April 13th Sycope

ew clerks weren’t here for this, but since we did talk about seizure and the discussion of loss of consciousness came up, thought I’d bring this up.

This approach is from symptom to diagnosis.

Level of consciousness requires four things

1.       Glucose

2.       Oxygen

3.       Blood pressure (to give the oxygen and glucose to the brain)

4.       Organized electrical activity

5.       Vascular conduit – the relates to a more rarer cause of syncope like vertebral basilar insufficiency

If presented with a patient with decreased level of consciousness we have lots of questions for them, As the history will give us the diagnoses the majority of time.  However, Some quick management tips

Always check our ABCs, are they breathing? Protecting their airway? Able to have a conversation?

What is there blood pressure, heart rate, temperature and oxygen saturation? These need to be addressed before taking a full history.

The 5^th vital sign is blood glucose, as we can see on our form browser that often it is done in emerge (appropriately so) as this is an easy test to do, and can dramatically change management – If going to give dextrose consider thiamine before, as not to precipitate  wernickes (though rarely seen these days). Also having a low threshold to consider a tox screen, and even just giving 0.4 mg of naloxone IV on speculation with decrease RR and pinpoint pupils.

In the seizure post I will run down the difference history of cardiac syncope vs seizure, but for the most part cardiac syncope happens suddenly, patient may have prodromes, but typically will wake up where they fell and will regain consciousness quickly.

So how does this cardiac syncope happen? I’ll give you the breakdown. Be aware that although neurocardiogenic  (also called vasovagal) are considered separate entities because one would likely require a pacemaker or ICD (cardiac syncope)… but in terms of understanding the causes they can be grouped in the below approach.

BP = cardiac output (CO) x total peripheral resistance (TPR

= Stroke volume x heart rate (CO) x TPR

= (EDV – ESV) [SV] x HR x TPR

So how can we affect the above variables?

1.       Low EDV

-          Hypovolemia – dehydration, diarrhea, excessive Lasix/diuretics

-          Blood loss

-          Tamponade (unable to fill properly)

-          PE – excessive pulmonary pressures means the RV isn’t getting blood through, therefore less filling in the left side of the heart. Think about this in the setting of syncope post op!

2.       Increase ESV: blood not leaving the heart

-          HOCM – young athlete fainting during exercise, LVH on ECG, with Valsalva mumur gets quieter and there is more obstruction of left ventricular outflow tract.

-          AS – look for the classic SAD triad: syncope, angina, dyspnea

HR

1.       Tachycardia

-          VT/Vib – think about this in patients with a history of CHF, old MI (scar), infiltrative disease of the heart – amyloid, sarcoid, hemochromatosis

-          Afib and AVRNT aren’t commonly associated with syncope as the ventricle can occasionally compensate for this – but could happen in the setting of low EF or diastolic dysfunction

2.       Bradycarida

-          Sinus brady from drugs, sick sinus syndrome

-          Heart blocks, third degree, second degree mobitz type II

-          Vasovagal bradycardia

Decrease in TPR

-          Drugs such as alpha blockers for prostate, alcohol is a vasodilator, opiates also venodilate and can lower bp.

-          Orthostatic hypotension potentially associated with adrenal insuff., parkinson’s (or multiple systems atrophy), diabetic autonomic neuropathy

-          Vasovagal vasodepressor type

-          Sepsis – rarely  just “syncope” on presentation

A note on vasovagal:

There is a variety of mechanism,  but how this happens is patient is a bit hypovolemic – standing for a while on a hot day, blood pooling in veins. Something happens (or nothing) and sympathetics increase heart rate, the low volume state in the ventricle activates mechanoreceptors which try to slow things down with parasympathetics – which can cause bradycardia, or a vasodepressor, or BOTH!
Harrison’s described NUMEROUS vasovagal types – *note I also group carotid sinus sensitivity with this.

The length of working this up is different in a healthy 16 year old who has a classic vasgovagal story, vs a 60 year old man with a history of MI, HTN and ECG abnormalities.

In our typical patient, a thorough history of what they were doing before, during, after, collateral history. VS and orthostatic VS (this should be done routinely in emerge for “syncope”), basic workup is looking at lytes BUN/CRE (pre-renal), CBC (for anemia), blood gas if suspected lung disease, CO2 is a vasodilator. ECG – looking for baseline abnormalities.

The San Franscisco Synope rule: Mneomnic is CHESS

CHF  (history of heart failure esp EF <30% could mean they are having epsidoes of Vfib/Vtach and may need and ICD)

Hematocrit <30 – they may be hemoconcrentrated initially so normal Hb doesn’t rule out bleed.

ECG abnormalities at baseline (long qt, brugada pattern)

Shortness of breath on admission

SBP <90 on triage VS

If all the above are negative, patients have a good prognosis.

When patients have a clear heart block on ECG… we know what to do. The trickier patients are recurrant vasovagal, and orthostatic hypotension not related to volume depletion.

Stolen from uptodate.

Vasovagal syncope treatment — Vasovagal syncope can usually be treated by learning to take precautions to avoid potential triggers and minimize the potential risk of harm. For example, if you faint while blood is being drawn, you may be instructed to lie down during the procedure. If you have a feeling that you will pass out during any activity, you should immediately lie down and elevate your legs.

Counter-pressure maneuvers — Counter-pressure maneuvers such as tensing your arms with clenched fists, leg pumping, and leg-crossing may stop a vasovagal syncopal episode, or at least delay it long enough that you can lie down with the feet elevated. Such maneuvers include:

●Leg crossing while tensing the leg, abdominal, and buttock muscles.

●Hand gripping, which involves gripping a rubber ball or similar object as hard as possible.

●Arm tensing, which involves gripping one hand with the other while simultaneously moving both arms away from the body.

For orthostatic hypotension first you often may not see a proportional increase in HR. One may consider sleeping with bed slightly elevated, getting up slowly (physio) and possibly fludrocortisone which is 0.1 mg po daily (starting) or mitodrine 5 mg po TID.