Myself and Grant were called to a 50yo male complaining of chest pain and the sensation of palpitations. On arrival we were presented with a male sitting on a step with a pallor sweaty complexion with no visible SOB. On initial assessment the patient had a weak, fast radial pulse and was moved to the ambulance for further assessment because of proximity. A 12 lead ECG was preformed which showed an SVT rhythm with a rate between 200-220. Further assessment of vital signs indicated the patient had moderate systemic compromise and two Valsalva manoeuvres were performed to no effect. Tatsu arrived immediately after the second Valsalva attempt and suggested we try the Modified Valsalva before we use any further invasive techniques. The Modified Valsalva was successful at reverting the SVT to a NSR, however immediately post Modified Valsalva the patient developed ventricular dysrhythmia which lasted for around 30 seconds.
The management of SVT in the pre-hospital environment is often varied throughout pre-hospital providers. The current trend for most providers in pre-hospital environment is to provide the least invasive treatment to terminate this rhythm. The Valsalva manoeuver has been identified as the preferred form of initial treatment for adults in SVT. Other more invasive treatments include adenosine or cardioversion which are both very invasive and often give the patient undesirable side effects.
The Valsalva manoeuvre has been used for many years and uses an increase in intrathoracic pressure to effect venous return, arterial pressure, heart rate and cardiac output. The end result is a parasympathetic response which causes a negative dromotropic response and a reduction in heart rate. The parasympathetic response starts with activation of the Vagus nerve which releases acetylcholine in the muscarinic receptors within the AV node. This causes an increase in intracellular cyclic adenosine monophosphate which affects the calcium and K channels, consequently increasing the action phase 0 of the heart. Slowing of action phase 0 decelerates conduction and increases the refractory period. The physiology of effect can be broken into four main action phases.
- During the first phase the patient exhales closes the glottis and contacts thoracic muscles. This initially causes an increased external pressure on the heart, aorta and Vena cava which causes an increase in vagal tone that subsequently causes the heart rate to drop.
- The second phase consists of the patient continuously exhaling. This causes the initial increase of heart to be shortly lived due to increased pressure on the vena cava reducing preload and cardiac output. The drop in cardiac output reduces the intra-aortic pressure which leads to activation of the baroreceptors and an increased heart rate.
- The third phase starts when the patient finishes exhaling. Aortic pressure briefly decreases due to the external pressure being removed from the thoracic vessels and the heart. The heart rate will briefly increase reflexively.
- The fourth phase starts with an increase in aortic pressure because of the sudden increase in cardiac output. The expected result of this and the Valsalva manoeuvre is a drop in heart rate.
Research has shown that although the Valsalva is often used by physicians it only has a success rate of between 5-20%. Due to the success rate of the Valsalva being very poor a modified version has been created and trialled. The modified Valsalva uses the same principles as the Valsalva manoeuvre but uses a modified postural position which exacerbates the vagal response. A recent study in the UK highlighted that 43% of patients that used the modified version reverted within 1 minute of the Valsalva being performed compared to 17% of the standard Valsalva manoeuvre.
How to perform the modified Valsalva:
- Monitor cardiac rhythm and ensure SVT.
- Sit patient on stretcher sitting upright in a comfortable condition.
- Get the patient to blow into a 10ml syringe for 15 seconds ensuring they have a good seal.
- At the end of the strain period lay the head of the stretcher flat and lift the legs to 45 degrees (hold this position for 15 seconds).
- Reassess the cardiac rhythm and ensure patient is comfortable.
Although research and trials involving the modified Valsalva is very limited a study by Appelboam, A, Reuben, A & Mann, C. (2015) found there to no serious adverse effects. Five subjects in this study showed electrocardiographic captured events such as asystolic pause and ventricular escape rhythms which were all transient and self-limiting.
Returning to the complex pattern of ventricular dysthymia and general arrhythmia post Valsalva manoeuvre of the patient within myself and Grants care, there seems to be little data/research suggesting why the patient had such an extensive but self-limiting cardiac response to the Modified Valsalva. Previous studies have shown that conditions such as myocardial infarction, coronary artery insufficiency, digitalis toxicity, hypokalaemia, hypoxemia, inadequate analgesia, old age and Halothane use can cause ventricular dysrhythmias. As we weren’t obviously aware of our patient having any of these conditions, a secondary cause to the post Valsalva dysrhythmias could be explained by the Trigeminocardiac reflex (TCR). TCR is a brainstem reflex which can be associated with a rapid onset of parasympathetic dysthymias due to stimulation of the sensory branches of the Trigeminal nerve. During the Valsalva manoeuvre TCR can be activated by changes in the intracranial pressure. Researchers are struggling to identify a thorough definition for TCR as TCR manifests in several different forms. On another note TCR has been found to have strong links with SIDS with further research needing to be completed to clarify this link.
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