CARDIAC ANESTHESIA

CARDIAC ANESTHESIA Dr. Jeffrey S. Sagel Anesthesia Attending, WRAMC Assistant Professor of Anesthesia, USUHS Education Director; Interns & Clerks, WRAMC Cardiovascular disease is the leading cause of death in the United States. Managano DT, Goldman L, Preoperative assessment of patients with know or suspected coronary disease. N Engl J Med 1995; 333:1750-1756 ANATOMY THE HEART LE RAISON D’ETRE ONE HEART OR TWO? 2 The Heart The Right Heart • The sole function of the right heart is to pump blood to the lungs. • Blood is received via the superior vena cava, the inferior vena cava, and the coronary sinus. The Right Heart • The blood enters and is collected into the right atrium • The ostium of the inferior vena cava is guarded by the eustachian valve. • The ostium of the coronary sinus is guarded by the thebesian valve. The Right Heart The Right Heart The Right Heart • The blood passes thru the right atrium via the tricuspid valve and into the right ventricle where it is collected. • The blood leaves the right ventricle via the pulmonic valve (also a trileaflet valve) and enters the pulmonary artery. The pulmonary circulation. The Right Heart The Right Heart • The pulmonary artery bifurcates into the left and the right pulmonary arteries. • Each lobe of the lung receives a pulmonary artery which will than branch into arterioles and capillaries. • These capillaries spread over alveolar surfaces. The Right Heart PRESSURES Vena Cava 0-5 mmHg Right Atrium 2-8 mmHg Right Ventricle 15-30 mmHg 2-8 mmHg The Right Heart PRESSURES Pulmonary Artery Mean Wedge 15-30 mmHg 4-12 mmHg 9-20 mmHg 6-12 mmHg The Right Heart VALVE AREAS Tricuspid Valve Pulmonic Valve 8-11 cm2 4 cm2 The Left Heart • The sole function of the left heart is to pump blood to the body. • Blood is received via three to five pulmonary veins. • The blood enters and is collected into the left atrium. The Left Heart The Left Heart • The blood passes to thru the left atrium via the mitral valve (a semilunar valve) and into the left ventricle where it is collected. • The blood leaves the left ventricle via the aortic valve (also a trileaflet valve) and enters the aorta. The systemic circulation. The Left Heart The Left Heart The Left Heart PRESSURES Left Atrium 2-10 mmHg Left Ventricle 100-140 mmHg 3-12 mmHg Aorta 100-140 mmHg 60-90 mmHg The Left Heart RESISTANCES Pulmonary Vascular Resistance <250 dyne/sec (cm)5 Systemic Vascular Resistance 700-1600 dyne/sec (cm)5 The Left Heart VALVE AREAS Mitral Valve Aortic Valve 4-6 cm2 3-4 cm2 The Heart Stroke Volume SVI Cardiac Output CI 60 – 100 ml / beat 33-47 ml / beat / M2 4 – 6 L / min 2.5 – 4.0 L / min / M2 The Heart OXYGEN CONSUMPTION 110-150[(L/min)M sq] The Heart 30’C 8-10 ml/100g/min (contracting) 22’C 2 ml/100gm/min (fibrillating) 22’C 0.3 ml/100gm/min (asystole) One more consideration. • If you look at the heart on a cross section and examine muscle thickness, one will see that the left heart is four times as thick as the right heart. The reason for this is that the left heart does four times the work as the right heart. This manifests itself in the individual vessel pressures as a 4:1 ratio. The Heart Points of note: The right heart does not care about the left heart. The left heart does not care about the right heart. The only issue between them is that the volume of blood entering the right heart must be the volume of blood leaving the left heart. If this issue does not occur…… HEART FAILURE Heart Failure Right heart failure manifests as peripheral edema. Heart Failure Left heart failure manifests a pulmonary edema Cardiac Blood Supply The heart receives its blood supply from the coronary arteries. The coronary arteries originate at the aorta from the sinuses of Valsalva. Cardiac Blood Supply Right Coronary Artery Left Coronary Artery Cardiac Blood Supply Right Coronary Artery The blood supply to the right heart. Branches include : SA Node AV Node Posterior Descending Posterior Lateral Cardiac Blood Supply Left Coronary Artery The blood supply to the left heart. Also known as the Left Main Coronary Artery Branches include: Left Anterior Descending > Diagonal, Septal Left Circumflex >Marginal Ramus (10% of pop.) Cardiac Blood Supply EKG MANIFESTATIONS OF CAD Left Anterior Descending Coronary Artery Changes in V3 – V5 (anterior wall) Cardiac Blood Supply EKG MANIFESTATIONS OF CAD Left Circumflex Coronary Artery Changes in I and AVL (lateral wall) Cardiac Blood Supply EKG MANIFESTATIONS OF CAD Right Coronary Artery Changes in II, III, AVF (inferior/posterior wall) Cardiac Blood Supply Coronary Dominance What is it? Cardiac Blood Supply Dominance is determined by which coronary artery crosses the junction between atria and ventricles to supply the posterior descending coronary branch (posterior wall). RCA 50% LCA 20% Balanced 30% Cardiac Blood Supply Coronary perfusion is autoregulated to maintain a constant flow over a range of perfusion pressure between 50 – 120 mmHg at any given myocardial oxygen demand. Auto regulation is strictly pressure dependant and unrelated to metabolism. Cardiac Blood Supply Right ventricular oxygenation can occur during systole or diastole. Left ventricular oxygenation can only occur during diastole. (hint; tachycardia bad) Cardiac Blood Supply Autoregulation is greater in the subepicardium than the subendocardium possibly because of the transmural gradient. Thus, the subendocardium is exposed to a greater risk of a hypoxic event. The Physiology Cardiac Electrophysiology Cardiac Conduction Affected by automaticity. Affected by interactions between sympathetic and parasympathetic innervations. Affected by intracellular vs.. extracellular ionic compositions; Ca+, Na+, K+. Cardiac Electrophysiology SA Node 60 – 100 beats per minute AV Node 40 – 60 beats per minute HIS Bundle 1/10 sec conduction delay Ventricular pacing cells 15 – 40 beats/min Cardiac Electrophysiology Right Atrium SA Node Discrete Inter Nodal Pathways AV Node Communication to Bundle of His Cardiac Electrophysiology Left Atrium Bockman’s Bundle Cardiac Electrophysiology Right Ventricle Right bundle branch Cardiac Electrophysiology Left Ventricle Left Bundle Branch -Anterior Fascicle -Posterior Fascicle Cardiac Electrophysiology Cardiac Electrophysiology The Action Potential Phase 0 Phase 1 Phase 2 Phase 3 Phase 4 Cardiac Electrophysiology Cardiac Electrophysiology Phase 0 Rapid Depolarization Increased Na+ Fast Channel Cardiac Electrophysiology Phase 1 Early Rapid depolarization Na+ permeability inactivated Cell repolarization 1 msec Cardiac Electrophysiology Phase 2 Plateau Repolarization delay Increased Ca+ conductance via slow channel 100 msec Cardiac Electrophysiology Phase 3 Rapid repolarization Ca+ permeability inactivated Increased K+ permeability Cardiac Electrophysiology Phase 4 Spontaneous diastolic depolarization All nodes; SA , AV, HIS, BB’s Ca+ inward & K+ out of sacrolemma Cardiac Electrophysiology So, why is this important? Cardiac Electrophysiology DRUGS DRUGS DRUGS DRUGS AND MORE DRUGS!!!!!!!!!!!!!!!!!!!!!!!!! Cardiac Anesthesia The Cardiac Cycle The Cardiac Cycle The rhythmic beating of the heart may be divided into distinct, repetitive cycles for analyzing cardiac function. Systole Diastole Both phases require energy. The Cardiac Cycle SYSTOLE The time period when contraction and tension development occur. Begins immediately prior to mitral valve closure and ends just after aortic valve closure. The Cardiac Cycle Phases of Systole Isovolumic Contraction Ejection The Cardiac Cycle Isovolumic Contraction  Occurs when the left ventricle pressure exceeds left atrial pressure but is less than aortic pressure.  Mitral valve is closed.  Left ventricle pressure rises rapidly without change in volume. The Cardiac Cycle Ejection  Occurs when left ventricle pressure exceed aortic pressure forcing the valve to open.  A period of rapid ejection occurs in which two-thirds of the stroke volume is ejected followed by a prolong slow ejection of the remaining one-third. The Cardiac Cycle Diastole The time period when blood is entering the ventricle at varying rates preparatory to the next systole. Relaxation of the ventricular myocardium requires energy in order to reaccumulate Ca+ in the sarcoplasmic reticulum. The Cardiac Cycle Phases of Diastole Isovolumic Relaxation Rapid Filling The Cardiac Cycle     Isovolumic Relaxation Begins when left ventricular pressure falls below aortic pressure and the aortic valve closes. Ends when left ventricular pressure falls below left atrial pressure and the mitral valve opens. Ventricular volume is unchanged. Approximately 50 – 60 ms. The Cardiac Cycle Rapid Filling  Begins when the mitral valve opens. This allows a rapid inflow of blood from the left atrium. Initially, a passive filling.  Atrial systole occurs at the end of diastole. The atrium contracts. This accounts for approx 15-20% of ventricular filling. The Cardiac Cycle Systolic time occupies about 1/3 of the cycle. Diastolic time occupies about 2/3 of the cycle. The duration of systole remains constant as heart rate increase. Thus, the duration of diastole is correspondingly shortened. (hint, tachycardia bad) The Cardiac Cycle The Pressure-Volume Model The Cardiac Cycle The Cardiac Cycle The pressure-volume loop model of the heart provides a functional graphic method of evaluating global cardiac function. The approach emphasizes one cardiac cycle. The model divides the cardiac cycle into 4 phases. The Cardiac Cycle PHASE 1 Ventricular filling (A=>B)  This portion of the loop encompasses all of ventricular filling and graphically depicts the pressure-volume relationship during the diastole of one cardiac cycle. The Cardiac Cycle The Cardiac Cycle PHASE 2 Isovolumic contraction (B=>C)  This phase begins at mitral valve closure and ends with the opening of the aortic valve.  Ventricular pressure rises rapidly.  Ventricular volume remains constant. The Cardiac Cycle The Cardiac Cycle PHASE 3 Ventricular ejection (C=>D)  The entire time during which the aortic valve is open.  This includes both rapid and slow ejection periods. The Cardiac Cycle The Cardiac Cycle PHASE 4 Isovolumic relaxation (D=>A)  The aortic valve closes.  Rapidly falling left ventricular pressure.  Left atrial pressure becomes greater than left ventricular pressure.  Mitral valve opens. The Cardiac Cycle The Cardiac Cycle The stroke volume equals the end-diastolic volume minus the end-systolic volume. This is graphically represented by the width of the pressure-volume loop. The ejection fraction equals the stroke volume divided by the end-diastolic. Cardiac Performance Initial studies were done using isolated stripes of cardiac papillary muscle. Cardiac Performance Determinants of cardiac performance     Preload Afterload Contractility Heart rhythm & rate Cardiac Performance PRELOAD Defined: The initial stretch (diastolic length) of muscle before contraction.  Best defined as the end-diastolic volume Cardiac Performance AFTERLOAD Defined: The force opposed contraction but has no effect until contraction begins.  A force that resists or impedes the flow of blood. Cardiac Performance CONTRACTILITY Defined: The intrinsic strength of the heart muscle.  Compliance; the ratio of change in volume to change in pressure (stiffness).  Elastance; the ration of change in pressure to change in volume. Cardiac Performance HEART RHYTHM & RATE Not depicted in pressure-volume loops. However, must be known prior to utilizing a pressure-volume loop. Invasive Monitoring Invasive Monitoring Pulmonary Artery Catheters Peripheral Artery Catheters Transesophageal Echocardiography Pulmonary Artery Catheters • Goals • Benefits • Risks Pulmonary Artery Catheter GOALS CONTROL Pulmonary Artery Catheter THE PRINICPLE Pulmonary Artery Catheter BENEFITS The PAC is an important monitor of ventricular function. The PAC is useful when large volume shifts are expected to occur intraoperatively and these volume shifts may be expected to adversely affect cardiac function. Pulmonary Artery Catheter BENEFITS A PAC will allow the patient’s preload to be optimized. Pulmonary Artery Catheter Pulmonary Artery Catheter Most procedures in patients with ischemic heart disease DO NOT REQUIRE a pulmonary artery catheter. Pulmonary Artery Catheter     RISKS Carotid Artery Injury Subclavian Artery Injury Hematoma Hemothorax Pulmonary Artery Catheter RISKS       Chylothorax Mediastinal Effusion Pleural Effusion Pneumothorax Brachial Plexus Nerve Injury Stellate Ganglion Injury Pulmonary Artery Catheter RISKS       Air Emboli Catheter Shearing Emboli Vena Cava Perforation Cardiac Perforation Cardiac Dysrhythmias Cardiac Conduction Block Pulmonary Artery Catheter       RISKS Tricuspid Valve Injury Pulmonic Valve Injury PAC Knotting Thromboembolism Thrombosis Endocarditis Pulmonary Artery Catheter RISKS     Sepsis Pulmonary Artery Rupture Pulmonary Infarction Etc………………………….. Pulmonary Artery Catheter PAC’s will show : Central Venous Pressures (systolic & diastolic) Pulmonary Artery Pressures (systolic & diastolic) Pulmonary Artery Occlusion Pressure Core Temperatures Thermodilution Cardiac Outputs Pulmonary Artery Catheter Accuracy??? The left heart pressure can be reflected by floating a flexible catheter into the pulmonary artery and using a balloon to occlude pulmonary artery pressure. Pulmonary Artery Catheter Pulmonary Artery Catheter YES, but you are making assumptions! Pulmonary Artery Catheter CVP  RAP Influenced by: Total blood volume Transfusions/ fluid infusions Vasopressor administration Increased peritoneal pressures Pulmonary artery hypertension COPD Pericarditis Catheter misdirection Venous blood volume Cardiac insufficiency/failure Increased intrathoracic pressures Pulmonary emboli Superior vena cava syndrome Pericardial tamponade Cor pulmonale Tricuspid valve incompetence Pulmonary Artery Catheter RAP  RVEDP Influenced by: RV dysfunction Tricuspid valve abnormalities Pulmonary valve abnormalities Compliance changes via external forces Pulmonary hypertension Pulmonary Artery Catheter RVEDP  PAEDP Influenced by: Pulmonary valve abnormalities Left ventricular septum Pulmonary hypertension/vascular resistance Compliance changes via external forces RV dysfunction, infarct Tachycardia (>120) Hypervolemia Pulmonary Artery Catheter PAEDP  PAOP Influenced by: Pulmonary vascular resistance Hypoxemia Emboli Lung zone Airway pressures Pulmonary Artery Pressure PAOP  LAP Influenced by: Airway pressures Peep Lung zone Pulmonary hypertension Pulmonary Artery Catheter LAP  LVEDP Influenced by: Mitral valve stenosis Premature valve closure Left atrial enlargement LV volume overload (AV insuff) Heart rate (tachycardia) Thrombus Mitral valve insufficiency Mitral valve prosthesis Reduced LV compliance Left atrial enlargement Heart rhythm Left atrial myxoma Pulmonary Artery Catheter LVEDP  LVEDV Influenced by: LV compliance Aortic valve stenosis LV filling LV wall thickness Myocardial composition RV dilation LV Function Aortic valve insufficiency LV volume Abnormal LV relaxation (ischemia) External ventricular compression Therapeutic interventions Pulmonary Artery Catheter LVEDV = Preload = LV Performance Thus, as shown, there are a lot of factors that can have an effect on values obtained from pulmonary artery catheterization! Yet, we still do it. Peripheral Artery Catheter • Goals • Benefits • Risks Peripheral Artery Catheter GOALS CONTROL Peripheral Artery Catheter BENEFIT Indicated for hemodynamic monitoring in patients where beat to beat visual arterial pressure wave and numerical pressure display enables prompt identification of trends or changes in blood pressure that could be potentially missed with noninvasive monitoring. Peripheral Artery Catheter BENEFIT Frequent blood sampling available in patients who are critically ill or are undergoing major surgery without having to expose the patient to multiple needle sticks for blood draws. Peripheral Artery Catheter       RISKS Arterial thrombosis Hemorrhage Air embolism Infection Hematoma Catheter embolism Peripheral Artery Catheter     RISKS HAND ISCHEMIA FOOT ISCHEMIA ARM ISCHEMIA LEG ISCHEMIA (depends on the site) Peripheral Artery Catheter SITES Radial artery Femoral artery Brachial artery Axillary artery Dorsalis pedis artery Ulnar artery Transesophageal Echocardiography • Goals • Benefits • Risks Transesophageal Echocardiography GOALS Transesophageal Echocardiography CONTROL Transesophageal Echocardiography A TEE provides a direct visual image of the heart, its valves, and its chambers. It will allow a REAL TIME VISUALIZATION as to the structure and function of the heart. Transesophageal Echocardiography Transesophageal Echocardiography BENEFIT Echocardiography evaluations focus on the functional outcome of coronary artery disease. i.e.: systolic wall thickening valvular competency ejection fraction Transesophageal Echocardiography BENEFIT Echocardiography offers a detailed functional assessment of segmental and global right ventricular and left ventricular function. Transesophageal Echocardiography BENEFIT Echocardiography allows diagnosis of acute myocardial events thru direct visualization. Late diagnosis Ekg findings; ectopy, rhythm changes ST monitoring Invasive monitors; PA cath, CVP, A-line Labs Transesophageal Echocardiography RISKS • • • • • • Dental trauma Esophageal trauma or perforation Bleeding Aspiration Dislodgement of ET tube Displacement of NG tube Transesophageal Echocardiography RISKS Mortality is less than 1 : 10,000 patients Transesophageal Echocardiography INTRAOPERATIVE USES Access cardiac function, both natural & prosthetic. Detect global & regional wall motion abnormalities. Detect interatrial & interventricular shunts. Measure atrial & ventricular size & ventricular preload Transesophageal Echocardiography INTRAOPERATIVE USES Detect atrial or ventricular masses or air. Detect pericardial effusions & cardiac tamponade. Examine the aorta for dissections, intimal irregularities, or friable plaques. Examine coronary flow distribution using specialize contrast techniques. FLOW VOLUME LOOPS FLOW VOLUME LOOPS MITRAL STENOSIS MITRAL REGURGITATION MITRAL VALVE PROLAPSE AORTIC STENOSIS AORTIC REGURGITATION Flow Volume Loops MITRAL STENOSIS Normal mitral valve area = 4 – 6 cm2  Moderate stenosis = 2 cm2  Severe stenosis = 1 cm2  Critical stenosis = 0.5 cm2 (25 mmHg) (50 mmHg) Flow Volume Loops MITRAL STENOSIS Etiology  Rheumatic fever 50%  Congenital  Carcinoid syndrome stenotic fibrous plaque  female to male preponderance 4:1 Flow Volume Loops MITRAL STENOSIS History  Asymptomatic x 20 yr  S/S 4th – 5th decade of life • acute CHF • paroxysmal atrial fib • pulmonary hypertension Flow Volume Loops MITRAL STENOSIS Goals      Preload Afterload Contractility Heart Rate PVR increase neutral neutral/increase decrease neutral/decrease Flow Volume Loops MITRAL STENOSIS Goals  Avoid atrial fib why????????????????? Flow Volume Loops MITRAL STENOSIS  The atrial kick provides up to 40% of your cardiac output. Flow Volume Loops MITRAL STENOSIS Flow Volume Loops MITRAL REGURGITATION Etiology  Disease of the valve leaflets alone.  Abnormalities of the papillary muscles.  Abnormalities of the cordae tendineae. Flow Volume Loops MITRAL REGURGITATION Causes:      Rheumatic disease Bacterial endocarditis Congenital abnormalities, i.e.; mvp Connective disorder Direct penetrating trauma Flow Volume Loops MITRAL REGURGITATION Causes:  Any disorder producing left ventricular dilation  Acute myocardial infarction cordae tendineae rupture  Papillary muscle dysfunction  ischemia Flow Volume Loops MITRAL REGURGITATION History: Acute vs.. Chronic Flow Volume Loops MITRAL REGURGITATION Acute  Fulminant pulmonary edema Flow Volume Loops MITRAL REGURGITATION Chronic  Asymptomatic 30 – 40 years.  Fatigue  Congestive heart failure (late) Flow Volume Loops MITRAL REGURGITATION When CHF signs and symptoms appear, the 5 years mortality is 50%.  Risks include a-fib, systemic emboli, & bacterial endocarditis.  The left atrium becomes massively dilated and compliant. Flow Volume Loops MITRAL REGURGITATION Goals;      Preload Afterload Contractility Heart Rate PVR increase decrease neutral/increase neutral/increase neutral/decrease Flow Volume Loops MITRAL REGURGITATION Flow Volume Loops MITRAL VALVE PROLAPSE An abnormal bulging of the mitral valve into the left atrium during systole. 10% incidence in the general population with 2:1 female preponderance. Flow Volume Loops MITRAL VALVE PROLAPSE Primary MVP is a structural abnormality  Chordae tendineae elongated  Redundant mitral leaflets Associated with marfan’s syndrome and other connective tissue diseases Flow Volume Loops MITRAL VALVE PROLAPSE Secondary MVP indicates an extravalvular cause  Distortion of ventricular geometry  Alteration in LV contraction pattern • Ischemia • Cardiomyopathy • Ventricular aneurysm Flow Volume Loops MITRAL VALVE PROLAPSE 15% go on to develop mitral insufficiency Flow Volume Loops MITRAL VALVE PROLAPSE Complications     Arrhythmia, SVT being the most common Systemic emboli Infective endocarditis Ruptured chordae tendineae  frank mitral regurgitation Flow Volume Loops MITRAL VALVE PROLAPSE Clinical Presentation  Majority are asymptomatic  Vague symptoms • Atypical chest pain • Fatigue • Light headedness Flow Volume Loops MITRAL VALVE PROLAPSE Goals  Preload increase  Afterload decrease  Contractility neutral  Heart Rate neutral/increase  PVR neutral Flow Volume Loops MITRAL VALVE PROLAPSE Flow Volume Loops AORTIC STENOSIS Normal Valve Area = 3-4cm2  Moderate stenosis 0.7-1.2cm2  Severe stenosis < 0.7cm2  Critical stenosis < 0.4cm2 50mmHg gradient Flow Volume Loops AORTIC STENOSIS Isolated aortic stenosis is the most common valvular abnormality Flow Volume Loops AORTIC STENOSIS Etiology  Congenital • Unicuspid • Bicuspid (50%) • Tricuspid  Acquired • Calcification of the valve Flow Volume Loops AORTIC STENOSIS History  Asymptomatic 50 years 4% incidence of sudden death  Angina 5 years to death  Syncope 3 years to death  CHF 2 years to death Flow Volume Loops AORTIC STENOSIS Goals      Preload Afterload Contractility Heart Rate PVR increase neutral/increase neutral/increase neutral/decrease neutral Flow Volume Loops AORTIC STENOSIS Flow Volume Loops AORTIC INSUFFICIENCY Etiology  Congenital  Acquired Flow Volume Loops AORTIC INSUFFICIENCY Congenital  Rarely an isolated lesion  Usually associated with other cardiac abnormalities Flow Volume Loops AORTIC INSUFFICIENCY Acquired       Rheumatic heart disease Endocarditis Aortic root dissection Cystic medionecrosis Takayasu’s disease Giant cell arteritis Flow Volume Loops AORTIC INSUFFICIENCY History  Usually occurs in the 4th – 5th decade of life.  Long (7-10 years) asymptomatic period during which the left ventricle undergoes progressive eccentric enlargement.  Then, CHF, angina, widen pulse pressure, decreased diastolic pressure. Flow Volume Loops AORTIC INSUFFICIENCY History  Acute aortic insufficiency  sudden left ventricular failure with both pulmonary congestion & systemic hypotension. • Usually lethal Flow Volume Loops AORTIC INSUFFICIENCY If patient presents with ;  LV enlargement  LVH on EKG  Large pulse pressure Flow Volume Loops AORTIC INSUFFICIENCY Then;     33% chance of CHF, angina, or death in 1 year 50% chance of CHF, angina, or death in 2 years 87% chance of CHF, angina, or death in 6 years 100% chance of CHF, angina, or death in 10 yrs if just 2 of these signs & symptoms Flow Volume Loops AORTIC INSUFFICIENCY Goals;      Preload Afterload Contractility Heart Rate PVR increase neutral/decrease neutral/increase neutral/increase neutral Flow Volume Loops AORTIC INSUFFICIENCY The Holy Grail BLOOD PRESSURE IS THE SECRET TO SUCCESS The Holy Grail B/P = CO x SVR The Holy Grail CO = HR x SV The Holy Grail B/P = HR x SV x SVR The Holy Grail SV  contractility SV  preload The Holy Grail SVR  tone SVR  viscosity The Holy Grail Now, what does this mean???????? The Holy Grail CONTROL The Holy Grail B/P = HR x SV x SVR HR  pace SV  contractility  beta receptors SV  preload  volume SVR  tone  alpha receptors SVR  viscosity  temperature Rx Therapy How ??????? Rx Therapy Increase beta agonist pacemaker vagolytic rx HEART RATE Decrease beta blocker diltiazem Rx Therapy CONTRACTILITY Increase Increase calcium theophylline amirone dopamine milarone norepinephrine dobutamine epinephrine digoxin glucagon Rx Therapy CONTRACTILITY Decrease halothane enflurane beta blocker Rx Therapy Increase volume tone PRELOAD Decrease diuresis vasodilate take blood off Rx Therapy SVRtone Increase Decrease epinephrine nitrates norepinephrine propofol phenylephrine hydralazine alpha agonist alpha antagonist ace inhibitor Rx Therapy Increase temperature colloid SVR  viscosity Decrease temperature crystalloid plasmaphoresis Rx Therapy Increase N2O PVR Decrease NO PGE2 PGI2 adenosine isopril nipride prostacylin priscolene phentolamine nitroglycerine Preoperative Evaluation Preoperative Evaluation There is nothing worse than a surprise!!! Preoperative Evaluation Why do we do coronary artery bypass surgery? Why do we do cardiac valve surgery? Why do we do aortic repair surgery? Preoperative Evaluation Because people do not want to die!!!!! Preoperative Evaluation What are the indications for cardiac surgery? Preoperative Evaluation Indications for cardiac surgery Symptomatic coronary artery disease unresponsive to medications or interventional cardiac therapies.  Myocardial Ischemia Preoperative Evaluation Indications for cardiac surgery Attempts to salvage stunned myocardium after an acute cardiac ischemic event. Preoperative Evaluation Indications for cardiac surgery Attempts to improve depressed myocardial function in patients with symptomatic decreased cardiac output syndromes.  Hibernating Myocardium Myocardial Ischemia:  A manifestation of the myocardial oxygen supply-demand imbalance.  Acute ischemic events are probably due to acute plaque disruption with subsequent thrombosis or spasm.  Chronic ischemic events are manifest as “classic angina” with exertional oxygen demand greater than oxygen supply. Of note; EKG changes associated with myocardial ischemia:  Subendocardial ischemia is associated with ST segment depression.  Transmural ischemia is associated with ST segment elevation. Myocardial infarction is never good regardless of where in the heart it occurs. Sudden cardiac death is generally associated with ischemia –induced arrhythmias. Stunned Myocardium:  An acute interruption of the coronary blood flow to the myocardium followed by a reperfusion of the coronary blood flow.  The cardiac muscle cell is injured but it has not died and recovery can occur with the proper support. [CABG,Rx,IABP] Hibernating Myocardium:  Chronic depression of the myocardium via a reduction in myocardial blood flow through stenotic coronary arteries.  The cardiac muscle cell receives only enough oxygen and nutrients to maintain a basal existence.  The cardiac muscle cell function is rapidly improved when the blood flow increases. Preoperative Evaluation The two risk factors identified to predict perioperative cardiac morbidity are recent myocardial infarction and the presence of congestive heart failure. Basics of Anesthesia, 4th ed. Stoelting & Miller p.248 Preoperative Evaluation  Of the adult patients who undergo surgery annually in the United States, it is estimated that 40% will either have or be at risk for coronary artery disease.  The presence of coronary artery disease in patients who undergo anesthesia for noncardiac surgery may be associated with increased morbidity and mortality. Basics of anesthesia, 4th ed Stoelting & Miller, p.248 Preoperative Evaluation Indications for valvular surgery When the patient is no longer stable with medical management of the valvular disease. When the risks outweigh the benefits of the valvular disease with worsening cardiopulmonary function . Preoperative Evaluation Indications for valvular surgery When the valvular disease has a greater risk to life than coexisting medical diseases. Preoperative Evaluation Indications for thoracic aneurysm surgery Acute injury; As a lifesaving procedure. Preoperative Evaluation Indications for thoracic aneurysm surgery Nonacute aneurysm; Judgmental with many considerations. What is the coexisting diseases? Location? Smaller is easier to repair. Rate of aneurysm expansion. Preoperative Assessment History Physical Examination Laboratory Studies Radiographic Studies Cardiac studies Preoperative Assessment HISTORY History of Presenting Illness Allergies Current medications Past Medical History Past Surgical History Family Anesthesia History Preoperative Assessment HISTORY Review of Systems      HEENT Cardiovascular Pulmonary Exercise tolerance Gastrointestinal Preoperative Assessment HISTORY Review of Systems      Urological Gynecological Endocrine Musculosketal Hematological Preoperative Assessment HISTORY Review of Systems  Neurological  Psychiatric  Pediatric Preoperative Assessment HISTORY Social  Tobacco  EtOH  Drugs Preoperative Assessment PHYSICAL EXAM Orientation Vital Sign’s Accurate Ht & Wt HEENT Chest Line sites Preoperative Assessment Why an accurate height & weight? Preoperative Assessment Drug dosages! BSA [(Ht x Wt)/3600]-2  to calculate indexes Preoperative Assessment LAB STUDIES CBC PT/PTT LYTES BUN/CREAT Type & Cross U/A [no universal agreement] Preoperative Assessment LAB STUDIES Cardiac Enzymes Rx levels Preoperative Assessment X-RAY STUDIES CXR Coronary Angiographies Dipyridamole Thallium Imaging Preoperative Assessment CARDIAC STUDIES EKG Holter Monitoring Echocardiography Stress Test Cardiopulmonary Bypass Why we are here!!! Cardiopulmonary Bypass GOALS To safely get the patient on to cardiopulmonary bypass. To safely get the patient off of cardiopulmonary bypass. Easy, huh? Cardiopulmonary Bypass STAGES OF THE SURGERY Preoperative Period Line Placement Induction Invasive Monitors Incision Sternal Splitting Pericardial Opening Cardiopulmonary Bypass STAGES OF SURGERY Vessel Harvesting Aortic Cannulation Venous Cannulation Cardiopulmonary Bypass Separation From Cardiopulmonary Bypass Protamine Cardiopulmonary Bypass STAGES OF SURGERY Removal of Cannulae Inspection for Bleeding Sternal Closure “Finished” Leaving the Operating Room Arrival into the ICU Cardiopulmonary Bypass PREOPERATIVE PERIOD Operating room preparation Patient evaluation Communication with surgeon Communication with perfusionist Anticipation Cardiopulmonary Bypass PREOPERATIVE PERIOD Patient preoperative medication requirements Patient transportation to the operating room Cardiopulmonary Bypass LINE PLACEMENT Venous access  Peripheral lines  Central lines Arterial access  Radial line  Femoral line All of this while avoiding ischemia.  How? Talk to the patient Use local anesthesia Supplemental oxygen Sedation as necessary Cardiac drugs as necessary And, be good at what you do!!!!!!!!!!!!!!!!!! Cardiopulmonary Bypass INDUCTION Monitors are placed Patient is masked preoxygenated Induce to a state of unconsciousness to take over the airway and maintain vitals Deepen the anesthesia to allow laryngoscopy & intubation while maintaining hemodynamic stability Cardiopulmonary Bypass INDUCTION This is a very dangerous period! Intubation can be associated with tachycardia and hypertension. This can lead to myocardial ischemia or arrhythmia which must be avoided. Slow & deliberate is the secret to success. Cardiopulmonary Bypass INVASIVE MONITORS Placement of additional peripheral lines. Placement of pulmonary artery catheter. Placement of any central venous access lines. Placement of transesophageal echocardiography probe. Cardiopulmonary Bypass The goal of anesthetic management in the precardiopulmonary bypass period is to achieve cardiopulmonary bypass with minimal hemodynamic variability Cardiopulmonary Bypass INCISION Incision can lead to a sympathetic response from which the patient must be protected. How?? Cardiopulmonary Bypass Drugs!!!!!!!!!!!     Narcotics Nitrates Beta blockers Volatile agents Cardiopulmonary Bypass STERNAL SPLITTING Avoid sympathetic response. Lungs down. Cardiopulmonary Bypass PERICARDIAL OPENING Risk of sympathetic response. Risk of vagal response. Cardiopulmonary Bypass PERICARDIAL OPENING Take the time to directly visualize the heart.  Observe movement; vigorous vs. sluggish  Observe size; enlarged vs. expected  Observe for aneurysms. Remember what you see!!!!!!!!! Cardiopulmonary Bypass VESSEL HARVESTING Vein grafts  Legs  Arms Arterial grafts  Internal mammary artery  Gastroepiploic artery  Radial artery Cardiopulmonary Bypass VESSEL HARVESTING Beware of papaverine administration by the surgeon on the field. Why? Cardiopulmonary Bypass VESSEL HARVESTING Hypotension Cardiopulmonary Bypass AORTIC CANNULATION Heparinization prior to placement of cannulae.  Done on field by surgeon via right atrial appendage. OR  Done via central line by anesthesiologist. Goal is Activated Clotting Time (ACT) greater than 400/480sec. (controversy) Cardiopulmonary Bypass AORTIC CANNULATION Sites:  Ascending aorta below innominate artery  Femoral artery  Axillary artery Avoid hypertension during cannulation. TEE can help find a safe cannulation site. Cardiopulmonary Bypass VENOUS CANNULATION Single cannula into the right atrial appendage. OR Double cannula into the right atrium & a vena cava. Patients are very sensitive to atrial manipulation. Cardiopulmonary Bypass VENOUS CANNULATION Risk of hypotension. Risk of arrhythmia. Cardiopulmonary Bypass INITIATION OF CPB Risk of hypotension from hypovolemia as the transition occurs. Turn off ventilator & disconnect expiratory limb to avoid inadvertant lung inflation. Pull PA catheter back 1-2cm. Turn TEE probe off. Cardiopulmonary Bypass CPB Assist the perfusionist. Monitor urine output. Monitor for electrical activity. Catch up on your paperwork. Cardiopulmonary Bypass Cardiopulmonary Bypass SEPARATION FROM CPB Inflate lungs & return patient to ventilator Pacemaker check Zero invasive monitors Check labs Cardiopulmonary Bypass SEPARATION FROM CPB Rate & rhythm Volume More Volume Rx IABP Ventricular Assist Devices Cardiopulmonary Bypass SEPARATION FROM CPB Goal is a cardiac index > 2.0 If index is > 2.0, life is good. If index is < 2.0, life sucks!!! Cardiopulmonary Bypass IABP Intra Aortic Balloon Counter Pulsation Indication: acute cardiac failure refractory to pharmacological intervention. Hemodynamic effects:  Peak aortic systolic pressure falls 10-15%  Can increase intra aortic diastolic pressure 70%  PAOP falls 10-15% Cardiopulmonary Bypass IABP Coronary blood flow effects ??? IABP will reduce myocardial oxygen demand. Conclusion: Refractory post-cardiotomy cardiogenic shock survival rate is 52-66% with IABP & maximal medical support. Cardiopulmonary Bypass VENTRICULAR ASSIST DEVICES Left Ventricular Assist Devices Right Ventricular Assist Devices Designed to replace a failed ventricle Capable of sustaining life while the heart recovers from reversible injury or until a donor heart can be obtained. Cardiopulmonary Bypass PROTAMINE Once the patient has been successfully weaned from CPB and is hemodynamically stable, it is time to reverse the heparin. The surgeon must be in agreement and the perfusionist must be aware. A protamine dose is decided upon. Cardiopulmonary Bypass PROTAMINE A test dose of protamine is given. Why? Cardiopulmonary Bypass PROTAMINE RISK  Protamine might have no hemodynamic effect.  There might be direct systemic vasodilatation.  There may be an anaphylactic reaction. OR Cardiopulmonary Bypass PROTAMINE Catastrophic pulmonary vasoconstriction  PA pressure increases  CVP increases  RV dilates  LV preload decreases  ABP decreases Cardiopulmonary Bypass PROTAMINE Treatment: Stop protamine Administer epinephrine Return to bypass if no immediate improvement Rxn is generally 5-10 min if properly tx’d Cardiopulmonary Bypass REMOVAL OF CANNULAE Atrial cannulae first.  Bleeding controlled  Arrhythmia risk Aortic cannulae second.  Remainder of pump volume infused  Surgeon will ask for temporary hypotension  Head of bed down. Cardiopulmonary Bypass INSPECTION FOR BLEEDING Final inspection before chest is closed. Bleeding can cause cardiac tamponade. Additional protamine as indicated. FFP, Cyro, Plts as indicated. Anastomoses are checked. Cardiopulmonary Bypass INSPECTION FOR BLEEDING Heart may be lifted!  Arrhythmias  Hypotension Cardiopulmonary Bypass STERNAL CLOSURE The chest is closed. Cardiac index is obtained.  > 2.0 is ideal TEE study performed looking for any changes. RWMA  Risk of graft kink. Cardiopulmonary Bypass FINISHED Dressings are placed. TEE probe removed. Pt monitors transferred to a transport monitor. Cardiopulmonary Bypass LEAVING THE OR Transport monitors in place. Emergency drugs available. Emergency airway equipment available. Patient switched to a transport vent. Patient leaves the OR. Now perfusion & instruments may be taken down. Cardiopulmonary Bypass THE ICU Patient to ventilator. Patient to monitors. Report to nurse. Report to physician. Watch chest tubes for bleeding. Cardiopulmonary Bypass RECOVERY PERIOD 3 – 8 % of patients return to OR for reoperation      Excessive bleeding Cardiac tamponade IABP placement or removal Acute myocardial ischemia Cardiac failure without identifiable etiology Cardiopulmonary Bypass QED A final thought……… “THE MIND CAN ONLY ABSORB WHAT THE GLUTEAL MUSCLES CAN TOLERATE”