Circulation and circulatory support in the critically ill

Cardiovascular dysfunction is common in the critically ill patient and is the primary cause of death in a vast array of illnesses. The prompt identification and diagnosis of its probable cause, coupled to appropriate resuscitation and (when possible) specific treatments, are cornerstones of intensive care medicine.

Cardiovascular monitoring and diagnosis—cardiovascular performance can be assessed clinically at the bedside and through haemodynamic monitoring, and with therapeutic or other proactive interventions. Diagnostic approaches or therapies based on data derived from invasive haemodynamic monitoring in the critically ill patient assume that specific patterns of derangement reflect specific disease processes, which will respond to appropriate intervention.

Interpretation of haemodynamic variables—the various adaptive cardiovascular controls and varying metabolic demands make rules about specific haemodynamic variables of limited clinical utility. It is simply not possible to say that, when looking after a critically ill patient, the central venous pressure, or any other single measurable variable, must be kept at x or y. Key points in this context are: (1) tachycardia is never a good thing; (2) hypotension is always pathological; (3) there is no such thing as a normal cardiac output; (4) central venous pressure is only elevated in disease; and (5) peripheral oedema is of cosmetic concern.

Oxygen delivery—while there is no level of cardiac output which is ‘normal’, there are oxygen delivery thresholds below which normal metabolism can no longer occur. One cardinal sign of increased circulatory stress is an increased O₂ extraction ratio, which manifests itself as a decreasing mixed venous O₂ saturation (Svo ₂): a value of less than 70% connotes circulatory stress, less than 60% identifies significant metabolic limitation, and less than 50% frank tissue ischaemia.

Pathophysiology of shock

Circulatory shock can be defined as a decreased effectiveness of circulatory blood flow to meet the metabolic demands of the body. Four basic functional aetiologies are recognized.

(1) Hypovolaemic shock (e.g. haemorrhage, dehydration)—effective circulating blood volume is inadequate to sustain a level of cardiac output necessary for normal function without supplemental sympathetic tone or postural changes to ensure adequate amounts of venous return.

(2) Cardiogenic shock (e.g. myocardial infarction)—pump dysfunction can be due to either left ventricular (LV) or right ventricular (RV) failure, or both. LV failure is usually manifest by an increased LV end-diastolic pressure, left atrial pressure and (by extension) pulmonary artery occlusion (‘wedge’) pressure, which must exist to sustain an adequate LV stroke volume.

(3) Obstructive shock—mechanical obstruction of blood flow (e.g. pulmonary embolism) or of ventricular filling (cardiac tamponade). In the acute setting, neither pulmonary vascular resistance nor mean pulmonary artery pressure need be grossly elevated for RV failure to occur. In cardiac tamponade, the cardinal sign is diastolic equalization of all pressures, central venous pressure, pulmonary arterial diastolic pressure, and pulmonary artery occlusion (‘wedge’) pressure.

(4) Distributive shock—loss of blood flow regulation occurs as the endstage of all forms of circulatory shock, but as the initial presenting process it is common in sepsis, neurogenic shock, and adrenal insufficiency. The haemodynamic profile of sepsis is one of increased cardiac index, normal pulmonary artery occlusion (‘wedge’) pressure, elevated Svo ₂, and a low to normal arterial pressure, consistent with loss of peripheral vasomotor tone.

Circulatory support of the haemodynamically unstable patient

If the cause of hypotension is intravascular volume loss, either absolute or relative, then cerebral and coronary perfusion pressures must be maintained while fluid resuscitation is begun, otherwise cardiac pump failure may develop and limit the effectiveness of fluid resuscitation.

Pharmacotherapies for cardiovascular insufficiency—these are directed at the pathophysiological processes that either induce or compound the problem. They can be loosely grouped into one of three types: (1) vasopressor therapy—agents that increase vascular smooth muscle tone include noradrenaline (norepinephrine), adrenaline (epinephrine), dopamine, and phenylephrine; (2) inotropic support—agents that that increase cardiac contractility include dobutamine, dopexamine, and phosphodiesterase inhibitors; (3) vasodilator therapy—agents that decrease smooth muscle tone include sodium nitroprusside and glyceryl trinitrate (nitroglycerine). It is important to recognize that most inotropes and vasopressors in clinical use are sympathomimetics that have direct effects on the adrenoreceptor system, and there is a quantitatively unpredictable variation in adrenoreceptor density and function in many pathophysiological states, hence agents acting upon them need to be titrated to effect rather than being given at a defined infusion rate.

Resuscitation strategies—the only prospective clinical trials documenting benefit from particular interventions were applied early in the course of sepsis or in high-risk surgical patients. However, it makes physiological sense to prevent organ ischaemia by maintaining blood flow, hence the following strategies seem warranted.

(1) Loss of vasomotor tone requires both fluid resuscitation to achieve the increased vascular volume needed to restore an effective pressure gradient for venous return, and increased α-adrenergic tone via sympathomimetic agents to restore arterial and venous vasomotor tone. Targets for resuscitation are an Svo ₂ less than 70% with a MAP greater than 60 mmHg.

(2) Impaired contractility requires afterload reduction, as tolerated, up to a decrease in MAP to approximately 70 mmHg, targeting pulmonary artery occlusion (‘wedge’) pressure less than 18 mmHg and Svo ₂ greater than 70%. In sepsis, Svo ₂ is usually elevated following fluid resuscitation, hence resuscitation targets usually focus on reaching elevated levels of oxygen delivery (e.g. >450 ml/min per m²).

(3) In RV failure, maintaining a MAP greater than pulmonary arterial pressure is essential to minimize RV myocardial ischaemia.

Acknowledgement: The author’s work was supported in part by NIH grants HL67181 and HL07820.