Hypovolemia Notes

Hypovolemia

Learning Objectives

• Be able to assess a patient with a DR ABCDE approach.
• List the ways in which the body maintains BP despite volume loss.
• Describe how to manage a hypovolemic patient acutely.
• Describe the basic physiology of the gastric mucosa.

Haemorrhage

• Haemorrhage is the loss of blood from the CVS (cardiovascular system), and it may be internal or external.
• The severity of haemorrhage is determined by the amount of blood lost and the rate of blood loss.

Blood Pressure Determinants

• Cardiac output (CO) is the product of stroke volume (SV) and heart rate (HR): Cardiac\ Output = Stroke\ Volume \times Heart\ Rate
• Blood pressure (BP) is the product of cardiac output (CO) and total peripheral resistance (TPR): Blood\ Pressure = Cardiac\ Output \times Total\ Peripheral\ Resistance
• Stroke volume is the difference between end-diastolic volume (EDV) and end-systolic volume (ESV): Stroke\ Volume = EDV - ESV
  • Normal EDV is approximately 120 ml.
  • Normal ESV is approximately 50 ml.

Stroke Volume

• Stroke volume is the amount of blood pumped by each ventricle per beat.
• Factors affecting stroke volume:
  • Preload and afterload
  • Inotropic state of the heart
  • Heart rate
  • Physical, nervous, and chemical factors

Importance of Maintaining Blood Pressure

• Adequate blood pressure is required to adequately perfuse organs, especially the brain and kidneys.
• Normal ABP (Arterial Blood Pressure) is approximately 120/80 mmHg.

Body's Monitoring of Blood Pressure

• Arterial Baroreceptors
• Kidneys
• Local stretch receptors in the heart (right atrium, left ventricle, and lungs)

Body Response to Hypovolemia

• The body responds to hypovolemia through baroreceptors.

Early Response to Hypovolemia

• Baroreceptors
  • PNS (Parasympathetic Nervous System) and SNS (Sympathetic Nervous System) responses
  • PNS:
    • Decreased cardiac stimulation (CN X - Vagus nerve)
    • Decreased heart rate
  • SNS:
    • Increased cardiac stimulation
    • Increased heart rate (SA node)
    • Increased contractility
    • Venous contraction
    • Arteriole contraction
    • Increased peripheral stimulation
  • The combined effects lead to increased cardiac output (CO), stroke volume (SV), heart rate (HR), and total peripheral resistance (TPR), ultimately increasing MAP (Mean Arterial Pressure).

Late Response to Hypovolemia

• Renal Responses
  • RAAS (Renin-Angiotensin-Aldosterone System) activation:
    • Hypoperfusion leads to renin secretion by JGA (Juxtaglomerular apparatus).
    • Renin cleaves angiotensinogen into Angiotensin I.
    • Angiotensin I is cleaved into Angiotensin II (AT2) by ACE (Angiotensin-converting enzyme).
    • AT2 causes vasoconstriction and increased cardiac contractility.
    • AT2 acts on adrenals to produce aldosterone.
    • Aldosterone acts on DCT (Distal Convoluted Tubule); ENaC channels are inserted, leading to salt and water retention.
  • ADH (Antidiuretic Hormone) Axis:
    • ADH is secreted by the posterior pituitary in response to multiple stimuli.
    • ADH acts on the V2 receptor.
    • AQP-2 channels are inserted into DCT & CD (Collecting Duct), leading to water retention.
• Stress Response
  • Adrenaline secreted by adrenal glands causes arterial vasoconstriction.
  • Cortisol secreted by adrenal glands acts on the aldosterone receptor, leading to salt and water retention.
• \text{CO} = HR \times SV
• \text{MAP} = CO \times TPR

Clinical Scenario: Jasmine

• Jasmine, a 62-year-old patient, is brought to the A&E (Accident & Emergency) in a semi-conscious state after vomiting a large amount of blood at home.
• Her regular medications include:
  • Aspirin 300mg
  • Analgesics for headache and back ache
  • Prednisolone for rheumatoid arthritis

Differential Diagnosis

• What is the most likely cause of her symptoms?
  • A. Bleeding gastric ulcer
  • B. Bleeding Oesophageal varices.
  • C. Mallory-Weiss tear
  • D. Gastroenteritis
  • E. Malignancy

Gastric Physiology

• Diagram of the stomach, esophagus, and duodenum, indicating the location of ulcers (Esophageal ulcer, Gastric Mucosa ulcer, and Duodenum ulcer), illustrating Peptic Ulcer Disease.

Gastric Barrier

• Gastro-irritant agents
  • NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) inhibit COX-1 and reduce prostaglandin production, leading to increased acid, decreased bicarbonate, and decreased mucus production.
  • Corticosteroids reduce prostaglandins.
  • H pylori

H. pylori

• H. pylori produces protease and ammonia.
• The inflammatory response induces G cells to produce gastrin.

Gastric Barrier (cont.)

• Gastro-protective agents
  • H2 receptor antagonists
  • Proton pump inhibitors
  • Antacids
  • Enteric coated drugs
• H2 receptor blockers block ECL cells, reducing histamine, which in turn reduces HCL production by parietal cells.
• G cells produce gastrin, which stimulates pepsin production by chief cells.
• Diagram illustrating the roles of carbonic anhydrase, HCO3-, H+, bile salts, and mucosal protection.