A 70-year old 70 kg man is scheduled for a transurethral prostatectomy. He suffered an acute myocardial infarction 16 months ago, complicated by shock and congestive heart failure. He smokes 5 packs of cigarettes a day, and has diffuse expiratory wheezes on auscultation. He is currently on metoprolol, isordil, nifedipine, and hydrodiuril. He is allergic to "Novocain". Vital signs are as follows: BP: 140/90 mmHg, P: 56. Hemoglobin is 17 and potassium is 3.1 mEq/l.
I. Cardiac evaluation:
1. Why is the HR 56?
The most likely cause, for this patient, is metoprolol therapy. Other causes of bradycardia include hypoxia, sinus node dysfunction, hypothermia, and hypothyroidism. Vagal maneuvers such as oculocardiac reflex, carotid sinus manipulations, reflex stimulation of the vagus nerve, reflex bradycardia from increased intracranial pressure, high subarachnoid or epidural block can also cause bradycardia. Drugs causing bradycardia include narcotics, calcium channel blockers, digoxin, antiarrhythmic drugs, anticholinesterase agents, succinylcholine, cholinergic agents and potent inhalational agents like halothane.
2. Is a more thorough preoperative cardiac evaluation needed?
A thorough preoperative cardiac evaluation is needed for this patient. Ischemic heart disease must be evaluated before surgery, as perioperative myocardial infarction has a mortality of up to 50%. The history should include the frequency, character, location, duration and any radiation of the chest pain. The presence of dyspnea, palpitations, or lightheadedness, and the effects of exertion should be ascertained. Subsequent revascularization procedures and the current cardiac medications should be discussed with the patient, and confirmed from medical records. Physical exam should include signs of congestive heart failure, arrhythmias, and evaluation of the heart rate and blood pressure. The electrocardiogram should be compared with a previous tracing, and the results of the treadmill electrocardiograms, cardiac catheterizations or thallium redistribution studies should be discussed with the cardiologist.
3. How will you manage his cardiac drugs preoperatively?
All of these drugs should be continued through the perioperative period, except the diuretic. Abrupt withdrawal of beta-blockers can cause rebound increases in heart rate and blood pressure. The nitrate therapy should be continued to increase the oxygen supply and decrease myocardial oxygen demand. The calcium channel blocker also should be continued in spite of the possibility of exaggerating the myocardial depressant effects of inhaled anesthetics.
4. How do beta-blockers help a heart in congestive failure?
They reduce myocardial oxygen demand by decreasing heart rate and allowing more diastolic filling time, by decreasing blood pressure, and myocardial contractility. In congestive heart failure, beta-receptors are down regulated, and beta-blockers normalize this.
1. What is the significance of the patient's wheezing?
He most likely has chronic obstructive pulmonary disease because of his history of heavy smoking. A reversible component of wheezing may necessitate bronchodilator therapy, and respiratory infection may also precipitate wheezing, and should be aggressively treated. Other causes of wheezing include asthma, pulmonary edema, and aspiration of gastric contents, allergic reactions, pulmonary embolism, and carcinoid syndrome. Drugs, which may cause wheezing, include anticholinergic drugs or beta-blockers.
2.Why is the hemoglobin 17?
The patient's polycythemia is probably related to his chronic hypoxemia due to chronic obstructive pulmonary disease. Polycythemia could be also due to a relative increase in the percentage of red blood cells in the circulation, caused by dehydration or diuretic use. Secondary polycythemia could be due to high altitude, cyanotic congenital heart disease, or alveolar hypoventilation. Primary polycythemia rubra vera, abnormal hemoglobins, and tumors producing erythropoietin may cause polycythemia.
3. Are pulmonary function tests indicated?
Evaluation of a reversible component and the extent of disease require pulmonary function tests in order to reduce the risk of postoperative complications by using aggressive therapy. The interpretation of the pulmonary function tests should take into account the history, physical exam, blood gas analysis, and chest radiograph.
4. Which pulmonary function tests would you use?
A standardized measurement of the patient's airflow and lung volumes is indicated. These values are reported as a percentage of the predicted normal value, which is calculated based on the age and height of the patient.
5. What would the pulmonary tests show?
Obstructive airway disease exhibits diminished expiratory airflow. The FEV1, FEV1/FVC ratio, and the FEF 25-75 are decreased.
6. The blood gas shows: PO2 = 58 mm Hg, PCO2 = 44 mm Hg, pH = 7.36 with an FIO2 of 0.21 and a respiratory rate of 16 breaths per minute. What is your interpretation?
The patient has mild hypoxemia with compensated respiratory acidosis. The alveolar-arterial oxygen gradient for this patient is elevated due to his chronic obstructive pulmonary disease. His hypoxemia should improve with supplemental oxygen.
III. Potassium management:
1. What are the manifestations of hypokalemia?
Hypokalemia decreases neuromuscular excitability, leading to muscle weakness, with quadriplegia, hypoventilation, adynamic ileus, and orthostatic hypotension. Renal effects include stimulation of renal ammonia production. Cardiac effects include atrial and ventricular arrhythmias, S-T segment depression, flattened T waves, prominent U-waves, and prolonged Q-T intervals. Severe hypokalemia can lead to rhabdomyolysis.
2. Should the potassium be increased preoperatively?
Yes. This patient is mildly hypokalemic. Not all patients with hypokalemia require potassium supplementation, but replacement is indicated if the potassium is less than 3.0 mEq/l with or without symptoms or associated disease, or if mild hypokalemia is associated with heart disease for which even mild hypokalemia can be life threatening.
3. How would you administer potassium replacement therapy?
The preferred choice for potassium therapy replacement in this patient is the intravenous route using 20 to 40 mEq/l of potassium diluted in a glucose-containing solution, given at a rate of 10 mEq/hour.
I. Choice of anesthesia:
Is regional anesthesia indicated?
1. Should you avoid using local anesthetics?
No. His "allergic" reaction could have been an intravascular injection, a reaction to epinephrine added to the solution, or a reaction to a derivative of para-aminobenzoic acid, from Novacaine's ester local anesthetic.
2. What determines potency of local anesthetics?
Lipid solubility determines potency. The higher the solubility, the more potent the agent is.
3. What determines duration of action of local anesthetics?
Protein binding determines duration of action. The more the protein binding, the longer the duration of action.
4. What determines onset of action of local anesthetics?
pKa determines onset of action. The closer the pKa is to the tissue pH, the faster the onset. All local anesthetics are weak bases, so those with a pKa near 7.4 have more molecules that are lipid-soluble and unionized.