2009B13 Explain the physiological processes that cause oliguria in response to hypovolaemic shock.

Oliguria

·      <0.5mL/kg/h

Hypovolaemic shock

·      Reduced blood volume resulting in failure to meet tissue metabolic requirement

·      Occurs at ~20% blood loss

Cause of oliguria

·      ↓Filtration

·      ↑Reabsorption

·      Acute tubular necrosis (or whatever it is that causes intrinsic renal failure)

Causal pathway

↓Blood volume -> ↓preload -> ↓cardiac output -> ↓mAP -> ↓P_c -> ↓GFR -> ↓UO

Relevant physiology

GFR = K[(P_C – P_B) – σ(π_C – π_B)]

·      P_c (capillary hydrostatic pressure) is the major variable in hypovolaemia

RBF = (mAP – CVP) / RVR

·      Effective autoregulation mAP 70-170mmHg

mAP – CVP = CO x TPR

·      Factors ↑CO: ↑preload, ↓afterload, ↑rate, ↑contractility

↑SNS

Stimulus: baroreceptor reflex

Effect:

·      Constrict efferent > afferent arterioles (α₁)

·      Hence ↓GFR but preserved GFP

·      ↑ proximal tubular reabsorption of Na⁺/H₂O (α₁)

↑ renin release (see RAAS) (β₁)

↑ADH

Source: hypothalamus -> posterior pituitary

Release stimuli:

·      Stress response from surgery

·      Many drugs

·      ↑osmolality (sensitive to ∆2%) – dehydration from pre-op fasting

·      ↓blood volume (sensitive to ∆10% but overrides osmolality)

·      ↓mAP

·      Angiotensin 2

Effects: ↑reabsorption

·      Insertion of aquaporin 2 into apical membrane of collecting ducts -> ↑H₂O reabsorption

·      Insertion of urea transporters -> ↑ medullary interstitial osmolarity

·      ↑Na+ reabsorption in thick ascending loop of Henle

↑RAAS

Source: granular cell of juxtaglomerular apparatus

Release stimuli:

·      ↑SNS activation of granular cells (β₁) - e.g. pain

·      ↓stretch of afferent arteriolar baroreceptors - i.e. hypotension

·      ↓ NaCl delivery to macula densa -> ↑PGE₂, ↓adenosine release - i.e. ↓GFR

Effects of angiotensin 2:

·      Constrict efferent > afferent arterioles

·      Hence ↓GFR with preserved GFP

·      ↑Na⁺/H₂O reabsorption from PT (via Na⁺/H⁺ exchange) (AGTR1)

·      ↑release of aldosterone

·      ↑release of ADH

Effects of angiotensin-3:

·      40% of pressor activity

·      100% of aldosterone induction

Effects of aldosterone:

·      ↑Na⁺ reabsorption from principal cells of connecting tubule and collecting ducts (MR)

·      Indirectly causes H₂O reabsorption via ↑ECF osmolality hence ↑ADH

Cause

·      ↓mAP -> ischaemia -> ATN

·      ? Other factors