Peri-op  TOC  

PERIOPERATIVE POCKET MANUAL 2005  (Contents)  - 3rd Edition
Maracus Magallanes, MD 2005



*Mild to moderate hypertension has NOT been shown to be a risk factor for perioperative morbidity/mortality. (Only severe hypertension is considered a major risk factor.)

In general, goal is to maintain SBP <180 and DBP <110 intraoperatively/postoperatively AND to avoid hypotension. (BP parameters are stricter in the presence of cardiac or cerebrovascular disease.) Postop, I will usually write prn med orders for SBP >170 or DBP >100.


  1. Hydralazine IV (10-20mg dose acutely; may be repeated after 15 minutes)-can write for prn dose q4hrs or standing dose 10mg up to 40mg) q6hrs.
  2. Metoprolol IV (5mg dose acutely; may be repeated after 5 minutes)-can write for prn dose q4hrs or standing dose (5mg up to 20mg) q6hrs, order to hold if HR<60.
  3. Enalapril IV (1.25-2.5mg dose acutely; may be repeated after 15 minutes)-can write for prn dose q4hrs or standing dose (1.25 to 2.5mg) q6hrs.
  4. Clonidine patch-it takes 1-2 days to maintain effect; lasts one week per patch. (For dose conversion, total daily oral dose = patch dose.)
  5. Nitroprusside drip (50mg in 250ccD5W=200mcg/cc)-begin @ 0.25 mcg/kg/min...60kg patient begins @ approximately 5cc/hr.
  6. NTG drip (50mg in 250cc NS or D5W=200mcg/cc)-begin @ 10mcg/min=3cc/hr, especially useful for CHF/CAD patients.
  7. Aldomet (250-500mg) IVPB q6hrs as standing dose.


  1. Hydralazine (25mg initial dose; 30 to 60 minute onset)-prn q4 or 6 hours.
  2. Clonidine (0.1-0.2mg initial dose; 30 to 60 minute onset)-prn q4 or 6 hours.
  3. Captopril (12.5-25mg initial dose; maximal effect at 1 hour)-prn q4 or 6 hours.



*CAD has been shown to be a definite risk factor for perioperative cardiac morbidity/mortality. (Prior successful angioplasty or CABG has been shown to be protective in patients who have had these procedures done and who have not had recurrence of cardiac symptoms or problems.)


  1. BETA-BLOCKER THERAPY-if patient is not already taking, initiate beta-blocker preoperatively and continue postop, unless there is some contraindication.
  2. NITRATES-may be beneficial in preventing perioperative myocardial ischemia, although not definitively proven in studies. Nitrates are recommended perioperatively if patient is on chronic nitrate therapy or has been symptomatic from coronary disease.
  3. ASPIRIN/PLAVIX-usually held for surgery, but if the patient has symptomatic coronary disease and/or known severe disease, then the benefit of continuing aspirin or plavix might outweigh the risk of increased surgical bleeding. *Inform the surgeon if aspirin or plavix will be given before surgery. Postop, aspirin/plavix can be resumed unless patient is actively bleeding or at high risk of bleeding. Rectal aspirin is an option if patient unable to take pills postop. (Effect of one aspirin will last at least 3 days.)
  4. ACE inhibitor-if patient is already taking, simply continue therapy preop and postop.
  5. HEPARIN DRIP or SQ ENOXAPARIN (1 mg/kg q12hr)-may be considered postop for very high-risk patients undergoing major surgery or for any patient with evidence of perioperative myocardial ischemia. *Must address the risk of postop bleeding with surgeon before initiating anticoagulation.
  6. BLOOD PRESSURE and HEART RATE CONTROL-the goal postoperatively is to keep patient normotensive and maintain heart rate at least under 100-preferably at 80 or less, especially for high-risk patients.
  7. POSTOP TRANSFUSION-goal is to maintain hemoglobin at or above 10 grams, especially for high- risk patients.
  8. SUPPLEMENTAL OXYGEN-goal is to maintain oxygen saturation over 90%.
  9. PAIN CONTROL-significant surgical pain may contribute to perioperative myocardial ischemia.

*A note about postoperative MI's: up to 60% are not associated with chest pain but instead present with unexplained hypotension, CHF, arrhythmia, or altered mental status; the mortality associated with postoperative MI is high (up to 50% in one study).


*CHF has been shown to be a definite risk factor for perioperative cardiac morbidity/mortality. Systolic LV dysfunction, even in the absence of clinical CHF, is also considered a risk factor (particularly if LV ejection fraction is under 35%).


  1. DIURETIC THERAPY-if patient has evidence of active CHF preoperatively, aggressive diuresis needs to be performed prior to surgery. Maintenance diuretic therapy should be continued postop.
  2. ACE INHIBITOR-if already taking, continue therapy preop and postop (IV enalapril is available if patient is unable to take pills postop). If initiating therapy, titrate up dose as blood pressure tolerates. If patient is unable to take ACE inhibitors for some reason, the combination of hydralazine and nitrate therapy has been shown to be effective in CHF management as an alternative.
  3. BETA-BLOCKERS-if already taking, continue therapy preop and postop (IV metoprolol is available if patient is unable to take pills postop). If initiating therapy, start at a low dose only. I would not recommend initiating beta-blocker therapy in-house if the patient has active CHF or if LV systolic function is severely depressed (unless deemed essential due to ischemic heart disease).
  4. ALDACTONE-if already taking, continue preop and postop; otherwise, no need to initiate this medication in-house, at least preoperatively. The dose is only 25mg daily.
  5. DIGOXIN-if already taking, continue preop and post-op; otherwise, no need to initiate this medication in-house, at least preoperatively.
  6. FLUIDS-run IV fluids relatively low in these patients.
  7. ELECTROLYTES-watch for low K, Mg, Na.
  8. POST-OP ARRHYTHMIAS-very common, both ventricular and supraventricular. Postop telemetry monitoring should be considered if patient has had significant arrhythmias in the past, if LV dysfunction is severe, or if patient has had recent active CHF.

VALVE DISEASE                    PERIOPERATIVE POCKET MANUAL 2005  (Contents)

*Valvular heart disease can be a significant risk factor for surgery, depending on the valve involved, the lesion and its severity. As a general rule, stenotic lesions are worse than regurgitant lesions, and aortic valve disease is worse than mitral valve disease (which is worse than right-sided disease).

*Patients with significant valve disease are much more likely to have arrhythmias, both ventricular and supraventricular. In addition, antibiotic prophylaxis is warranted if undergoing oral/GI/GU or ob/gyn procedure.

Severe aortic stenosis (AV area <1cm2, mean gradient >50) confers a high surgical risk, even worse if LV dysfunction is present. Unfortunately, there are no effective medical options to manage aortic stenosis. Treat underlying CHF if present. Avoid overaggressive IVF hydration postoperatively, but hypovolemia must also be avoided. No benefit of spinal over general anesthesia. (General may actually be preferable because of the hypotension associated with spinal anesthesia due to peripheral vasodilation.)

Severe mitral stenosis (MV area <1cm2) confers a significantly increased surgical risk, but it can be well-tolerated as long as heart rate is controlled. The absolute key to management is heart rate control (keep HR <80) whether the patient is in sinus rhythm or in atrial fib. Beta-blockers are particularly effective for this; calcium-channel blockers can also be used. Digoxin is useful only in atrial fib. Additionally, regarding chronic anticoagulation, if the patient has both atrial fib and mitral stenosis, the risk of thromboembolization is significantly higher than if patient has atrial fib alone, so resumption of anticoagulation postop should be instituted once surgically safe to do so.

This lesion is usually well-tolerated for surgery as long as it is chronic and LV function is preserved. (The prognosis for surgery is actually more dependent on the LV function than on the severity of the aortic regurgitation.) Afterload reduction (ACE inhibitors or hydralazine) is indicated even if LV function is normal.

This lesion is usually well-tolerated for surgery, again as long as it is chronic and LV function is preserved. Afterload reduction (ACE inhibitors or hydralazine) is indicated even if LV function is normal.

Mitral valve prolapse itself is not a significant concern for surgery. (Furthermore, antibiotic valve prophylaxis is not warranted unless mitral regurgitation is present.)

If prosthetic valve is functioning well and LV function is preserved, then the main issues are maintenance of anticoagulation and antibiotic prophylaxis. Mechanical mitral valves are much more thrombogenic and require more prompt resumption of anticoagulation postop than mechanical aortic valves. (Porcine and homograft valves do not require chronic anticoagulation.) Prosthetic valves are considered high-risk with regard to antibiotic prophylaxis.

ARRHYTHMIAS                     PERIOPERATIVE POCKET MANUAL 2005  (Contents)

Chronic atrial fibrillation alone is not a significant risk factor for surgery, as long as heart rate is controlled. Other cardiac problems, however, may be identified which would confer increased surgical risk (such as LV dysfunction, coronary artery disease, valve disease, etc.). Rate-control can be achieved with beta-blockers, calcium-channel blockers, or digoxin. *In patients who suddenly develop rapid ventricular response after surgery, do not forget to consider the multiple possible etiologies of postop tachycardia (such as hypoxia, anemia, ischemia, pneumonia, PE, etc.).

The development on new atrial fibrillation is particularly common after cardiac and thoracic procedures, but may occur after any major surgery. In general, anticoagulation is not necessary within the initial 48 hours of new atrial fibrillation, and a majority of these patients can be successfully cardioverted within that timeframe (many are spontaneous). Beta-blockers are effective for controlling rate and may also convert to sinus rhythm. Other agents for postoperative cardioversion: IV procainamide (loading dose followed by infusion), amiodarone (slow IV or PO), flecainide 300mg single PO dose (not recommended for elderly patients, atrial flutter, or patients with pre-existing cardiac disease or conduction abnormalities), IV ibutilide (NOTE multiple potential, severe drug interactions), and PO sotalol. Electrical cardioversion is another option if chemical cardioversion is unsuccessful or if immediate cardioversion is necessary due to symptoms, ischemia, CHF, or hemodynamic compromise.

Anticoagulation for new atrial fibrillation is highly recommended after 48 hours, but in the postoperative setting the patient's immediate bleeding risk needs to be addressed with the surgeon before starting anticoagulation. If anticoagulation is initiated and the patient remains in atrial fibrillation beyond 48 hours, the current ACC/AHA recommendation is not to attempt cardioversion for another 3 to 4 weeks while on anticoagulation, then to continue for at least 3 to 4 weeks post-cardioversion. Furthermore, even for patients who successfully cardiovert to sinus rhythm within the first 48 hours (without anticoagulation), there is consideration of post-cardioversion anticoagulation for 3 to 4 weeks depending on assessment of cardioembolic risk. (Although it has been common practice not to anticoagulate this group, data supporting this practice is very limited.)

Patients with PVC's (>5/min) statistically do have some increased risk of perioperative cardiac death; however, the cause of death is not due to arrhythmia. In fact, the increased surgical risk is not due to the ectopy at all, but rather to the underlying cause of the arrhythmia. Patients with asymptomatic PVC's/bigeminy/ trigeminy should not have the ectopy treated preoperatively because suppression of the PVC's has not been shown to reduce perioperative morbidity/mortality. Instead, an underlying cause of the arrhythmia should be investigated (such as CHF, hypoxia, electrolyte abnormality, coronary disease, valve disease, drug-induced, etc.). In the absence of any significant underlying disease, the arrhythmia is likely to be benign.

Postoperative ventricular ectopy is very common, and the same principle applies with regard to management. There is no need to treat asymptomatic PVC's themselves, unless the patient develops ventricular tachycardia or has documented ischemia (which itself needs to be treated acutely). In high-risk or elderly surgical patients, asymptomatic PVC's may sometimes be an indicator of post-op ischemia, but the likelihood of this is variable. A 12-lead EKG can quickly and reliably resolve the issue.

Asymptomatic patients with chronic sinus bradycardia (HR <60) in general do not require any intervention preop or postop. Patients with sick sinus syndrome (inappropriate tachycardia followed by bradycardia, or vice-versa) or with symptomatic bradycardia should have a pacemaker placed before surgery, unless the bradycardia is medication-related and simply resolves by withholding the causative drug. (The most common causative drugs are beta-blockers, calcium-channel blockers, and clonidine.) Intraoperative/postoperative bradycardia is well-described after succinylcholine administration and after ophthal-mologic procedures. It is also commonly associated with spinal/epidural anesthesia. If necessary, atropine is the first drug of choice to acutely treat bradycardia.

In the absence of underlying cardiac or pulmonary disease, the surgical risk associated with SVT is unclear. (It is probably a similar situation to that of atrial fibrillation, which alone is not a significant risk factor for surgery as long as the heart rate is controlled.) Postoperative SVT is a common occurrence, and management is identical to that in nonsurgical patients. Beta-blockers, in particular, have been proven to be better than calcium-channel blockers in controlling postop SVT and converting to sinus rhythm.


Isolated LBBB, RBBB, bifascicular block, 1st degree AV block, and 2nd degree AV block-Type 1 have NOT been shown to progress to complete heart block intraoperatively or postoperatively.

2nd degree AV block-Type 2 (either intermittent or constant) and 3rd degree AV block carry a high surgical risk of cardiac arrest. These problems require pacemaker placement.


*Cardiac pacemakers themselves do not increase operative risk, as long as they are functioning properly.


  1. Magnet should be made easily accessible intraoperatively in case of pacemaker malfunction.
  2. Electrocautery electrode should be kept distant from pacemaker site during surgery, with grounding away from the pacemaker. (For hip surgery, ground on the leg or the opposite hip.)
  3. If necessary, preop and postop interrogation can be performed readily by checking EKG with and without magnet application. The magnet converts the pacemaker to its programmed back-up mode. If pacing spikes are not apparent, this may indicate battery malfunction.

* A note regarding Implanted Cardioverter Defibrillator (ICD) devices. As a general rule, these should be deactivated just prior to surgery and re-activated postop. The newer ICD models are deactivated by placing an overlying magnet, and then instantly re-activated by removing the magnet. If unsure of a particular ICD, the manufacturer can be contacted for technical support or a cardiologist experienced with ICD's may be able to manage instead. (For the Bellflower Medical Center / Tricentral service area, Dr. Naheed Olsen is the cardiologist in charge of the ICD clinic and would be the physician to contact.)

         PERIOPERATIVE POCKET MANUAL 2005  (Contents)