Valsalva vs. Muller's Maneuver

The Basics

Valsalva Maneuver - In Depth

1. Patient exhales forcefully against a closed glottis (or bears down as if defecating)
2. Intrathoracic pressure rises sharply
3. Venous return to the right heart decreases (compressed vena cava)
4. Cardiac output falls -> preload drops
5. As the maneuver is sustained, vagal tone increases -> SA and AV nodal conduction slow

• Phase I (onset): Brief BP rise from aortic compression
• Phase II (strain): Decreased venous return -> drop in BP and cardiac output; reflex tachycardia
• Phase III (release): Sudden drop in BP as intrathoracic pressure normalizes
• Phase IV (overshoot): Rebound increase in venous return -> BP overshoot -> reflex bradycardia (vagal)

• Patient supine with cardiac monitor
• Take a deep breath, close lips around thumb (or blow into a syringe), and attempt to exhale without expelling air
• Bear down for 10-20 seconds, or passively raise legs simultaneously (modified Valsalva)

1. Terminating SVT - the vagal phase (Phase IV) slows AV nodal conduction. Mean success greatest with Valsalva + diving response among vagal maneuvers (Roberts & Hedges' Clinical Procedures in Emergency)
2. Diagnosing heart murmurs - by reducing preload:
   • Most murmurs decrease in intensity and duration during Valsalva strain phase
   • Two key exceptions that increase with Valsalva:
     • HOCM (hypertrophic obstructive cardiomyopathy) - murmur becomes much louder because decreased preload worsens LV outflow tract obstruction
     • MVP (mitral valve prolapse) - click and murmur move earlier and often become louder (leaflets prolapse sooner with smaller LV volume)
   • After release: right-sided murmurs return to normal earlier than left-sided murmurs (Harrison's Principles of Internal Medicine, 22e, Table 246-1)
3. Equalizing ear pressure (e.g., during flight or diving)
4. Diagnosing hernias and varicoceles - radiologists perform with and without Valsalva to demonstrate small defects (Sleisenger & Fordtran's GI Disease)
5. Provocative test for presyncope / autonomic dysfunction

Muller's Maneuver - In Depth

• Patient inspires forcefully against a closed glottis (mouth and nose closed)
• Intrathoracic pressure becomes strongly negative
• This simulates the negative airway pressure during obstructive sleep apnea
• Pharyngeal walls are sucked inward -> dynamic airway collapse becomes visible

• Mouth closed, nose pinched
• Patient asked to inhale forcefully
• Examiner observes pharyngeal collapse via fiberoptic nasendoscope

1. OSA (Obstructive Sleep Apnea) evaluation - primary use. Done with flexible fiberoptic endoscopy (nasopharyngoscopy) in awake patients, both sitting and supine, to identify the level and degree of pharyngeal collapse:
   • Retropalatal collapse
   • Retrolingual collapse
   • Hypopharyngeal collapse Used preoperatively to predict success of UPPP (uvulopalatopharyngoplasty). Sher et al. found that patients with palatal collapse had 73% chance of >=50% reduction in RDI after UPPP (Cummings Otolaryngology, 6e).
2. Respiratory muscle assessment - measuring maximal inspiratory pressure (MIP/PImax) and transdiaphragmatic pressure during maximum static inspiratory effort. Note: activates intercostals, diaphragm, and sternomastoid (Fishman's Pulmonary Diseases).
3. Mueller-Hillis maneuver (obstetrics variant) - used to predict dystocia in the second stage of labor.

• Poor inter- and intra-rater reliability for OSA assessment
• Low correlation with intraoperative findings
• Low positive-predictive value for surgical outcomes
• Findings in awake patients differ from sleep (hence drug-induced sleep endoscopy [DISE] is gaining favor)

Key Comparison Summary

"HOCM and MVP go UP with Valsalva" - everything else goes down because preload falls; but HOCM worsens with less blood (cavity collapses), and MVP's leaflets prolapse earlier with a smaller ventricle.

Differentiating MVP vs. HOCM by Auscultation Maneuvers

The Underlying Logic

Maneuver-by-Maneuver Breakdown

The Critical Differentiator: Handgrip

• Handgrip increases systemic vascular resistance (afterload). This increases LV volume (the LV empties less completely against greater resistance) AND increases aortic pressure.
• In HOCM: increased LV volume relieves outflow obstruction → murmur decreases
• In MVP: increased LV volume delays prolapse → click moves toward S2 and murmur shortens → but the murmur intensity is often increased due to greater MR from elevated LV-LA pressure gradient

The Click: MVP's Unique Signature

• Standing (small LV): click moves closer to S1 - murmur longer
• Squatting (large LV): click moves closer to S2 - murmur shorter

The systolic murmur of HOCM behaves similarly to MVP on standing/squatting - but HOCM has no click. The click is the distinguishing feature.

Other Differentiating Features (Non-Maneuver)

Quick Memory Rule

"Both go UP with Valsalva and standing - but only MVP has a CLICK, and only HOCM has an S4 + LVH."

Handgrip = the separator: HOCM down, MVP click goes toward S2 (shorter murmur).

ECG Findings: HOCM vs. MVP

HOCM - ECG is Almost Always Abnormal

1. Left Ventricular Hypertrophy (LVH)

• Increased QRS voltage (large R in lateral leads, deep S in V1-V3)
• Left axis deviation
• ST depression and T-wave inversion in lateral leads (the classic "strain pattern")

2. Septal Q Waves ("Pseudoinfarction Pattern")

• Deep, narrow Q waves (>0.3 mV) in anterior, lateral, or inferior leads (I, aVL, V4-V6, or II, III, aVF)
• These are caused by hypertrophied septal depolarization, not scar
• They can mimic Q waves of prior MI - but the T-wave polarity is the key differentiator:
  • HOCM: T waves are upright in the same leads that have the septal Q waves (QS or QR complexes with upright T)
  • Myocardial infarction: T waves are inverted in leads with Q waves

Real HOCM ECG:

3. Left Atrial Enlargement

• Broad, notched P waves in lead II (P mitrale) or biphasic P in V1
• Reflects the stiff, non-compliant LV requiring high filling pressures

4. Arrhythmias

• Atrial fibrillation - seen in up to 20-25% of HOCM patients; can be catastrophic (loss of atrial kick dramatically worsens obstruction)
• Ventricular arrhythmias - non-sustained VT on Holter; a major risk factor for sudden cardiac death
• WPW pattern (delta waves + short PR) - seen in some HOCM patients, especially those with PRKAG2 mutations (glycogen storage type)

5. Giant Negative T Waves

• A specific variant: Apical HOCM (Yamaguchi syndrome) - predominantly affects the LV apex rather than septum
• Hallmark ECG: giant symmetric T-wave inversions in precordial leads V3-V5, often >10 mm deep
• This variant is more common in Japanese patients and is typically non-obstructive

MVP - ECG Usually Normal

"The ECG is usually normal. If suspecting mitral valve prolapse, refer the patient for outpatient echocardiography to confirm the diagnosis." (Tintinalli's Emergency Medicine)

1. T-Wave Inversions in Inferior Leads (II, III, aVF)

• The most characteristic MVP-associated ECG finding
• Flat or inverted T waves in inferior leads
• Can mimic inferior ischemia
• Clinically important: T-wave abnormalities in inferior leads have been associated with malignant arrhythmias in MVP patients - these patients have a higher risk of sudden death (Fuster & Hurst's The Heart, 15e)

2. Biphasic/Inverted T Waves in V5-V6

• Less common, nonspecific
• May suggest significant mitral regurgitation if present alongside LA enlargement

3. QTc Prolongation (mild)

• Can occur in some MVP patients, contributing to arrhythmia risk

4. Arrhythmias

• PVCs - frequent and complex PVCs are associated with the "malignant arrhythmic phenotype" of MVP
• Atrial fibrillation - less common than in HOCM unless significant MR has caused LA enlargement
• PSVT/SVT - due to accessory pathways more common with connective tissue predisposition

Side-by-Side ECG Summary

The One-Line Differentiator

HOCM: LVH + narrow septal Q waves + upright T waves in those Q-wave leads = pseudoinfarction pattern. ECG almost never normal.

MVP: ECG usually clean. If abnormal, look for T-wave inversions isolated to inferior leads - and take them seriously as a marker of arrhythmic risk.