Cardiovascular problems during anesthesia
Picture the acutely hypotensive, tachycardic patient (BP 80/50 HR 120 bpm), a fairly common observation. How should you go about treating this patient? After the ABCs,5 we recommend a physiologic approach, rather than a mnemonic laun-dry list of possible causes. First, there are three main ways a patient can become hypotensive: low preload (not enough blood to push forward through the system), low contractility (inadequate force pushing the blood), and low resistance (dilated vascular bed). Other categories are less common and include severe bradycardia, lack of atrial kick, and valvular anomalies, to name a few. To distinguish between these, we start with situational awareness. Did the cross-clamp just come off the aorta? Did we just induce a sympathectomy with a high spinal anesthetic?
Add to that a quick physical examination to rule out abnormal rhythm or valvular or cardiac dysfunction and review of the patient’s medical history (chronic CHF or recent myocardial infarction (MI)?). If these do not lead to a high-probability diagnosis, invasive monitoring may be indicated.
The invasive monitors we have available, in addition to the arterial catheter for blood pressure monitoring, include:
· filling pressure as an inference of ventricular volume/preload: central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP);
· cardiac output: thermodilution via a pulmonary artery catheter (PAC).
For example, consider the hypotensive, tachycardic patient above. Assume a CVP of 1 mmHg (normal 5–12 mmHg) and cardiac output of 6.5 L/min. A low filling pressure (low preload) translates into low ventricular volume – but contractility appears to be good (a cardiac output of 6.5 L/min is not consistent with a poorly contracting heart). With a look at the systemic vascular resistance (SVR) equa-tion above, we see that a low MAP (small numerator) and high cardiac output (denominator) implies a very low SVR. The baroreflex, though, should be railing against the low BP and raising the SVR – we cannot measure the baroreflex activ-ity but assume that it is straining to raise resistance, without success. Thus, our attention is drawn to vasodilation (via endotoxin as in septic shock, or blockade of sympathetic outflow as in spinal shock or neuraxial anesthesia).
Such a physiologic approach allows tailoring of intervention to the specific problem. While intravenous fluid administration is routinely our first choice in a hypotensive patient – particularly in the post-operative setting – and proves the correct choice 99 times out of 100, it does no favor for the patient hypotensive from CHF. Thus, with an unclear etiology or a troubling response to initial treatment, invasive monitoring may be helpful (Table 9.2).
We see from the table that the typical general inhalation anesthetic can affect blood pressure from top to bottom, decreasing preload by venous pooling, decreasing contractility by a direct negative inotropic effect on the heart, decreas-ing SVR by depressing sympathetic outflow and, with some agents, even decreas-ing the baroreceptor reflex. The treatment of hypotension under anesthesia – when not attributed to primary heart disease, hypovolemia from hemorrhage or sepsis – still consists of “filling up the tank” by giving fluids, lightening anes-thesia to improve cardiac function. and giving sympthomimetic drugs, such as ephedrine, to raise SVR and contractility.
Rhythm disturbances occur in up to 70% of patients subjected to general anesthe-sia. Fortunately, the majority of these, in the otherwise healthy patient, are benign and transient. A number of factors can be blamed: the effects of anesthetic agents on the SA and AV nodes, peri-operative ischemia, and increased sympathetic activity during light anesthesia, e.g., laryngoscopy, hypoxemia, and hypercarbia (not uncommon during induction of general anesthesia). In addition to adher-ing to ACLS protocols, potential triggers must be sought and eliminated: correct ventilation, alter anesthetic agent selection (no halothane), increase oxygenation, deepen anesthetic, etc.
The differential diagnosis of intraoperative hypertension is lengthy, but should be approached by considering the patient and procedure first (Table 9.3).
Management of intra-operative hypertension should focus on three things:
(i) Fix the underlying problem: correct anesthetic depth, treat hypercarbia, drain the bladder, etc.
(ii) Where correction is not possible: treat according to the physiologic derange-ment. For example, volume overload should not be treated with beta-blockade nor anxiety with diuretics.
(iii) Consider the time course of the treatment: if a patient’s hypertension results from a transient surgical stimulus, a long-acting anti-hypertensive may cause refractory hypotension when the stimulus ends.
See the pharmacology section to review a selection of the myriad anti-hypertensive agents at our disposal.
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