Physiology Compare
Compare how different clinical states and vasoactive agents affect hemodynamics.
Compare how different clinical states and vasoactive agents affect hemodynamics.
Potent α1 agonism → arterial/venous vasoconstriction; modest β1 → increased contractility. Minimal β2 effect.
V1 receptor agonism → vascular smooth muscle contraction. Non-adrenergic; no direct cardiac β1 effect.
Pure α1 agonism → arterial vasoconstriction. No β1 activity. Reflex bradycardia from baroreceptor activation.
Potent β1 + β2 + α1 agonism. Dose-dependent: lower doses β-dominant (inotropy/chronotropy), higher doses α-dominant (vasoconstriction).
Predominant β1 agonism → increased contractility. Mild β2 → peripheral vasodilation. No significant α1 effect.
PDE-3 inhibitor → increased cAMP → inotropy + vasodilation (inodilator). Non-adrenergic mechanism.
Dihydropyridine calcium channel blocker → arterial smooth muscle relaxation → afterload reduction.
GABA-A agonism → venodilation + arterial vasodilation + negative inotropy. Direct cardiac depression.
Intravascular volume expansion → increased mean systemic filling pressure (MSFP) → increased venous return gradient → enhanced ventricular end-diastolic volume and stroke volume.
Inflammatory vasodilation → decreased SVR. Capillary leak → reduced effective preload. Septic cardiomyopathy may depress contractility.
Pump failure → decreased CO → compensatory sympathetic activation → increased SVR and HR. Elevated filling pressures.
Acute RV pressure overload → RV dilation → interventricular septum bowing → LV underfilling → decreased CO.
Reduced circulating volume → decreased venous return → decreased preload → decreased CO. Compensatory sympathetic response.
Diffuse alveolar damage → V/Q mismatch + intrapulmonary shunt. Hypoxic pulmonary vasoconstriction → elevated PVR → RV strain.
Chronic or acute elevation of PVR → RV pressure overload → RV dilation and failure → decreased LV filling.
Pericardial fluid compresses cardiac chambers during diastole → impedes ventricular filling → reduced stroke volume → compensatory tachycardia and vasoconstriction. Pulsus paradoxus: inspiratory drop in SBP >10 mmHg.
Airflow obstruction → incomplete exhalation → progressive air trapping (auto-PEEP) → increased intrathoracic pressure → compressed vena cava → reduced venous return → severe preload reduction and decreased CO.
One-way valve pleural air accumulation → positive intrathoracic pressure → mediastinal shift → vena cava kinking/compression → catastrophic collapse in venous return → obstructive shock.
IgE-mediated mast cell degranulation → massive histamine and cytokine surge → profound arterial/venular vasodilation + diffuse capillary leak + bronchospasm.
Acute RV afterload/pressure spike → RV dilatation → interventricular septal flattening/bowing (D-sign) → LV diastolic compression → low cardiac output.
Inadequate tissue oxygen delivery (DO₂) relative to cellular demand → anaerobic glycolysis → pyruvate conversion to lactate via LDH → high anion gap metabolic acidosis.
Positive intrathoracic pressure during inspiration and high PEEP → increased right atrial pressure → decreased pressure gradient for venous return (MSFP - RAP) → decreased LV preload.
Elevated extracellular K⁺ depolarizes resting membrane potential → inactivates sodium channels → slows cardiac conduction velocity → wide QRS, sine wave, and arrest.
Absolute insulin deficiency → unchecked lipolysis and hepatic ketogenesis → ketoacidosis + severe osmotic diuresis (5–8 L deficit) with profound total body potassium depletion.