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Stokes Adam Syndrome is seen with which AV Block

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"Stokes-Adams Syndrome"[MeSH Terms] OR "atrioventricular block"[MeSH Terms]

Stokes-Adams syndrome is classically seen with third-degree (complete) AV block. Mobitz type II second-degree block, which can progress to complete block, can also cause it.
  • Bradley and Daroff's Neurology in Clinical Practice (Atrioventricular Block section) says: "The term Stokes-Adams attack describes disturbances of consciousness occurring in association with a complete AV block." Complete block occurs mainly in elderly patients and often in those with aortic valve disease.
  • The same book, in its Syncope section, describes the typical attack. With sudden-onset third-degree heart block, the patient loses consciousness and falls without warning, with no prodrome.
  • Ganong's Review of Medical Physiology (Therapeutic Highlights) says that in third-degree block the ventricles are slow, which causes cerebral ischemia, dizziness and fainting (Stokes-Adams syndrome). Causes include septal myocardial infarction and damage to the bundle of His during surgical repair of ventricular septal defects.
  • Adams and Victor's Principles of Neurology, 12th Edition, lists "AV block (second and third degree) with Stokes-Adams attacks" among the bradyrhythmias that cause syncope.
Mechanism: In complete block the escape rhythm is slow, and there is a pause before it takes over (ventricular standstill). Cardiac output and cerebral perfusion fall abruptly. The patient collapses suddenly, looks pale, and may have brief seizure-like jerks. Recovery is quick, often with a flush as the escape rhythm or conduction resumes.
Treatment: Permanent pacemaker.
My quick PubMed check of the last 2 years turned up no new systematic reviews that change this. The three results were on AV block in Takotsubo cardiomyopathy, with immune checkpoint inhibitors, and in hyperthyroidism. None of them bear on this question.

Why does dyspnea occur in patient with Afibrillation

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"Atrial Fibrillation"[MeSH Terms] AND "Dyspnea"[MeSH Terms]

Dyspnea in AF comes mainly from a rise in left atrial and pulmonary venous pressure, which causes pulmonary congestion. Several mechanisms contribute.
1. Loss of the atrial kick
  • Atrial contraction normally supplies about 20-30% of ventricular filling. In AF the atria quiver and stop contracting effectively.
  • Cardiac output falls and left atrial and end-diastolic pressures rise. The loss matters most when the ventricle is stiff or the mitral valve is narrowed.
  • Braunwald's Heart Disease (Resting Cardiac Function) says AF-induced loss of the atrial boost to diastolic filling aggravates age-related diastolic filling impairment. Older patients with AF are therefore more likely to have reduced cardiac output, dyspnea and fatigue.
  • Goldman-Cecil Medicine (HFpEF section) says atrial contraction supplies a disproportionately large share of filling into a noncompliant ventricle, so AF can exacerbate symptoms in diastolic dysfunction.
2. Rapid, irregular ventricular rate
  • A fast rate shortens diastole, so the ventricle fills less. Left atrial pressure rises and the pressure is transmitted back to the pulmonary veins and capillaries.
  • Interstitial and alveolar edema stiffens the lungs, increases the work of breathing and stimulates J-receptors, which causes dyspnea.
  • Irregular beat-to-beat filling also reduces stroke volume on short cycles.
3. Underlying structural disease, especially mitral stenosis
  • Goldman-Cecil Medicine says patients with mitral stenosis who develop AF usually decompensate. The rapid rate shortens diastolic filling time, raises left atrial pressure and lowers cardiac output.
  • Creasy & Resnik's Maternal-Fetal Medicine says the same: a faster heart rate means less time for ventricular filling and higher left atrial pressure, which causes exertional dyspnea.
  • Mulholland and Greenfield's Surgery says loss of the atrial kick in AF increases the transmitral gradient and atrial pressure, and patients tolerate it poorly.
4. Other contributors
  • Tachycardia-induced cardiomyopathy: sustained fast AF can reduce LV systolic function.
  • Reduced cardiac output causes fatigue and poor exercise tolerance. Exertion worsens the rate and filling problems, so dyspnea tends to appear on effort first.
  • AF is also a marker of, or coexists with, HFpEF, hypertension, valvular disease, thyroid disease, lung disease and sleep apnea. These add to dyspnea independently.
Management:
  • Control the rate (beta-blocker, diltiazem or verapamil, digoxin) or restore sinus rhythm.
  • In unstable patients, use synchronized cardioversion.
  • Treat the underlying cause.
The quick PubMed check of the last 2 years returned no systematic review that changes this explanation. The results covered dyspnea in ventilated patients, asthma with AF, and sleep apnea in heart failure.

Cardiac output falls and left atrial and end-diastolic pressures rise. Explain this point

The explanation rests on the Frank-Starling relationship and on how the left atrium and ventricle are linked in series.
Step 1: Normal filling in two phases
  • Early diastole is passive. The mitral valve opens and blood flows from the left atrium to the left ventricle (LV) along the pressure gradient. This gives about 70-80% of the filling.
  • Late diastole is the atrial kick. The atrium contracts and adds about 20-30% of the filling volume.
  • The kick lets the LV reach its end-diastolic volume at a low mean atrial pressure.
Step 2: What AF removes
  • In AF the atria fibrillate and have no coordinated contraction, so the late-diastolic boost is gone.
  • Rapid ventricular rates also shorten diastole. The passive phase then has less time to fill the ventricle.
Step 3: Why cardiac output falls
  • Cardiac output = stroke volume x heart rate.
  • Stroke volume depends on preload (end-diastolic volume), as the Frank-Starling mechanism describes.
  • With less filling, end-diastolic volume drops, so stroke volume drops. A faster rate does not compensate, because the shorter diastole reduces filling further.
  • Irregular R-R intervals add to this. A beat that follows a short cycle has little filling time and ejects a small stroke volume.
Step 4: Why left atrial pressure rises
  • Blood still arrives from the pulmonary veins, but the LV cannot take it in as efficiently.
  • The atrium must generate a higher pressure to push the same volume across the mitral valve in a shorter time.
  • Blood that is not emptied stays in the atrium, so left atrial pressure and volume rise.
  • If the mitral valve is stenotic, this effect is magnified. The valve is a fixed obstruction, so the gradient needed to maintain flow is larger when flow time is short.
Step 5: Why end-diastolic pressure rises
  • The relationship between LV volume and pressure is nonlinear. A stiff or hypertrophied ventricle sits on a steep part of the curve, so a small change in volume produces a large change in pressure.
  • In a noncompliant LV (hypertension, aging, HFpEF), the ventricle relies on the atrial kick to reach adequate volume without a high mean atrial pressure.
  • Without the kick, the LV needs a higher filling pressure to reach the same volume. If the LV also does not relax fully during a short diastole, end-diastolic pressure goes up even when volume does not.
  • This is why Braunwald's Heart Disease and Goldman-Cecil Medicine highlight older patients and HFpEF as the group most affected.
Step 6: How this becomes dyspnea
  1. Left atrial and LV end-diastolic pressures rise.
  2. The pulmonary veins and capillaries have no valves, so the pressure passes back to them.
  3. Capillary hydrostatic pressure rises. Once it passes the oncotic pressure (about 25 mmHg), fluid leaks into the interstitium and alveoli.
  4. The lungs become stiffer and gas exchange worsens, and J-receptors fire. The patient feels breathless.
  5. Low cardiac output also reduces perfusion to muscles and organs, which adds fatigue and exercise intolerance.
Summary chain: AF → no atrial kick plus short diastole → less LV filling → lower stroke volume and cardiac output, with blood backing up into the left atrium → higher left atrial and end-diastolic pressure → pulmonary congestion → dyspnea.

What is the pathophysiology of Atrial fibrillation

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