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

Urine output determinants

= filtration + secretion – reabsorption

Normal urine output

0.5mL/kg/h

Peri-op effects

↓filtration: hypotension

↑Reabsorption: stress response, dehydration

Hence ↓urine output

Starling equation

GFR = [K(P_c – P_B) – σ(π_c – π_B)]

·      P_c (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

↓mAP

↓Cardiac output

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

·      ↓inotropy (e.g. propofol)

↓SVR:

·      General anaesthesia

·      Neuraxial anaesthesia

↑CVP

·      IPPV

·      Heart failure

·      Raised intra-abdominal pressure

↑RVR

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

↑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

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

↑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

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

↑SNS

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)