Hemodynamics: Delivery, Responsiveness & Congestion

Everything from two equations

There are twenty numbers on a hemodynamic monitor. There are two equations underneath all of them.

Working the equation backwards

Given a hypotensive patient, ask in order:

1. Is the rate wrong? Too slow — no output despite a good stroke volume. Too fast — no diastolic filling time, so stroke volume collapses. Either extreme drops cardiac output.
2. Is the stroke volume low? If so, is it a preload, afterload, or contractility problem? Those are the only three inputs to stroke volume.
3. Is the tone low? SVR below roughly 800 dyn·s·cm⁻⁵ points to a distributive process — sepsis, anaphylaxis, neurogenic, liver failure, adrenal crisis, post-bypass vasoplegia.

That single walkthrough separates the four shock categories without a single monitor beyond an arterial line and an echo.

The derived numbers, and what each actually is

Pressure is not flow

The most consequential idea in this module, and the one most often skipped:

A blood pressure tells you about pressure. It tells you almost nothing about flow.

A patient with a MAP of 75 on high-dose norepinephrine and a cardiac index of 1.6 has a beautiful number and is dying of low output. A patient with a MAP of 62 and a cardiac index of 3.8 who is warm, making urine and mentating is fine. Organs are perfused by flow, not pressure; pressure is only the driving force, and it can be manufactured with vasoconstriction at flow's expense.

Autoregulation, and why MAP targets exist at all

Brain, heart and kidney maintain roughly constant blood flow across a range of perfusion pressures — the classic cerebral autoregulation range is a MAP of about 60–150 mmHg — by constricting and dilating their own arterioles. Below the lower limit, flow falls linearly with pressure and the organ becomes pressure-dependent.

Two clinical consequences:

• Chronic hypertension shifts the whole curve to the right. A chronically hypertensive patient may be genuinely ischemic at a MAP of 65 that is fine for someone else. This is the physiology behind individualizing MAP targets.¹
• Injured brain loses autoregulation. In TBI and stroke the curve flattens toward pressure-passive, which is why cerebral perfusion pressure (CPP = MAP − ICP) becomes the target rather than MAP alone.

Preload and the Frank–Starling curve

What preload actually is

Preload is the myocardial fiber length at end-diastole — how stretched the ventricle is just before it contracts. The true measure is end-diastolic volume, not pressure.

Otto Frank and Ernest Starling showed that within limits, greater end-diastolic stretch produces a more forceful contraction. The molecular basis is worth knowing because it explains the shape of the curve: stretching the sarcomere toward its optimal length (~2.2 μm) improves actin–myosin overlap and increases the calcium sensitivity of troponin C. Past that length, overlap and sensitivity both fall off, and further stretch does not help — it just raises filling pressures.

The curve you can actually move

The Frank–Starling curve is not one curve. It is a family of curves, and contractility selects which one you are on.

• Steep, high curve = good contractility. Small increases in preload produce large increases in stroke volume. This patient is fluid responsive.
• Flat, low curve = poor contractility. The same fluid produces little stroke volume gain and a large rise in filling pressure — congestion without benefit.

Two patients with identical CVPs can be at opposite ends of this behavior. That is precisely why a single filling pressure cannot predict fluid responsiveness, and why the profession moved to dynamic testing.

Venous return: the other half that gets forgotten

Cardiac output cannot exceed venous return. Guyton's framing: venous return is driven by the difference between mean systemic filling pressure (the pressure in the venous reservoir) and right atrial pressure, divided by the resistance to venous return.

VR ∝ (MSFP − RAP) ÷ resistance to venous return

Three practical consequences follow:

1. A fluid bolus works by raising MSFP. It converts unstressed volume (blood sitting in venous capacitance, generating no pressure) into stressed volume (blood under pressure that can flow). This is why only some of a liter of fluid does anything hemodynamically.
2. A vasopressor also raises MSFP through venoconstriction. This is the underappreciated mechanism by which norepinephrine can increase cardiac output — it recruits unstressed volume, an internal autotransfusion.
3. Anything that raises right atrial pressure reduces the gradient for venous return. Positive-pressure ventilation, high PEEP, auto-PEEP, tamponade, tension pneumothorax and abdominal compartment syndrome all obstruct flow this way. It explains why the hypotension after intubation, the hypotension from auto-PEEP, and the hypotension of tamponade share a mechanism.

The evidence that ended the CVP era

Marik's systematic reviews found essentially no relationship between CVP and blood volume, and that CVP performed no better than a coin flip at predicting who would respond to a fluid bolus — an area under the ROC curve of roughly 0.56.^3,4 Later large sepsis trials (ProCESS and its companions) found that protocolized care built on CVP and ScvO₂ targets did not improve mortality over usual care with good clinical judgment.⁵

The Surviving Sepsis Campaign 2021 accordingly recommends against using static physical examination or static measures alone to guide resuscitation, favoring dynamic measures, capillary refill and lactate clearance.¹

Afterload, contractility and the pressure–volume loop

Afterload

Afterload is the wall stress the ventricle must overcome to eject. By Laplace's law:

Wall stress ∝ (Pressure × Radius) ÷ (2 × Wall thickness)

That formula has three teaching points hidden in it:

• Afterload is not the same as SVR. SVR is a contributor; ventricular size is another. A dilated ventricle has higher wall stress at the same blood pressure — one reason dilated cardiomyopathy is self-perpetuating.
• Hypertrophy reduces wall stress by increasing thickness. It is initially adaptive, and eventually maladaptive (diastolic dysfunction, impaired subendocardial perfusion).
• Reducing afterload increases stroke volume in a failing ventricle, and does so more effectively than in a normal one. This is why afterload reduction is such a powerful intervention in acute decompensated heart failure — and why it does relatively little in a healthy heart.

RV afterload is pulmonary vascular resistance, and the RV — a thin-walled volume pump — tolerates increases in it very poorly. Hypoxia, hypercarbia, acidosis, high PEEP, and pulmonary embolism all raise PVR acutely, and the RV can fail within minutes.

Contractility (inotropy)

Contractility is the intrinsic force of contraction at any given preload and afterload. It is the property that selects which Frank–Starling curve you are on.

Increased by: catecholamines and other cAMP-raising drugs, calcium, digoxin, and increasing heart rate (the Bowditch or treppe effect). Decreased by: ischemia, acidosis, hypoxia, hypocalcemia, hyperkalemia, beta blockade, calcium-channel blockade, myocardial stunning, sepsis-induced cardiomyopathy, and myocarditis.

Ejection fraction is the number we use clinically, but it is load-dependent — a mitral regurgitation patient can have a "normal" EF ejecting mostly backwards into a low-pressure atrium, and a patient on high-dose vasopressors can have a falsely low EF because afterload is enormous. The load-independent measure is the slope of the end-systolic pressure–volume relationship, which you will not measure at the bedside but should understand exists.

The pressure–volume loop

One cardiac cycle plotted with LV pressure against LV volume makes a loop that runs counterclockwise through four phases:

1. Mitral valve closes → isovolumic contraction (vertical rise, pressure up, volume unchanged)
2. Aortic valve opens → ejection (volume falls as blood leaves)
3. Aortic valve closes → isovolumic relaxation (vertical fall)
4. Mitral valve opens → filling (volume rises along the diastolic compliance curve)

Reading changes in the loop is the fastest way to see what an intervention did:

Diastolic function

Roughly half of heart failure has a preserved ejection fraction. A stiff ventricle fills poorly, so:

• Filling pressures are high at any given volume — pulmonary congestion at "normal" volumes.
• Atrial contraction matters much more — losing the atrial kick to atrial fibrillation can drop cardiac output substantially in a stiff ventricle.
• Tachycardia is poorly tolerated — shortened diastole means less filling time, in a ventricle that already fills slowly.
• Fluid tolerance is narrow. These patients flip from dry to congested over a very small volume range.

The University of Minnesota Atlas of Human Cardiac Anatomy physiology tutorial has free videos of the cardiac cycle in reanimated human hearts that make the valve timing in the pressure–volume loop concrete.⁶

Oxygen delivery and consumption

The entire cardiovascular system exists to deliver oxygen to mitochondria. Two numbers describe whether it is succeeding.

Oxygen delivery (DO₂)

DO₂ = CO × CaO₂ × 10

where CaO₂ = (1.34 × Hgb × SaO₂) + (0.003 × PaO₂)

Normal DO₂ is roughly 900–1100 mL/min (about 500–600 mL/min/m² indexed).

Read the CaO₂ equation carefully, because it tells you where oxygen actually lives:

• 1.34 = mL of O₂ each gram of fully saturated hemoglobin carries
• Hgb × SaO₂ = the hemoglobin-bound oxygen — essentially all of it
• 0.003 × PaO₂ = dissolved oxygen — at a PaO₂ of 100 that is 0.3 mL/dL out of roughly 20. About 1.5%.

Oxygen consumption (VO₂)

VO₂ = CO × (CaO₂ − CvO₂) × 10

Normal at rest is roughly 200–250 mL/min. It rises with fever (about 10% per °C), shivering, agitation, work of breathing, seizures, pain, and burns — and falls with sedation, cooling, paralysis and mechanical ventilation. Reducing VO₂ is a legitimate therapeutic strategy when delivery cannot be raised: this is the physiologic argument for intubating a patient whose respiratory muscles are consuming a large fraction of cardiac output, and for treating shivering during targeted temperature management.

The extraction ratio and what ScvO₂ tells you

O₂ER = VO₂ ÷ DO₂, normally about 25%.

The body extracts a quarter of delivered oxygen and returns the rest — which is why mixed venous saturation is normally 60–80% (central venous, ScvO₂, runs slightly higher, 70–80%).

When delivery falls, the tissues compensate by extracting more, and venous saturation falls. That makes ScvO₂ an elegant global marker of the supply–demand balance.

Anaerobic threshold and lactate

Normally VO₂ is supply-independent — as delivery falls, extraction rises to compensate, and consumption is unchanged. Below a critical DO₂, extraction can rise no further, VO₂ begins to fall with delivery, and anaerobic metabolism takes over. Pyruvate is shunted to lactate, and lactate rises.

But lactate is not a pure hypoxia marker. It also rises from β₂-adrenergic stimulation (endogenous stress or an epinephrine infusion), impaired hepatic clearance, thiamine deficiency, metformin, malignancy and seizures. Interpret the trend alongside perfusion, not in isolation — a falling lactate is one of the most reliable signs that a resuscitation is working, and the Surviving Sepsis Campaign suggests guiding resuscitation to decrease lactate in patients with an elevated level.¹

Fick's principle

CO = VO₂ ÷ [(CaO₂ − CvO₂) × 10]

Rearranged from the VO₂ equation. It underlies thermodilution cardiac output measurement, the estimated-Fick calculation in the cath lab, and — most usefully at the bedside — the intuition that for a fixed VO₂, the arteriovenous oxygen difference is inversely proportional to cardiac output. A widened A-V difference means the tissues are extracting more, which means flow has fallen. That is the physiology behind reading an ScvO₂ as a cardiac output surrogate.

Fluid responsiveness: static is dead, dynamic is the standard

Only about half of hemodynamically unstable ICU patients are fluid responsive. Giving fluid to the other half produces edema, worsened oxygenation, raised intra-abdominal pressure, delayed weaning, and — as the accumulating literature shows — worse outcomes. So the question is no longer "is this patient dry?" but "will a fluid bolus increase this patient's stroke volume?"

Why the static indices failed

CVP, PAOP, and the echocardiographic end-diastolic areas are all static measurements of a filling pressure or volume at one moment. To predict responsiveness they would need to tell you the slope of the Frank–Starling curve at that point — and a single point on an unknown curve cannot do that. Marik's meta-analyses put CVP's performance at roughly the level of chance.^3,4

The dynamic indices: using the ventilator as the test

Positive-pressure ventilation cyclically compresses the vena cava and the pulmonary vasculature. In a preload-dependent patient, that cyclic change produces a visible cyclic change in stroke volume — the swings are big. In a preload-*independent* patient, the swings are small.

• Pulse pressure variation (PPV) = (PP_max − PP_min) ÷ PP_mean × 100. A threshold above about 13% predicts responsiveness with good accuracy in validated conditions.^8,7
• Stroke volume variation (SVV) = the same computation on stroke volume rather than pulse pressure; the usual threshold is about 10–13%.

On the arterial line, PPV is literally the respiratory "swing" you can see with your own eyes on the waveform.

Passive leg raise: the test that works almost everywhere

Tilt the patient from a 45° semi-recumbent position to supine with the legs elevated to 45°, which shifts roughly 300 mL of blood centrally — a reversible, self-limited autotransfusion that requires no fluid at all.

Done right, it is the single most useful bedside test of preload responsiveness because it is valid in spontaneous breathing, in arrhythmia, and at low tidal volumes.⁷

How to do it properly:

• Start semi-recumbent, not flat — the trunk-down component is what recruits splanchnic volume. Starting supine loses much of the effect.
• Move the bed, not the patient. Lifting the legs by hand causes pain and adrenergic stimulation that confound the result.
• Measure a real-time flow variable — stroke volume, cardiac output, velocity–time integral on echo, or end-tidal CO₂. Blood pressure alone is not adequate; it changes late and unreliably.
• Measure within 30–90 seconds. The effect peaks within a minute and dissipates.
• A ≥10% increase in cardiac output or stroke volume is a positive test.

Other dynamic tests

• End-expiratory occlusion test: a 15-second expiratory hold removes the cyclic impediment to venous return; a >5% rise in cardiac output predicts responsiveness. Requires a patient who tolerates the hold.
• Mini-fluid challenge: 100 mL over one minute with a real-time flow measurement — small enough to be nearly harmless, big enough to detect.
• IVC distensibility/collapsibility on ultrasound: carries the same limitations as PPV in spontaneously breathing patients and in RV failure. Useful at the extremes (a fully collapsing IVC in a hypotensive patient is informative), unreliable in the middle.
• Capillary refill time: simple, and in the ANDROMEDA-SHOCK trial performed at least as well as lactate for guiding resuscitation. Standardize the technique (firm pressure on the index finger for 10 seconds, refill <3 seconds).

What the change in practice looks like

The FRESH trial randomized patients with septic shock to dynamic-assessment-guided resuscitation versus usual care and found less positive fluid balance and less need for renal replacement therapy and mechanical ventilation in the dynamic-assessment arm.⁹ The Surviving Sepsis Campaign recommends dynamic measures over static physical examination or static parameters alone.¹

Fluid tolerance, congestion and VExUS

Fluid responsiveness answers will the stroke volume go up? Fluid tolerance answers a different and equally important question: what will the fluid do to everything else?

Both can be true at once. A patient can sit on the steep part of the Starling curve and be so congested that additional volume causes kidney injury, gut edema and worsening oxygenation. Recognizing that pairing is the modern refinement in resuscitation, and it is where point-of-care ultrasound earned its place.

What venous congestion does

Organ perfusion pressure is arterial inflow minus venous outflow pressure. Raising central venous pressure narrows that gradient from the wrong end, and encapsulated organs suffer first:

• Kidney: the renal capsule cannot expand, so rising renal venous pressure raises interstitial pressure and collapses tubules. Elevated CVP has been associated with acute kidney injury more consistently than low cardiac output has — congestive nephropathy, or "cardiorenal syndrome type 1."
• Liver: congestive hepatopathy, rising transaminases and bilirubin.
• Gut: bowel wall edema, impaired absorption, feeding intolerance, translocation, and rising intra-abdominal pressure — which in turn further reduces venous return, a closing loop.
• Lung: interstitial and alveolar edema, worse compliance, prolonged ventilation.

VExUS: grading congestion instead of guessing at it

The Venous Excess Ultrasound grading system, described by Beaubien-Souligny and colleagues in 2020, turns venous congestion into a reproducible grade using four ultrasound views.¹⁰

Step 1 — the gate: IVC diameter. If the IVC is < 2 cm, the score is Grade 0 and you stop. Congestion severe enough to matter distends the IVC.

Step 2 — if the IVC is ≥ 2 cm, interrogate three venous Doppler waveforms:

Step 3 — assign the grade:

• Grade 0 — IVC <2 cm. No congestion.
• Grade 1 — IVC ≥2 cm, but no severely abnormal waveform. Mild.
• Grade 2 — IVC ≥2 cm and one severely abnormal waveform. Moderate.
• Grade 3 — IVC ≥2 cm and two or more severely abnormal waveforms. Severe.

The four-quadrant framework

Combine the two questions and you get a practical grid:

The PA catheter and its waveforms

Pulmonary artery catheter use has fallen sharply since ESCAPE and similar trials showed no mortality benefit from routine use in heart failure and general ICU populations.¹² But it remains in use in cardiogenic shock, complex right ventricular failure, pulmonary hypertension, transplant evaluation and mechanical circulatory support — and the CCRN exam still tests it, because the waveforms teach cardiac physiology better than anything else at the bedside.

The trip through the heart

Every chamber has a signature pressure and waveform. Watching them change as the catheter floats is how placement is confirmed.

The CVP waveform: a, c and v

• a wave — atrial contraction (follows the P wave on the ECG)
• c wave — tricuspid valve bulging into the atrium during early ventricular systole
• x descent — atrial relaxation
• v wave — atrial filling against a closed tricuspid valve (occurs around the T wave)
• y descent — tricuspid opens, atrium empties

Read at end-expiration, at the level of the phlebostatic axis, with the transducer zeroed.

Wedging safely

Inflate the balloon slowly with no more than 1.5 mL of air while watching the waveform, and stop the moment the tracing changes to a wedge. Then deflate immediately — the balloon should be up for no longer than 2–4 respiratory cycles.

Interpreting the numbers

• PAOP ≈ left atrial pressure ≈ LV end-diastolic pressure, under the assumption of an uninterrupted column of blood between the catheter tip and the left atrium. That assumption fails with mitral stenosis, mitral regurgitation, high PEEP (if the tip is not in West zone 3), pulmonary venous obstruction, and severe pulmonary hypertension.
• PA diastolic pressure normally sits within a few mmHg of PAOP. When PVR rises (pulmonary hypertension, PE, ARDS, hypoxia), that gap widens — and a widening PAd–PAOP gradient is a useful signal of rising pulmonary vascular resistance.
• The RV picture in RV failure: a high CVP with a low or normal PAOP is the classic pattern; the right heart is congested while the left is underfilled.

Cardiac output by thermodilution

Inject a known volume of cold saline into the proximal port; the distal thermistor plots the temperature change over time, and the area under that curve is inversely proportional to flow. Errors matter and are testable:

• Falsely high CO: too small an injectate volume, injectate that is too warm, a slow injection, intracardiac shunt.
• Falsely low CO: too large a volume, injectate colder than programmed.
• Unreliable in tricuspid regurgitation — some indicator regurgitates and recirculates.
• Inject at a consistent point in the respiratory cycle, ideally end-expiration, and average three measurements within 10% of each other.

Monitoring technology and its errors

Every hemodynamic number is only as good as the system that produced it. The CCRN exam tests this heavily, because managing the equipment is nursing work.

Arterial line fundamentals

Zeroing references the transducer to atmospheric pressure — do it at setup, at shift change, after any disconnection, and whenever a number is implausible.

Leveling references the transducer to the phlebostatic axis: the fourth intercostal space at the mid-axillary line, approximating the level of the right atrium.

The square wave (dynamic response) test

Fast-flush the line and watch what happens to the waveform. This tests whether the system is transmitting pressure faithfully.

Allen's test before radial cannulation assesses collateral ulnar flow; its predictive value is debated but it remains standard practice in many units. Monitor the hand distal to any arterial line for perfusion.

Cuff versus arterial line

They disagree, and the direction of disagreement is predictable. In vasoconstricted shock states, the cuff typically underestimates true intra-arterial pressure. In vasodilated states it may overestimate. The arterial line, correctly zeroed and leveled with a good square-wave test, is the more reliable measurement in an unstable patient — and the reason it is placed.

A cuff that is too small reads falsely high; too large, falsely low.

Less invasive cardiac output

• Pulse contour analysis (calibrated and uncalibrated systems) derives stroke volume from the shape of the arterial pressure waveform. It requires a good arterial waveform — damping, arrhythmia, aortic regurgitation, an intra-aortic balloon pump and severe vasoconstriction all degrade accuracy. Calibrated systems drift less; uncalibrated systems are least reliable in exactly the vasoplegic patients you most want to measure.
• Esophageal Doppler measures descending aortic velocity; operator- and position-dependent.
• Bioreactance / bioimpedance — completely noninvasive, and accuracy in critically ill patients is variable.
• Critical care echocardiography — increasingly the reference at the bedside: LVOT velocity–time integral for stroke volume, visual assessment of RV size and function, IVC assessment, and a look for tamponade and valve disease.¹³ It answers "what kind of shock is this?" in minutes, which no pressure number can.

Sources of error worth memorizing

Shock profiles and mechanical support

The four shock categories by number

Learn the pattern, not the rows. Distributive shock is the only one with a low SVR. Obstructive shock is the only one where the CVP is high while the patient is functionally underfilled on the left. Cardiogenic shock is the only one with high pressures on both sides plus low output.

Forrester subsets: the two-by-two you will actually use

Forrester and colleagues described four hemodynamic subsets in acute MI in 1976, and the framework survives as warm/cold, wet/dry:¹⁴

You can assign this at the bedside with an exam — warmth of the extremities, capillary refill, pulse pressure, JVD, crackles, orthopnea — before any catheter goes in. That is why it survived the decline of the PA catheter.

Cardiogenic shock and SCAI stages

The SCAI classification (updated 2022) stages severity A through E and adds a three-axis framework of shock stage, cardiac arrest, and risk modifiers.¹⁵ It appears in full in the vasopressors module. Its clinical value is a shared vocabulary between the ICU, cardiology and the shock team, and a trigger for escalation: a patient moving from stage C to D is the moment for the shock team, not after.

Mechanical circulatory support

Nursing actions the exam tests

The assessment that beats the monitor

Before any number, five observations that take under a minute and are remarkably informative:

1. Mentation. Cerebral perfusion, assessed for free.
2. Capillary refill and the temperature line. Where on the limb does warm become cool? A mottling line that recedes from mid-thigh to the knee over an hour is a resuscitation working.
3. Urine output. Renal perfusion, integrated over time.
4. Pulse pressure. Narrow suggests low stroke volume; wide suggests vasodilation or a stiff aorta.
5. Skin mottling and JVD. Congestion and tone in one look.

The Surviving Sepsis Campaign explicitly includes capillary refill in resuscitation guidance, and the ANDROMEDA-SHOCK trial found capillary-refill-guided resuscitation performed at least as well as lactate-guided.¹

Documentation that is actually useful

Charting "MAP 62" is a data point. Charting a pattern is clinical judgment:

"MAP 62 on norepinephrine 12 mcg/min, up from 6 at 0400. CI 1.9, ScvO₂ 52%, lactate 4.8 rising from 3.1. Mottling now to mid-thigh, cap refill 5 sec, urine 12 mL/hr over 3 hours. PLR produced no change in cardiac output. Discussed with Dr. — echo ordered."

That paragraph tells the next clinician what is happening, what you tested, and what the plan is. It is also the observable form of the Clinical Judgment domain the exam is measuring.

Evaluating whether an intervention worked

For a fluid bolus:

• Stroke volume or cardiac output up ≥10%? (Not blood pressure alone.)
• Lactate trending down over hours?
• Urine output improving?
• Capillary refill shortening, mottling receding, extremities warming?
• And the tolerance side: oxygenation unchanged or better? Peak/plateau pressures not rising? Abdomen not distending? No new crackles or rising oxygen requirement?

A "successful" bolus that raised the MAP by 4 mmHg and dropped the P/F ratio by 60 was not successful.

Alarm management

Hemodynamic alarms are where alarm fatigue does the most harm. The nursing competencies here:

• Customize limits to the patient, not the unit default. A patient whose baseline systolic is 90 does not need an alarm at 90.
• Fix the artifact rather than widening the limit. Re-zero, re-level, run a square-wave test, resite a positional line.
• Verify with a second method before acting on an implausible number — cuff versus arterial line, a manual pulse, a look at the patient.
• Never act on a number you have not validated. Titrating a pressor to a damped arterial line is a real, documented harm.

Safety with invasive lines

• Arterial lines: labeled clearly, never used for drug administration, tubing and connections Luer-locked, distal perfusion checked each assessment, pressure bag maintained around 300 mmHg.
• CVCs: maximal barrier precautions at insertion, chlorhexidine site care, daily necessity review, scrub the hub — the CLABSI bundle is nursing-executed.
• Blood conservation: closed sampling systems and reduced draw volumes; iatrogenic anemia in the ICU is real and reduces oxygen delivery — a direct link back to the DO₂ equation.
• Air embolism prevention on line insertion and removal: Trendelenburg or supine, occlusive dressing, patient exhaling or performing Valsalva during removal. If air embolism is suspected: left lateral decubitus with head down, 100% oxygen, call for help.

Connecting back to the blueprint

Hemodynamic reasoning appears throughout the exam, not only in the Cardiovascular section: sepsis and shock states in Multisystem (16%), fluid and electrolyte balance in Multisystem, hemodynamic effects of ventilation in Respiratory, cerebral perfusion pressure in Neurological, and abdominal compartment syndrome in Gastrointestinal. Learning it as physiology rather than as a list of numbers is what lets it transfer across all of them — which is the whole argument of this site.