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Table 1 Systemic consequences of cardiac arrest

From: Pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest

 

Pathophysiology

Clinical consequences

Ischemia -reperfusion injury

Free radical formation

Apoptosis, necrosis

“Sterile inflammation”

Impaired resistance to infection

Endothelial damage

Impaired vasoregulation

Adrenal suppression

Electrolytes disturbances

Acidosis, hypoxia, catabolism

Multiorgan failure

Infection/sepsis

Microbiome disturbances

Tissue hypoxia/ischemia

Hyperglycemia

Increase of intra-abdominal pressure

Development of abdominal compartment syndrome

Brain injury/global cerebral ischemia (GCI)

Calcium homeostasis disruption

No reflow

Pyrexia

Hyperglycemia

Hyperoxygenation

Impaired cerebrovascular autoregulation

Impairment of hypothalamic-pituitary-adrenal axis

Raised corticotropin releasing factor (CRF)-blood flow changes

Damage of blood-brain barrier (BBB) (endothelial dysfunction and capillary permeability)

Coma

Seizures

Cognitive dysfunction

Stroke

Brain death

Pulmonary complications following cerebral ischemia (neurogenic pulmonary edema, acute distress respiratory syndrome, pneumonia)

Myocardial dysfunction

Global hypokinesis

Preserved coronary blood flow

Elevated systemic and pulmonary vascular resistance

Impaired ventricular function

Decreased venous return, cardiac compliance, and cardiac output.

Decreased contractility

Acute myocardial infarction (AMI)

Arrhythmias

Cardiomyopathies: dilated, restrictive, hypertrophic

Cardiovascular collapse

Arrest related lung injury

Reperfusion injury

Endothelial damage

Systemic inflammation

Activation of clotting cascades

Ventilation-perfusion mismatch (ventilatory pressure)

Basal atelectasis

Pneumonia

Acute respiratory distress syndrome

Pulmonary thromboembolism

Arrest related liver and kidney injury

Reperfusion injury

Reduced blood flow

Reduced urine output

Hypoxic hepatitis/acute liver failure

Acute kidney injury