Hypovolemia Notes

Hypovolemia

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.

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 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

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

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).

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

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

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

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

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.