Pulmonary Hypertension - Anesthesiologist's view

Pulmonary Hypertension Anesthesiologist's View : 

Pulmonary Hypertension Anesthesiologist's View Dr.J.Rajesh,D.A.,DNB., Anesthesiologist - Pain & Palliative care Physician Meenakshi Mission Hospital & Research Centre Madurai

Basics : 

Basics Pulmonary circulation Walls of PA & large branches are 30% as thick as aorta Small arterial vessels – small endothelial tubes with little muscle in wall Post capillary vessels – smooth muscles +

Pressures : 

Pressures

Definition : 

Definition Progressive increase in mean pulmonary arterial pressure (PAP) >25mmHg at rest or 30mmHg during exercise PAP > 30/15 mmHg Estimated PA systolic pressure >½ systemic systolic pressure

Classification : 

Classification Primary Secondary

Classification : 

Classification Pulmonary arterial HTN Primary pulm HTN (sporadic, familial) Pulm arterial HTN (related to collagen vascular disease- scleroderma, lupus, RA) Congenital systemic-to-pulmonary shunts (Eisenmenger syndrome), Porto pulmonary HTN HIV, drugs, toxins Pulmonary HTN associated with disorders of respiratory system and/or hypoxemia Parenchymal lung disease (COPD, interstitial pulmonary fibrosis) Chronic alveolar hypoxemia (exposure to long-term low oxygen tension such as in high altitudes)

Classification : 

Classification Pulmonary venous HTN Mitral valve disease Chronic LV dysfunction Pulm veno occlusion disease Pulmonary HTN due to chronic thrombotic and/or embolic disease Thromboembolic obstruction of prox pulm arteries Obstruction of distal pulm arteries Pulmonary HTN due to disorders directly affecting the pulm vasculature Inflammatory Pulm capillary hemangiomatosis

Haemodynamic profiles : 

Haemodynamic profiles Pre capillary Pulmonary Hypertension Post capillary Pulmonary Hypertension Mixed Selective or Nonselective increase in Pulmonary blood flow

Calculations : 

Calculations PBF = (MPAP-MPCWP)/ PVR MPAP = PVR X PBF + MPCWP PBF – liters per minute MPCWP , MPAP– mm of Hg PVR - Dynes per sec per 5 cm

Pathology : 

Pathology Muscularization of terminal portion of pulmonary arterial vasculature due to SMC hyperplasia Elevation of pulmonary pressure → Medial hypertrophy & Intimal fibrosis Morphological changes in vasculature are due to reactivity of vessels to high pressure Changes are variable

Pathophysiology : 

Pathophysiology Acute  RV afterload ( Sudden & severe)  EDV  EF of RV SV of RV

Chronic : 

Chronic Progressive systolic pressure overload of RV RV dilates and hypertrophies - gradual RV dysfunction venous return compromises RV preload and pulmonary blood flow - results from positive intrathoracic pressure (ex. PEEP) which also causes alveolar overdistension which PVR and  pulm blood flow

Chronic PHTN : 

Chronic PHTN Paradoxical movement of IVS due to raised RV pressure LV compression due to septal bowing Impaired left ventricular filling Low cardiac output state Reduced arterial pressure Reduced coronary blood flow to RV

Pathophysiologic mechanics in Secondary PHTN : 

Pathophysiologic mechanics in Secondary PHTN Hypoxic vasoconstriction Decreased area of pulmonary vascular bed Volume/Pressure overload

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Abnormally high BP in pulmonary arteries Increased pressure damages large and small pulmonary arteries Blood vessel walls thicken Cannot transfer oxygen and carbon dioxide normally Levels of oxygen in blood fall Constriction of pulmonary arteries Further increase in pressure in pulmonary circulation

Pathophysiology : 

Pathophysiology PVR limits RV SV and the volume for LV filling LV compressed by intraventricular septum during systole  LV volume/filling CO/BP BP leads to coronary perfusion which can lead to myocardial ischemia/R sided failure

Pathophysiology : 

Pathophysiology Coronary blood flow to RV usually occurs during diastole and systole Decreased if RV pressures are equal to or higher than systemic pressures Hypoxemia from CO/pulm blood flow or from R to L intracardiac shunt (if RA pressures higher than LA)

Etiology - Pediatrics : 

Etiology - Pediatrics Persistent pulm htn of the newborn: meconium, RDS, pneumonia, sepsis, severe hypoxia Congenital cardiac lesions: L to R shunt Post cardiac surgery (CPB induces a pulmonary inflammatory response) Chronic lung disease (2º Pulm HTN) Idiopathic

Signs and symptoms : 

Signs and symptoms Exertional Dyspnea & Fatigue – due to low fixed cardiac output Cool extremities Poor peripheral pulse Quiet Precordium early & systolic murmur over pulmonary area in late stage Prominent a waves in jugular vein

Physical Exam : 

Physical Exam Loud P2 (increases PAP) Left parasternal heave (R sided overload) Pulm valve regurgitation (dilatation of pulm valve annulus) S3 gallop (advanced RV failure)

Functional assessment : 

Functional assessment I – No limitation of physical activity II – Slight limitation of physical activity III – Marked limitation of physical activity IV – Symptoms at rest

Signs of Disease Severity : 

Signs of Disease Severity Dyspnea at rest Low cardiac output with metabolic acidosis Hypoxemia Signs of right heart failure (large V wave on jugulars vein, periph edema, hepatomegaly) Syncope (poor prognosis) Chest pain (2 to RV ischemia)

Evaluation of suspected PHTN : 

Evaluation of suspected PHTN History, Physical examination, ECG,CXR ↓ Pulmonary Hypertension Suspected ↓ 2D ECHO with Doppler flow studies ↓ Proceed

PHTN confirmed without heart disease : 

PHTN confirmed without heart disease Complete blood count LFT PT, aPTT HIV ABG Nocturnal & Exercise oximetry Sleep study

Pulmonary Function Testing : 

Pulmonary Function Testing Normal/near normal V-P scan ↓ > 1 segment defect ↓ Pulmonary angiography < 1 segment ↓ CT chest Restriction CT chest ↓ Normal /mediastinal fibrosis ↓ Complete cath.study Parenchymal lung tissue- Referral for tissue diagnosis

Pulmonary Hypertension with Heart disease : 

Pulmonary Hypertension with Heart disease Complete cardiac catheterization

Test indicators : 

Test indicators ECG – RVH, Right atrial enlargement CXR – Prominent MPA, Cardiomegaly ECHO- ? TR, ?PFO, estimation of pulm pressure, RV hypertrophy, dilatation of RV with impairment of LV filling, paradoxical movement of IV septum

Tests : 

Tests Cath study – Pulmonary hypertension ± cause of the disease, pulm pressures, CO, response to vasodilators, ?PFO, status of coronary circulation Ventilation – Perfusion scan – R/O Embolism Pulmonary angiogram Pulmonary Functional Test ABG

Treatment : 

Treatment Treat the cause Oxygen Diuretics in RV failure Vasodilators Calcium channel blockers ACEI Epoprostenol, Trepstinil Sildenafil – phophodiesterase 5 inhibitor

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Prostacyclin Nitric oxide Atrial septostomy Transplant Anticoagulation

Management strategies : 

Management strategies Post capillary Pulmonary Hypertension Reduction of PCWP (Diuretics, Venodilators, Mixed arteriolar & veno dilators) Decrease PVR Pulmonary vasodilators - NTG, SNP, ACEI, NO, Prostacyclin, Endothelin antagonists Treat the cause

Management strategies : 

Management strategies Pulmonary hypertension due to selective or nonselective increase in PBF Correct the cause Reduce the ratio of SVR/PVR - Arteriolar vasodilators (Hydralazine, Phentolamine)

Precapillary Pulmonary Hypertension : 

Precapillary Pulmonary Hypertension Vasodilators – CCB, Prostacyclin, Endothelin antagonists Treatment of RVF – Digitalis, Diuretics, ACEI,Dobutamine, Phosphodiesterase inhibitors Adjunctive therapy – Anticoagulants, Supplemental Oxygen Surgical therapy

Investigational therapies : 

Investigational therapies Prostacyclin analogues ( Iloprost, Baroprost) Endothelial antagonists Nitric oxide donors – L-arginine Gene therapy Phosphodiesterase – 3,5 inhibitors

Recommended Tests before Anesthesia : 

Recommended Tests before Anesthesia Complete blood count, Coagulation profile, LFT ECG CXR ABG ECHO Cardiac Catheterization

Pre-operative care : 

Pre-operative care Pre operative assessment of severity Maintain all pulm vasodilators Heparin Premedication – Benzodiazepines Avoid Hypotension ,Respiratory acidosis

Preoperative care : 

Preoperative care Sildenafil (0.1mg/kg daily up to 0.5mg/kg q6hrs, adults 50-100mg daily, IV 0.2mg/kg/hr) l-arginine (15gm daily) if clinical signs of pulm HTN or poor ex tolerance

Pre operative care : 

Pre operative care Oxygen Digoxin Diuretics – caution Avoid Vasoactive medications

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Sudden stoppage of Pulmonary vasodilators in chronic Pulmonary hypertension is dangerous as it will lead to Vasoconstriction, Hypoxia & Death

Anesthetic Goals : 

Anesthetic Goals Maintain NSR Avoid tachycardia Avoid hypotension/hypertension Avoid all factors that increase PVR: Hypoxia Hypercarbia Acidosis Pain/noxious stimuli Low lung volumes/overdistension

Monitoring : 

Monitoring Basic monitoring of ASA standards Arterial line CVP or PAC TEE if available

Anesthetic technique : 

Anesthetic technique Regional or General anesthesia????? Regional block for peripheral surgeries Combination of Epidural + General anesthesia is a good choice in view of postoperative analgesia

Anesthetic technique : 

Anesthetic technique Epidural anesthesia can be given safely Reduce the local anesthetic dosage with opioids to avoid haemodynamic fluctuations Spinal anesthesia with L.A is not technique of choice

General Anesthesia Induction : 

General Anesthesia Induction Opioids used at a dose to block the response of intubation have no direct effect on pulm vessels Lidocaine (1mg/kg) can help suppress response to intubation Propofol, Thiopentone or etomidate may be used Depolarizing or nondepolarizing muscle relaxants could be used (avoid MR releasing histamine)

Pulmonary vasoreactivity : 

Pulmonary vasoreactivity Propofol – No problem Ketamine –SNS activation,↑catecholamine Ketamine & Etomidate – selectively attenuates endothelial dependent pulmonary vasorelaxation by inhibiting NO

Maintenance : 

Maintenance Isoflurane Most common volatile agent Attenuates magnitude of hypoxic pulm vasoconstriction Potentiates vasodilator response to B1 adrenoceptor activation No effect on alpha 1 vasoconstriction Desflurane Potentiates pulm vasoconstriction to adrenoceptor activation Sevoflurane can be used safely

Maintenance : 

Maintenance Halothane reduce pulmonary vasodilator effect mediated by ATP sensitive K+ channel agonist Nitrous oxide depress myocardial contractility – use in caution

Maintenance : 

Maintenance Maintain opioids at a surgical analgesic level Maintain muscle relaxation Avoid Histamine releasing drugs

Treatment of Entrap. Pulmonary Hypertension crisis : 

Treatment of Entrap. Pulmonary Hypertension crisis Inhaled NO (20-40 ppm) Milrinone (50ug/kg bolus then 0.5-0.75ug/kg/min) Dypiridamole (0.2-0.6 mg/kg IV over 15min q 12hrs) Inhaled prostacyclin (nebulized or IV 2-20 mcg/kg/min) Mg: smooth muscle relaxant, attenuates the effect of hypoxia on PVR (serum conc 3-5mmol/L)

Nitric Oxide : 

Nitric Oxide Selective pulmonary vasodilation, improves oxygenation ↑ cGMP Used in ARDS, PPHN, cardiogenic shock, post CPB Risks: methemoglobinemia and carboxyhemoglobinemia, rebound pulm HTN when stopped Requires closed inhalational circuit

Phosphodiesterase inhibitors : 

Phosphodiesterase inhibitors Inhibition of nitric oxide degradation Sildenafil (PDE-5 inhibitor): ↓ PAP/PVR Min effects on systemic vasculature Synergistic with NO Reduction in RV mass - role in prevention or reversal of remodeling of RV Milrinone (PDE-3 inhibitor): ↓ PVR/PAP/SVR in setting of shock Nebulized minimizes systemic vasodilation

Prostacyclins : 

Prostacyclins Potent pulm and systemic vasodilators with antiplatelet properties Epoprostenol (IV): ↓ PVR, better CO/ex. Tolerance S/E: ↓BP, need for central line (risk of infection) Beraprost (PO): Longer duration Iloprost (nebulized)

Endothelin receptor antagonists : 

Endothelin receptor antagonists Endothelin-1 Neurohormone that causes pulm vasoconstriction, smooth muscle proliferation, fibrosis Stimulates endothelin receptors A & B (A: vasoconstriction & B: vasodilation) Nonselective: Bosentan A selective: sitaxsentan, ambrisentan Chronic pulm htn tx given long ½ life and no IV preparation s/e: hepatic toxicity

Ca channel blockers : 

Ca channel blockers Chronic pulm HTN Rx s/e: hypotension causing reflex tachycardia Only 15-25% of pts respond Need to undergo vasoreactivity testing prior to starting

Post-op care : 

Post-op care Optimal analgesia with continuous epidural, regional block or parenteral opioids Avoid hypoxemia, ↓BP, hypovolemia Risk of acute pulm vasospasm, PE, arrhythmia, fluid shifts, ↑ sympathetic tone, ↑ pulm vascular tone Wean any pulmonary vasodilators progressively

Obstetric Anesthesia : 

Obstetric Anesthesia Epidural anesthesia Risk of ↓ venous return/BP from sympathetic blockade Keep BP within 15% of baseline and below basal level Systemic pressure should always be higher than pulmonary pressure

C-section : 

C-section Uterine contraction: large bolus of blood to circulation may be poorly tolerated if severe pulm HTN or MS Vasodilators e.g.. NTG Diuretics

Pulm HTN Crises : 

Pulm HTN Crises Rapid ↑ in PVR where PAP > Systolic BP RVF →↓PBF, ↓ CO, hypoxia and Biventricular failure Rx 100% O2 Hyperventilation Attenuation of noxious stimuli Pulmonary vasodilators

PCWP : 

PCWP

PCWP : 

PCWP Pulmonary capillary wedge pressure Normal – 4-12mmHg Elevated in Cardiogenic Pulmonary edema PAWP Measurement needs Swan Ganz catheter placement

PCWP : 

PCWP Pulmonary Capillary Wedge Pressure (PCWP) PCWP = left atrial pressure (LAP) = left-ventricular end-diastolic pressure (LVEDP) (Left Ventricular Preload)

PAWP : 

PAWP

Waveforms of chamber pressures : 

Waveforms of chamber pressures

PAWP - Swan Ganz : 

PAWP - Swan Ganz Measurement is obtained when inflated balloon impacts into smaller branch of PA Balloon stops the flow Catheter tip senses pressure transmitted backward through static column of blood from pulmonary vein Vascular channel between catheter tip and left atrium should be patent

Wedge : 

Wedge Wedge position is confirmed by withdrawing and testing blood specimen from distal lumen → Mean oxygen saturation should be >95%

PAWP Waveform : 

PAWP Waveform Similar to Rt. atrial waveform – a, c, v waves and x, y descents v wave slightly larger than a wave

PCWP monitoring When it is ideal? : 

PCWP monitoring When it is ideal? Assessment of respiratory distress ( Cardiogenic vs Noncardiogenic P.edema) Assessment of shock Management of complicated MI Assessment of fluid requirements in critically iIl Perioperative monitoring of fluid status Assessment of therapy in selected individuals Severe preeclampsia management

Shock state : 

Shock state

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