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Systemic HTN
- BP: 140/90
- Essential: 95% (presumed to have ischemia)
- Secondary: 5%
- Path: Final pathway is salt and water retention.
- Risk: ischemic heart disease and a major cause of congestive heart failure, cerebral vascular accident (stroke), arterial aneurysm, and ESRD.
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Causes of Essential Hypertension
- Increased sympathetic response (stress)
- High Na Intake
- Inadequate K and Ca intake
- Increased Renin (RAA pathway)
- Vasodilator deficiencies (NO&prastaglandins)
- Diabetes Mellitus
- Obesity
- Alcohol and tobacco use
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Treatment of Essential Hypertensionn (Pharmacological)
- 1. Thiazide diuretics: often initial
- 2. ACE inhibitors: useful for pts w/ heart failure.
- 3. If monotherapy is unsuccessful, a drug from a different class is used.
- 4. Consider ARBs, Aldosterone antagonist, diuretics (thiazide, loop, K sparing), B-Blockers, vasodilators, or Ca Channel Blockers,
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Antihypertensives in Perioperative
- 1. Continue antihypertensives to decrease risk of rebound HTN (B-blockers, clonidine)
- 2. Discontinue ACE inhibitors, as they do not cause rebound HTN.
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Treatment for a Hypertensive Emergency
- Sodium Nitroprusside 0.5-10mcg/kg/min
- Nicardipine
- Dopamine
- Esmolol
- Labetalol
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Hypertensive Emergency
- Patients with evidence of acute or ongoing target organ damage.
- Parturient patients w/ diastolic >100
- Normal patients >150
- Goal: decrease diastolic pressure promptly & gradually. Rapid decrease may provoke coronary/cerebral ischemia. 20% decrease in the first hour.
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Treatment of Primary Aldosteronism
- Spironolactone: for women. May cause gynecomastia in men.
- Amiloride: for men
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ACE Inhibitors
- Risk of preoperative hemodynamic instability and hypotension.
- Fluid maintenance is critical.
- Discontinue ACEi 24-48 hours prior to surgery
- Anesthetics: depress autonomic response
- ACEi: blunt the renin-angiotensin-aldosterone system
- Vasopressin system: only available system to regulate BP following loss of RAA and autonomic systems. Likely to be volume dependent.
- May cause hyperkalemia.
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Angiostensin Receptor Blockers (ARBs)
- Prevent Angiotensin II from binding to its receptor.
- Blockade of the renin-angiotensin-aldosterone system increased potential for hypotension during surgery.
- Discontinue ARBs 24 hours prior to surgery
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Preoperative Evaluation of a Hypertensive Patient
- No evidence of increased postoperative complications when a hypertensive patient undergoes elective sx.
- Try to make patient normotensive prior to surgery,
- Co-existing HTN may increase postop incidence of MI w/ previous history and near complications iduring endarterectomy.
- If there is end organ damage, an elective procedure may need to be postponed to improve end-organ damage.
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Induction of Anesthesia
- Rapid IV induction may produce an exaggerated decrease in BP
- IV induction drugs do not predictably suppress circulatory response of tracheal intubation
- High risk ischemia patients may benefit from maneuvers that blunt the autonomic response to intubation: deep inhalation anesthetics opioid, lidocaine, B-blocker, or vasodilator.
- Minimize DL time.
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Intraoperative HTN
- Often due to increased surgical stimulation (light anesthesia)
- BP control w/ any volatile anesthetic (decreasd SVR and contractility), opioids+N2O
- Any muscle relaxant can be used.
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Intraoperative Hypotension
- Tx by decreasing depth of anesthesia and increasing fluid infusion.
- Pt taking ACEi or ARBs is still responsive to IV fluids, sympathomimetics, and vasopressin
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Pulmonary Arterial Hypertension
- Pulmonary HTN: MAP > 25mm Hg
- Average: MAP 12-16 mm Hg (18-25/6-10 mm Hg)
- At risk for RV Failure, hypoxemia, and coronary ischemia.
- S/S: breathlessness, fatigue, murmurs of pulmonic insufficiency or tricuspid regurgitation, S3 gallops, peripheral edema, hepatomegaly, ascites
- Physio: Increased RV after load, decreased RV stroke volume, low systemic output, and hypotension
- Hypoxemia Risk: 1.Increased Right-sided pressure increases R-L shunting through a patent foramen ovale, 2.During fixed CO, the increased oxygen extraction with exertion will produce hypoxemia, 3.V/Q mismatch can result in perfusion of poorly ventilated alveoli.
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Treating Pulmonary Hypertension
- Oxygen, Anticoagulation, and Diuretic Therapy: O2 reduces hypoxic pulmonary vasoconstriction, diuretics decrease preload, and anticoagulation decreases risk of thrombus and thromboembolism.
- Ca Channel Blockers: For those responsive to vasodilator trial (Nifedipine, nicardipine, and amilodipine)
- Phosphodiesterase inhibitor: Produce pulmonary vasodilation and improve CO
- Inhaled Nitric Oxide: Smooth muscle relaxation and vasodilation in well-ventilated alveoli which improves V/Q mismatch.
- Prostacyclins: Systemic and pulmonary vasodilators (also antiplatelet). May lead to bronchospasm, rebound HTN,
- Endothelin Receptor Antagonists: Lower PA pressure ad PVR and improve RV function, exercise tolerance
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Anesthetic Management of Pulmonary Hypertension
- Increased risk of right heart failure: increased RV after load, hypoxemia, hypotension, and inadequate RV preload.
- Sedatives with caution since respiratory acidosis may increase PVR.
- Medications for PAH should be continued throughout the perioperative period: infusions of pulmonary vasodilators, diuretics to control edema.
- Reduced SVR by volatiles or sedatives may be dangerous due to fixed CO.
- Ketamine and etomidate may suppress vasorelaxation and should be avoided.
- Hypoxia, hypercarbia, and acidosis must be controlled since they increase PVR.
- Inhalationals, neuromuscular blockers, and opioids (except histamine release) can be used safely
- Pulmonary vasodilators: milrinone, NTG, or prostacyclin should be available.
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Induction for Patient with Pulmonary Hypertension
- Sidafenil or L-arginine may be useful for newly diagnosed.
- Opioids (except histamine), propofol, thiopental, and depolarizing/non-depolarizing neuromuscular blockers may be used.
- Avoid: ketamine and etomidate since they may suppress pulmonary vasorelaxation.
- Hypotension: Treated with NE, phenylephrine, or fluids.
- Severe pulmonary HTN: Tx with pulmonary vasodilator such as milrinone, NTG, NO, or prostacyclin.
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Meds that may cause HTN
- MAOIs
- TCAs
- SNRIs
- COMT Inhibitors
- Amphetamines: Adderall,
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Hypertensive Emergency (Encephalopathy)
- Primary: Nitroprusside, labetolol, fenolodopam, nicardipine
- Caution: Cerebral ischemia may occur due to drop in BP
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Hypertensive Emergency (Myocardial ischemia)
- Primary: NTG
- Caution: Avoid B-blockers in acute CHF
- Notes: Include morphine and oxygen (MONA- morphine, oxygen, NTG, aspirin)
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Hypertensive Emergency (Acute pulmonary Edema)
- Primary: NTG, nitroprusside, fenoldopam
- Caution: Avoid B-blockers in acute CHF
- Notes: Include morphine, diuretic, and oxygen
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Hypertensive Emergency (Aortic Dissection)
- Primary: Esmolol, vasodilators, trimethaphan
- Caution: vasodilators cause reflex tachycardia
- Goal: Lessen pulsatile force of LV contraction.
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Hypertensive Emergency (Renal Insufficiency)
- Primary: Fenoldopam, nicardipine
- Caution: Tachyphlaxis with fenoldopam
- Notes: Avoid ACEis and ARBs. May require hemodialysis
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Hypertensive Emergency (Preeclampsia/eclampsia)
- Primary: Methyldopa, hydralazine, Mg-sulfate, labetalol, nicardipine
- Caution: Lupus-like syndrome w/ hydralazine, risk for flash pulmonary edema, Ca channel blocker may reduce uterine flow.
- Notes: Definitive is delivery. ACEIs and ARBs are contraindicated due to teratogenic effect
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Hypertensive Emergency (Pheochromocytoma)
- Primary: Phentolamine, phenoxybenzamine, propanolol
- Caution: Unopposed alpha stimulation following B-block worsens HTN
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Hypertensive Emergency (Cocaine intoxication)
- Primary: NTG, nitroprusside, phentolamine
- Caution:Unopposed alpha stimulation following B-block worsens HTN
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