CVD

Question 1

What is the brain’s energy source

How much CO goes to the brain

How much 02 is consumed

Answer 1

AEROBIC metabolism

20% of cardiac output

15% of O2 consumption

Question 2

After cerebral ischemia, how much time can elapse to…

maintain normal brain function?

before irreversible damage occurs?

Two main causes of cesseation of blood flow:

Answer 2

For normal brain function: 8-10 seconds

Irreversible damage after 6-8 minutes

NO 02 reserve in the brain, a constant supply of 02 is needed

*hypotension (reduction in the perfusion pressure)

*occlusion (small or large vessel)

Question 3

Which cells are most sensitive to ischemia?

Which neurons are more susceptible to ischemia?

Answer 3

Neurons > oligodendrocytes > endothelial cells > astrocytes

Variable neuronal susceptibility to ischemia:

Pyramidal neurons in CA1 region of hippocampus, purkinje cells of cerebellum and certain layers in the cortex

Question 4

What are the major etiologies of global cerebral ischemia? (4)

Answer 4

1. Low perfusion (atherosclerosis, near or compete occlusion)
2. Acute decrease in blood flow (cardiogenic shock)
3. Chronic Hypoxia (although the brain is less sensitive to hypoxia vs ischemia)
4. Repeated episodes of hypoglycemia

Question 5

What type of damage can occur in a global cerebral ischemia:

Mild global ischemia –?

Severe –?

Mododerate –

Answer 5

Mild – usually no permanent damage

Severe – DIFFUSE damage, vegetative state

Moderate – increased vulnerability in watershed areas (anterior and middle cerebral arteries) and selecively vulnerable regions

Question 6

Global Cerebral ischemia

When can damage be seen histologically?

What is the underlying pathology and associated changes to the cell (3):

Answer 6

Histological changes appear 6-12 hours after insult

Pathology: RED DEAD nucleus

cytoplasmic eosinophilia, loss of Nissl substance, shrunken/dark pyknotic nuclei

Question 7

Global Ischemia:

Where are areas of neuronal vulnerability in adults (3) and in infants (4)?

Answer 7

Adults: “big neurons”, cortical layers 3&5, CA1 of hippocampus, Purkinje cells of cerebellum

Infants: Subiculum, Thalamus, pontine nuceli, white matter (cerebellum)

Question 8

What type of histology can be observed with laminar cortical necrosis?

which areas are highly vulnerable?

Answer 8

Brown discoloration, pitting of cortex, band-like fashion, and microscopically will show loss and vaculation

Less vulnerable superficial cortex is preserved

Selective vulnerability: CA1 area of hippocampus (Sommer’s sector), watershed or border zone infarcts

Question 9

What are the three types of ischemic strokes and what are their major affected arteries (3)?

Answer 9

1. Thrombic- in situ thrombosis, atherosclerotic plaque (75%) esp at bifurcation of internal cartoid and MCA
2. Embolic (10%) - cardioembolic (Afib, MI –>MCA), atheroembolic (carotid, vertebra from damaged endothelium)
3. Small vessel disease (HTN, DM, vasculitis) - lacunar stroke (lenticulostriate vessels, cystic infarct <1.5 cm), internal capsule - motor or thalamus - sensory

Question 10

What type of vasular insult is pictured?

What is the major artery affected?

What are the major associated sx:

Answer 10

Ischemic hemispheric infarct

MCA territory

SX: midline shift, contralateral hemiparesis affecting the lower face and upper extremity more than the leg, similar distribution contralateral hemisensory loss, contralateral visual field deficits,

Dominant hemisphere infarct highly associated with expressive aphasia, whereas non-dominant infarct is associated with neglect sydrome

Question 11

What are major differences between acute, subacute and chronic ischemic infarcts?

Answer 11

Acute - indistinct borders, bluring of the cortex, white matter

Subacute - boarders more distinct, tissue liquefaction; early PMNs and late macrophages, vascular proliferation

Chronic - cystic spaces, +/- hemosiderin, gliosis

Question 12

Typical characteristics of embolic infarcts (4):

Answer 12

Smaller, centered at gray-white junction

can be single or multiple

may invovle more than one vascular territory

MCA is the most common artery invovled

Question 13

Lacunar infarcts:

usually occurs secondary to ______, complication of long standing ______.

most commonly involved ______ artery which leads to small _____ areas of infraction, aka _____.

Common locations (4)

involvement of the internal capsule –> pure _____ stroke

involvement of the thalamus —> pure _____ stroke

Answer 13

Lacunar infarcts:

usually occurs secondary to hyaline atherosclerosis, complication of long standing HTN

most commonly involved lenticulostriate vessels which leads to small, cystic areas of infraction (up to 1.5 cm in size) = small-lake infractions

Common locations: putamen, thalamus, pons, cerebellum

involvement of the internal capsule –> pure MOTOR stroke

involvement of the thalamus —> pure SENSORY stroke

Question 14

What are the different intracranial hemorrhages that can occur above the arachnoid and below the arachnoid?

Answer 14

Above the arachnoid:

mostly traumatic in nature

–> epidural and subdural hematomas

Below the arachnoid:

underlying cerebrovascular disease

–> aneurysms => subarachnoid hemorrhages (SAH)

–> HTN => parenchymal hemorrhages

Question 15

Intraparenchyma hemorrhages:

Common locations (4)-

microscopic changes (3)-

Intraparenchymal hemorrhages are secondary to rupture of _______ also called ______

(highly seen at _____ arteries)

Similar distribution to _____ infarcts

Common vessels (4)

Answer 15

Common locations: putamen, thalamus, pons, cerebllum

Microscopic: recent hemorrhage surrounded by central edema, minimal tissue necrosis, resolution leaves behind cystic space with macrophages containing hemosiderin

Intraparenchymal hemorrhages are secondary to rupture of pseudoaneurysms also called charcot-bouchard (highly seen at the lenticulostriate arteries, with rupture after hyline arterosclerosis)

Similar distribution to LACUNAR infarcts

Common vessels (4): lenticulostriate arteries, paramedial pontine vessels, short circumferential vessels of the cerebellum and in teh central white matter (end arteries)

Question 16

Subarachnoid Hemorrhage

Etiologies (3):

CSF will show _________, yellow hue due to bilirubin

Pathology:

Answer 16

bleeding into the subarachnoid space

Causes:

1. Berry aneurysm: common cause of non-traumatic spontaneous subarachnoid hemorrhage

2. AVM (arterious-venous malformations)

3. Anticoagulated state

CSF shows XANTHOCHROMIA

Question 17

Pathology of subarachnoid hemorrhage:

gross: thin-walled no_____ outpouching from arterial branching points

site of rupture is at the _____

associated vascular spasms produced _________

Answer 17

gross: thin-walled no MEDIA outpouching from arterial branching points

site of rupture is at the DOME

associated vascular spasms produced GLOBAL CEREBRAL ISCHEMIA

Question 18

Saccular (BERRY) Aneurysms - due to a defect in/lack of ____ within the arterial wall

Etiology & associations (3)

Prevalence: female vs male

SX, fatality

Most are in ______ circle of willis @ ____ communicating artery

Answer 18

Saccular (BERRY) Aneurysms

Etiology: unclear, congenital defect in MEDIA hypothesized; genetic component associated with AD polycystic kidney disease, Ehler’s-Danlos, IV, NF I, Marfans

Prevalence: FEMALE > male

most are ASMPYMPTOMATIC until rutpure, with 50% mortality in the first 24 hours

Most are in ANTERIOR circle of willis @ ant communicating artery

Question 19

Intraventricular Hemorrhages

Site of hemorrhage is in _______ matrix located beneath the _____ which easily ruptures into the ventricles

massive are instantenously fatal

Seen in ______ (young/old)

Answer 19

Intraventricular Hemorrhages

Site of hemorrhage is in GERMINAL matrix located beneath the EPENDYMA which easily ruptures into the ventricles

massive are instantenously fatal

Seen mostly in PREMATURE INFANTS, very rare in adults

Question 20

Duret Hemorrhages

are seen secondary to _____ from ______ of the medial temporal lobe that —> stretching and ischemia of ______ arterioles

Etiologies (3):

Answer 20

are seen secondary to COMPRESSION from HERNIATION of the medial temporal lobe that —> stretching and ischemia of PERFORATING arterioles –> break = duret hemorrhages

Etiologies (3): from mass lesions producing herniation such as…hemorrhages, inflammation, neoplasms

Question 21

Epidural Hematoma:

Is blood between _____ and _____

Classically seen due to fracture of ______ bone with associated rupture of the _______ artery

CT:

SX:

Complication:

Answer 21

Epidural Hematoma:

Is blood between DURA and SKULL

Classically seen due to fracture of TEMPORAL bone with associated rupture of the MIDDLE MENINGEAL artery

CT: lens-shaped lesion (lenticular/convex shape)

SX: lucid interval that preced neurological signs

Complication: herniation is a lethal complication

Question 22

Subdural Hematoma:

Blood located __________

Secondary to tearing of _______ between _____ & _____

Usually due to _____

CT:

SX:

Population at-risk:

Complications:

Answer 22

Subdural Hematoma:

Blood located underneath the dura covering brain surface

Secondary to tearing of BRIDGING VEINS between DURA & ARACHNOID

Usually due to TRAUMA

CT: crescent-shaped lesion (takes shape of brain)

SX:progressive neurological signs

Population at-risk: eldery due to age-related cerebral atrophy, which stretches bridging veins

Complications: herniation is a lethal complication

Question 23

Herniations lead to….

Types (3)

Answer 23

= displacement of the brain due to mass effect or increased intracranial pressure

• Types:*
  1. Tonsillar herniation
  2. Subfalcine herniation
  3. Uncal herniation

Question 24

____ Herniation –> displacement of cerebellar tonsils into _______ –> compression of ______ and cardiopulmonary arrest

Answer 24

TONSILLAR herniaiton

–> displacement of cerebellar tonsils into foramen magnum–> compression of BRAIN STEM and cardiopulmonary arrest

Question 25

________ herniation –> displacement of the cingulate gyrus under the falx cerebri —> compression of _______ –>Infarction

Answer 25

Subfalcine herniation —-> displacement of the cingulate gyrus under the falx cerebri —> compression of the ACA –> infarction

Question 26

______ herniation —> displacement of the ____ /medial temporal lobe under the tentorium cerebelli –> compression of CN ___ –> SX (2) and compression of _____ artery —-> occipital lobe infarct —–> SX (1)

Question 27

What is the underlying pathogenesis of ischemic CVD?

what are major and minor predisposing factors to ischemic cerebrovascular disease:

Where does atherosclerotic changes predominate?

Answer 27

Atherosclerosis is one of the major underlying pathologies of CVD

artherosclerosis, with predispositions such as HTN, heart disease, DM, smoking, hyperlipidemia, and family history of vascular disease

Minor contributing factors include: obesity, lack of exercise, and excessive alcohol conspumption

Atherosclerotic changes predominate at the bifurcation points of large, major cervical adn intracranial artiers (more turbulent blood flow?) –> intravascular atheromas or arterial plaques develop from subintimal lipid deposition, smooth muscle proliferation and fibrosis –> enlarging atheromas or plaques may narrow or occlude an artery or may ulcerate (or both) – an ulceration dirupts the intima, the coagulation process is initiated –> local occlusion (thrombosis0 or distal propagation (embolization) of blood clot, platelets, fibrin, cholesterol or calcified elements (emboli), which can occlude smaller caliber arteries downstream

TWO basic mechanisms of ischemic infarction are: local arterial thormbosisi of an atheroma or embolic arterial occlusions form proximal resources

Question 28

what causes lacunar infarcts?

Answer 28

THROMBOSIS (not emboli) of perforator or lenticulostriate arteries that supply deeper structures (basal ganglia, thalamus, internal capsule, corona radiata) –> ischemic infarction that such lesion in the internal capsule may cause a disabling hemiparesis

Question 29

TIA is an ___ from an arterial or cardiac source that obstructs branches of _____ or ______, lasting less than 24 hours.

One type of cartoid territory TIA is called ________, which causes _____ due to the involvement of _____ artery or _____ branches. SX include:

Vertebrobasilar territory TIAs cause ischemia of: (3) –> symptoms such as:

Answer 29

TIA is an EMBOLUS from an arterial or cardiac source that obstructs branches of INTERNAL CAROTID or VERTEBROBASILAR ARTERY lasting less than 24 hours.

One type of cartoid territory TIA is called AMAUROSIS FUGAX, which causes MONOCULAR BLINDNESS due to the involvement of OPTHALMIC ARTERY or RETINAL BRANCHES branches. Symptoms include: lowered dark shade in one eye, which gradually lightenes up; hemispheral ishcemia –> hemiparesis or aphasia

Vertebrobasilar territory TIAs cause ischemia of: BRAIN STEM, CEREBELLUM OR VISUAL/OCCIPITAL CORTEX –> symptoms such as: ATAXIA, HOMONYMOUS HEMIANPOSIA, HEMIPARESIS asscoiated with crossed brain stem syndromes

Question 30

What “stroke syndromes” would suggest occlusion of larger arteries or branches:

hemiparesis with greater weakness of hte face and upper limb –> ?

Hemiparesis with greater weakness of the lower limbs –> ?

Sensory deficits limited to the face and upper limb –> ?

Other MCA artery findings:

Answer 30

hemiparesis with greater weakness of hte face and upper limb –> precentral MCA territory

Hemiparesis with greater weakness of the lower limbs –> precentral ACA

Sensory deficits limited to the face and upper limb –> postcentral ACA

Other MCA artery findings: aphasia or homonymous visual field deficits

Cerebellar hemispheral syndryomes or “crossed” brain stem syndromes - Weber syndrome, Wallenberg syndrome, due to occlusion of large vertebrobasilar arterial branches

Question 31

What are the classic lacunar syndrome symptoms?

Answer 31

if it involves tiny infarcts in the internal capsule, corona radiata or basilar pons –> Pure motor hemiplegia, ataxic-hemiparesis and clumsy hand-dysarthia

If it involved small vessel occlusions inolving the thalamus –> pure sensory stroke

Question 32

Treatment for TIAs:

Answer 32

Younger pt / pt that lack stroke risk factors: work up for caogulopathy or non-atherosclerotic causes of ischemica should be done.

Pt that is stroke-prone: echocardiograph (determine cardiac source of emboli), ultrasound imaging,

MRA, CTA or catheter angiograph for carotid or vertebrobasilar

Question 33

what patient would benefit from a carotid endarterectomy?

Answer 33

symptomatic atheromatous lesions of 70-99% stenosis at teh origin of the internal carotid artery – surgically remove the lesion, unless life-limiting health conditions exist

Question 34

Meds to use to reduce stroke risk:

..in patients wtih chornic atrial fib?

— with no afib?

Answer 34

w/ CHORNIC atrial fib: WARFARIN (target INR 2.5), if no contraindications for anticoagulation exists

Other pt: antiplatelet drugs such as aspirin, clopidogrel, or aspirin/dipyridamole

Statin durgs reduce the risk of stroke even in the absence of hyperlipidemia

other means: medical control of BP and diabetes, cessation of smoking and other stroke preventative measures

Question 35

What medication could be used for an acute ischemic infarction and a moderate neurological deficit to help improve recovery?

Within what time period must this medication be administered?

What conditions prohibit the administration of this medication?

What is the greatest risk to using this drug?

Answer 35

What medication could be used for an acute ischemic infarction and a moderate neurological deficit to help improve recovery?

IV tPA, a thormbolytic drug

Within what time period must this medication be administered?

three hours

What conditions prohibit the administration of this medication?

rapidly improving or post-ictal deficits, presence of hemorrhage on a brain CT scan, uncontrollable HTN, extreme hypo or hyper- gylcemia, concurrent use of warfarin or increased bleeding risk from recent surgical or invasive procedures.

What is the greatest risk to using this drug?

intracranial hemorrhage, can be fatal

Question 36

What could be done in those patients who cannot use

Answer 36

Brain CT or MRI scans help indicate whether a large artery occlusion occurred in which embolic sources must be investiaged for hte possible need for WARFARIN, CAROTID ENDARTERECTOMY OR INTEREVNTIONAL PROCEDURES, veruss a small arter occlusion, where antiplatelet drugs and medical therapy is used.

Question 37

What important parameters needs to be monitored?

Answer 37

GLUCOSE- hyperglycemia during an acute ischemic infarction is associated with a poorer prognosis. Saline without dextrose is prefered, insulin to ensure normal glucose levels (if pt develops impaired consciousness withouth hypoglycemia - increased ICP may be considered - mechanical hyperventilation heps reduce ICP; hypocapnia induces cerebral OR IV mannitol

Blood Pressure - should be carefully monitored yet not over treated since further reduction in cerebral perfusion may further worsen an area of focal ishchemia

Avoid Warfarin - temporarily withheld to avoid complications

*antiplatelet meds are used in patients where warfarin is not indicated.

*ALL PT should be prevented from complications that may accompany the neurological deficits of stroke, such as seizures, aspiration or choking and pulmonary emboli from DVT

Question 38

What are some symptoms of intracranial hemorrhage?

Pathology behind hemorrhage?

Answer 38

SX: severe H/A, impairment or loss of consciousness, focal neurological deficit (depending on the location of the bleeding)

sudden rupture of arterial blood into the brain parenchyma –> increasing ICP –> edema around the hematoma, potentially leading to a fatal shifting or herniation of the brain

deeply located hemorrhage suggests hypertension as the cause, while more superficial hemorrhages at the poles of the frontal, temporal or occipital lobes often occur from head trauma.

Question 39

What does cerebral hemorrhage appear as?

Answer 39

dark red clot with surrounding edema and occasional dissection into the ventricular system if the bleeding is deep and extensive

The clot gradually liquefies, edema resolves, and the remianing cyst or slit appears to be peripherally staned brown from hemosiderin

Question 40

When is bleeding from venous sources become a problem?

Answer 40

In the elderly patients, who normally have some degree of brain atropy. Mild or trivial head trauma may tear taut bridging coritcal veins which empy into largersinuses.

Such VENOUS bleeding normally accumulates in the SUBDURAL space- NOT within the brain parenchyma –> SUBDURAL HEMATOMA

progressive growth of the hematoma could lead to cognitive and consciousness impairments

Question 41

What are some etiologies of cerebral hemorrhages?

Answer 41

Traumatic hemorrhage - obvious with HX and other physical signs

INR (prothrombin time) should be checked if the patient takes warfarin for anotehr medical conditiona nd other blood test for a bleeding disorder

Cocaine and other sympathomimetic drugs which abruptly iincrease blood pressure may also cause cerebral hemorrhage - screen the urine for illicit drugs

HTN is the MOST COMMON cause of cerebral hemorrhage [weakened walls of small lenticulostriate arteries rupture, bleeding most often into the striatum and thalamus and less often into the subcortical white matter, pons and cerebellum]

Cerebral amyloid angiopathy - recurrent lobar hemorrhages usually in the posterior cerebral hemisphers;

Congenital vascular abnormalities such as arteriovenous malformations (AVMs)

Brain tumors or ischemic infarcts

Question 42

Treatment of cerebral hemorrhage:

Answer 42

control of BP and increased intracranial pressure

Surgical evaculation of hte hematoma is warranted generally only for worsening cerebellar hemorrhages

Question 43

Subarachnoid hemorrhage - Etiologies and signs

Answer 43

Trauma is the most common cause of bleeding into the subarachnoid space

w/out trauma, ruptured congenital berry aneurysm is the most common cause of SAHs

[congenital berry or saccular aneurysms arise in the circle of Willis at the base of the brain, esp anteriorly, beg as bulges or thinned out-pouching at arterial bifurcations INC risk for rupture beyond 7 to 10 mm – some patients have a sentinel H/A or warning leak from a mild to moderate amount of bleeding – SAH “worst h/a of my life” due to increased ICP and meningeal irritation by the blood]

NUCHAL RIGIDITY** and meningeal signs are usually preset, often with **N/V and impaired consciousness

• • localizing neurological signs are often absent, since the hemorrhage does not involve the brain parenchyma itself*
• presence of a third cranial/oculomotor nerve palsy suggest that the berry aneurysm is near the posterior communicating artery*

Question 44

SAH evaluation and treatment:

Answer 44

suspected patients should have a NON-CONTRASTED CT Brain Scan, which often shows blood in the cisterns and sulci around the base of the brain

If the CT brain scan appears normal - LP is necessary to exclude a small volume of SA blood yet bleeding from a traumatic LP procedure itself makes teh diagnosis of SAH difficult

a yellow coloration = Xanthochromia of the CSF indicates breakdown of hte blood within the CSF prior to the LP vs with a traumatic LP, the amount of blood typically decreases in serial tubes but the blood from SAH is fairly constant from tube to tube

EMERGENT ANGIOGRAPHY - should be done to locate aneurysm

the neck of the aneurysm should be surgically clipped to prvent further rebleeding

if the patient cannot tolerate surgery or the aneurysm is surgically inaccessible, an intravascular catheter may be used to occlude the anerusym with metallic coils

COMPLICATIONS: the patietn may over the next days, even after successful surgery, develop the complication of cerebral vasospasm – reduced blood flow from teh cerebral vasospasm creates ischemic inffarctions and is more likely to occur after a large volume SAH

RX: post operatively, cerebral vasospasm is minimized by TRIPLE H THERAPY = consisting of hypertension (induced by vasopressor medication), hypervolemia (generous intravenous hydration), and hemodilution (phlebotomy to remove blood)

ORAL NIMODIPINE also improves patient outcome, perhaps more from a neuroprotective effect than any vasoactive property as a calcium-channel blocker