Anesthetic Considerations for Diastolic Dysfunction

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Presentation transcript:

Anesthetic Considerations for Diastolic Dysfunction Suneel.P.R Associate Professor SCTIMST Trivandrum

Dysfunction: systolic vs. diastolic Systolic function is intuitively meaningful Diastology is a relative newcomer

Diastolic damages Nearly 50% of all cardiac failures Prognosis and mortality same as systolic Mortality is four times when compared with normal population

Diastolic heart failure The Ejection Fraction will be normal Called Heart failure with normal EF (HFnlEF) Diastolic dysfunction can occur along with systolic dysfunction

Diastology When does diastole begin ? Anatomical -when aortic valve closes Molecular level- dissociation of the actin- myosin cross-bridges The heart begins the relaxation process in systole !!

Relaxation-requires energy BJA 98 (6): 707–21 (2007

Diastolic dysfunction definition Inability of the ventricles to fill at low pressure The end-diastolic pressure is 16-26 mm Hg (normal EDP is < 12 mm Hg) The atrial pressures that are needed to complete filling are even higher

Pathophysiology- two key terms Increased filling pressures are due to Abnormality of relaxation Decreased compliance

Physiology: The stages Isovolumic relaxation Rapid filling Diastasis Atrial contraction

Physiology

Isovolumetric relaxation AoVC MVO

Isovolumetric contraction Occurs between two closed valves Active relaxation occurs during this time The ventricular pressures continue to fall Mitral valve opening creates “suction effect”

Physiology

Rapid filling phase

Diastasis

Atrial “kick”

Active diastolic dysfunction Abnormality of relaxation Failure of energy dependent part of diastole Myocardial ischemia Hypertension Aortic stenosis Hypertrophic cardiomyopathy

Passive diastolic dysfunction Increase in chamber stiffness Infiltrative disorders ( amyloidosis) Myocardial fibrosis Progression from impaired relaxation

Physiology End systole End Diastole

Physiology

Impaired relaxation

Diagnosis of diastolic dysfunction Echocardiography

Transmitral Pulse Wave Doppler

Transmitral Pulse Wave Doppler

Stage I of diastolic dysfunction Impaired relaxation

Stage II diastolic dysfunction Pseudonormalization

Stage III of diastolic dysfunction Restrictive filling

Improvement to a worse grade Tachycardia Loss of atrial contraction Volume excess

Improvement to a milder grade Reduction in preload Reverse Trendelenburg Diuresis Amyl nitrate inhalation Valsalva maneuver Relief of tachycardia Return from AF to Sinus

Stage IV diastolic dysfunction Irreversible restrictive filling pattern

Pulmonary venous Doppler

Pulmonary venous Doppler

Pulomnary venous Doppler Impaired relaxation D wave decreases in size S/D ratio >1 Pseudonormal and Restrictive filling Increase in D S/D < 1 Increase in A wave duration

Other echocardiographic tools Tissue Doppler imaging to assess mitral annular movement Color M mode of the Mitral valve to assess the propagation velocity

Diastolic dysfunction vs. failure Dysfunction is a physiologic or preclinical state Abnormal relaxation and increased chamber stiffness compensated by increased LAP The LV preload is maintained When these mechanisms are stressed, diastolic heart failure ensues

Braunwald 8th edition

Diastolic heart failure Definite C/F of heart failure Within72 hours Echo evidence of normal LVEF Echo evidence of diastolic dysfunction

Most likely diastolic heart failure SBP >160 mm Hg DBP> 100 mm Hg Concentric LVH Worsened by Tachycardia Volume bolus Improved by Reducing HR Restoring sinus rhythm

When to suspect diastolic dysfunction History of previous diastolic heart failure Age > 70 years Female sex Uncontrolled hypertension Myocardial ischemia Diabetes mellitus Comorbidities: Obesity, renal failure

Echo Specifically documented If not then, look for LVH –absence does not rule out! LA enlargement RV enlargement Pulmonary hypertension

Perioperative worsening Deterioration in diastolic dysfunction Myocardial ischemia Directly affects relaxation Induces rhythm disturbances Hypovolemia Tachycardia Rhythms other than sinus

Perioperative worsening Shivering Anemia Hypoxia Electrolyte imbalances

Perioperative worsening Post-op sympathetic stimulation Post-op hypertensive crisis

Periop-risks Delayed weaning from mechanical ventilation Difficulty weaning from CPB More use of vasoactive agents Prolonged ICU stay & mortality

Conducting the anesthetic Pre-operative evaluation Functional status & exercise tolerance Optimizing the perioperative drugs

Perioperative drugs Diuretics Beta blockers, calcium channel blockers ACEI & ARBs Statins Antiplatlets

Monitoring - Major surgeries Standard monitoring tools Invasive arterial pressures Monitoring volume status is important Central venous pressures or Pulmonary artery catheter or TEE ?

GA or Regional No definite recommendation either way Epidural vs. spinal ? Epidural wins

General anesthesia IV induction & maintained with volatile agents and opioids Greater hemodynamic instability

General anesthesia Good induction practices Consideration for age Titrate to effect Smooth take over from spontaneous-bag mask Hpoxia, hypercarbia worsens PHT

GA-control of BP Systolic BP within 20 % of baseline Maintain diastolic BP Keep pulse pressure < DBP

Control of BP Rule of the 70s Age >70 years Pulse rate around 70s DBP >70 Pulse pressure < 70

Drug combination for hemodynamics Low dose nitroglycerin and titrated phenylephrine Either agent alone can worsen the hemodynamics

Nitroglycerine + Titrated phenylephrine Preserves vascular distensibility Avoids reduction in preload Maintains coronary perfusion pressure Maintains stroke volume with minimal cardiac work

Management of hypertensive crisis Sound anesthetic practices Plan for post-op analgesia Prevention of shivering Intravenous calcium channel blocker IV nitroglycerin

Post-op diastolic heart failure Reduce preload Diuretics Use of nitrates CPAP Use of adrenaline, dobutamine, dopamine

Specific drugs for diastole Milrinone Phosphodiesterase III inhibitor Inotropic, vasodilatory with minimal chronotropy Increases calcium ion uptake to SR

Milrinone Lusitropic effect more evident in heart failure Bolus dose of 50µgm/Kg over 60 minutes Infusion of 0.5 to 0.75µgm/Kg/min

Specific drugs for diastole Levosimendan Sensitizes the contractile elements to calcium Has a vasodilator effect Improves both systolic and diastolic function

Thank you