Pathophysiology
P-II-22. Circulatory shock, Case 1
循環性ショック 症例1
Case Presentation
A 63-year-old man was taken to the emergency department by ambulance, as he had been vomiting blood since the morning hours.
Medical history:
- Hypertension and coronary heart disease
- Coronary artery stent treatment 15 years ago
- Takes 100 mg of Aspirin daily
- Deep vein thrombosis (DVT) in 2018, on Warfarin since then
- Long-standing drinking problem; dismissed from his job
- Fails to take medications as prescribed, and usually makes an attempt to take the medication he missed taking earlier
Presenting complaint: This morning he was woken up by pain which developed in his stomach, and the pain radiated toward the midline of his abdomen. He has vomited several times since then — initially his vomit was rather dark in colour, and later he vomited fresh blood as well. He arrived at the emergency department at noon.
Laboratory results on admission:
- White blood cell count: 10.7 g/L
- Haemoglobin: 128 g/L (low)
- Haematocrit: 0.39 L/L (low)
- Thrombocyte: 132 g/L (low)
Imaging: The abdominal CT scan showed liver cirrhosis and an abnormal fluid accumulation in the abdominal cavity.
Course in the ICU
He was taken to the ICU immediately after the CT scan. The patient was alert and oriented to person, place, and time, however, he complains of intermittent headaches.
- Blood pressure 70/30 mmHg, pulse 120 beats/min
- Oxygen administration raised to 40% to maintain arterial oxygen saturation above 90%
- Central intravenous catheter inserted; rapidly given 3 litres of normal saline, 3 units of fresh frozen plasma, and vitamin K
- Only 50 ml of urine passed via the urine catheter
Laboratory results after fluid treatment:
- White blood cell count: 13.4 g/L (high)
- Hb: 89 g/L (low)
- Ht: 0.30 (low)
- Thr: 115 G/L (low)
Deterioration: The patient’s condition deteriorates. His skin is pale, cold, and clammy. His blood pressure is unmeasurable, his pulse rate is 150/min. He has heavy breathing, and his finger pulse oximetry result is 86%, despite the administration of 40% oxygen. The patient developed shock.
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| Vomit “initially … dark in colour, and later … fresh blood” | Hematemesis from upper-GI bleeding; dark = partially digested blood, fresh red = active brisk bleed |
| CT: “liver cirrhosis and an abnormal fluid accumulation in the abdominal cavity” | Cirrhosis → portal hypertension → ascites and esophageal/gastric varices (the likely bleeding source) |
| “100 mg of Aspirin daily … on Warfarin” | Combined antiplatelet + anticoagulant therapy aggravates bleeding and impairs clotting |
| Hb 128 → 89 g/L; Ht 0.39 → 0.30 | Progressive fall confirms significant ongoing blood loss (partly dilutional after saline) |
| BP 70/30 → unmeasurable; pulse 120 → 150/min | Hypotension with compensatory, then decompensated, tachycardia |
| Skin “pale, cold, and clammy” | Intense peripheral vasoconstriction (sympathetic compensation) → high SVR; hallmark of hypovolemic shock |
| “only 50 ml of urine” | Oliguria from renal hypoperfusion |
| SpO₂ 86% despite 40% O₂ | Decompensated shock with tissue hypoperfusion and impaired oxygen delivery |
Key Points
- Type of shock: Hypovolemic (hemorrhagic) shock from upper-GI variceal bleeding secondary to liver cirrhosis / portal hypertension.
- Aggravating factors: Chronic alcohol use, poor medication compliance, and combined Aspirin + Warfarin therapy.
- Pathophysiology: Loss of circulating volume → ↓venous return → ↓cardiac output → compensatory sympathetic vasoconstriction and tachycardia → eventual decompensation.
- Clinical signature: Cold, clammy, pale skin (high systemic vascular resistance) distinguishes hypovolemic shock from warm distributive shock.
- Course: Progressed despite aggressive resuscitation (3 L saline, 3 U FFP, vitamin K) — indicates severe ongoing hemorrhage requiring definitive source control.
一問一答
▶What type of shock is caused by haematemesis from variceal bleeding in a cirrhotic patient?
Hypovolaemic (haemorrhagic) shock.
▶How does liver cirrhosis lead to upper GI bleeding?
Cirrhosis causes portal hypertension, producing oesophageal/gastric varices that can rupture and bleed.
▶What is the pathophysiology of hypovolaemic shock?
Loss of circulating volume reduces venous return and cardiac output, impairing tissue perfusion.
▶Why is the skin pale, cold, and clammy in hypovolaemic shock?
Compensatory sympathetic vasoconstriction shunts blood away from the skin (high systemic vascular resistance).
▶How does cold, clammy skin distinguish hypovolaemic from distributive (e.g. septic) shock?
Hypovolaemic shock has high SVR (cold skin); early distributive shock has vasodilation (warm skin).
▶Why does the heart rate rise to 120–150/min in haemorrhagic shock?
Sympathetic compensation increases heart rate to maintain cardiac output as volume falls.
▶Why is the urine output low (50 mL) in shock?
Renal hypoperfusion reduces glomerular filtration, causing oliguria.
▶How do combined aspirin and warfarin worsen this patient's bleeding?
Aspirin impairs platelet function while warfarin reduces clotting-factor synthesis, compounding the haemorrhage.
▶Why was fresh frozen plasma and vitamin K given to this patient?
To reverse warfarin's anticoagulation and replace clotting factors to help control bleeding.
▶What are the stages/classes of hypovolaemic shock based on blood loss?
Class I (<15%), II (15–30%), III (30–40%), and IV (>40%), with progressively worsening vital signs.
▶Why might the initial haemoglobin (128) underestimate the blood loss?
In acute haemorrhage haemoglobin concentration falls only after fluid shifts/resuscitation dilute the blood.
▶What defines decompensated (irreversible) shock?
When compensatory mechanisms fail, blood pressure becomes unmeasurable, and tissue/organ injury progresses despite resuscitation.
▶Why does chronic alcohol use predispose to this presentation?
It causes cirrhosis (→ varices) and can impair clotting, increasing bleeding risk.
▶What does the ascites (abdominal fluid) on CT indicate?
Portal hypertension and hypoalbuminaemia from cirrhosis, supporting a variceal source of bleeding.
▶What is the definitive management of bleeding oesophageal varices?
Endoscopic band ligation/sclerotherapy, vasoactive drugs (e.g. terlipressin), and antibiotics; balloon tamponade or TIPS if refractory.
▶Why does SpO2 fall to 86% despite oxygen in decompensated shock?
Severe hypoperfusion impairs oxygen delivery and gas exchange, and poor peripheral perfusion degrades the oximetry signal.
▶What is the immediate resuscitation priority in haemorrhagic shock?
Restore circulating volume with IV fluids and blood products while achieving source control of the bleeding.
▶Why is lactic acidosis expected in prolonged shock?
Inadequate tissue oxygen delivery forces anaerobic metabolism, producing lactate.
▶What is the role of the baroreceptor reflex in early shock?
Falling blood pressure reduces baroreceptor firing, triggering sympathetic activation to raise heart rate and vasoconstriction.
▶Why can ongoing haemorrhage progress despite large-volume fluid resuscitation?
Without source control, continued bleeding outpaces replacement and dilutes clotting factors, worsening the shock.