Perioperative HTN increases risk for ischemia, infarction, heart failure, and cerebrovascular accident.

BP of less than 180/110 mmHg without end organ disease is not a risk factor for perioperative cardiac complications.

Pulse pressure >80 mmHg is a more sensitive indicator for cardiovascular and cerebrovascular risk than SBP or DBP.

Aggressive reduction in BP >20% may cause ischemic damage to brain, heart, and kidney.

Hypertensive urgency – BP >180/120 mmHg without organ damage. Treated with oral/IV medications [1, 2].

Hypertensive emergency – BP >180/120 mmHg with end organ damage (e.g., chest pain, changes in vision, confusion, nausea/vomiting), require hospitalization and rapid decrease in BP (MAP reduction 25% first hour and to target BP over the next 6 hours) to limit organ damage with IV medications [1, 2].

Intraoperative high BP – stop stimulus and confirm BP. Clinician should ensure an adequate level of sedation, profound local anesthesia, and optimal oxygenation. Treat with antihypertensives.

Ultra-short acting beta-1 selective blocker.

Broken down via RBC esterase in the cytosol (not dependent on renal or hepatic clearance).

5–10 mg over 1 minute every 3 minutes with a maximum dosage of 300 mg.

Onset within 1 minute with duration 10–20 minutes.

Excellent agent for HTN with tachycardia.

Non-selective beta-blocker and selective alpha-1 blocker.

Good for HTN with tachycardia.

5–10 mg IV every 10 minutes with a maximum dosage of 300 mg.

Onset within 5 minutes with a duration 3–6 hours.

Direct arterial vasodilator.

Causes reflex sympathetic activation and tachycardia.

Good treatment of choice for HTN with bradycardia (avoid in patients at risk for myocardial ischemia).

2.5–5 mg IV over 2 minutes (redose every 10 minutes) with a maximum dosage of 25 mg.

Onset 5 minutes with duration of action of 2 hours.

Venodilator at low doses, which reduces preload and cardiac output.

Arterial vessel dilator at high doses, which decreases afterload allowing blood entry to the aorta.

5–10 mcg/min with increase by 5–10 mcg/min every 5 minutes IV.

Onset 2–5 minutes with a duration 10–20 minutes.

Must ask if the patient has used erectile dysfunction medications within 48 hours (washout period) as it can lead to hypotension unresponsive to vasopressors.

May use 0.4 mg sublingual every 5 minutes for a total of three doses.

Good for HTN with bradycardia.

Initial medication of choice for treatment of angina.

Contraindicated for patients with hypotension (SBP <90 or ≥30 mmHg below baseline) and use of phosphodiesterase inhibitors.

Generally said to be a BP <90/60 mmHg. No widely accepted definition intraoperative but widely held as a drop of systolic arterial blood pressure >25% from baseline [3].

Leads to inadequate tissue perfusion to vital organs.

Place the patient in supine position and elevate the legs.

Administer supplement 100% oxygen.

250–500 cc NS or LR infusion (cautious use in patients with CHF or severe renal disease as to prevent volume overload).

Check oxygenation and ventilation with auscultation of heart and lungs.

Recheck blood pressure often.

Attempt to determine the source (allergic reaction, hypovolemia, anesthesia depth, pulmonary embolism, pneumothorax, etc.) .

Cholinergic antagonist.

Most useful in hypotension with bradycardia.

0.5 mg increments every 2–3 minutes to a max of 3 mg.

0.5 mg IM or sublingual every 5 minutes to max 3 mg.

Hypotension with normal heart rate.

α and β agonist.

2.5–5 mg IV every 5–10 minutes to a 50 mg max dose.

25 mg IM or sublingual q 5–10 minutes to a 50 mg max dose.

Onset 1 minute (peak 15 minutes) with a duration 1 hour.

Available as 50 mg/mL (need to dilute 9 cc of sterile saline with 1 mL solution to obtain a concentration of 5 mg/mL) .

Selective α agonist.

Used to treat hypotension with tachycardia or if an increase in heart rate should be avoided.

Available as 10 mg/mL (need a 1% solution, dilute 1 mL in 9 mL of saline then take 1 cc and further dilute in 9 mL of saline allowing for a 100 mcg/mL).

100 mcg/mL q 5 minutes.

Onset 2–3 minutes .

Tachycardia is a heart rate >100/min.

Symptomatic tachycardia is tachycardia with symptoms: shortness of breath, angina, dyspnea on exertion, and mental status change or clinical signs such as pulmonary edema, rhonchi, hypotension, peripheral edema, jugular distension, ischemic EKG changes (Fig. 25.2).

Heart rates >150/min not considered a normal physiological response to stress.

Obtain ECG and ensure IV access.

Rule out common causes of sinus tachycardia including pain, dehydration, and hypoxia.

Supraventricular (SVT) origin – QRS complex is narrow with an origin at or above AV node. E.G. – Sinus tachycardia, A-Flutter, A-fib, paroxysmal supraventricular tachycardia (PVST).

Ventricular origin – QRS wide with a ventricular origin. E.G – ventricular tachycardia.

Always rule out the Hs and Ts (Table 25.1).

Normal HR for adults 60–100/min.

Bradycardia – HR < 60/min (generally rate <50/min associated with symptoms).

Bradycardic rhythm’s examples include sinus bradycardia, first degree AV block, second degree type I (Wenckebach/Mobitz I), second degree type II (Mobitz II), and third degree AV block (Fig. 25.3).

Symptomatic bradydysrhythmia’s signs: hypotension, CHF, pulmonary congestion, and acute MI. Symptoms: angina, fatigue, altered mental status, light-headedness. (See Fig. 25.4 for treatment algorithm) .