- Section 1 ICU organization and management
- Section 2 Pharmacotherapeutics
- Section 3 Resuscitation
- Section 4 The respiratory system
- Section 5 The cardiovascular system
- Part 5.1 Physiology
- Part 5.2 Cardiovascular monitoring
- Part 5.3 Acute chest pain and coronary syndromes
- Part 5.4 Aortic dissection
- Part 5.5 The hypotensive patient
- Chapter 149 Pathophysiology of shock
- Chapter 150 Diagnosis and management of shock in the ICU
- Part 5.6 Cardiac failure
- Part 5.7 Tachyarrhythmias
- Part 5.8 Bradyarrhythmias
- Part 5.9 Valvular problems
- Part 5.10 Endocarditis
- Part 5.11 Severe hypertension
- Part 5.12 Severe capillary leak
- Part 5.13 Pericardial tamponade
- Part 5.14 Pulmonary hypertension
- Part 5.15 Pulmonary embolus
- Section 6 The gastrointestinal system
- Section 7 Nutrition
- Section 8 The renal system
- Section 9 The neurological system
- Section 10 The metabolic and endocrine systems
- Section 11 The haematological system
- Section 12 The skin and connective tissue
- Section 13 Infection
- Section 14 Inflammation
- Section 15 Poisoning
- Section 16 Trauma
- Section 17 Physical disorders
- Section 18 Pain and sedation
- Section 19 General surgical and obstetric intensive care
- Section 20 Specialized intensive care
- Section 21 Recovery from critical illness
- Section 22 End-of-life care
(p. 695) The hypotensive patient
Shock remains a major cause of intensive care unit admission. Initially categorized into hypovolaemic, cardiogenic, and distributive shock, understanding of the pathophysiology has recently evolved such that tissue hypoperfusion in all shock states leads to a dysregulated inflammatory response. After 24 hours, septic shock and ischaemiareperfusion related to hypovolaemic and cardiogenic shock share similar haemodynamic and pro-inflammatory profiles. Vascular hyporesponsiveness to catecholamines is a major consequence of this common pathophysiology, which is focused upon activation of NF-κb with subsequent NO overproduction. Myocardial dysfunction is a frequent complication of the cytokine storm that follows septic shock and ischaemiareperfusion. It may worsen haemodynamic status, but nevertheless, remains transient and totally reversible.
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- Section 1 ICU organization and management
- Section 2 Pharmacotherapeutics
- Section 3 Resuscitation
- Section 4 The respiratory system
- Section 5 The cardiovascular system
- Part 5.1 Physiology
- Part 5.2 Cardiovascular monitoring
- Part 5.3 Acute chest pain and coronary syndromes
- Part 5.4 Aortic dissection
- Part 5.5 The hypotensive patient
- Chapter 149 Pathophysiology of shock
- Chapter 150 Diagnosis and management of shock in the ICU
- Part 5.6 Cardiac failure
- Part 5.7 Tachyarrhythmias
- Part 5.8 Bradyarrhythmias
- Part 5.9 Valvular problems
- Part 5.10 Endocarditis
- Part 5.11 Severe hypertension
- Part 5.12 Severe capillary leak
- Part 5.13 Pericardial tamponade
- Part 5.14 Pulmonary hypertension
- Part 5.15 Pulmonary embolus
- Section 6 The gastrointestinal system
- Section 7 Nutrition
- Section 8 The renal system
- Section 9 The neurological system
- Section 10 The metabolic and endocrine systems
- Section 11 The haematological system
- Section 12 The skin and connective tissue
- Section 13 Infection
- Section 14 Inflammation
- Section 15 Poisoning
- Section 16 Trauma
- Section 17 Physical disorders
- Section 18 Pain and sedation
- Section 19 General surgical and obstetric intensive care
- Section 20 Specialized intensive care
- Section 21 Recovery from critical illness
- Section 22 End-of-life care