HYPOPERFUSIONSTATES
CAUSES
Cerebral perfusion pressure (CPP) is dependent on mean arterial blood pres-
sure (MAP) and intracranial pressure (ICP), and is represented by the formula:
CPP = MAP – ICP. Hypoperfusion may logically result from an increased ICP
or decreased MAP.
Hypoperfusion stroke is a diffuse process with regional variability depending on
state of vasculature and brain in any given region. Prolonged hypoperfusion
will result in permanent injury.
Stroke symptoms may wax and wane as these variables change.
SYMPTOMS/EXAM
■ Symptom onset varies with stroke type.
■ Sudden and maximal at onset with embolic
■ More gradual or preceded by TIA with thrombotic
■ Waxing and waning with hypoperfusion state
■ Location of symptoms varies with location of obstruction (see Table 15.1).
■ Amaurosis fugax: Transient monocular blindness from embolization of
carotid plaque to the ophthalmic artery
■ Transient ischemic attack (TIA):Neurologic deficit that has complete
clinical resolution within 24 hours.
■ Wernicke aphasia(receptive aphasia): There is inability to comprehend
language input. Speech is fluent but disorganized, due to ischemia/infarct
in Wernicke’s area of temporal lobe.
■ Broca’s aphasia (expressive aphasia): There is inability to communicate ver-
bally. Speech is halting and produced with great effort, due to infarct/ischemia
of Broca’s area in the frontal lobe.
DIAGNOSIS
■ Suspect based on history and examination.
■ Confirmed based on CT or MRI
■ Appears as area of hypodensity on noncontrast CT (see Figure 15.2)
■ Perfusion-weighted CT angiography can identify the ischemic penumbra.
■ Ischemic stroke will not be visible on noncontrast CT until >6 hours.
■ Glucose to rule out hypoglycemia
■ ECG to evaluate rhythm
■ Coagulation studies if coagulopathy suspected
TREATMENT
■ ABCs (including intubation for decreased level of consciousness)
■ Hypotension:Restore euvolemia, then use pressors (if necessary).
■ Hypertension
■ Aggressive lowering of BP in chronically hypertensive patients (who
have cerebral autoregulation curve shifted to right) may limit flow to
the ischemic penumbra.
■ Treat if BP persistently elevated (systolic >220 or diastolic >140).
■ Goal = BP ≤185/115 mmHg.
■ Use titratable agent such as labetalol or nitroprusside.
NEUROLOGYThe hallmark of posterior
circulation stroke is crossed
deficits (face vs body).In stroke, treat BP if
persistently elevated
>220/140.
Goal BP is ≤18 5 /115