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TCU

Ron Anderson, M.D.

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hypertension cardiology anesthesia medical notes

Summary

This document presents a comprehensive overview of systemic and pulmonary hypertension, with a focus on providing practical information on the anesthetic management of such conditions. The presentation dives into various aspects of the disease, encompassing its pathophysiology, diagnosis, treatment strategies from a medical and surgical standpoint, as well as covering special considerations, including intraoperative and postoperative management.

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SYSTEMIC AND PULMONARY HYPERTENSION PERICARDIAL DISEASE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 SYSTEMIC HYPERTENSION General Essential HTN Secondary HTN Treatment Hypertensive Crisis Anesthetic Management 2 SYSTEMIC HYPERTENSION Hypertension >140/90 Prehypertension Systolic 120 - 139 Diastolic...

SYSTEMIC AND PULMONARY HYPERTENSION PERICARDIAL DISEASE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 SYSTEMIC HYPERTENSION General Essential HTN Secondary HTN Treatment Hypertensive Crisis Anesthetic Management 2 SYSTEMIC HYPERTENSION Hypertension >140/90 Prehypertension Systolic 120 - 139 Diastolic 80 - 89 Incidence ~ 25% of adults in U.S. Increases with increasing age Higher in African Americans Risk Factor for: CAD, CHF, CVA, ESRD, and arterial aneurysm 3 INCIDENCE OF HYPERTENSION HINES 4 INCIDENCE OF CARDIOVASCULAR EVENTS RELATIVE TO BLOOD PRESSURE 5 HINES PATHOPHYSIOLOGY OF ESSENTIAL HYPERTENSION Contributing Factors: – Increased SNS activity in response to stress – Overproduction of: Vasoconstrictors Sodium retaining hormones – – – – – High sodium intake Low K+ and Ca++ intake Increased renin secretion Decreased endogenous vasodilators Concurrent disease Diabetes Obesity – Modulation of the autonomic nervous system – Disruption of natriuretic peptide release and/or receptor responsiveness HINES 6 OBESITY AND HYPERTENSION 7 OBESITY AND HYPERTENSION 8 EVIDENCE OF END-ORGAN DAMAGE Ischemic heart disease LVH CHF Cerebrovascular disease (TIA, RIND, CVA) Renal insufficiency 9 TREATMENT OF ESSENTIAL HTN CATEGORY SYSTOLIC DIASTOLIC OPTIMAL < 120 and NORMAL < 130 and < 85 or 85 - 89 HIGH NORMAL 130 - 139 < 80 Treatment Goals – Standard < 140/90 – Coexisting disease < 130/80 HYPERTENSION STAGE 1 140 - 159 or 90 – 99 STAGE 2 160 - 179 or 100 – 109 STAGE 3 > 180 or > 110 10 A COUPLE DEFINITIONS Resistant hypertension – Uncontrolled despite three or more antihypertensives of different classes Refractory hypertension – Uncontrolled despite 5 or more antihypertensive drugs Note on compliance – Study looked at what appeared to be treatment-resistant HTN in patients “taking” 3 – 5 drugs. 25% had no detectable drug in their system 11 TREATMENT OF ESSENTIAL HTN Lifestyle Modification – Reasonable first approach in patients without associated risk factors or evidence of end organ damage. Weight loss Increased physical activity Smoking cessation Decrease alcohol intake Adequate dietary Ca++ and K+ Dietary salt restriction 12 TREATMENT OF ESSENTIAL HTN Pharmacologic Guidelines for Initial Therapy – Non-black with or without diabetes ACEI, ARB, CCB, or thiazide diuretic – Black with or without diabetes CCB or thiazide diuretic – Chronic kidney disease ACEI or ARB – Beta blockers generally not indicated for initial therapy in the absence of CAD or tachydysrhythmia. Often useful in a multi-drug regimen in resistant HTN 13 SECONDARY HYPERTENSION Has a known cause < 5% of all hypertension – But much higher percentage in certain age groups Often amenable to surgical therapy Common Etiologies Renovascular disease Hyperaldosteronism Aortic coarctation Pheochromocytoma Cushing’s syndrome Renalparenchymal disease Peripartum HTN 14 SECONDARY HTN BY AGE GROUP – Child shows up preop with HTN – that’s unusual 75% or more of the time it’s going to be secondary Usually renal artery stenosis or maybe coarctation of the aorta – Teenagers – coarct becomes more likely – Young adults – drugs, hyperthyroidism, renal – Middle age – OSA, pheo, hyperaldosteronism – Elderly – atherosclerotic renal vascular disease, renal failure 15 HYPERTENSIVE CRISIS BP typically > 180/120 Higher blood pressures tolerated in patients with chronic hypertension Hypertensive urgency Elevated BP without evidence of target organ damage Hypertensive emergency Evidence of target organ damage Treatment Goal Gradual reduction in blood pressure – 20% reduction in first hour – Reduce to 160/110 range over next 2-6 hours* 16 MANAGEMENT OF HYPERTENSIVE EMERGENCY 17 HINES ANESTHETIC MANAGEMENT OF SYSTEMIC HYPERTENSION Surgical/Anesthetic Risk Perioperative Drug Therapy Induction Maintenance Postoperative Care 18 SURGICAL / ANESTHETIC RISK Hypertension is associated with an increased risk of silent ischemia and infarction Incidence and magnitude of perioperative hypertensive and hypotensive events is increased in patients with HTN Little evidence that blood pressures < 180/110, but > normal increase complication rate in elective surgery – Exceptions Reinfarction following prior MI Neurologic complications in CEA patients Have you just diagnosed a “secondary” etiology of HTN rather than poorly controlled essential HTN? 19 SURGICAL / ANESTHETIC RISK Bottom Line Is there end-organ damage or risk for it, that can be reduced by delaying a case or, would further evaluation change your anesthetic management? RISK OF GENERAL ANESTHESIA AND ELECTIVE SURGERY IN HYPERTENSIVE PATIENTS Preoperative Blood Pressure Incidence of Perioperative Hypertensive Episodes (%) Incidence of Postoperative Cardiac Complications (%) Normotensive 8 11 Treated/ Rendered Normotensive 27 24 Treated/ Remain Hypertensive 25 7 Untreated/ Hypertensive 20 12 20 HINES SURGICAL/ANESTHETIC RISK Risk of Hypotension – Hypertensive patient Decreased vascular elasticity Volume depletion Baroreceptor desensitization Altered cerebral autoregulation End organ damage due to long-standing HTN – Transient hypotension can result in significant injury to myocardial, renal or cerebral tissue 21 PERIOPERATIVE DRUG THERAPY Good evidence for continuation of most antihypertensive drugs throughout the perioperative period. Questions to ask: Have the drugs been controlling your BP? Do you take them regularly? Did you take them this morning? 22 SPECIFIC DRUG CLASSES Diuretics – Take morning of surgery? – Acceptable K+ levels? Beta Blockers – Do not discontinue! – Initiate new therapy acutely? Clonidine ACE Inhibitors – Controversy ARBs – Controversy – Often discontinued prior to surgery Calcium Channel Blockers 23 INDUCTION CONCERNS Hypotension Fluid status – NPO – Chronic volume depletion with untreated HTN Antihypertensives Hypertension Laryngoscopy and intubation – Duration – Pharmacologic blunting of response to tracheal instrumentation 24 MAINTENANCE GOALS Minimize wide swings in blood pressure common to patients with hypertension Central neuraxis anesthesia requires special attention to fluid status due to the associated sympathetic block 25 INTRAOPERATIVE MANAGEMENT Hypertension Volatile anesthetics Antihypertensives Hypotension Anesthetic depth Fluid resuscitation Sympathomimetics – Ephedrine – Phenylephrine *Note on ACE Inhibitors and ARBs 26 POSTOPERATIVE HYPERTENSION Multifactorial Not uncommon Results in increased mortality Highest incidence occurs following surgery which may disrupt normal function of baroreceptors or chemoreceptors: – – – – Carotid endarterectomy Intracranial Radical neck dissection Abdominal aortic surgery 27 POSTOPERATIVE HYPERTENSION Determine etiology Pain, agitation, shivering Bladder or bowel distention Emergence excitement Pre-existing hypertension Hypercapnia Increased ICP Autonomic dysreflexia Postoperative hypertension should be anticipated in a patient who experienced episode of intraoperative hypertension Appropriate orders for antihypertensives should be written 28 PULMONARY HYPERTENSION Definition Etiology Determination of Severity and Response Pathophysiology Treatment Anesthetic management Obstetric Management 29 PULMONARY HYPERTENSION Normal pulmonary artery pressures Systolic 18 – 25 mmHg Diastolic 6 – 10 mmHg Mean 12 – 16 mmHg Definition of pulmonary arterial hypertension Mean PA pressure > 25 mmHg at rest Or Mean PA pressure > 30 mmHg with exercise 30 31 UPDATED CLASSIFICATION OF PULMONARY HYPERTENSION HINES NOTES ON CLASSES OF PULMONARY HYPERTENSION Group 1 – Idiopathic (1.1) primarily young women and survival is poor – Familial (1.2) Rare. < 3% of cases – Connective tissue disorders (1.4.1) extremely poor prognosis when associated with scleroderma Group 3 (Associated with lung diseases or hypoxia) – Increasing 20 obesity. PH estimated to exist in: 20% of OSA patients 50% of OHS patients Overall, much more common than we previously believed 32 DETERMINATION OF SEVERITY AND RESPONSE TO VASODILATORS Right heart catheterization with calculation of pulmonary vascular resistance (PVR) (mean PAP – PAOP) CO mmHg/L/min = Wood units Responsiveness to vasodilators determined by administration of prostacyclin, NO, adenosine, or prostaglandin E1 Responsiveness defined as a decrease in PVR and mean PA pressure of > 20% ~ 25% of patients with primary pulmonary hypertension will have a positive response to vasodilators 33 PATHOPHYSIOLOGY PULMONARY VASOCONSTRICTION VASCULAR REMODELING THROMBOSIS PULMONARY ARTERIAL HYPERTENSION INCREASED RV WALL STRESS RV DILATATION TRICUSPID REGURG DECREASED RV STROKE VOLUME DECREASED RV MYOCARDIAL PERFUSION PULMONIC REGURG DECREASED LV FILLING DECREASED CARDIAC OUTPUT 34 RISKS OF HYPOXEMIA IN PULMONARY HYPERTENSION Right-to-left shunting through a patent foramen ovale Exertion resulting in increased oxygen extraction in light of a relatively fixed cardiac output Perfusion of poorly ventilated alveoli due to V/Q mismatch Hypoxemia hypoxic pulmonary vasoconstriction further pulmonary HTN 35 36 TREATMENT OF PAH Oxygen Anticoagulation Diuretics Calcium Channel Blockers Phosphodiesterase Inhibitors – Sildenafil, tadalafil Nitric Oxide/Guanylate cyclase – Inhaled NO – Riociguat – oral guanylate cyclase stimulant Prostacyclins – Epoprostenol, iloprost, beraprost, treprostinil Endothelin Receptor Antagonists – Bosentan, ambrisentan, macitentan Surgery – RV assist device – Balloon atrial septostomy – Heart-lung transplant HINES PREOPERATIVE ASSESSMENT Known or suspected PH – Further evaluation of functional status Exercise capacity RV function Pulmonary function tests Moderate or severe PH by history or echo, or significant comorbidities – Right heart cath prior to moderate or high-risk procedures If PAH, vasoreactivity testing during right heart cath – 10-15% will respond to inhaled nitric oxide 37 ANESTHETIC MANAGEMENT General Guidelines – Continuation of medications for PAH – Availability of a pulmonary vasodilator – Sedation Judicious to avoid hypoxia, hypercapnia Supplemental oxygen – Mixed feelings about invasive monitors Procedures requiring special consideration – – – – Orthopedic Laparoscopy Thoracic Emergency surgery 38 PROCEDURES REQUIRING SPECIAL CONSIDERATION Orthopedic – Significant increase in morbidity and mortality with PH Showers of emboli Amenable to neuraxial anesthesia but avoid excessive sedation Laparoscopy – Effects on filling pressure and afterload can further increase PA pressure and impair RV function Pneumoperitoneum, Trendelenburg, increased inspiratory pressure Thoracic – – – – Transient pressurization of chest to facilitate collapse of lung Potential for systemic hypoxia Increased RV afterload due to HPV Removal of lung tissue (and vasculature) may result in long-term increases in PVR 39 PRIMARY GOAL Maintain optimal mechanical coupling of the RV and the pulmonary circulation which will allow adequate filling of the LV and systemic perfusion Consider effects of your interventions on: – – – – RV preload Inotropy Afterload Oxygen supply/demand relationships 40 OBSTETRIC MANAGEMENT OF PRIMARY PULMONARY HYPERTENSION Labor and Delivery Epidural analgesia with dilute local anesthetic and opioid Cesarean Section General anesthesia – Previously recommended – If necessary, likely best to avoid nitrous oxide due to increases in PVR Spinal anesthesia – Avoid due to sudden decrease in SVR Epidural – Likely the best choice in a non-emergent setting Monitoring – Controversial Maternal mortality 30 - 55% (depends on severity obviously) Primarily due to right heart failure in labor and the early postpartum period 41 PERICARDIAL DISEASE Acute Pericarditis Pericardial Effusion and Cardiac Tamponade Constrictive Pericarditis Pericardial Laceration and Cardiac Contusion 42 ACUTE PERICARDITIS Acute benign pericarditis Viral etiology? Does not involve a significant effusion or tamponade Rarely progressive Pericarditis following MI – Acute presentation 1 – 3 days following transmural MI – Delayed presentation (Dressler’s Syndrome) Weeks to months after an MI 43 ACUTE PERICARDITIS Diagnosis Chest pain Friction rub ECG changes Treatment Salicylates NSAIDs Corticosteroids 44 ACUTE PERICARDITIS Relapsing pericarditis Takes 2 forms, incessant and intermittent May require treatment with immunosuppresive drugs Post-cardiac surgery pericarditis Infective or autoimmune High frequency (10 – 40%) More common in pediatrics Rarely progressive Treatment as above 45 CAUSES OF ACUTE PERICARDITIS AND PERICARDIAL EFFUSION TRANSUDATIVE Infectious Post MI Drug induced Autoimmune disease EXUDATIVE (serosanguinous) Metastatic disease Tuberculosis Post radiation Post traumatic 46 PERICARDIAL EFFUSION AND CARDIAC TAMPONADE When does a pericardial effusion result in tamponade? When the pressure in the pericardial space interferes with cardiac filling Dependent on size and acuity of effusion Normally the pericardial space holds 15 – 50 ml of fluid. HINES 47 PERICARDIAL EFFUSION AND CARDIAC TAMPONADE Symptoms – Related to compression of adjacent structures – – – – Dyspnea Cough ---- hoarseness Anorexia ---- dysphagia Chest pain – Related to pericardial restraint – – – – Tachycardia Jugular venous distention Hepatomegaly Peripheral edema 48 CARDIAC TAMPONADE Mechanism Diastolic collapse due to pressure imposed by the pericardium impairs diastolic filling of the chambers, thereby reducing stroke volume and cardiac output Compensatory mechanisms Tachycardia Peripheral vasoconstriction Physical Findings Kussmauls sign Pulsus paradoxus Beck’s Triad – Quiet heart sounds – Increased jugular venous pressure – Hypotension 49 CARDIAC TAMPONADE BARASH 50 CARDIAC TAMPONADE Diagnosis – Echocardiography* – CT/ MRI – ECG Treatment Removal of fluid – Pericardiocentesis – Pericardiostomy (pericardial window) Temporizing measures – Intravascular volume expansion – Increase contractility – Correction of any metabolic acidosis 51 ANESTHETIC MANAGEMENT General anesthesia and positive-pressure ventilation in the presence of hemodynamically significant cardiac tamponade can result in lifethreatening hypotension. 52 53 HINES ANESTHETIC MANAGEMENT Goal Maintenance of cardiac output – – – – – – Maintain contractility Avoid decreases in systemic vascular resistance Avoid decreases in venous return Maintain adequate preload Avoid bradycardia Maintain sinus rhythm Monitors Arterial line and + central venous pressure Induction and Maintenance – – – – Inhalational? Ketamine Benzodiazipines? Muscle relaxants? 54 CONSTRICTIVE PERICARDITIS Pericardium becomes a rigid shell due to adhesions and/or scarring Over time may become calcified Impaired diastolic filling as in cardiac tamponade Treatment Stripping of the pericardium which may be closely adherent to the myocardium May involve significant blood loss May require cardiopulmonary bypass 55 ANESTHETIC MANAGEMENT Goals Maintenance of heart rate, contractility, SVR, and venous return Anesthetic drug selection will depend on severity of hemodynamic compromise With severe hemodynamic compromise this should be treated similar to cardiac tamponade If patient not hypotensive a broader selection of techniques is reasonable within the stated goals above 56 PERICARDIAL LACERATION Common in rapid deceleration injuries to the chest wall If associated with laceration of adjacent structures may result in cardiac herniation In patients with pericardial laceration: – 18% have diaphragmatic tears – 9% have right-sided pleural tears – 9% have mediastinal tears 30% of this group had cardiac herniation (1/3 survived) Cardiac herniation would be managed similar to cardiac tamponade 57 CARDIAC CONTUSION Maintain a high index of suspicion in rapid deceleration injuries LOC or narcotics may limit value of chest pain as a sign Be alert to ECG changes – ST-T abnormalities – Dysrhythymias Troponin levels may be indicated Patients may have multiple injuries and significant blood loss and fluid shifts Keep this in your differential diagnosis and be prepared to treat dysrhythmias or hemodynamic compromise 58 COMMOTIO CORDIS A high impact chest injury during ventricular repolarization producing an unsynchronized impulse resulting in V Fib Football helmet, baseball, steering wheel, etc to the chest Treatment is defibrillation 59 SOURCES Anesthesia and Coexisting Disease. Hines, Marschall. 8th Edition. 2022 Kaplan’s Cardiac Anesthesia. Kaplan. 7th Edition. 2016 Clinical Anesthesia. Barash. 8th Edition. 2017 Miller’s Anesthesia. Miller. 9th Edition. 2020 60

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