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

 

List:

·     Intro

·     Glomerular filtration physiology

·     Factors decreasing filtration

·     Factors increasing reabsorption

 

Intro:

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

 

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:

↓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

 

Factors increasing reabsorption:

↑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)