricle quivers but does NOT contract!  NO cardiac output , and no pulses; Cardiac Arrest!! grossly disorganized pattern.

56. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class I Antidysrhythmic

57. Class 1B: Lidocaine Ventricular Dysrhthmias

62. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class III Antidysrhythmic

68. Management of Cardiac Dysrhythmias REMEMBER: Many drugs used to treat dysrhythmias also may worsen them or cause new ones!

69. Coronary Heart Disease & Acute Myocardial Infarction (MI or AMI)

71. Coronary Circulation LV LV

73. Ischemic Heart Disease a.k.a Coronary Heart Disease a.k.a Coronary Artery Disease Angina Myocardial Infarction

77. Collateral Circulation

87. “ Severe” coronary stenosis and vulnerable plaques co-exist Califf, Atlas of Heart Diseases 2001

90. An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis

99. Angina Typically precordial, substernal Usual distribution of pain Less common sites of pain distribution

101. Hamon M and Hamon M. N Engl J Med 2006;355:2236 A 38-year-old man was scheduled to undergo invasive coronary angiography after cardiac scintigraphy revealed silent ischemia of the anterior myocardial wall Variant or Vasospastic Angina

102. Acute Coronary Syndrome (ACS) NSTEMI STEMI Unstable or ruptured plaque

103. Acute Coronary Syndrome (ACS)

105. Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392 .

106. Acute Coronary Syndrome (ACS)

108. ECG : STEMI vs NSTEMI

109. Non ST Segment Elevation Myocardial Infarction (NSTEMI) How is this different from unstable angina or STEMI? Unstable angina , plaque disruption but no thrombus or occlusion of the coronary artery, therefore no myocardial cell death (no MI). NSTEMI , a thrombus partially occludes a coronary artery. Depending on the degree of occlusion and oxygen demand of downstream heart cells, there may be myocardial cell death (an MI) but insufficient to produce ST segment elevations.

110. Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392 .

112. Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392 .

122. Cardiac Markers Hr 1 2 3 4 5 6 7 8 9 10 11 12 Day 2 3 4 5 Troponin CK-MB

123. NSTEMI Unstable angina No ECG  s Elevation of serum markers Unstable Angina Pain is severe No ECG  s No change in markers ACS No ST Elevation STEMI

129. Reperfusion McCance 5 th Ed, 2006 Figure 30-2

130. Reperfusion – Balloon Angioplasty, Possibly with Stenting Copyright © 2005 Nucleus Communications, Inc. All rights reserved. www.nucleusinc.com http://www.orbusneich.com/patients/genous/treatment/stenting/?PHPSESSID=d3bf5eb0eed5f6a353d73c

131. Complication of PCI N Engl J Med 2011;364:453-64.

132. Administration of Thrombolytic Therapy Must be Done Promptly Giugliano & Braunwald, Circulation 2003;108;2828-2830 IRA = infarct-related artery

133. PCI (angioplasty ± stenting) must be done promptly Nallamothu B et al. N Engl J Med 2007;357:1631-1638

149. You having an MI ??

153. Need a break?

154. Heart Failure

157. Cardiac Output Stroke Volume Heart Rate Preload LVEDV Afterload SVR Contractility LVSWI Determinant of Cardiac Output

158. SV Contractility CO O 2 to Organs Trigger Compensatory Mechanisms Blood volume Vascular resistance Cardiac work HF

159. Vicious Cycle of Heart Failure Lehne, 2009, Pharmacology for Nursing Care, 7th ed., Elsevier, p. 518

167. Systolic Dysfunction Impaired ejection  cardiac contractility   CO Conditions that  contractility: ischemic heart disease,  preload,  afterload Symptoms mainly result of  CO  “ forward” flow Porth 2005 28-4  EF

168. Diastolic Dysfunction Porth 2005 28-4 Impaired filling  LV Filling   CO Conditions that cause diastolic dysfunction: conditions that restrict diastolic filling - MV stenosis -  ventricular hypertrophy - Delay diastolic relaxation (aging)  EF

169. Right-sided vs Left-sided Failure Classified according to side of heart that is affected

170. “ Backward” “ Forward”

171. Right Heart Failure (RHF)  fluid accumulation in systemic venous system  venous congestion  peripheral edema Causes : Pulmonic valve stenosis or regurgitation RV infarction Cardiomyopathy PE (or anything else  PVR) Cor Pulmonale: RHF caused by lung disease Signs &Symptoms :

175. HF Classifications ACC/AHA NYHA Functional Class A High Risk; no structural disease or symptoms B Structural disease; no symptoms I Asymptomatic C Structural disease with symptoms II Symptomatic w/ moderate exertion III Symptomatic w/ minimal exertion D Advanced structural disease; severe symptoms; invasive tx needed IV Symptomatic at rest

177. Diuretics Preload Vasodilators Afterload

180. Afterload Reduction in HF  Vasodilation - Decrease resistance to ventricular ejection of blood - Improves forward blood flow - Reduce cardiac workload - Reduce compensatory myocardial remodeling

183. ALL Heart Failure Patients SHOULD BE ON an ACE-I or ARB !!!!!!!! American College of Cardiologists, TJC, NQF, AHRQ

190. Need a break?? Can’t make it any longer….

191. Disorders of Heart Valves

197. Diagram in Handout- Use it to figure out murmurs & Problems with blood flow d/t valvular defects!

199. Mitral Stenosis: Signs & Symptoms When would you hear a murmur? DIASTOLE

206. Valve Disease Summary

208. Kathryn !!! Pleeeaaase! Release the students! Mmmm…excellent!

209. Shock: The rude unhinging of the machinery of life!

212. Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen Consumption 100%

213. Aerobic Metabolism Anaerobic Metabolism 36 molecules ATP 2 molecules ATP Supports normal cell function Eventual cell dysfunction

218. Cardiogenic Shock

219. Preload SV Restore Cardiac Pump  Ventricular Contractility Positive Inotropic Agents Depressed Normal Enhanced

224. Cardiogenic Shock Vasodilators Afterload

228. Hypovolemic Shock

230. Frank-Starling Curve: Preload SV LVEDV LV dysfunction Hypovolemia Normal

238. Continuum of S epsis SIRS with a suspected or confirmed infx Sepsis SIRS Septic Shock ≥ 2 of the following: Temp: >38°C or < 36 °C H R: >90 beats/min Resps: >20/min WBC : >12,000/mm 3 , or < 4,000/mm 3 1992 Consensus Conf Bone et al. Chest. 1992;101:1644-1654. ; 2001 SCCM/ESICM/ACCP/TS/SIS International Sepsis Definition Conference. Crit Care Med 2003 31(4):1250-1256. Sepsis + Hypotension despite fluid + perfusion abnormalities + MODS (>1 organ failure, inability to maintain homeostasis w/o tx) Severe Sepsis Sepsis + > 1 organ dysfunction

241. Catecholamines: Adrenergic Agonists Alpha 1 Beta 1 Beta 2 Dopamine Vasoconstrict Cardiac stimulation Bronchodilate Renal artery dilation Phenylephrine Epinephrine Norepinephrine (Levophed) Dobutamine Dopamine Dopamine Dopamine

243. Cardiac Output Stroke Volume Heart Rate Preload Afterload Contractility Management of Shock: Oxygen Delivery SaO2 & Hgb X Reverse the causative factor(s) Restore perfusion to cells, tissues, organs

244. Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen Consumption 100%

248. SaO 2 /Hb CO O 2 Utilization Extraction & VO 2 Venous Return SvO 2 O 2 Delivery

249. Questions?