Hemodynamics & Waveforms
Arterial, CVP and PA waveforms; pressure-volume loops; fluid responsiveness; echo-derived hemodynamics; and integrated shock physiology.
Core Topics
1 topicsHemodynamic Monitoring & Waveforms
From arterial and venous waveforms to PA catheterization, echo, fluid responsiveness, pressure-volume loops, and integrated shock phenotyping.
Physiology Modules & Waveforms
24 conceptsOxygen Delivery
Arterial oxygen content is dominated by hemoglobin-bound oxygen (1.34 mL O2/g Hb × Hb[g/dL] × SaO2[fraction]), with dissolved oxygen (0.003 mL O2/dL/mmHg × PaO2[mmHg]) contributing very little at normal atmospheric pressure. Because hemoglobin saturation dominates the equation, the clinically important drop in CaO2 only becomes steep once SaO2 falls below roughly 90% — the shoulder of the oxyhemoglobin dissociation curve. DO2 then scales linearly with cardiac output, so a fall in either CO or CaO2 alone can be compensated by a rise in the other, up to a point.
Oxygen Consumption
Under normal conditions, VO2 is set by metabolic demand, and the body adjusts oxygen extraction (and, if needed, cardiac output) to meet it — DO2 normally exceeds VO2 several-fold, leaving a wide margin of reserve. Critical illness increases metabolic demand (fever, sepsis, increased work of breathing) while simultaneously threatening the ability to increase DO2 to match, narrowing that reserve. Extraction ratio (VO2/DO2) rises as this margin shrinks, which is reflected clinically as a falling mixed or central venous oxygen saturation (SvO2/ScvO2).
DO2/VO2 Relationship
This produces a two-part relationship: a flat plateau where VO2 is supply-independent, and a steep segment below the critical DO2 threshold where VO2 falls linearly with DO2. The transition point is the critical DO2 — below it, tissues can no longer meet metabolic demand through extraction alone, and anaerobic metabolism begins, producing lactate. The critical threshold isn't fixed; it shifts with metabolic demand, so a febrile, agitated, or septic patient reaches supply-dependency at a higher DO2 than one who is sedated and afebrile.
Preload
By the Frank-Starling mechanism, increasing preload stretches sarcomeres toward their optimal length for force generation, increasing stroke volume — up to a point. Beyond that point, further stretch no longer increases (and can even reduce) stroke volume, which is why the Frank-Starling curve plateaus rather than rising indefinitely. Preload is commonly estimated at the bedside using surrogates like central venous pressure, inferior vena cava diameter and collapsibility, or dynamic measures such as pulse pressure variation — none of which measure ventricular volume directly, which is why 'volume responsiveness' testing (e.g. passive leg raise) is generally more informative than any single static number.
Afterload
For a fixed contractility and preload, a rising afterload reduces stroke volume, because more of the ventricle's generated force is spent overcoming resistance rather than ejecting volume. A healthy ventricle tolerates afterload changes well; a failing or acutely strained ventricle (especially the thin-walled right ventricle) is far more afterload-sensitive, and a sudden rise in afterload can precipitate acute decompensation.
Contractility
Reduced contractility (from ischemia, sepsis-associated cardiomyopathy, or chronic heart failure) shifts the Frank-Starling curve downward and to the right: for any given preload, stroke volume is lower, and the curve plateaus earlier. Increased contractility (endogenous catecholamines, inotropic drugs) shifts the curve upward. Because contractility is a separate axis from preload, a patient can be both volume-overloaded and have poor contractility at the same time — more fluid won't help, and may worsen congestion, while an inotrope shifts the whole curve rather than just moving along it.
Cardiac Output
Because CO is a product of rate and volume, the body can maintain it in more than one way — a fall in stroke volume can be partly compensated by a rise in heart rate, which is why early compensated shock often presents with tachycardia and a preserved blood pressure before stroke volume failure becomes clinically obvious. Beyond a certain heart rate, however, shortened diastolic filling time reduces stroke volume enough that further tachycardia no longer helps, and can even reduce CO.
Systemic Vascular Resistance
Blood pressure is the product of cardiac output and SVR (MAP ≈ CO × SVR), so the same blood pressure can arise from very different underlying physiology — a high-CO, low-SVR state (distributive/septic shock) versus a low-CO, high-SVR state (cardiogenic shock). Vasodilation from inflammatory mediators (sepsis, SIRS) or from vasodilating drugs lowers SVR; compensatory sympathetic vasoconstriction, or vasopressor therapy, raises it.
Venous Return
Venous return falls when mean systemic filling pressure falls (hypovolemia, venodilation) or when right atrial pressure rises enough to reduce the driving gradient — which is exactly what happens with elevated intrathoracic pressure from auto-PEEP, high PEEP, or tension pneumothorax. This is the physiologic link between ventilator settings and hemodynamics: positive-pressure ventilation raises intrathoracic and right atrial pressure, which can reduce venous return and, downstream, cardiac output, especially in a volume-depleted patient.
RV Failure Physiology
A sudden rise in pulmonary vascular resistance — from hypoxia, hypercapnia, acidosis, high intrathoracic pressure (high PEEP, auto-PEEP), or pulmonary embolism — can acutely overwhelm the RV's limited ability to generate pressure. As the RV dilates to compensate, it shifts the interventricular septum leftward (ventricular interdependence), impairing left ventricular filling and reducing left-sided cardiac output even though the primary problem is right-sided. This creates a self-reinforcing cycle: falling systemic pressure reduces RV coronary perfusion (which occurs throughout the cardiac cycle, not just diastole), further impairing RV function.
Septic Shock: From Infection to Hemodynamic Failure
Pathogen-associated molecular patterns (PAMPs) — lipopolysaccharide from gram-negatives, peptidoglycan from gram-positives, fungal glucans — bind Toll-like receptors on macrophages and neutrophils, activating NF-κB. This drives massive transcription of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and inducible nitric oxide synthase (iNOS). The resulting nitric oxide surge causes vascular smooth muscle relaxation, systemic vasodilation, and a precipitous fall in SVR. Simultaneously, endothelial activation increases permeability, allowing protein-rich fluid to extravasate into the interstitium. This reduces effective circulating volume and venous return, compounding the MAP fall despite compensatory tachycardia and a hyperdynamic cardiac output. The clinical picture is warm, vasodilated extremities with rapid, bounding pulses — the hallmark of distributive shock. Cardiac function may also be directly impaired by sepsis-induced myocardial depression (cytokine-mediated), which becomes clinically significant in patients who cannot sustain the compensatory increase in cardiac output. As shock deepens, tissue hypoxia drives lactate accumulation, further impairing myocardial and vascular function in a self-reinforcing cycle.
Cardiogenic Shock: LV Failure and Circulatory Collapse
Loss of LV contractility — whether from myocardial infarction, decompensated cardiomyopathy, acute myocarditis, or arrhythmia — reduces stroke volume. Cardiac output falls. Baroreceptors sense the drop in MAP and trigger sympathetic activation: tachycardia (which partially compensates CO), increased SVR (which raises afterload), and sodium and water retention (which raises preload). These compensatory mechanisms sustain MAP in early decompensation but at the cost of worsening LV workload. As stroke volume falls further, left ventricular end-diastolic pressure rises, is transmitted to the left atrium and pulmonary veins, and eventually exceeds pulmonary capillary oncotic pressure. The result is cardiogenic pulmonary oedema, alveolar flooding, and hypoxaemia — which in turn worsens myocardial ischaemia in the case of AMI-related shock. Falling coronary perfusion pressure and rising myocardial oxygen demand from tachycardia and increased wall tension create a death spiral: ischaemia → more contractile failure → worse shock → more ischaemia. This bidirectional pathophysiology explains why the haemodynamic target in cardiogenic shock differs fundamentally from other shock types: reducing afterload can improve stroke volume more than vasopressors, but the choice depends on whether MAP is already critically low.
RV Failure: Afterload, Interdependence, and Treatment Pitfalls
The normal RV operates at low pressure (~25/5 mmHg) and fills easily at low end-diastolic pressures. When PVR rises acutely — from massive PE, severe ARDS, acute hypoxia, hypercapnia, or acidosis — RV wall stress increases. The RV initially compensates by dilating (Frank-Starling) to maintain stroke volume, but in the non-hypertrophied RV, dilation quickly becomes maladaptive. RV dilation causes leftward displacement of the interventricular septum (ventricular interdependence), mechanically compressing the LV cavity. LV end-diastolic volume falls despite adequate systemic venous filling, reducing LV stroke volume and MAP — a paradox where the LV appears 'underfilled' even though the problem is entirely right-sided. The RV is uniquely vulnerable to coronary ischaemia during failure: unlike the LV, the RV receives coronary perfusion throughout the entire cardiac cycle (both systole and diastole). As RV pressure rises and MAP falls, the aorta-to-RV pressure gradient narrows in both phases, critically reducing RV coronary perfusion. This creates a vicious cycle: ischaemia → worse contractility → more dilation → more septal shift → lower MAP → worse ischaemia.
Positive-Pressure Ventilation: Cardiovascular Effects
During spontaneous inspiration, intrathoracic pressure falls below atmospheric, increasing the pressure gradient from the peripheral venous system to the right atrium. This augments venous return and RV filling — the natural respiratory 'bellows' effect on circulation. The LV simultaneously faces increased transmural pressure (intracavitary pressure minus intrathoracic pressure) because pleural pressure is sub-atmospheric; this functionally increases LV afterload. Positive-pressure ventilation reverses these relationships. Raised intrathoracic pressure narrows the venous return gradient (mean systemic filling pressure minus right atrial pressure), reducing RV preload. If tidal volumes are large enough to cause lung overdistension, alveolar capillaries are compressed and PVR rises, increasing RV afterload further. The consequences are most severe in hypovolaemic or RV-failure patients who are already near the limit of their RV reserve. However, PPV simultaneously helps the left ventricle. Positive pleural pressure raises the external pressure on the LV, reducing transmural pressure for the same intracavitary pressure — the LV effectively 'works less' against a lower afterload. For patients with severe LV failure, PPV can be dramatically beneficial: reducing LV afterload increases stroke volume and reduces pulmonary oedema. This is why non-invasive ventilation in acute cardiogenic pulmonary oedema improves haemodynamics within minutes.
Obstructive Shock: Massive Pulmonary Embolism & Acute Cor Pulmonale
The normal right ventricle is a thin-walled, compliant volume pump unaccustomed to acute pressure overloads. When acute mechanical obstruction and neurohumoral vasoconstrictors (thromboxane A2, serotonin) double or triple pulmonary vascular resistance, RV systolic pressure cannot exceed 50–60 mmHg. The RV acutely dilates and its wall tension spikes (Laplace's Law), dramatically increasing RV myocardial oxygen consumption while compressing right coronary artery capillary perfusion in the wall. As the RV dilates within the non-compliant pericardial sac, ventricular interdependence causes the interventricular septum to shift leftward ('D-shaped LV'), restricting left ventricular diastolic filling. LV stroke volume collapses, MAP plummets, and systemic hypotension extinguishes aortic root driving pressure to the right coronary artery, completing a fatal ischemic spiral.
Cardiac Tamponade: Intrapericardial Pressure & Equalization
The normal pericardial space contains 15–50 mL of lubricating fluid. When fluid accumulates faster than the fibroelastic pericardium can stretch, intrapericardial pressure rises exponentially along its steep volume-pressure curve. Elevated intrapericardial pressure compresses all four cardiac chambers, equalizing diastolic filling pressures across the right atrium, right ventricle, left atrium, and left ventricle (equalization of diastolic pressures). During inspiration, negative intrathoracic pressure increases venous return to the right heart. Because total cardiac volume is fixed within the tense pericardium, RV expansion can only occur by bowing the interventricular septum into the LV cavity. This sharply reduces LV end-diastolic volume and stroke volume, producing the clinical sign of Pulsus Paradoxus (>10 mmHg inspiratory drop in systolic blood pressure).
Hyperkalemia: Membrane Excitability, Shifting, and Elimination
The cardiac resting membrane potential (Em) is determined primarily by the Nernst equilibrium for potassium: Em = -61.5 × log([K+]in / [K+]out). As extracellular potassium rises, the ratio [K+]in / [K+]out decreases, making the resting membrane potential less negative (e.g., from -90 mV toward -70 mV). This resting depolarization partially inactivates fast voltage-gated sodium channels (Nav1.5), slowing phase 0 depolarization velocity (dV/dt) and prolonging intraventricular conduction (peaked T waves → PR prolongation → QRS widening → sine wave → VF/asystole). Management requires a three-pillar physiological strategy: 1. Stabilize: IV Calcium raises the cardiac threshold potential, restoring the normal safety margin between resting and threshold potentials without lowering serum K+. 2. Shift: Regular Insulin + Dextrose, Beta-2 agonists (Albuterol), and Sodium Bicarbonate activate the Na+/K+ ATPase, rapidly pumping potassium into cells for 2–4 hours. 3. Eliminate: Loop diuretics, potassium binders (Patiromer, ZS-9), or Hemodialysis remove potassium from the body permanently.
Aortic Dissection: Shear Stress (dP/dt), Beta-Blockade, and Vasodilation
The mechanical force driving propagation of an intimal flap is not merely mean arterial pressure, but the velocity of pressure rise during early ventricular systole: dP/dt (the rate of change of left ventricular pressure over time), combined with absolute systolic blood pressure and heart rate. Administering a direct arterial vasodilator (such as Nicardipine, Hydralazine, or Nitroprusside) without prior beta-blockade triggers baroreceptor-mediated reflex sympathetic activation. Circulating catecholamines increase myocardial contractility and heart rate, dramatically steepening the dP/dt slope. This increased pulsatile shear wave collides with the aortic root with each heartbeat, propagating the dissection flap proximally or distally and dramatically increasing the risk of fatal rupture. IV beta-blockers (Esmolol, Labetalol) directly depress LV contractility and slow heart rate, flattening the dP/dt curve before blood pressure is lowered.
Cerebral Perfusion Pressure: CPP = MAP − ICP Dynamics
In the healthy brain, Cerebral Autoregulation maintains a constant Cerebral Blood Flow (CBF) across a wide range of CPP (50–150 mmHg) by dynamic arteriolar vasoconstriction and vasodilation. In severe traumatic brain injury, subarachnoid hemorrhage, or intracranial hypertension, autoregulation is frequently impaired or shifted rightward. Cerebral blood flow becomes passively dependent on perfusion pressure. When ICP rises (e.g., to 35 mmHg) and MAP is low or normal (e.g., 75 mmHg), CPP drops to 40 mmHg, below the critical ischemic threshold. Microvascular collapse occurs in the ischemic penumbra surrounding the brain contusion, triggering cellular ATP depletion, cytotoxic edema, and secondary brain infarction. Conversely, excessive CPP (>70–80 mmHg) drives vasogenic edema and increases the incidence of Acute Respiratory Distress Syndrome (ARDS).
Oxygen Delivery (DO2): The 3 Pillars & Failure Modes
Arterial oxygen content (CaO2) is determined overwhelmingly by hemoglobin-bound oxygen; dissolved oxygen in plasma (0.003 × PaO2) contributes less than 2% of total content under normobaric conditions. Oxygen Delivery can fail through three distinct physiological mechanisms: 1. Flow Failure (Cardiogenic/Hypovolemic Shock): Cardiac output collapses, but hemoglobin and arterial oxygen saturation are normal. (Treated with inotropes, vasopressors, or fluids). 2. Anemic Failure (Severe Hemorrhage / Critical Anemia): Hemoglobin drops below critical thresholds, halving CaO2 despite hyperdynamic cardiac output. (Treated with red blood cell transfusion). 3. Hypoxic Failure (Severe ARDS / Shunt / Hypoventilation): SaO2 plummets due to severe alveolar gas exchange impairment, desaturating available hemoglobin. (Treated with PEEP, recruitment, FiO2, prone positioning). When DO2 drops below the critical oxygen delivery threshold (DO2crit), tissue oxygen consumption (VO2) becomes supply-dependent, forcing cells into anaerobic glycolysis with lactate generation and cellular death.
Venous Return & Mean Systemic Filling Pressure
Intravascular blood volume is partitioned into unstressed volume (volume required to fill the vascular tree without generating wall tension, ~70% of total volume) and stressed volume (volume stretching vessel walls, generating MSFP, ~30%). In vasoplegic and hypovolemic shock, loss of vascular tone or volume reduces stressed volume and drops MSFP. Conversely, positive-pressure ventilation raises intrathoracic pressure and RAP, narrowing the (MSFP - RAP) gradient and acutely reducing venous return. Vasopressors with alpha-1 activity (such as norepinephrine) recruit blood from unstressed to stressed volume via venoconstriction of the splanchnic venous capacitance reservoir, raising MSFP and restoring venous return without requiring excessive fluid administration.
RV-PA Coupling & Acute Afterload Mismatch
The right ventricle is thin-walled, compliant, and adapted to low afterload (PVR is ~1/10th of SVR). In acute massive PE, ARDS, or high-PEEP ventilation, sudden afterload spikes uncouple the RV from the pulmonary artery (Ees/Ea < 0.8). The RV dilates acutely to preserve stroke volume via heterometric autoregulation. However, excessive dilation increases RV wall stress, shifts the interventricular septum leftward (D-sign), compresses the LV, and impairs LV filling. Critically, the right coronary artery (RCA) supplies the RV during both systole and diastole under normal conditions because aortic root pressure far exceeds RV intracavitary pressure. When RV cavity pressure rises and systemic aortic MAP drops, RV coronary perfusion pressure (MAP - RVSP) collapses, inducing RV ischemia and precipitating acute circulatory arrest.
Oxygen Extraction Ratio & Critical DO2-VO2 Supply Dependence
Under normal physiological conditions, oxygen consumption (VO2) is supply-independent: when DO2 falls (due to anemia, hypoxemia, or low cardiac output), microvascular beds recruit capillaries and increase O2ER (up to 60–70%), maintaining stable tissue VO2 while ScvO2 drops. However, once DO2 drops below the critical oxygen delivery threshold (DO2crit, ~300–400 mL/min/m2), maximal tissue oxygen extraction is exhausted. Beyond this point, VO2 becomes supply-dependent (pathologic supply dependency): oxidative phosphorylation fails, cellular dysoxia occurs, anaerobic glycolysis takes over, and blood lactate rises exponentially.
Lactate Kinetics & Cellular Dysoxia in Shock
Type A Hyperlactatemia is caused by tissue hypoperfusion and anaerobic metabolism. In the absence of oxygen, mitochondrial pyruvate dehydrogenase (PDH) is inhibited and NADH accumulates, shifting pyruvate to lactate via lactate dehydrogenase (LDH) with an elevated lactate-to-pyruvate ratio (>20:1). Type B Hyperlactatemia occurs with preserved tissue oxygenation: - Type B1: Underlying disease (liver failure, malignancy, thiamine deficiency). - Type B2: Drugs and toxins (epinephrine, linezolid, metformin, beta-2 agonists via Na+/K+-ATPase stimulation). - Type B3: Inborn errors of metabolism. In sepsis, endogenous and exogenous adrenergic stimulation accelerates aerobic glycolysis via beta-2 receptors faster than PDH can process pyruvate, generating lactate despite adequate tissue PO2.
Clinical Reasoning Cases
2 casesSeptic Shock Resuscitation
2026 SSC-aligned fluids, early norepinephrine, dynamic reassessment, and perfusion endpoints
Mixed Septic and Cardiogenic Shock
Sepsis-induced myocardial dysfunction with vasoplegia and low forward flow