Increases in venous tone decrease venous capacitance, redistributing blood volume centrally and thereby increasing venous return to the heart. Common causes of hyperdynamic shock include sepsis, anaphylaxis, some drug intoxications, spinal shock, and adrenal insufficiency.
The primary metabolic defect in circulatory shock is impaired oxidative metabolism with resulting cellular and organ failure. : Die Definitionen der Schockformen. : Acute adrenal insufficiency in cervical spinal cord injury. Mutschler M, Nienaber U, Brockamp T, et al. The primary metabolic defect in circulatory shock is impaired oxidative metabolism with resulting cellular and organ failure.
For most vital organs, autoregulatory and neuronal mechanisms maintain blood flow independent of blood pressure at a mean arterial pressure of 60 to 130 mm Hg.
At that level of oxygen delivery (DO2crit), VO2 becomes linearly dependant on DO2, and anaerobic metabolism manifested by lactic acidosis ensues.
MANAGEMENT OF SHOCK 2. When oxygen extraction is maximized, a critical level of oxygen delivery (DO2crit) is reached below which oxygen consumption decreases and anaerobic metabolism ensues.
13 This classification can be simplified into two categories with typical hemodynamic profiles .
Critical Care 2016; 20: 100, Aoki K, Yoshino A, Yoh K, et al. Similarly, patients in cardiogenic shock after myocardial infarction and cardiac surgery may demonstrate significant vasodilation due to the activation of mediator cascades while on cardiopulmonary bypass.1,18. Vasopressin and activation of the renin-angiotensin system serve to enhance water and sodium retention, thereby protecting intravascular blood volume.
Crit Care 2013, 17: R42, Deitch E, Condon M, Feketeova E, et al. Nitric oxide (NO), peroxynitrite (ONOO−), and superoxide (O2−) are potential inhibitors of the electron transfer chain. This pathophysiology is altered in patients with hyperdynamic forms of circulatory failure such as septic shock, where inflammatory mediators play a prominent role. Hinshaw and Cox proposed a classification of circulatory shock involving four subsets: hypovolemic, cardiogenic, distributive, and obstructive shock.13 This classification can be simplified into two categories with typical hemodynamic profiles (Table 90-1).
I am merely delighted to have my shock classifications spontaneously organise themselves into HASH and NACHOS. Increases in systemic vascular resistance are due to vasoconstriction and represent compensatory mechanisms directed at maintaining blood pressure in the setting of decreased cardiac output.
This impairment is most commonly due to decreases in tissue oxygen supply caused by either global decreases in blood flow or maldistribution of blood flow on a regional or microcirculatory level. Acute myocardial infarction involving 40% or more of the ventricular mass is the most common cause of cardiogenic shock.14 Cardiomyopathies and severe valvular lesions are other important causes of cardiogenic shock. Circulatory shock represents a final common pathway of cardiovascular failure.
These measurements correlate poorly with blood volume, end-diastolic volumes, and fluid responsiveness.9,10 Filling pressures are determined by ventricular compliance, venous return, and systolic function. Intensivmed 2001; 38: 54153. Burns 2010; 36: 10805, Singer M, Deutschmann CS, Seymour CW, et al. Pharmacotherapy 2014; 34: 8993, Furer A, Wessler J, Burkhoff D: Hemodynamics of cardiogenic shock.
Systemic vascular resistance is an indicator of arterial tone and is calculated from cardiac output and arterial pressure. Interv Cardiol Clin 2017; 6: 35971, Werdan K, Russ M, Buerke M et al. Oxygen consumption/oxygen delivery relationships. The mortality rate remains high, particularly for patients in cardiogenic and septic shock, for whom the overall mortality rate approximates 50%.1,2 From a physiologic perspective, circulatory shock can be defined as a syndrome in which tissue perfusion is reduced such that blood flow is inadequate to meet cellular metabolic requirements. The opening of arteriovenous connections which bypass the capillary network may play a role in tissue hypoperfusion. There are four major types of shock, each of which can be caused by a number of different events. A low cardiac output may be adequate when metabolic requirements are decreased—for example, deep sedation or hypothermia.
In most cases, changes in venous tone will parallel changes in arterial tone.
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