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Pharmacologic Considerations in the Cardiac Patient Wayne E. Ellis, Ph.D., CRNA.

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Presentation on theme: "Pharmacologic Considerations in the Cardiac Patient Wayne E. Ellis, Ph.D., CRNA."— Presentation transcript:

1 Pharmacologic Considerations in the Cardiac Patient Wayne E. Ellis, Ph.D., CRNA


3 1/15/2014 Treatment of Ischemia(primary) ASA 325 mg immediately Thrombolytics (Retevase) –> flow rate than TPA –2 30 min intervals –lyse clots through the activation of plasminogen

4 1/15/2014 Primary Treatment Antiplatelet agents(abciximab, eptifibatide, tirofiban, integullin) GPIIb-IIIa antagonists inhibit platelet function by blocking the GPIIb-IIIa receptor, the final pathway of platelet aggregation thereby decreasing thrombi development and prevents arterial vessel occlusion

5 1/15/2014 Percutaneous Coronary Intervention Advantages include: higher recanulazation rates improved blood flow through the infarct-related vessel improved LV function lower in-hospital mortality rates

6 Anesthetic Technique Goals of Anesthesia loss of consciousness amnesia analgesia suppression of reflexes (endocrine and autonomic) muscle relaxation

7 Preoperative Preparation Angina Medications to control it Blood pressure controlled Diastolic < 95 torr Congestive heart failure treated Diuretics Afterload reduction Bed rest if indicated Control diabetes

8 Preoperative Medications Sedation Prevent tachycardia Hypertension Prepared for hypoxia Supplemental oxygen Calcium channel blockers not protective of perioperative ischemia Antihypertensives continue on day of surgery Stop Diuretics

9 1/15/2014 Low Molecular Weight Heparin Enoxaparin, Dalteparin Anticoagulant activity by binding to antithrombin III, which further binds and inactivates the coagulation factors IIa (thrombin) and Xa Advantages include dosed per body wt. Given q12 sub q. Less trombocytopenia and bleeding

10 1/15/2014 Opioids Advantage relates to the relative lack of myocardial depression –Exception Sufenta, Carfentanil, and high dose fentanyl They maintain stable hemodynamics and reduce heart rate A primary opioid technique may be of value in the patient with severe myocardial dysfunction

11 Opioids Advantages Excellent analgesia Hemodynamic stability Blunt reflexes Can use 100% oxygen

12 Opioids Disadvantages May not block hemodynamic and hormonal responses in patients with good LV function Do not ensure amnesia Chest wall rigidity Respiratory depression

13 1/15/2014 Vasoconstrictors are useful in the prevention and treatment of ischemia r/t the ability to increase systemic BP Phenylephrine improves coronary perfusion pressure, at the expense of increasing afterload and Mv02

14 1/15/2014 Vasoconstrictors At the same time, phenylephrine causes venoconstriction, increasing venous return and left ventricular preload. The increase in CPP more than offsets the increase in wall tension

15 Inhalation Agents Advantages Myocardial oxygen balance altered favorably by reductions in contractility and afterload Easily titratable Can be administered via CPB machine Rapidly eliminated

16 1/15/2014 Inhalational Agents Disadvantages include myocardial depression systemic hypotension with possible tachycardia lack of postoperative analgesia

17 Inhalation Agents Disadvantages Significant hemodynamic variability May cause tachycardia or alter sinus node function Possibility of coronary steal syndrome

18 Inhalation Agents Potential for coronary steal Alters coronary autoregulation Alters regional blood flow Little influence on outcome

19 Coronary Steal Arteriolar dilation of normal vessels diverts blood away from stenotic areas Commonly associated with adenosine, dipyridamole, and SNP Forane causes steal and new ST-T segment depression May not be important since Forane reduces SVR, depresses the myocardium yet maintains CO

20 1/15/2014WE Ellis20 Antianginal medications Beta-blockers Calcium Channel Blockers Nitrates Nitropaste morning of surgery

21 1/15/2014 Nitrates Nitroglycerin = venodialator, reduces venous return, decreases wall tension(Mv02) also a coronary arterial dialator. Drug of choice for coronary vasospasm Although primarily is a systemic venodialator, at high doses causes arterial dilatation and systemic hypotension

22 Cardioactive drugs Nitroglycerin Lower LVEDP Vasodilator Poor ventricular function

23 1/15/2014 Beta Blockers Beta blockers reduce myocardial workload(Mv02), and oxygen consumption(V02) by reducing HR,BP, and contractility, and they increase the threshold for ventricular fibrillation. Indications for beta blockers include: sinus tachycardia, supraventricular dysrhythmias and hyperdynamic states

24 Beta Blockers Negative inotropic effects Withdrawal following stoppage of beta blocker Unstable angina Myocardial infarction

25 1/15/2014 Beta Blockers Propranolol (non-selective) t 1/2 = 4-6 hours Metoprolol (B 1 selective) t 1/2 = 4-6 hours Labatelol (1:7 ratio) t 1/2 = 2-4hours Esmolol (Beta1 selective) t 1/2 = 9.5 minutes

26 Esmolol Control heart rate and blood pressure Induction Emergence

27 Labetalol Mixed alpha and beta Control hypertension Heart rate management

28 1/15/2014 Ca Channel Blockers Evidence for beneficial effects post mi is less compelling Nifedipine treatment is associated with a trend towards increased mortality and reinfarction Verapamil does not reduce mortality or reinfarction Verapamil - useful for slowing the ventricular response in atrial fibrillation/flutter

29 1/15/2014 Ca Channel Blockers Cardizem- in pts with non-Q wave infarction seems to reduce the reinfarction rate during the 1st 6 months after the infarction, but incidence of late infarction was similar to a placebo. Cardizem increases cardiac events in pts with LVEF<40%, but decreases their incidence in pts with preserved LV function

30 1/15/2014 Ca Channel Blockers All Ca blockers depress contractility, reduce coronary and systemic tone, decrease sino-atrial node firing, and impede atrioventricular conduction. The negative inatropic effect is greatest with verapamil Nifedipine + Cardizem are used in the prevention of coronary vasospasm

31 Nifedipine Controlling hypertension Manage coronary artery spasm

32 1/15/2014 ACE Inhibitors Are effective in reducing ischemic effects after MI Treatment should be instituted within the 1 st 24 hours of all pts with acute mi complicated by symptomatic or asymptomatic left ventricular dysfunction

33 1/15/2014 ACE Inhibitors Contraindicated in pts with hypotension, bilateral renal artery stenosis, history of a cough or angio- edema with ace inhibitors

34 1/15/2014 Aspirin ASA benefit well established as a secondary prevention Antiplatelet therapeutic dose ( mg/day) other antiplatelet agents such as dipyridamole are not supported in the literature except in pts with allergies to ASA who are poor candidates to oral anticoagulants

35 1/15/2014 Anticoagulants Studies of anticoagulant treatment after mi show reduction in death, recurrent MI, and thromboembolitic complications However, trials comparing warafin to ASA for secondary prevention show no difference in recurrent infarction or death

36 1/15/2014 Anticoagulants Are indicated for pts with ASA intolerance and for those at risk of embolisation from left ventricular or atrial clot(i.e. persistent atrial fib)

37 1/15/2014 Lipid Lowering Agents meta analysis of clinical trials show that lipid lowering agents produce a reduction in fatal and non-fatal MIs and cardiovascular deaths Should be given to pts with LDL concentration >3.37 mmol/1

38 Clonidine Less hypertension Decreased anesthesia requirements

39 Anesthetic Management Regional vs. general Anesthetic management skills more important than technique Safest technique is the one the practitioner does best

40 Regional Anesthesia Monitor patient more accurately Control sympathetic responses Fluids Esmolol

41 General anesthesia Avoids sympathectomy Risks with intubation Sympathetic stimulation Hypoxia Increased catecholamines Loss of subjective monitor Chest pain Ischemia

42 General Anesthesia required Narcotics Effective control of catecholamines Respiratory depression Prolonged ventilation

43 Lidocaine Blunt effects of intubation 1.5 mg/kg 4-6 minutes prior to intubation

44 Nitrous Oxide Rarely used due to: increased PVR depression of myocardial contractility mild increase in SVR air expansion

45 Induction Drugs Barbiturates Benzodiazepines Ketamine Etomidate

46 Avoid Ketamine Hypertension Tachycardia Use in trauma

47 Etomidate Painful to inject More CV stability

48 Barbiturate Direct depressant Extended duration of activity Smaller doses 1-2 mg/kg Add benzodiazepines and narcotic

49 Benzodiazepines Quell anxiety Hemodynamic stability Extended duration of action Potential for hypoxia Lidocaine Esmolol

50 Muscle Relaxants Used to: facilitate intubation prevent shivering attenuate skeletal muscle contraction during defibrillation

51 Muscle Relaxants Avoid pancuronium Tachycardia ST segment changes consistent with ischemia Doxacurium Duration similar to pancuronium No cardiovascular effects

52 Avoid Histamine releasing drugs Curare Atracurium Mivacurium <15 mcg/kg Hypotension Tachycardia

53 Nitrous Oxide Constricts coronary arteries Aggravates myocardial ischemia High FiO2 recommended Maintain saturation at %

54 Intraoperative predictors Choice of anesthetic Site of surgery Duration of Anesthesia Emergency Surgery

55 Intraoperative predictors Choice of Anesthetic No difference in infarction rate GETA vs. Regional No significant hypotension No significant tachycardia TURP Regional decreased risk post MI Reinfarction rate SAB < 1% GETA 2-8%

56 Intraoperative predictors Choice of Anesthetic Patient with CHF will benefit from regional technique Sympathectomy Decreased preload Coronary Steal Potent inhalation agents vs. narcotics

57 Intraoperative predictors Site of Surgery Thoracic and upper abdominal 2-3 Xs risk of extremity procedures Duration of Anesthetic > 3 hours > risk of morbidity & mortality Emergency Surgery Xs greater risk than nonemergent surgery

58 Postoperative Management Maintain analgesia Balance supply and demand Supplemental oxygen Continue monitoring into postoperative period Early transfusion

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