Shock

Definitions

• Acute circulatory failure causing inadequate tissue perfusion and oxygen delivery to meet cellular metabolic needs, leading to cellular hypoxia, cellular death and organ dysfunction
• Impaired perfusion causes hypoxia and anaerobic metabolism leading to buildup of lactate and decreased ATP stores
• Dysfunciton of cell membrane ion pumps, causing intracellular oedema, 3rd space leakage and altered intracellular pH and function
• Systmemic acidosis leads to endothelial dysfunction and activation of inflammatory cascades
• Compensatory mechanisms initially provide a reversible situation
• Progression of shock leads to overwhelmed compensatory mechanisms and symtpoms of organ dysfunction occur, eventually irreversible end - organ damage

Classification

Distributive	Septic	- Bacterial - Fungal - Viral - Parasitic - Mycobacterium
	Nonseptic	- Inflammatory shock - Burns, trauma, pancreatitis, postmyocardial infarction, post-coronary bypass, post-cardiac arrest, viscus perforation, amniotic fluid embolism, fat embolism, idiopathic systemic capillary leak syndrome - Neurogenic shock: Traumatic brain injury, spinal cord injury (quadriparesis with bradycardia or paraplegia with tachycardia), neuraxial anesthesia - Anaphylactic shock: IgE-mediated (eg, foods, medications, insect bites or stings), IgE-independent (eg, iron dextran), nonimmumnologic (eg, exercise- or heat-induced), idiopathic - Other: Liver failure, transfusion reactions, vasoplegia (eg, vasodilatory agents, cardiopulmonary bypass), toxic shock syndrome, toxicologic (eg, heavy metals), beriberi
Cardiogenic	Cardiomyopathic	- Myocardial infarction (involving >40% of the left ventricle or with extensive ischemia) - Severe right ventricle infarction - Acute exacerbation of severe heart failure from dilated cardiomyopathy - Stunned myocardium from prolonged ischemia (eg, cardiac arrest, hypotension, cardiopulmonary bypass) - Stress-induced cardiomyopathy (eg, Takesubo cardiomyopathy, sepsis) - Advanced septic shock - Myocarditis - Myocardial contusion - Drug-induced (eg, beta blockers)
	Arrhythmogenic	- Tachyarrhythmia: Atrial tachycardias (fibrillation, flutter, reentrant tachycardia), ventricular tachycardia and fibrillation - Bradyarrhythmia: Complete heart block, Mobitz type II second degree heart block
	Mechanical	- Severe valvular insufficiency, acute valvular rupture (papillary or chordae tendineae rupture, valvular abscess), critical valvular stenosis, acute or severe ventricular septal wall defect, ruptured ventricular wall aneurysm, atrial myxoma
Hypovolemic	Hemorrhagic	- Trauma, gastrointestinal bleeding (eg, varices, peptic ulcer), intraoperative and postoperative bleeding, retroperitoneal bleeding (eg, ruptured aortic aneurysm), aortic-enteric fistula, hemorrhagic pancreatitis, iatrogenic (eg, inadvertent biopsy of arteriovenous malformation or left ventricle), tumor or abscess erosion into major vessels, ruptured ectopic pregnancy, postpartum hemorrhage, uterine or vaginal hemorrhage (eg, infection, tumors, lacerations), spontaneous peritoneal hemorrhage from bleeding diathesis
	Nonhemorrhagic	- Gastrointestinal losses (eg, diarrhea, vomiting, external drainage), skin losses (eg, heat stroke, burns, dermatologic conditions), renal losses (eg, excessive drug-induced or osmotic diuresis, salt-wasting nephropathies, hypoaldosteronism), third space losses into the extravascular space or body cavities (eg, postoperative and trauma, intestinal obstruction, crush injury, pancreatitis, cirrhosis)
Obstructive	Pulmonary vascular	- Hemodynamically significant pulmonary embolus, severe pulmonary hypertension, severe or acute obstruction of the pulmonic or tricuspid valve, venous air embolus
	Mechanical	- Tension pneumothorax or hemothorax (eg, trauma, iatrogenic), pericardial tamponade, constrictive pericarditis, restrictive cardiomyopathy, severe dynamic hyperinflation (eg, elevated intrinsic PEEP), left or right ventricular outflow tract obstruction, abdominal compartment syndrome, aorto-caval compression (eg, positioning, surgical retraction)
Mixed/unknown		- Endocrine (eg, adrenal insufficiency, thyrotoxicosis, myxedema coma) - Metabolic (eg, acidosis, hypothermia) - Other: Polytrauma with more than one shock category, acute shock etiology with pre-existing cardiac disease, late underresuscitated shock, miscellaneous poisonings

Distributive

• Septic shock - see Sepsis Syndrome
• SIRS
  • Pancreatitis
  • Burns
• Neurogenic shock
• Anaphylactic shock
• Endocrine shock
• Drug and toxin induced shock

Cardiogenic shock

• Cardiomyopathic
• Arrhythmic
• Mechanical

Hypovolemic shock

• Hemorrhagic shock
• Non-hemorrhagic
  • Dehydration

Obstructive shock

• Pulmonary vascular
• Mechanical
  • Tension pneumothorax
  • Pericardial tamponnade
  • Constrictive pericarditis
  • Restitive cardiomyopathy

Pathophysiology

• Cellular hypoxia
  • Reduced tissue perfusion and/or increase oxygen consumption
• The major physiologic determinants of tissue perfusion (and systemic blood pressure) are cardiac output (CO) and systemic vascular resistance (SVR)
  • ΒP = CO X SVR
• CO is the product of heart rate (HR) and stroke volume (SV)
  • CO = HR X SV
• The stroke volume is determined by:
  • Preload
  • Myocardial contractility
  • Afterload
• SVR is governed by:
  • Vessel length
  • Blood viscosity
  • Vessel diameter (ie, vessel tone)

Physiologic variable	Preload	Pump function	Afterload	Tissue perfusion
Clinical measurement	Pulmonary capillary wedge pressure	Cardiac output	Systemic vascular resistance	Mixed venous oxyhemoglobin saturation
Hypovolemic	↔ (early) or ↓ (late)	↔ (early) or ↓ (late)	↑	>65% (early) or <65% (late)
Cardiogenic	↑	↓	↑	<65%
Distributive	↔ (early) or ↓ (late)	↑ or ↓ (occasionally)	↓	>65%
Obstructive
PE, PH, tension pneumothorax	↔ (early) or ↓ (late)	↔ (early) or ↓ (late)	↑	>65%
Pericardial tamponade	↑	↓	↑	<65%

Differentiation

• Clinical Features of the causes of shock - main things
  • Obstructive causes have specific clinical signs from ATLS/ACLS
    • Tamponade distended neck veins and hypotension with muffled heart sounds
    • Tension PTX distended neck veins and hypotension with hypertympany and tracheal deviation
    • Spinal vs Neurogenic shock
• Distinguishing features
  • All except distributive - (cardiogenic, obstructive, hypovolaemic)
    • REDUCED CO
    • INCREASED SVR
  • Distributive
    • INCREASED CO
    • REDUCED SVR (peripheral vasodilation)

Vasopressors and inotropes

Receptors

• α1-Adrenergic: Vasoconstriction (increased systemic vascular resistance, SVR).
• β1-Adrenergic: Increased heart rate (chronotropy) and contractility (inotropy).
• β2-Adrenergic: Vasodilation (especially in vascular muscle).
• Dopamine (D1/D2): Vasodilation in renal, mesenteric, coronary, and cerebral vessels (D1).
• V1 (Vasopressin): Vasoconstriction independent of adrenergic pathways.

Drugs

Vasopressors

• Primarily increase vascular tone (vasoconstriction) to raise blood pressure.

1. Norepinephrine
   • Receptors: α1 > β1
   • Effects: Vasoconstriction (↑ SVR) with moderate inotropy.
   • Clinical Use: First-line for septic shock, hypotension.
2. Epinephrine
   • Receptors: β1 > β2 > α1
   • Effects: Low dose: ↑ cardiac output. High dose: ↑ vasoconstriction (α1).
   • Clinical Use: Anaphylaxis, cardiac arrest, refractory shock.
3. Phenylephrine
   • Receptors: Pure α1
   • Effects: Vasoconstriction without cardiac stimulation.
   • Clinical Use: Hypotension, particularly in patients with tachyarrhythmias.
4. Dopamine (High Dose)
   • Receptors: α1
   • Effects: Vasoconstriction at high doses.
   • Clinical Use: Hypotension with bradycardia or shock (rarely used due to side effects).
5. Vasopressin
   • Receptors: V1
   • Effects: Potent vasoconstriction independent of adrenergic receptors.
   • Clinical Use: Septic shock (adjunct to norepinephrine), diabetes insipidus.
6. Metaraminol
   • Receptors: α1
   • Effects: Vasoconstriction

Inotropes

• Enhance cardiac contractility to improve cardiac output.

1. Dobutamine
   • Receptors: β1 > β2
   • Effects: Strong inotropy, mild chronotropy, and mild vasodilation (β2).
   • Clinical Use: Acute heart failure, cardiogenic shock.
2. Milrinone
   • Mechanism: PDE-3 inhibitor (↑ cAMP).
   • Effects: Positive inotropy and vasodilation (↓ SVR).
   • Clinical Use: Acute heart failure with high SVR or pulmonary hypertension.
3. Dopamine (Medium Dose)
   • Receptors: β1
   • Effects: Increased cardiac contractility and heart rate.
   • Clinical Use: Cardiogenic shock with compromised cardiac output.
4. Isoproterenol
   • Receptors: β1 = β2
   • Effects: Increased heart rate and contractility with β2-mediated vasodilation.
   • Clinical Use: Bradycardia, heart block, rarely used in shock.

Drugs with Combined Effects

(Some drugs have significant vasopressor and inotropic actions.)

• Epinephrine
  • Inotropic effect at lower doses (β1, β2); vasopressor effect at higher doses (α1).
• Norepinephrine
  • Primarily a vasopressor (α1), but also has moderate inotropic activity (β1).
• Dopamine
  • Dose-dependent effects:
    • Low dose: Vasodilation (D1).
    • Medium dose: Inotropic (β1).
    • High dose: Vasopressor (α1).