2011B15 Outline the physiological changes that might explain why an otherwise well patient
may have a reduced urine output intra-operatively.



·      Intro

·      Glomerular filtration physiology

·      Factors decreasing filtration

·      Factors increasing reabsorption



Urine output determinants

= filtration + secretion – reabsorption

Normal urine output


Peri-op effects

↓filtration: hypotension

↑Reabsorption: stress response, dehydration

Hence ↓urine output


Glomerular filtration physiology:

Starling equation

GFR = [K(Pc – PB) – σ(πcπB)]

·      Pc (capillary hydrostatic pressure) is the major variable peri-operatively

·      Dependent on a) renal blood flow b) afferent and efferent arteriolar tone

Renal blood flow

RBF = mAP – CVP / renal vascular resistance (RVR)

·      Myogenic autoregulation effective if mAP 70-170mmHg

Mean arterial pressure

mAP – CVP = CO x TPR

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


Factors decreasing filtration:


↓Cardiac output

·      ↓preload (general or neuraxial anaesthesia, IPPV, dehydration)

·      ↓inotropy (e.g. propofol)


·      General anaesthesia

·      Neuraxial anaesthesia


·      IPPV

·      Heart failure

·      Raised intra-abdominal pressure


Angiotensin 2 (AGTR1) and SNS (α1) -> efferent > afferent arteriolar constriction


Factors increasing reabsorption:


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

Renal effects:

·      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


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

Renal effects of angiotensin 2

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

·      ↑release of aldosterone

·      ↑release of ADH

Actions of angiotensin-3:

·      40% of pressor activity

·      100% of aldosterone induction

Renal effects of aldosterone

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

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


Stimulus: baroreceptor reflex

Renal effects:

·      Constrict efferent > afferent arterioles(α1)

·      Hence ↓GFR but preserved GFP

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

·      ↑ renin release (see RAAS) (β1)




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