Pathophysiology – Shock

Definition & General Concepts

• 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).

Pathogenesis of Shock

Impaired Tissue Oxygenation

• 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).

Stages & Compensatory Mechanisms

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.
2. Progressive Stage
   • Compensatory mechanisms fail → hypotension, worsening hypoxia.
   • Anaerobic metabolism dominates (↑ lactate, acidosis).
   • Cell swelling, dysfunction, death; cytokines & clotting cascade amplify injury.

Cardiogenic Shock

Etiology & Pathogenesis

• Severe ventricular dysfunction after myocardial infarction most common.
• Others: cardiomyopathy, ventricular rupture, congenital defects.

Clinical Picture

• ↓ 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.

Early Reflexes for Low CO

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

Management Goals

• 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).

Hemorrhagic Classification (Table 20.3)

• Class I (
• Class II (750–1500 mL / 15–30 %) – tachycardia, tachypnea, cool skin.
• Class III (1500–2000 mL / 30–40 %) – ↓ SBP, mental status changes.
• Class IV (>2000 mL / >40 %) – profound hypotension, coma.

Obstructive Shock

• 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).

Hypovolemic Shock

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

Distributive Shock

Anaphylactic

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

Neurogenic

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

Septic

• 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.

Updated Definition of Sepsis

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

Assessment & Hemodynamic Monitoring

• 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.

Complications of Shock

• 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.

Acid–Base Physiology: Bicarbonate Buffer

• 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.

Nursing Plan of Care Considerations (NGN)

• Insert large-bore IV for rapid fluid/blood infusion.
• Begin albumin (colloid) therapy as ordered.
• Administer Lactated Ringer’s (or NS) crystalloid.
• Monitor/infuse dextran if prescribed.
• Maintain supplemental O$_2$ (optimize arterial content).
• Type & cross-match; prepare for rapid PRBC transfusion.
• Assess serum Ca$^{2+}$ (citrate in blood products can induce hypocalcemia).