Critical Care Nephrology · Two-Week Intensive · Lecture 2 of 9
Renal Hemodynamics, Shock & ICU Monitoring
Perfusion pressure, venous congestion and the vulnerable kidney — reading both sides of the gradient
40 minutesNephrology FellowsWeek 1
Based on Koyner, Handbook of Critical Care Nephrology (2021) · NTUH Yunlin Branch
Learning objectives
By the end of this session you will be able to…
Explain why the outer medulla is the kidney's watershed and how autoregulation defends it.
Calculate renal perfusion pressure from MAP, CVP and intra-abdominal pressure — and act on it.
Choose a fluid-responsiveness test that is valid for the patient in front of you.
Match shock phenotype to first-line vasopressor and quote the renal evidence for each.
Recognise venous congestion and hypertensive emergency as the two extremes that both injure kidneys.
Koyner Ch 1–2, 13, 40, 43, 45 · Ronco Ch 4, 18
01
Renal perfusion physiology
A high-flow, low-extraction organ with one region living permanently on the edge of hypoxia.
Koyner Ch 2 · Ronco Ch 18
The kidney's energy paradox
20–25%of cardiac output — ~1.0–1.2 L/min for 0.5% of body mass
~10%of whole-body oxygen consumption
~99%of filtered sodium is reabsorbed — the metabolic bill
10–20mmHg medullary PO₂ vs ~50 in the cortex
Key point
Blood flow is delivered for filtration, not for oxygenation. Global renal oxygen extraction is low, which is exactly why a "normal" renal blood flow tells you nothing about medullary oxygenation.
The countercurrent architecture that concentrates urine also shunts oxygen from descending to ascending vasa recta
The medullary thick ascending limb and the S3 segment of the proximal tubule sit in the lowest-PO₂ zone and do the most transport work
Oxygen consumption is flow-dependent: more GFR → more filtered sodium → more reabsorptive work → more O₂ demand
This is why loop diuretics are theoretically medulla-protective (less mTAL transport) and why that theory has never translated into outcome benefit
The clinical consequence
Anaemia, hypoxaemia, sepsis and vasoconstrictors do not have to abolish renal blood flow to injure the kidney. They only have to tip a region that already runs at PO₂ 10–20 mmHg.
Ronco Ch 18 · Brezis M, Rosen S. N Engl J Med 1995;332:647 · Koyner Ch 2
Autoregulation: the kidney defends its own flow
Two mechanisms
Myogenic response — afferent arteriole constricts to a stretch stimulus within 3–10 s
Tubuloglomerular feedback — macula densa senses distal NaCl and releases adenosine to constrict the afferent arteriole over 10–60 s
Pharmacology at the two arterioles
NSAIDs block prostaglandin-mediated afferent dilation → the afferent cannot open
Give both to a hypotensive patient and autoregulation is disabled from both ends
Effective over MAP ≈ 80–180 mmHg — not down to 65
The curve shifts right in chronic hypertension: these patients need a higher MAP for the same flow
Autoregulation is blunted or lost in sepsis, after CPB, in CKD and in the elderly
Ronco Ch 18 · Koyner Ch 2 · Burke M et al. Am J Physiol Renal Physiol 2014
Perfusion pressure: it is never just MAP
RPP = MAP − CVP (renal perfusion pressure)
APP = MAP − IAP (abdominal perfusion pressure, target ≥ 60 mmHg) Use whichever back-pressure is higher. MAP 75 with CVP 18 gives an RPP of 57 — a number no one charted.
The venous side is the neglected half
The kidney is encapsulated. Raised renal venous pressure raises interstitial pressure, collapses tubules and peritubular capillaries, and reduces net filtration — with a perfectly acceptable MAP on the chart.
The abdominal side
Intra-abdominal hypertension transmits directly to the renal veins and parenchyma. Oliguria is the earliest sign — it precedes any change in blood pressure.
Ronco Ch 18 · Koyner Ch 2, 43 · Mullens W et al. J Am Coll Cardiol 2009;53:589
Four haemodynamic patterns, four different reasons the same creatinine goes up.
Koyner Ch 2 · Ronco Ch 4
Four shock types — one kidney at risk
Type
CO
SVR
CVP
ScvO₂
Renal mechanism
Hypovolemic
↓
↑
↓
↓
Prerenal → ATN if uncorrected; responds to volume
Distributive (sepsis)
↑ or normal
↓↓
variable
↑ or normal
Microcirculatory failure + inflammation; flow may be normal
Cardiogenic
↓↓
↑
↑↑
↓↓
Low output and venous congestion — the cardiorenal trap
Obstructive
↓
↑
↑↑
↓
Impaired filling and outflow; fix the obstruction, not the pressure
Common pitfall
Mixed shock is the ICU norm. A septic patient with pre-existing heart failure has a low-output and a vasodilated component — one vasopressor strategy will not serve both.
Koyner Ch 2 · Vincent JL, De Backer D. N Engl J Med 2013;369:1726
Sepsis: the map says 65, the kidney says otherwise
Macrocirculation (MAP, cardiac output) can be fully restored while the microcirculation stays deranged — haemodynamic incoherence
Regional shunting preserves cortical flow at the medulla's expense
Tubular cells downregulate metabolism to survive — GFR falls as an adaptive response, not only as damage
What follows from this
Resuscitating harder past the point of macrocirculatory adequacy does not reopen the microcirculation — it just adds venous congestion. Perfusion targets need an endpoint, not a ceiling.
Koyner Ch 2, 36 · Ince C. Crit Care 2015;19:S8 · Ronco Ch 89–90
Perfusion endpoints we actually use
Signal
What it reflects
Caveat
Urine output
Perfusion + function, continuously
Blunted by diuretics; non-oliguric injury is common
Lactate clearance
Global dysoxia and hepatic clearance
Liver failure, epinephrine, metformin, malignancy raise it without hypoperfusion
Hard to read in dark skin and in peripheral vascular disease
ScvO₂ / SvO₂
Oxygen supply–demand balance
Low in cardiogenic, normal-to-high in distributive despite dysoxia
Creatinine trend
Functional GFR
Lags 24–72 h and is diluted by resuscitation
ANDROMEDA-SHOCK · JAMA 2019
Capillary-refill-targeted resuscitation vs lactate-targeted in septic shock: 28-day mortality 34.9% vs 43.4% (p = 0.06) with less organ dysfunction at 72 h and less fluid. A cheap bedside endpoint held its own against a laboratory one.
Koyner Ch 1–2 · Hernández G et al. JAMA 2019;321:654
03
Hemodynamic monitoring
Which numbers deserve a decision, which deserve a trend, and which deserve to be ignored.
Koyner Ch 1 · Ronco Ch 21–26
The monitoring ladder — use the least invasive step that answers the question
1
Clinical exam + non-invasive BP — mottling, capillary refill, temperature gradient, mentation. Free, repeatable, underrated.
2
Arterial line — continuous MAP, waveform-derived SVV/PPV, blood gases. The minimum for any patient on vasopressors.
3
Central venous catheter — CVP as a congestion signal, ScvO₂, drug and KRT access.
4
Echocardiography — biventricular function, filling, valvular disease, tamponade. The modern workhorse; repeat it rather than trend a number.
5
Cardiac output monitoring — transpulmonary thermodilution or pulse contour when the diagnosis is genuinely unclear.
6
Pulmonary artery catheter — no longer routine; still valuable in mixed shock, pulmonary hypertension, RV failure and pre-transplant assessment.
Koyner Ch 1 · Ronco Ch 21–26
CVP: the most popular, least reliable number
The hard truth
CVP does not predict fluid responsiveness. Across studies the area under the ROC curve is ≈ 0.56 — "equivalent to flipping a coin". No CVP value should ever generate a fluid order by itself.
What CVP is still good for
The back-pressure term in renal perfusion pressure
A congestion signal: CVP >12–15 mmHg is consistently associated with AKI across cardiac and septic cohorts
Its waveform: large v-waves, RV failure, tamponade physiology
Its trend during decongestion
What it cannot do
Estimate blood volume
Predict the response to a bolus
Be interpreted without knowing intrathoracic and intra-abdominal pressure
Marik PE, Cavallazzi R. Crit Care Med 2013;41:1774 · Legrand M et al. Crit Care 2013;17:R278 · Koyner Ch 1
Venous congestion — the half of the gradient nobody monitors
Raise renal venous pressure and GFR falls, even with cardiac output held constant. In decompensated heart failure, CVP predicts AKI better than cardiac index does.
Hepatic vein Doppler: systolic blunting then systolic reversal
Intrarenal venous flow: continuous → biphasic → monophasic (the worst pattern, and the one that tracks AKI)
Combined with a plethoric IVC these give the VExUS grade 0–3 (Lecture 4)
Why this changes your plan
A congested kidney needs decongestion, not perfusion pressure. Giving fluid or raising MAP in VExUS grade 3 makes the kidney worse — this is the physiology behind diuresis-first management in cardiorenal syndrome.
Mullens W et al. J Am Coll Cardiol 2009;53:589 · Beaubien-Souligny W et al. Ultrasound J 2020;12:16 (VExUS) · Ronco Ch 109–111
Fluid responsiveness: ask a question the test can answer
Tests that work in most patients
Passive leg raise — semi-recumbent to legs-up 45°, measure stroke volume (not BP) within 60–90 s; ≥10% rise predicts response. Valid with arrhythmia and spontaneous breathing.
End-expiratory occlusion — 15 s hold; ≥5% SV rise. Needs a ventilated patient who tolerates the hold.
Mini-fluid challenge — 100 mL over 1 min, measure SV.
PPV / SVV — valid only if all are true
Fully controlled ventilation, no spontaneous effort
Tidal volume ≥8 mL/kg predicted body weight
Sinus rhythm
Normal intra-abdominal pressure, closed chest, no RV failure
In the real ICU these conditions hold in well under half of patients
Key point
"Fluid responsive" only means the stroke volume will rise — it never means fluid is indicated. Roughly half of haemodynamically stable people are fluid-responsive; that is normal physiology, not a prescription.
ResuscitationMinutes–hours. Life-threatening shock; boluses, positive balance is acceptable.
→
O
OptimisationHours. Titrate to organ perfusion; test responsiveness before every bolus.
→
S
StabilisationDays. Neutral balance; fluid only for ongoing losses. Maintenance and drug volumes now dominate.
→
E
EvacuationDays–weeks. Active de-resuscitation: diuretics or net ultrafiltration to remove the accumulated fluid.
Common pitfall
Most ICU fluid is given in phases S and E — as maintenance, drug diluents and flushes — long after the patient stopped being fluid-responsive. Count and prescribe it as deliberately as you prescribe vasopressors.
Malbrain MLNG et al. Ann Intensive Care 2018;8:66 · Koyner Ch 10
POCUS answers binary questions well ("is this a plethoric IVC with B-lines?") and continuous questions badly. Use it to change a decision, not to generate a number.
Koyner Ch 1, 18 · Ronco Ch 33
MAP targets: 65 is a starting point, not dogma
SEPSISPAM · NEJM 2014
MAP 80–85 vs 65–70 in septic shock: no mortality difference. In the chronic hypertension subgroup the higher target reduced doubling of creatinine and KRT use — at the cost of more atrial fibrillation.
The 65 Trial · JAMA 2020
Permissive hypotension (MAP 60–65) in patients ≥65 y on vasopressors: no increase in 90-day mortality, with less vasopressor exposure. Adjusted analysis favoured the lower target.
How to apply it
Start at 65. Go higher for chronic hypertensives, patients with raised IAP or CVP (the gradient, not the number), and where oliguria improves with the trial. Go lower in the elderly with vasopressor-limiting arrhythmia. Then reassess the target daily — it is a prescription, not a constant.
Asfar P et al. N Engl J Med 2014;370:1583 · Lamontagne F et al. JAMA 2020;323:938 · Evans L et al. Crit Care Med 2021 (SSC)
04
Vasopressors & inotropes
What each agent does at the two arterioles, and what the trials actually showed for the kidney.
Koyner Ch 2, 13
First-line by shock type
Shock
First-line
Add / alternative
Renal note
Distributive (sepsis)
Norepinephrine
Vasopressin 0.03 U/min → epinephrine → angiotensin II
Restoring perfusion pressure is protective; excess α-load is not
Cardiogenic
Norepinephrine + inotrope
Dobutamine, milrinone (renally cleared), mechanical support
Decongestion often matters more than the pressor
Hypovolemic
Volume first
Norepinephrine as a bridge while replacing
Do not use pressors to mask ongoing bleeding
Obstructive
Relieve the obstruction
Vasopressor only as a bridge
Pressure without flow will not perfuse anything
Practical conversion
Norepinephrine-equivalent dose lets you compare patients: epinephrine 1:1 · phenylephrine ÷10 · dopamine ÷150 · vasopressin 0.04 U/min ≈ 0.1 µg/kg/min. Above ~0.5 µg/kg/min NEE, mortality rises steeply — escalate the diagnosis, not just the dose.
Koyner Ch 2, 13 · Evans L et al. Crit Care Med 2021 · Goradia S et al. J Crit Care 2021 (NEE)
Norepinephrine — the workhorse
Pharmacology
Potent α₁ with modest β₁ — raises MAP with little chronotropy
Constricts the efferent arteriole more than the afferent → preserves or raises filtration fraction
Also increases venous return by recruiting unstressed splanchnic volume
Start 0.05–0.1 µg/kg/min; titrate every few minutes to the MAP target
Practice points
Start early — CENSER showed earlier shock control with norepinephrine begun alongside, not after, fluids
Peripheral administration is acceptable short-term through a well-sited proximal large vein with close monitoring
Rising dose with a falling MAP means a missed diagnosis: bleeding, tamponade, acidosis, adrenal insufficiency, abdominal pressure
Koyner Ch 13 · Permpikul C et al. Am J Respir Crit Care Med 2019;199:1097 (CENSER) · SSC 2021
Vasopressin — a sparing agent with a renal story
Rationale
Relative vasopressin deficiency develops in septic shock
V₁ receptor vasoconstriction is catecholamine-independent and preserved in acidosis
Preferential efferent arteriolar constriction — a filtration-friendly profile
Fixed dose 0.03 U/min; not titrated as a rescue pressor
Evidence
VASST (2008): no overall mortality difference; benefit signal in less severe shock
VANISH (2016): kidney-failure-free days not different, but less KRT use (25.4% vs 35.3%)
Watch: digital and mesenteric ischaemia, hyponatraemia, hepatic effects
Russell JA et al. N Engl J Med 2008;358:877 · Gordon AC et al. JAMA 2016;316:509 (VANISH) · Koyner Ch 13
Renally cleared — accumulates in AKI; long half-life means slow reversal of hypotension
Dopamine
Dose-dependent DA/β/α
Essentially never
"Renal-dose" dopamine is dead: no protection, more arrhythmia (ANZICS 2000)
Koyner Ch 13 · Bellomo R et al. Lancet 2000;356:2139 · SSC 2021
Angiotensin II and refractory vasoplegia
ATHOS-3 · NEJM 2017
Angiotensin II vs placebo in vasodilatory shock on ≥0.2 µg/kg/min norepinephrine equivalents: MAP response at 3 h 69.9% vs 23.4%. In the pre-specified AKI-on-KRT subgroup, KRT discontinuation by day 7 was 38% vs 15% — hypothesis-generating, not practice-defining.
Other rescue options
Hydrocortisone 200 mg/day — faster shock resolution (ADRENAL); with fludrocortisone, a mortality benefit in APROCCHSS
Methylene blue 1–2 mg/kg — NO-pathway inhibition in post-cardiotomy or refractory vasoplegia; avoid with serotonergic drugs and in G6PD deficiency
Correct the reversible: severe acidaemia, hypocalcaemia, hypothyroidism, adrenal insufficiency
Before escalating, exclude
Ongoing haemorrhage or unrecognised source of sepsis
Tamponade, tension pneumothorax, auto-PEEP
Abdominal compartment syndrome
Anaphylaxis or drug error
Khanna A et al. N Engl J Med 2017;377:419 · Tumlin JA et al. Crit Care Med 2018;46:949 · Venkatesh B et al. N Engl J Med 2018;378:797 (ADRENAL) · Annane D et al. N Engl J Med 2018;378:809 (APROCCHSS)
05
The kidney in specific contexts
Cardiorenal, hepatorenal, lung–kidney and the abdomen — the consult service's daily work.
Koyner Ch 3, 40, 42–43 · Ronco Ch 109–128
Cardiogenic shock and cardiorenal syndrome: a two-sided problem
Forward failure
Low cardiac output → reduced renal perfusion pressure → prerenal physiology → ATN if prolonged. Real, but the minority mechanism in most admissions.
Backward failure (dominant)
Raised CVP → renal venous and interstitial pressure → tubular collapse and reduced net filtration. In the ESCAPE and Mullens cohorts, CVP predicted AKI where cardiac index did not.
Key point
In most cardiorenal patients, decongestion is the renal therapy. A rising creatinine during effective diuresis of a congested patient often reflects haemoconcentration and better outcomes — not injury. Watch the CVP, weight and lung ultrasound, not the creatinine alone.
Mullens W et al. J Am Coll Cardiol 2009;53:589 · Bart BA et al. N Engl J Med 2012;367:2296 (CARRESS-HF) · Koyner Ch 40 · Ronco Ch 109–111
Hepatorenal physiology: everything dilates in the wrong places
Compensatory RAAS, sympathetic and ADH activation → intense renal vasoconstriction with a bland sediment and FeNa <1%
Cirrhotic cardiomyopathy blunts the cardiac compensation
Systemic inflammation from bacterial translocation adds a septic component — spontaneous bacterial peritonitis is a classic trigger
Diagnosis is exclusion
HRS-AKI requires cirrhosis with ascites, KDIGO-defined AKI, no shock, no nephrotoxins, no proteinuria/haematuria or structural disease, and no response to 2 days of albumin 1 g/kg with diuretic withdrawal.
Angeli P et al. J Hepatol 2019;71:811 (ICA) · Koyner Ch 42 · Ronco Ch 128
Lung–kidney crosstalk: ventilation changes the kidney
Mechanical effects
Positive intrathoracic pressure ↓ venous return and cardiac output
High PEEP ↑ CVP and pushes the diaphragm down, raising intra-abdominal pressure — a double hit on the venous side
Neurohormonal: ↑ renin, ADH and sympathetic tone → sodium and water retention
Gas-exchange effects
Hypoxaemia → renal vasoconstriction
Permissive hypercapnia → renal vasodilation but systemic acidaemia; net renal effect is usually tolerable
Ventilator-induced lung injury releases cytokines that injure the kidney directly (biotrauma)
Oliguria appears at IAP ≈ 15 and anuria near 30 — before blood pressure changes
Clinical pearl
Measure bladder pressure in any tense, oliguric abdomen — pancreatitis, massive resuscitation, burns, post-laparotomy. Vasopressors cannot fix a perfusion pressure problem created by the abdomen.
Kirkpatrick AW et al. Intensive Care Med 2013;39:1190 (WSACS) · Koyner Ch 43
06
The other extreme: hypertensive emergencies
Blood pressure management has two edges — and the kidney is injured by both.
Koyner Ch 45
Hypertensive emergency — the kidney is both target and victim
Definition: severe hypertension with acute end-organ damage — brain, heart, aorta, retina or kidney. The number alone is not an emergency.
Renal presentation: acute microangiopathy with haematuria, proteinuria, rising creatinine, sometimes a thrombotic microangiopathy picture
Target: reduce MAP by ≤25% in the first hour
then to ~160/100–110 over the next 2–6 h Autoregulation is right-shifted — normalising the pressure infarcts the brain and the kidney.
Four exceptions to "go slow"
Aortic dissection — SBP <120 and HR <60 within 20 min; β-blockade before vasodilator
Thrombolysis-eligible stroke — <185/110 before lysis
Scleroderma renal crisis — the treatment is an ACE inhibitor (captopril), not a titratable drip
Preeclampsia/eclampsia — labetalol, hydralazine or nifedipine plus magnesium; delivery is definitive
Koyner Ch 45 · Whelton PK et al. Hypertension 2018 · van den Born BH et al. Eur Heart J Cardiovasc Pharmacother 2019
Agents that respect the kidney
Agent
Use
Renal / ICU note
Nicardipine
First-line titratable IV for most emergencies
No dose change in renal failure; predictable, easy to titrate; reflex tachycardia
Clevidipine
Ultra-short-acting alternative
Lipid emulsion — count the calories and watch triglycerides
Labetalol
Dissection, pregnancy, hyperadrenergic states
Avoid in decompensated heart failure, severe asthma, bradycardia
A. Give fluid — PPV >13% means fluid-responsive · B. Do not give fluid — CVP 14 is too high · C. PPV is not interpretable here; do a passive leg raise · D. Start an inotrope
Hands up — then name which validity condition fails
Two pitfalls that undo good haemodynamics
Pitfall 1 — chasing MAP while ignoring the venous side
A "good" MAP with a high CVP or IAP is still a badly perfused kidney. Read both sides of the gradient before every fluid and vasopressor decision.
Pitfall 2 — using a valid test in an invalid patient
PPV/SVV in low tidal volumes, arrhythmia, spontaneous effort or intra-abdominal hypertension; IVC collapsibility in a ventilated patient; CVP as a volume estimate. A confidently wrong number is more dangerous than no number.
The kidney needs perfusion pressure (MAP − CVP or IAP), oxygen supply, and low tubular workload — the medulla lives at PO₂ 10–20 mmHg.
CVP predicts fluid responsiveness about as well as a coin flip, but it is a genuine congestion signal — use it as back-pressure, never as volume.
Pick a fluid-responsiveness test that is valid for that patient; PLR with stroke volume works when PPV does not.
Norepinephrine first, vasopressin to spare it (less KRT in VANISH); "renal-dose" dopamine is dead and fenoldopam did not replace it.
MAP 65 is the starting prescription — higher in chronic hypertension or high back-pressure, lower in the frail elderly. Reassess daily.
Congestion injures kidneys: cardiorenal syndrome and abdominal compartment syndrome are perfusion problems solved by removing fluid.
References & further reading
Where to go deeper
Asfar P, Meziani F, Hamel JF, et al. High versus low blood-pressure target in patients with septic shock (SEPSISPAM). N Engl J Med. 2014;370:1583–1593.
Lamontagne F, Richards-Belle A, Thomas K, et al. Effect of reduced exposure to vasopressors on 90-day mortality in older critically ill patients (65 Trial). JAMA. 2020;323:938–949.
Gordon AC, Mason AJ, Thirunavukkarasu N, et al. Effect of early vasopressin vs norepinephrine on kidney failure in septic shock (VANISH). JAMA. 2016;316:509–518.
Khanna A, English SW, Wang XS, et al. Angiotensin II for the treatment of vasodilatory shock (ATHOS-3). N Engl J Med. 2017;377:419–430.
Hernández G, Ospina-Tascón GA, Damiani LP, et al. Effect of a resuscitation strategy targeting peripheral perfusion vs lactate levels (ANDROMEDA-SHOCK). JAMA. 2019;321:654–664.
Mullens W, Abrahams Z, Francis GS, et al. Importance of venous congestion for worsening renal function in advanced decompensated heart failure. J Am Coll Cardiol. 2009;53:589–596.
Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with POCUS: the VExUS grading system. Ultrasound J. 2020;12:16.