Hemorrhage
- Hemorrhage decreases blood volume.
- Hemorrhage decreases venous return.
- Hemorrhage decreases end-diastolic volume.
- Hemorrhage decreases stroke volume.
- Hemorrhage decreases cardiac output.
- Hemorrhage-induced arterial pressure fall decreases baroreceptor firing.
- Decreased baroreceptor firing during hemorrhage increases sympathetic activity.
- Tachycardia helps compensate for hemorrhage.
- Increased contractility helps compensate for hemorrhage.
- Arteriolar vasoconstriction helps compensate for hemorrhage.
- Venoconstriction helps compensate for hemorrhage.
- Reduced renal flow helps preserve cerebral and coronary perfusion during hemorrhage.
- Reduced splanchnic flow helps preserve cerebral and coronary perfusion during hemorrhage.
- Renin is activated during hemorrhage.
- Angiotensin II is activated during hemorrhage.
- Aldosterone is activated during hemorrhage.
- Antidiuretic hormone is activated during hemorrhage.
- Thirst is activated during hemorrhage.
- Fluid shifts during hemorrhage move fluid from the interstitium into capillaries.
- Renal salt and water retention helps restore extracellular volume after hemorrhage.
- Severe hemorrhage causes hypotension.
- Severe hemorrhage causes tissue hypoxia.
- Severe hemorrhage causes metabolic acidosis.
- Severe hemorrhage causes shock.
- Shock is inadequate tissue perfusion, and metabolic acidosis can develop when poorly perfused tissues rely more on anaerobic metabolism.
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