From the Guidelines
Shock is a life-threatening condition that requires immediate recognition and intervention, characterized by signs including low blood pressure (systolic below 90 mmHg), hypoperfusion, and organ dysfunction, as defined by the latest guidelines 1. The signs of shock can vary depending on the type, but generally include:
- Low blood pressure (systolic below 90 mmHg) for more than 30 minutes
- Requirement of vasopressors to maintain systolic BP ≥90 mm Hg or mean BP ≥60 mm Hg
- Hypoperfusion defined by:
- Decreased mentation
- Cold extremities, livedo reticularis
- Urine output <30 mL/h
- Lactate >2 mmol/L These signs are critical to recognize, as shock can rapidly progress to organ failure and death if not promptly treated, as emphasized in the 2022 AHA/ACC/HFSA guideline for the management of heart failure 1. The underlying mechanism involves insufficient oxygen delivery to tissues, triggering compensatory mechanisms like increased heart rate and respiratory rate as the body attempts to maintain adequate perfusion. The most recent and highest quality study recommends that systolic BP and hypoperfusion criteria need to be met for the shock diagnosis 1. In clinical practice, it is essential to prioritize the signs of shock and hypoperfusion, as they are critical for early recognition and intervention, and to seek immediate emergency medical attention if shock is suspected, as this is a true medical emergency requiring rapid intervention.
From the FDA Drug Label
In patients with vasodilatory shock vasopressin in therapeutic doses increases systemic vascular resistance and mean arterial blood pressure and reduces the dose requirements for norepinephrine. Vasopressin tends to decrease heart rate and cardiac output.
The signs of shock that vasopressin may help with include vasodilatory shock, characterized by:
- Low systemic vascular resistance
- Low mean arterial blood pressure
- High requirements for norepinephrine
- Possibly high heart rate and high cardiac output. Vasopressin may help alleviate these signs by increasing systemic vascular resistance and mean arterial blood pressure, and reducing the need for norepinephrine 2.
From the Research
Signs of Shock
- Early signs of shock include:
- Decrease in pulse pressure
- Decrease in urine output
- Decrease in urine sodium concentration
- Decrease in alertness
- Increase in urine osmolarity
- Tachypnea
- Tachycardia 3
- Late signs of shock include:
- Systolic hypotension
- Oliguria
- Metabolic acidosis
- Cold clammy skin 3
- Shock is characterized by hypotension, oliguria, and poor peripheral perfusion, with a systolic blood pressure less than 90 mmHg or a mean arterial pressure less than 60 mmHg or reduced by greater than 30%, for at least 30 minutes 4
Pathophysiology of Shock
- Early hypovolemic shock includes:
- Hyperventilation
- Vasoconstriction
- Cardiac stimulation
- Fluid shifts into the vascular system
- Platelet aggregation 3
- Late shock is characterized by:
- Lysosomal breakdown
- Release of kinins (especially bradykinin)
- Impaired cell metabolism and organ function
- Fluid shifts out of the vascular system due to capillary endothelial damage
- Intravascular coagulation 3
Management of Shock
- The primary cause of shock should not be neglected in favor of treating signs, symptoms, and laboratory data 3
- Resuscitation from shock involves correction of pathophysiologic changes, based on objective trends and responses rather than isolated measurements 3
- A suggested outline of therapies in order of their use includes:
- Correction of the primary problem
- Ventilation and oxygen
- Fluid-loading
- Inotropic agents
- Correction of acid-based and electrolyte abnormalities
- Steroids
- Vasopressors
- Vasodilators
- Diuretics
- Heparin 3
- Management of hypovolaemic shock requires urgent management of the underlying defect and replacement of the intravascular volume loss 4
- Management of cardiogenic shock has changed with the use of percutaneous coronary revascularisation techniques, including emergency cardiac catheterisation with urgent myocardial reperfusion and use of glycoprotein IIb/IIIa antagonists 4