the complications of simplicity
So I go to where the BLS truck crew was, an Intermediate and a Basic. The Basic is just about to finish his paperwork. Quick rundown of the patient--- 40's male, BP of 198/118 hr of 58, headache, nausea (but no vomitting), seems a slight bit lethargic (but unable to tell if that's baseline, it being 2am, medications, or the BP) no CP, no SOB, pupils are fine, lungs clear, no other medical history aside from psych. Nurse states his BP's been elevated since Friday. (Keep in mind this is a generally good psych hospital). They've given Norvasc with little change in BP.
As I follow the thread I see a lot of honing in on Cushing's triad and the potential for CVA. I would just like to kindly add a few words on this.
I would like to fist define what cushing's traid is:
1. irregular respirations
2. widening pulse pressures
3. bradycardia
Cushing's triad is seen in head injuries ( late stages), it does not mean there is a head injury.
It is also manifests in When chemoreceptors in the brain and baroreceptors are receiving mixed inputs.
In hypertension patients the heart must overcome the resistance of the reverse flow in order to adequetely eject blood and achieve perfusion pressure.
In the findings posted by Linuss. There was no evidence of intracranial shift. Pupils were normal, a bit of lethargy (possibly baseline at 2 am) and no irregular breathing pattern.
These findings (or lack of findings) rule out cushing's triad. As only 2 of the 3 criteria are met. The fact the pt is still conscious at any level also plays a strong role in this finding. There is also only one set of vitals so there is no way to tell if the pulse pressure is widening.
Now when we add a drug into the mix the dynamic completely changes.
Norvasc is a calcium chanel blocker that acts non specifically on both the heart and vascular smotth muscle. Depending on the underlying cause and patients level of compensation, norvasc is known to cause negative inotropic effect. (lack of contractility) In addition, as any CCB it can also produce negative chronotropic effects because Ca channels are part of the normal cardiac cycle. But I think the bradycardia in this case has a slightly different mechanism, more along the lines of something Dr. Cushing would be proud of.
In a well compensated patient with HTN, the body maintains perfusion to end tissues over the vascular resistence with increased inotropic or chronotropic response. (which opposes)
Decreasing the rate/pressure the heart beats at, decreases cerebral perfusion pressure. Which leads to a catecholamine response. (increased peripheral resistance to maintain central perfusion in addition to increased rate.) Having said that, the baroreceptor reflex in the carotid sinus would detect and attempt to regulate the arterial pressures by decreasing heart rate. All together central baroreceptor acting in contra to peripheral catecholamine, with chemical blockage of central catecholamine effect. Epi in particular affects cerebral arterioles.
Cushing's reflex + pharm.
Another important pharm finding is that headache is the most commonly reported side effect of norvasc. The peripheral HTN cold also produce the same effect and when adding in the nausea, it looks to me that norvasc is not the best choice here to regulate hypertension by trying to normalize numbers instead of patient condition. Norvasc is also not a first line therapy anywhere I have seen.
when you add in the nausea that is a nonspecific finding but I would think in this case it does point to a problem with cerebral perfusion and subthreshold stimulation of the vomiting reflex. Certainly a potential for CVA exists, but it seems more like an anoxic brain insult (from perfusion issues after chemically knocking out the patient's compensatory reflexes) than an ischemic or hemorrhagic insult from the limited information provided here.
But for all my musings, it doesn't change the EMS treatment... BLS ambulance to hospital where it can all be sorted out for sure.
