Shock

Shock is reduced perfusion of tissues that impairs their oxygenation. Blood pressure is the product of cardiac output and systemic vascular resistance (MAP ≈ CO × SVR), and cardiac output depends on venous return (preload) and pump function. Each type of shock begins with a different one of these failing: hypovolemic (too little volume), cardiogenic (the pump), obstructive (flow blocked through the heart or lungs) and distributive, of which septic shock is the main example (vessel tone and capillary integrity lost; also anaphylactic and neurogenic shock).

Some signs are shared by every type. Oliguria (urine < 0.5 mL/kg/h) reflects low renal blood flow and GFR plus ADH and aldosterone; if prolonged it becomes acute tubular necrosis. Lactic acidosis, a high anion gap metabolic acidosis, reflects tissue oxygen debt; a lactate above 2 mmol/L is abnormal and above 4 mmol/L signals severe hypoperfusion. Altered mental status reflects brain hypoperfusion.

Read each profile by walking the circuit from the primary disturbance: venules and vena cava (CVP, right-sided filling), lungs and left atrium (PCWP, left-sided filling), left ventricle and aorta (CO), arterioles (SVR), and back through the tissues (SvO₂, mixed venous oxygen saturation: how much oxygen the tissues left behind). The lecture's diagrams do exactly this; the lecture calls SVR “PVR” and SvO₂ “MVO₂”.

Lecture slide

Lecture slide

Lecture slide

Lecture slide

Hypovolemic shock follows loss of blood or sodium-containing fluid: external or internal hemorrhage (ruptured spleen or liver, ruptured abdominal aortic aneurysm), vomiting and diarrhea, massive sweating, and burns, where capillaries in burned and unburned tissue leak plasma into the interstitium and fluid evaporates from the wound. Cardiac output and left ventricular end-diastolic pressure fall; catecholamines, ADH and angiotensin II constrict arterioles, so SVR rises; SvO₂ falls because tissues extract more from the slow flow. The patient is cold and clammy with a rapid weak pulse, low urine output and a high anion gap lactic acidosis.

In acute hemorrhage the hemoglobin and hematocrit do not fall at first, because whole blood is lost: red cells and plasma leave in the same proportion. Over hours to days, interstitial fluid moves into the plasma (and intravenous fluids add more), diluting the red cells that remain and uncovering the deficit. The marrow answers with a reticulocytosis that becomes evident over several days and peaks about a week later. In burns the opposite happens: plasma is lost without red cells, so the hematocrit rises.

Cardiogenic shock is pump failure, most often from a large acute myocardial infarction; other causes are myocarditis, acute valvular failure (for example a cusp destroyed by infective endocarditis or papillary muscle rupture) and cardiomyopathy. The damaged ventricle ejects less, so CO falls; blood accumulates in the left ventricle, raising LVEDP and PCWP (pulmonary edema) and eventually CVP. Catecholamines, ADH and angiotensin II raise SVR, which adds afterload to the failing ventricle. Clinically: chest pain, then cold clammy skin, hypotension, low urine output and crackles.

Dying myocytes leak their contents into the blood (the membrane damage of irreversible injury, Chapter 1). Cardiac troponins I and T are the most sensitive and specific markers: they rise about 3–4 hours after onset, peak around 24–48 hours and stay elevated for 7–10 days (troponin I) to 10–14 days (troponin T). CK-MB rises within about 4–6 hours, peaks near 24 hours and returns to normal by 48–72 hours, which makes it useful for detecting a reinfarction a few days after the first event, when troponin is still high.

Septic shock follows bloodstream infection and is the most common cause of death in intensive care units. The lecture's figures: Gram-positive organisms in about 65% of cases (coagulase-negative staphylococci, Staphylococcus aureus; lipoteichoic acid), Gram-negative in about 25% (most often E. coli; endotoxin, lipopolysaccharide), and fungi in about 9% (Candida). Sepsis is now defined as life-threatening organ dysfunction caused by a dysregulated host response to infection; septic shock adds vasopressor-requiring hypotension with a lactate above 2 mmol/L despite fluid.

Early septic shock is warm: the skin is warm and flushed, the pulse is strong and bounding, and cardiac output rises to compensate for the low resistance. Blood races through dilated beds, and cells poisoned by cytokines extract oxygen poorly, so lactate rises even though venous blood stays relatively oxygen-rich. Hematologic findings in the lecture: anemia (bleeding and venipuncture), thrombocytopenia (platelets trapped and consumed in thrombi) and neutropenia (neutrophils marginated by activated adhesion molecules), although neutrophilia is more typical early.

ARDS is the same endothelial and epithelial injury in the lungs: activated neutrophils and cytokines damage alveolar capillaries, a protein-rich exudate floods the alveoli and hyaline membranes form (diffuse alveolar damage). It is a permeability edema with a normal PCWP, which separates it from the pressure edema of left heart failure (4.5).

In obstructive shock blood cannot get through the heart or lungs: massive pulmonary embolism, tension pneumothorax (rising intrathoracic pressure kinks and compresses the great veins), cardiac tamponade and constrictive pericarditis (the heart cannot fill). Pressure rises upstream of the block, so the neck veins distend (CVP ↑); the left heart is underfilled, so CO falls and SVR rises. A saddle embolus is the version you meet in 4.6: sudden collapse with raised JVP after immobility.

Neurogenic shock follows high spinal cord injury (above about T6) or spinal anesthesia. Sympathetic outflow to vessels and heart is lost: arterioles and veins dilate (SVR ↓, venous pooling, CVP ↓) and the heart rate is slow because vagal tone is unopposed. The skin is warm and dry. Bradycardia with hypotension in a trauma patient points here rather than to hemorrhage, which causes tachycardia.