Management of different type of shock with mechanism of shock and drug m/a
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Harrison's Principles of Internal Medicine, Twenty First Edition
Page 8234
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Harrison's Principles of Internal Medicine, Twenty First Edition
Page 8253
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Management of Shock: Types, Mechanisms & Drug Actions
Classification of Shock
Shock is a state of inadequate oxygen delivery (DO₂) relative to oxygen consumption (VO₂), leading to cellular hypoxia and end-organ dysfunction. All types share a final common pathway but differ in their primary physiologic derangement.
(Harrison's Principles of Internal Medicine, 21st Ed., p. 8234)
Four Major Types of Shock
1. 🔴 Hypovolemic Shock
Mechanism
- Loss of intravascular volume → ↓ preload → ↓ CO → ↓ MAP → ↓ tissue perfusion
- Baroreceptors trigger compensatory tachycardia and vasoconstriction (↑ SVR)
- Subtypes:
- Hemorrhagic: trauma, GI bleed, ruptured AAA
- Non-hemorrhagic: vomiting, diarrhea, burns, third-spacing
Hemodynamic Profile
| Parameter | Finding |
|---|---|
| CO/CI | ↓ |
| SVR | ↑ |
| PCWP/CVP | ↓ |
| HR | ↑ |
Management
| Priority | Intervention |
|---|---|
| 1st | Identify and control the source of volume loss |
| 2nd | IV fluid resuscitation — crystalloids (Normal Saline / Lactated Ringer's) |
| Hemorrhagic | Packed RBCs, FFP, platelets in 1:1:1 ratio (massive transfusion protocol) |
| Permissive hypotension | Target MAP 50–65 mmHg in uncontrolled hemorrhage until surgical control |
| Vasopressors | Only as bridge after volume resuscitation |
Drugs Used
| Drug | Mechanism of Action |
|---|---|
| Norepinephrine | α1 > β1 agonist → ↑ SVR + mild ↑ CO; used if refractory despite volume |
| Vasopressin | V1 receptor agonist → direct vasoconstriction, SVR-independent of adrenergic system |
| Tranexamic acid | Antifibrinolytic — inhibits plasminogen activators → stabilizes clot in hemorrhagic shock (given within 3 hrs) |
2. 🔵 Cardiogenic Shock
Mechanism
- Primary pump failure → ↓ CO → ↓ MAP → compensatory ↑ SVR (worsens afterload)
- Causes: acute MI (most common), acute severe MR/VSD, myocarditis, arrhythmias, DCM
- High PCWP (pulmonary congestion) distinguishes it from other shock types
- "Cold and wet" phenotype — poor perfusion + pulmonary edema
Hemodynamic Profile
| Parameter | Finding |
|---|---|
| CO/CI | ↓↓ |
| SVR | ↑↑ |
| PCWP/CVP | ↑ |
| HR | ↑ |
Management
| Priority | Intervention |
|---|---|
| Revascularization | Urgent PCI in AMI-related cardiogenic shock |
| Inotropes | Increase contractility |
| Vasopressors | If MAP critically low |
| Mechanical support | IABP, Impella, VA-ECMO in refractory cases |
| Diuresis | Carefully if volume-overloaded (↑ PCWP) |
Drugs Used
| Drug | Mechanism of Action |
|---|---|
| Dobutamine | β1 > β2 agonist → ↑ contractility (↑ cAMP) → ↑ CO; mild ↓ SVR via β2 |
| Dopamine | Dose-dependent: low dose (dopaminergic → renal vasodilation); moderate (β1 → ↑ CO); high dose (α1 → ↑ SVR). Less preferred now due to arrhythmia risk |
| Norepinephrine | α1 + β1 → ↑ MAP; preferred over dopamine (lower arrhythmia risk) |
| Milrinone | PDE-3 inhibitor → ↑ cAMP → ↑ contractility + vasodilation (↓ SVR, ↓ PCWP); "inodilator" |
| Levosimendan | Calcium sensitizer → ↑ myofilament sensitivity to Ca²⁺ → ↑ contractility without ↑ O₂ demand; also opens K⁺_ATP channels (vasodilation) |
| Vasopressin | V1 agonist → ↑ SVR; adjunct if catecholamine-refractory hypotension |
3. 🟠 Distributive Shock
The most common type in ICU. Characterized by maldistribution of blood flow despite normal or elevated CO.
Subtypes & Mechanisms
a) Septic Shock
- Pathogen → innate immune activation → massive cytokine release (TNF-α, IL-1, IL-6)
- ↑ iNOS → ↑ NO → profound vasodilation (↓ SVR)
- Capillary leak → relative hypovolemia
- Myocardial depression (cytokine-mediated)
- "Warm shock" early → "cold shock" late (decompensated)
b) Anaphylactic Shock
- IgE-mediated mast cell/basophil degranulation → histamine, leukotrienes
- Histamine → H1 + H2 → vasodilation, ↑ capillary permeability, bronchoconstriction
c) Neurogenic Shock
- Spinal cord injury (T6 and above) → loss of sympathetic tone below injury
- Unopposed parasympathetic → vasodilation + bradycardia (distinguishing feature)
Hemodynamic Profile
| Parameter | Finding |
|---|---|
| CO/CI | ↑ (high output) |
| SVR | ↓↓ |
| PCWP/CVP | ↓ (relative) |
| HR | ↑ (bradycardia in neurogenic) |
Management & Drugs
Septic Shock (Surviving Sepsis Campaign)
| Step | Action |
|---|---|
| Within 1 hour | Blood cultures × 2, IV broad-spectrum antibiotics, 30 mL/kg crystalloid bolus |
| Vasopressor | Start if MAP < 65 mmHg despite fluid |
| Steroids | If refractory to vasopressors |
| Source control | Drain abscess, remove infected catheter, etc. |
| Drug | Mechanism |
|---|---|
| Norepinephrine (1st line) | α1 >> β1 → potent ↑ SVR with minimal ↑ HR; preferred in septic shock (Harrison's, p. 8253) |
| Vasopressin (2nd line, 0.03–0.04 U/min) | V1 receptor → ↑ SVR; catecholamine-sparing effect; does not increase HR |
| Epinephrine | α1 + β1 + β2 → ↑ SVR + ↑ CO; used as 2nd/3rd line or adjunct |
| Hydrocortisone 200 mg/day | Reverses relative adrenal insufficiency; restores adrenergic receptor sensitivity (catecholamine-refractory shock) |
| Antibiotics | Source-specific; early administration ↓ mortality |
Anaphylactic Shock
| Drug | Mechanism |
|---|---|
| Epinephrine IM (1st line) | α1 → ↑ SVR (reverses vasodilation + edema); β2 → bronchodilation; β1 → ↑ CO; also inhibits mast cell degranulation |
| IV fluid bolus | Replaces capillary leak |
| Diphenhydramine (H1 blocker) | Blocks H1 receptors → reduces vasodilation, urticaria, bronchoconstriction |
| Ranitidine/Famotidine (H2 blocker) | Blocks H2 → reduces gastric effects and vasodilatation |
| Hydrocortisone / Methylprednisolone | Anti-inflammatory → prevents biphasic reaction; not for acute reversal |
| Salbutamol (nebulized) | β2 agonist → bronchodilation (adjunct for bronchospasm) |
Neurogenic Shock
| Drug | Mechanism |
|---|---|
| Norepinephrine / Phenylephrine | α1 → ↑ SVR; restores vascular tone lost due to absent sympathetics |
| Atropine / Vasopressin | For refractory bradycardia |
| Methylprednisolone | In acute spinal cord injury (within 8 hrs — controversial, NASCIS protocols) |
4. 🟡 Obstructive Shock
Mechanism
- Mechanical obstruction of blood flow into or out of the heart
- CO falls due to physical blockage, not pump failure or volume loss
- Causes:
- Massive PE: obstruction of RV outflow, RV failure
- Cardiac tamponade: pericardial fluid compresses heart → ↓ ventricular filling (↓ preload)
- Tension pneumothorax: mediastinal shift → kinks SVC/IVC → ↓ preload; also compresses RV
Hemodynamic Profile
| Parameter | Finding |
|---|---|
| CO/CI | ↓ |
| SVR | ↑ |
| PCWP/CVP | ↑ (tamponade, PE) or ↓ effective |
| HR | ↑ |
Management & Drugs
Massive PE
| Intervention | Detail |
|---|---|
| Anticoagulation | IV heparin immediately (UFH bolus 80 U/kg, then infusion) |
| Systemic thrombolysis | Alteplase 100 mg IV over 2 hrs (if hemodynamically unstable) |
| Surgical embolectomy / catheter-directed thrombolysis | If thrombolysis contraindicated |
| Vasopressors | For RV failure-driven hypotension |
| Drug | Mechanism |
|---|---|
| Alteplase (tPA) | Activates plasminogen → plasmin → fibrinolysis → clot dissolution |
| Unfractionated Heparin (UFH) | Binds antithrombin III → inhibits thrombin (IIa) and Factor Xa → prevents clot propagation |
| Norepinephrine | α1 → ↑ SVR → improves RV coronary perfusion pressure in RV failure |
| Inhaled NO / Epoprostenol | Pulmonary vasodilation → ↓ RV afterload |
Cardiac Tamponade
| Intervention | Detail |
|---|---|
| Pericardiocentesis | Definitive — needle drainage of pericardial fluid (immediate relief) |
| IV fluids | Temporizing — volume loading maintains preload until drainage |
| Vasopressors | Temporizing — norepinephrine as bridge |
| Avoid negative inotropes / diuretics | These worsen the hemodynamic compromise |
Tension Pneumothorax
| Intervention | Detail |
|---|---|
| Needle decompression | 2nd ICS, MCL (immediate) |
| Chest tube insertion | Definitive management |
| No drugs replace mechanical intervention | Vasopressors only as bridge |
Summary Comparison Table
| Shock Type | CO | SVR | PCWP | Key Drug | Drug Mechanism |
|---|---|---|---|---|---|
| Hypovolemic | ↓ | ↑ | ↓ | Fluids → Norepinephrine | α1 → ↑ SVR |
| Cardiogenic | ↓↓ | ↑↑ | ↑ | Dobutamine + Norepinephrine | β1 → ↑ CO; α1 → ↑ MAP |
| Septic | ↑ | ↓↓ | ↓ | Norepinephrine → Vasopressin | α1 → ↑ SVR; V1 → vasoconstriction |
| Anaphylactic | ↑ | ↓↓ | ↓ | Epinephrine IM | α1 + β1 + β2 → vasoconstriction + bronchodilation |
| Neurogenic | ↑/N | ↓↓ | ↓ | Norepinephrine/Phenylephrine | α1 → restores lost sympathetic tone |
| Obstructive (PE) | ↓ | ↑ | ↑ | Alteplase + Heparin | Fibrinolysis; anti-Xa/IIa |
| Obstructive (Tamponade) | ↓ | ↑ | ↑ | Pericardiocentesis (procedure) | — |
Key Drug Receptor Summary
| Drug | Receptors | Net Effect |
|---|---|---|
| Norepinephrine | α1 >> β1 | ↑ SVR, mild ↑ HR |
| Epinephrine | α1 = β1 + β2 | ↑ SVR, ↑ HR, bronchodilation |
| Dopamine | Dose-dependent: D1 → β1 → α1 | Varies by dose |
| Dobutamine | β1 > β2 | ↑ CO, mild ↓ SVR |
| Phenylephrine | Pure α1 | ↑ SVR only (reflex bradycardia) |
| Vasopressin | V1 | ↑ SVR (catecholamine-independent) |
| Milrinone | PDE-3 inhibitor (↑ cAMP) | ↑ CO + ↓ SVR (inodilator) |
| Levosimendan | Ca²⁺ sensitizer + K⁺_ATP | ↑ CO without ↑ O₂ demand |
| Atropine | mAChR antagonist | ↑ HR (used in neurogenic bradycardia) |
| Hydrocortisone | Glucocorticoid receptor | ↑ vascular responsiveness to catecholamines |
Sources: Harrison's Principles of Internal Medicine, 21st Ed. (pp. 8234, 8253); Surviving Sepsis Campaign Guidelines; AHA/ACC Guidelines on Cardiogenic Shock; ACLS Anaphylaxis Protocol.
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