The
Cushing`s Triad is a triad of three signs, which is typically seen in the late
stages of patients with elevated intracranial pressure (ICP). Both the
sympathetic and parasympathetic nervous system plays important roles in the
triad, which consists of:- Hypertension (increased blood pressure)
- Bradycadria (decreased heart rate)
- Irregular breathing pattern
Why
hypertension?
When there
is an elevated ICP due to for example intracranial bleeding or edema, cerebral
vasculature will be increasingly compressed with rising ICP, leading to
cerebral ischemia. To combat this the sympathetic nervous system is activated.
The increased sympathetic tone will primary constrict the arterioles of the
body, mediated by alpha 1 adrenergic receptors. Since our mean arterial blood
pressure (MABP) is the product of cardiac output (CO) and systemic vascular
resistance (SVR), the MABP will rise, in other words, the patient will develop
hypertension. An increased pulse pressure (difference between systolic and
diastolic blood pressure) is also seen, because primary the systolic blood
pressure rises, whereas the diastolic pressure remains the same. The cerebral
vessels are not affected by this vasoconstriction, protecting the brain form
ischemia.
The hypertension
seen in patients with increased ICP is part of the cerebral autoregulation, trying
to keep cerebral perfusion pressure (CPP) relatively constant, even though the
ICP increases. CPP is the difference between MABP and ICP (CPP=MABP-ICP), so
increasing MABP by contracting arterioles makes sense when the ICP is elevated.
The brain also shunts away cerebrospinal fluid in order the combat the rising
ICP. If these and other compensatory mechanisms are inadequate, ICP will continue
to rise, reducing CPP to levels leading to global ischemia of brain tissue.
When ICP equals MABP, the CPP will be 0, and there will be no circulation to
the brain, a state known as brain tamponade.
Why
bradycardia?
The initial
sympathetic tone will initially cause tachycardia, and increased contractility
of the heart mediated primarily by beta 2 adrenoreceptors. This will increase
cardiac output, and thus increasing MABP together with the increased systemic
vascular resistance. The increased MABP will stretch and activate the high
pressure baroreceptors in the aortic arch and carotid sinus, which via the
vagus and glossopharyngeal nerve respectably, will signal that there is and
increased MABP to the cardiovascular control center in medulla oblongata. When
there is an elevated MABP sympathetic tone will be reduced and parasympathetic
tone will be increased, leading to bradycardia. The signal to the arterioles to
constrict, due to the high ICP, remains leaving the patient with both hypertension
and bradycardia.
Why
irregular breathing pattern?
The
irregular breathing pattern seen in patients with elevated ICP is due to
inadequate function of the respiratory control center located in the medulla
oblongata, because of the reduced cerebral perfusion pressure, or direct damage
to important structures. Often Cheyne-Stokes respirations are seen.
Sources:
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