Rapid Review·Cardiovascular
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PHYSIOLOGY
T2High yieldCardiac Output Variables
FA P288
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Focus on
The three levers on stroke volume, and the molecular chain that makes contractility move.
Key takeaways
Cardiac output and its levers
Cardiac output (CO)
the volume of blood the heart pumps through the circulatory system per minute (∼ 5 L/min at rest). Cardiac output = Stroke volume x Heart rate.Stroke volume
has exactly three determinants, by "SV CAP": Contractility, Afterload, Preload.- Stroke volume rises with increased contractility (anxiety, exercise), increased preload (early pregnancy), and decreased afterload.
Contractility (inotropy)
What it is
how strongly the heart contracts at the same preload. ↑ Contractility = ↑ Ca²⁺ inside cardiac cells → ↑ stroke volume = ↑ COIncreased by
- β₁ stimulation / catecholamines → ↑ cAMP → ↑ Ca²⁺
- Digoxin → inhibits Na⁺/K⁺ ATPase → ↓ Na⁺/Ca²⁺ exchanger → ↑ intracellular Ca²⁺
- Dobutamine
- Milrinone → PDE-3 inhibitor → ↑ cAMP
Decreased by
- β-blockers
- Systolic heart failure
- Acidosis, hypoxia, hypercapnia
- Non-DHP CCBs (verapamil, diltiazem)
| Raises contractility | Lowers contractility |
|---|---|
| Catecholamines (beta-1, raising cAMP) | Beta-1 blockade (lowering cAMP) |
| Digoxin (raising intracellular Ca2+) | Heart failure with systolic dysfunction |
| Raised intracellular Ca2+ | Acidosis |
| Exercise, anxiety | Hypoxia and hypercapnia |
| Nondihydropyridine calcium channel blockers |
Preload and afterload
Preload
is approximated by ventricular EDV, and depends on venous tone and circulating blood volume. Venous vasodilators such as nitroglycerin lower it.Afterload
is approximated by MAP. Arterial vasodilators such as hydralazine lower it. ACE inhibitors and ARBs lower both preload and afterload.Why chronic hypertension thickens the ventricle
the LV compensates for increased afterload by thickening, which lowers wall stress. This is why chronic hypertension produces LV hypertrophy.Stroke work
SV × MAP. A failing heart has a reduced SV, from systolic dysfunction, diastolic dysfunction, or both.| Formula | Meaning |
|---|---|
| Wall tension = pressure × radius | A dilated ventricle has higher wall tension at the same pressure |
| Wall stress = (pressure × radius) / (2 × wall thickness) | Thickening reduces wall stress, which is the rationale for hypertrophy in chronic hypertension |
| Factor | Why |
|---|---|
| Contractility | More force per beat |
| Afterload | Proportional to arterial pressure |
| Heart rate | More beats per minute, and less diastolic perfusion time |
| Ventricular diameter | Raises wall tension by Laplace |
The cardiovascular response to exercise
Cardiac changes
summarised on the Exercise overview and the Cardiac changes figure.- Exercise → ↑ sympathetic activity + ↓ vagal tone → ↑ HR + ↑ contractility + ↑ SV → ↑ cardiac output.
- Early exercise: HR + SV both increase CO.
- Intense exercise: HR becomes the main driver of further CO increase.
Vascular changes
- Sympathetic stimulation → vasoconstriction in non-exercising tissues
- Active muscle metabolites → local vasodilation → more blood flow to working muscle
- Local vasodilators: Adenosine, K⁺, CO₂, lactate, ATP
Blood pressure
- ↑ SBP → due to ↑ cardiac output
- ↓/same DBP → due to ↓ systemic vascular resistance
- Therefore, MAP increases only slightly
A patient is started on digoxin. Which pump does it block, and why does intracellular calcium rise?
The Na+/K+ ATPase. Intracellular Na+ rises, so the Na+/Ca2+ exchanger stalls, and the calcium that cannot leave is the extra contractility.
How it's tested
Digoxin increases contractility by blocking the Na+/K+ ATPase, which raises intracellular sodium and thereby shuts down the Na+/Ca2+ exchanger. The calcium that cannot leave is the inotropy, and stating that chain in order is what the question rewards, because the distractors offer direct calcium channel agonism. Note the pattern running through the contractility table: anything that impairs cellular energetics lowers contractility, which covers acidosis, hypoxia, and hypercapnia in one idea.
Go deeper
First Aid 2026 — CV/Physiology (p.288) · B&B — Cardiac output & SV determinants · Mehlman — HY Cardio (preload vs afterload), HY Arrows (inotropy)
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