Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
GFR
Baroreceptors in
bloodvessels of
SNS
systemic circulation
Autoregulation
Kidney can maintain a nearly constant GFR despite fluctuations
in in systemic arterial BP
Arterial pressure range from 80 to 180 mmHg
Outside autoregulation limits RBF becomes pressure dependent
Directly regulated the diameter of afferent (and lesser extent
efferent) arterioles
Mechanism: 2 types of control
Myogenic mechanism
General tendency for vascular smooth muscle to contract when stretched
Increased BP afferent arterioles constrict (decreased blood flow into glomerulus) and decrease in
glomerular pressure
Decreased BP dilatation of afferent arterioles and increase in glomerular hydrostatic pressure
Tubuloglomerular feedback mechanism
Directed by macula densa cells of juxtaglomerular apparatus
Located in walls of distal tubules – responds to filtrate flow rate and osmotic signals
Either allows or prevents release of chemicals that produces intense vasoconstriction of afferent
arterioles
Eg if macula densa exposed to slow flowing filtrate or low osmolarity filtrate vasodilatation of
afferent arterioles promoted ie allows more blood flow into glomerulus and therefore increases NFP
and GFR
Main Functions of the Kidneys
Salt & Water Balance or Homeostasis
Toxin Removal
Calcium & Phosphate Homeostasis
Acid Base Homeostasis
Stimulation of Erythropoiesis
Salt & Water Balance
Water Homeostasis
Controlled by ADH: Increase nr of aquaporins within
collecting ducts (Facilitates greater water reabsorption)
Sodium Balance
2 most NB mechanisms:
RAAS: Aldosterone increases NA reabsorption by increases nr of NA channels
and Na pumps (DCT and collecting duct)
ANP :Released with atrial stretch (salt &water overload) and Increases Na
excretion by INHIBITING the RAAS
Potassium Balance
K freely filtered by glomerulus and most of it reabsorbed by PCT (not
respond to differing plasma K concentration)
DCT and collecting ducts regulates K balance
Aldosterone : Stimulates K secretion by increasing Na reabsorption
K-H exchange pump: Collecting duct stimulates pump in response to
hypokalaemia (H secreted into collecting duct in exchange for reabsorning K ions)
A
D
H
A
N
P
ALDOSTERONE
Toxin Removal
• 2 Mechanisms:
- Filtration
- Secretion
• Most water soluble toxins e.g
creatinine are freely filtered and not
reabsorbed
• Ie the levels should remain
constant and at non-toxic levels in
blood unless
- Ingestion
- Production changes
- GFR changes
Calcium & Phosphate Homeostasis
Acid Base Homeostasis
Bicarbonate Reabsorption
Distal nephron reclaims any HCO3 that remains in the filtrate after passing through PCT
Acid Base Balance
Enzyme systems are very pH sensitive
Excess acid generation by metabolism that body needs to excrete
Vast majority excreted as CO2 in lungs but NB fraction
(phosphate and sulfate ions) excreted by collecting ducts
Bicarbonate main buffer in human body
When filtrate reaches the collecting ducts it is acidic (dt HCO3
reabsorption and NOT excretion of acid)
H ions are actively secreted by H-K antiporter (urine acidity
would increase if H not buffered)
All HCO3 has been reabsorbed ie H ions are now buffered
primarily by ammonia (metabolised glutamine) and filtered
phosphate ions
Stimulation of Erythropoiesis
ANAESTHESIA FOR PATIENTS
WITH KIDNEY FAILURE
CKD
Preoperative Evaluation
Intraoperative
Considerations
Postoperative
Considerations
Pharmacologic
Considerations
CKD
Incidence of ESRD (aka CRF) increasing worldwide – in USA
prevalence of ESRD more than doubled between 1990 and 2001
4 –Year survival for ESRD patients in UK only 48%
Approximately 26 million Americans have some form of CKD
(pre-dialysis kidney disease) and many remain undiagnosed
The CKD patient population fits the “2nd hit injury” paradigm
because they have some stable chronic baseline organ dysfunction
that is disproportionately worsened when exposed to acute
physiologic stress such as hypotension, hypovolaemia, or drug
toxicity
Definition CKD
2002 National Kidney Foundation Kidney Disease Outcomes
Quality Initiative (K/DOQI) guidelines proposed a 5 stage
classification for CKD based on GFR
GFR < 60mL/min/1,73m2 for > 3 months where there is
evidence of kidney damage or
Evidence of kidney damage for > 3 months based on pathologic
specimen, imaging or laboratory tests (e.g proteinuria)
irrespective of GFR
RIFLE criteria
Aetiology of CKD
ENDOC
GASTRO
INTESTINAL
UREMIA RINE
ACIDOSIS
ANOREXIA & NV (malnutrition)
• Less clearance H and HAGMA
DELAYED GASTRIC EMPTYING (RSI)
FLUID & ELECTROLYTE ABN’s
HYPERACIDITY (PUD – PPI)
• Hyperkalaemia – NB acidosis (avoid
MUCOSAL ULCERATIONS
(urea mucosal irritant) META hypercarbia in GA)
• Sodium balance – NB diuretic use
HAEMORRHAGE
ADYNAMIC ILEUS BOLIC and cardiac function
Ca & PO4 DERANGEMENT
Preoperative Evaluation
Reversal Agents
NEOSTIGMINE Renal excretion. Halflife prolonged. Inadequate reversal
often related to other effects (“recurarizaton’)
ATROPINE & Safe for use.
GLYCOPYROLLATE Repeated doses potential for accumulation (50% drug excreted in
urine)
Opioids
MORPHINE Active metabolites (morphine-6-glucoronide) may have
greater activity than parent drug and may accumulate
Start at lower suggested dosage and titrate dosage
upwards slowly and increase dose intervals
FENTANYL Inactivated by liver and excreted by urine
REMIFENTANYL Significant accumulation does not occur
ALFENTANYL No active metabolites
Benzodiazepines
MIDAZOLAM & Hepatic metabolism with urine elimination
DIAZEPAM Active metabolites accumulate
Protein bound ; increased sensitivity in
hypoalbuminaemic patients
Dose reduction 30 – 50%
Inhalation Agents
ACE inhibitors
No data to support benefit
CCB’s
Data insufficient to support benefit
N -Acetyl Cysteine
Prevention of contrast nephropathy (high risk in CKD)
Combination with adequate hydration
Data fails to show benefit when used as renoprotective agent during major surgery
References
Butterworth JF, Mackey DC, Wasnick JD. Morgan and Mikhail’s Clinical Anaesthesiology
5th Edition. Ch 29 pg 631 – 652 (Renal Physiology and Anaesthesia) and Ch 30 pg 653 –
670 (Anaesthesia for patients with kidney disease) 2013 The McGraw Hill Companies,
Inc.
Marieb EN. Human Anatomy and Physiology 5th Edition. Ch 26 pg 1013 – 1029 (The
Urinary System: kidney physiology) 2001 Pearson Education, Inc publishing as Benjamin
Cummings
McPhee SJ & Papadakis MA. Lange Current Medical Diagnosis & Treatment. 2012
McGraw Hill Companies, Inc.
Wallace K. Renal Physiology. Update in Anaesthesia (www.worldanaesthesia.org)
Milner Q. Pathophysiology of chronic renal failure. British Journal of Anaesthesia 2003;
3; 130 – 133 (http://ceaccp.oxfordjournals.org)
Salifu MO. Perioperative Management of Patients with Chronic Renal Failure. Jun 7
2013 (emedicine.medscape.com/article/284555)
Rang ST, West NL, Howard J, Cousins J. Anaesthesia for Chronic Renal Disease and
Renal Transplantation. EAU-EBU Update Series 4 (2006) 246 – 256
Eilers H, Liu KD, Gruber A, Niemann CU. Chronic kidney disease: implications for the
perioperative period. Minerva Anestesiologica 2010;76:725 – 736
Google Images