Medical brain notes 7

  Anesthesia and the cardiovascular system Surgical procedures and anesthesia confront the cardiovascular system with a triple threat: trauma, blood loss, and depressant drugs. Trauma triggers a cascade of hormones; if that were not enough, the surgeon might constrict the vena cava, compress a lung, trigger reflexes, and handle the gut, causing sequestration of fluid in traumatized tissue. Exposed pleural and peritoneal lining lets water evaporate, not to mention blood loss and the potential of small clots. To this onslaught, anesthesia adds depressant drugs, induces ventilation/perfusion mismatches with mechanical ventilation (which turns respiratory mechanics upside-down by imposing positive pressure during inhalation), and then infuses cold solutions that are never quite the same as the real thing. Aware of all of these factors, the anesthesiologist appreciates the stresses imposed on the patient and does his or her best to keep the system as close as possible to “how Mother Nat...

  Blood pressure and its determinants To understand how surgery and anesthesia affect blood pressure, we must con-sider its basic components (Fig.  9.1 ). First,  afterload , the combination of all resis-tances against which the heart must eject. Its aliases include systemic vascular resistance (SVR) and total peripheral resistance (TPR). This parameter cannot be measured, but rather is calculated based on the relationship of pressure to flow: 1 where MAP  =  mean arterial pressure, CVP  =  central venous pressure, and CO  =  cardiac output. The vasomotor center influences the diameter of peripheral vessels through sympathetic α 1  innervation. SVR, then, changes with anything that affects the  vasomotor center (the baroreflex (see below), anesthetics), the sympathetic chain (neuraxial (epidural or spinal) anesthesia), α 1  receptors (catecholamines, vaso-pressors), or smooth muscle of the vessel wall directly (histamine, anest...

  Hypertension When we do not know the etiology, we hide behind the technical term “essential.” Thus, we call “essential” the hypertension afflicting some 95% of patients. The pathophysiology of essential hypertension is probably multi-factorial including renal, vascular, cardiac, and neurohumoral factors – and reflex control problems thrown in for good measure. Chronic hypertension leads to left ventricular hypertrophy with consequent stiffening of the ventricle. A “stiffer,” less compliant ventricle will exhibit a large rise in intraventricular pressure during diastole. This increased diastolic pressure (wall tension) both increases myocardial oxygen demand and limits coronary  perfusion. All organ perfusion depends on the upstream and downstream pres-sures. Thus, for the coronary perfusion pressure (CorPP): CorPP  =  DBP  −  RAP or LVEDP where DBP  =  diastolic blood pressure (because the majority of coronary perfu-sion occurs during diastole),...

  Hypotension 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...