Pathophysiology – Shock

Shock = life-threatening state produced by an imbalance between O$2$ supply and cellular O$2$ demand.
- Leads to inadequate tissue perfusion, impaired aerobic metabolism, progressive organ dysfunction.
Four major clinical categories:
- Cardiogenic – pump failure.
- Obstructive – mechanical blockage to forward flow.
- Hypovolemic – absolute fluid loss.
- Distributive – pathological vasodilatation/maldistribution (anaphylactic, neurogenic, septic).

Universal feature across all shock types.
↓ O$_2$ delivery → cells shift from aerobic pathways to glycolysis; consequences include:
- ↓ ATP production.
- ↑ lactate → metabolic acidosis.
- Generation of oxygen-derived free radicals.
- Activation of inflammatory cytokines (e.g., TNF-α, IL-1).

Compensatory Stage
- Baroreceptors detect ↓ BP → sympathetic discharge.
  - Vasoconstriction (↑ SVR), tachycardia, bronchodilation.
  - Skin cool/clammy, pupils dilated, urine output ↓.
  - BP may stay normal despite falling CO.
Progressive Stage
- Compensatory mechanisms fail → hypotension, worsening hypoxia.
- Anaerobic metabolism dominates (↑ lactate, acidosis).
- Cell swelling, dysfunction, death; cytokines & clotting cascade amplify injury.

↓ Cardiac output, ↑ LV end-diastolic pressure, S$_3$ gallop, pulmonary edema.
SNS response → tachycardia, vasoconstriction, narrow pulse pressure.
↓ SvO$_2$ (venous oxygen saturation) due to high extraction.

Aortic/carotid baroreceptors → medullary center → SNS → β$_1$ stimulation ↑ HR/contractility.

Improve CO & myocardial O$_2$ delivery while reducing workload.
Pharmacology
- Inotropes (e.g., dobutamine).
- Afterload reducers (e.g., nitroprusside).
- Preload reducers (e.g., nitrates/diuretics).
Mechanical support
- Impella, ECMO, Ventricular Assist Devices (VADs).

Mechanism: external impedance to cardiac filling/outflow.
Causes: pulmonary embolism, cardiac tamponade, tension pneumothorax.
Clinical signs: right-sided HF (JVD, hepatomegaly), sudden hypotension.
Trauma pearl: Chest trauma → pneumothorax → mediastinal shift → LV preload ↓ → shock; immediate decompression essential.
Therapy: Remove/relieve obstruction (thrombolysis, pericardiocentesis, chest tube).

Pathogenesis: absolute loss of blood/plasma (hemorrhage, burns, dehydration, third-spacing).
Compensation: tachycardia, vasoconstriction, ↑ contractility.
Treatment: Stop loss + fluid resuscitation (crystalloids, colloids, blood).

Antigen → mast-cell degranulation → histamine, leukotrienes → vasodilation, ↑ permeability, bronchospasm.

Brain/spinal injury → loss of sympathetic tone → vasodilation, bradycardia, hypotension.

Systemic infection + SIRS; bacteremia common.
Cytokine storm (TNF-α, IL-1) → excess nitric oxide → profound arterial/venous vasodilation → pooling, hypotension.
DIC risk: widespread microthrombi.
Progressive phase may switch to hypodynamic state (↓ CO, cold skin, narrow pulse pressure).
Lactic acidosis hallmark of tissue hypoxia.

Presence of viable organisms in bloodstream plus systemic inflammatory response.
Severe hypotension is common consequence but not definitional criterion.

Tissue O$_2$ adequacy depends on:
- Cardiac Output (CO)
- Arterial O$_2$ content
- Blood-flow distribution
Invasive/non-invasive monitoring guides manipulation of preload, afterload, contractility to optimize CO.

Acute Respiratory Distress Syndrome (ARDS) – respiratory failure; hyperventilation → risk of respiratory alkalosis.
Disseminated Intravascular Coagulation (DIC) – systemic microvascular clots.
Acute Renal Failure – ischemic tubular necrosis.
Multiple Organ Dysfunction Syndrome (MODS)
- Primary – direct initial insult.
- Secondary – consequence of sustained inflammation/hypoperfusion.

Core reaction: CO2 + H2O \leftrightarrow H2CO3 \leftrightarrow H^{+} + HCO_3^{-}
- Lungs: adjust CO_2 via respiratory rate.
- Kidneys: secrete H^{+} / reabsorb HCO_3^{-}.
- Buffer reserve: plasma bicarbonate neutralizes added acids/bases.