Essential Hypertension

What percent? What is the cause?

95%

No Identifiable Cause

Perhaps sympathetic dysfunction is a component

Hypertension

How many it affects in US?

Leading cause of death and disability

2/3 of people over 65 have HTN

Classifications of HTN

Normal

Pre

Stage 1

Stage 2

Normal    <120/<80

  Pre            120-139/80-89

Stage 1    140-159/90-99

Stage 2         >160/>100

Patients > 50 yrs, who have SBP > ___ is more significant than DBP

140 mmHg

Patients who are normotensive at 55 yrs still have a 90% lifetime risk of developing HTN as they age

Chronic vasoconstriction

-dehydration

Renin release

   -conversion of angiotensin I to angiotensin II

-Aldosterone secretion from adrenal cortex

Cerebrovascular effects of HTN

Rightward shift of autoregulation

-Compensatory to reduce CBF

-Prevent increases in ICP

-Normal is 50-150??

(vessels hypetrophy, happens over time, takes 1-2 months to shift curve)

What drugs makes BP control challening in the OR and suggest holding for the day of surgery?

What % of baseline should your BP goal be intraop?

ACE inhibitor

ARA (ARB)-particularly challenging b/c blocks ADH

20%

Generally can proceed with surgery if BP is less than??

180/110

if higher then it is controversial

PROLIFERATIVE

B/C endothelial injury --> plt aggregation

Release of platelet-derived growth factor resulted in smooth muscle proliferation

Served as a site for plaque formation

Inflammatory Process (not injury first)

Smooth Muscles

Immune cells

Immune mediators

Identified criticality of cholesterol

New view has helped in patient management

Arterial Stenosis

Thrombosis

Ischemia

Aneurysm formation (aortic space)

Hypercholesterolemia

Elevated triglycerides

Smoking

HTN

DM

Obesity

Genetic predisposition

Sex (males > females)

Impaired glucose regulation

Homocysteine

C-Reactive protein

Statins

C-reactive protein?

Anti-inflammatory agents?

Genomic treatment/recognition?

Surgical

-embolectomy

-angioplasty

-endarterectomy

-stenting

-bypass

-resection

Vasculopathic (cardiac)

HTN (meds, control, end organ effects)

DM

Smoking

COPD

Renal

Unstable coronary syndromes

decompensated CHF

significant dysrhthmias

severe valvular disease

Mild angina

prior MI

compensated CHF

DM

Renal Insufficiency

Advanced age

Abnormal ECG

Non-sinus rhythm

low functional capacity

CVA Hx

Uncontrolled HTN

3 or more clinical risk factors

(ischemic heart disease, compensated or prior HF, DM, renal insufficiency, and cerebrovascular disease)

AND

Vascular surgery

If it would change management!

CEA

(CVA's 3rd leading cuase of death in US)

CEA performed in patients with stenotic and ulcerative lesions in what vessels?

What is the most common?

Common carotid

Internal carotid

External carotid

Most common is Carotid bifurcation (where internal and external divide and cause turbulent flow)

CVA Rates in CEA

Periop MI Rate

What are high risk factors for complications?

CVA <3% asymptomatic

5% in symptomatic

10% in CVA patients

Periop MI 2-5% (is most common CEA problem)

Mortality is 0.5-2.5%

Risks

Age > 75, Inexperienced surgeon, Previous CVA, Angina, DBP >110, CEA in prep for CABG, ICA thrombus, Contralateral occlusion

Diagnosis of carotid pathology

What are the tests?

1) Neurological symptoms that warrent investigation

2) Incidental finding from

       -carotid bruit

       -Amaurosis fugax (25% in high grade) monocular 

         blindness from blockage in opthalmic artery

3) Tests

     -Duplex US (sensitive)

     -Arteriography for anatomical detail

     -CT or MRI if alternative comorbidities also investigated

Increases in CO2 cause ________ in vessels in the brain.

What is this related to?

Vasodilation

(Related to H+ concentration surrounding arterioles)

Cerebral blood flow autoregulates at what pressures?

Normal CBF is _____?

50-150 mmHg

CBF 50 ml/100g/min

Carotid stenosis jeopardizes flow (considerations are BP and PaCO2)

Blood flow to continue to brain tissue despite reduced flow in another vessel.

It is protective.

Anterior cerebral arteries (2)

Anterior communicating artery

Internal carotid arteries (2)

Posterior cerebral arteries (2)

Posterior communicating arteries (2)

CAD and carotid artery disease go hand in hand

NEED a risk assessment

Neurologic baseline assessment

HTN

Directed by patient status and medication regimen

Glucose

Potassium

CBC

Coagulation studies

ECG, other cardiac studies

Anti-hypertensive agents

Clopidogrel (if on it, keep them on it)

ASA (benefits may outweigh risk of bleeding)

Is sedation suggested preop for CEA?

Why or why not?

Suggested minimal or none

Anesthesia provider should use calming influence

Need to maintain normal CBF

-avoid Hypotension, hyper or hypocarbia

-CPP=MAP-ICP

Protect heart and brain

Maintain hemodynamic stability (middle ground)

Provide for prompt emergence

Want eucarbia, normothermic

Shivering post-op Increases SNS activity and Myocardial O2 demand

Arterial line

EEG

Transcranial doppler

SSEP

Cerebral Oximetry

high normal level (within 20% of baseline)

arterial line usually placed before patient is asleep

hypoperfused areas of brain lose ability to autoregulate

EEG monitor during CEA is to identify_______?

Describe sensitivity

When do you see EEG changes and then shunt?

Limitations?

Areas of focal ischemia

Limited sensitivity

Complicated by use of anesthetic agents (keep MAC <1)

May help limit shunt use or BP augmentation

CBF < 15ml/min/100g brain tissue

Doesn't monitor deep brain structures, false negatives, affected by temp, BP and anesthesia, doesn't prove to improve outcomes

Transcranial Doppler during CEA measures ______?

what is the limitation?

Middle cerebral artery flow velocity

Detect and quantify emboli

Can predict neuro events despite normal EEG

Low prediction during cross clamping

Somatosensory Evoked Potential during CEA detects_____?

What is the limitation?

cortical potentials after electrical stimuli presented to peripheral nerve

**evaluates deep brain structures

Affected by all anesthetics, must maintain light plain of anesthesia

value is questioned

Keep normal glucose

Patient population often has DM

High glucose implicated in poor neurologic outcomes (from cerebral lactic acidosis from anaerobic glycolysis of increased glucose stores in brain)

**Avoid dextrose-containing solutions**

General anesthesia considerations for CEA

What induction agent?

Use of narcotic?

Give what drug for hypotension?

What can cause bradycardia and even asystole?

Use Propofol or etomidate

restrict use of narcotic or use remifentanil (rapid exam)

Be alert for hypotension after induction (dehydrated but weigh fluid load with cardiac condition)

Consider local by surgeon

Phenylephrine for hypotension

Baroreceptor activation (treat with lidocain 1% to inactivate receptor or atropine/glyco)

Muscle relaxation as needed

Patient should be able to do what 3 things upon extubation from CEA?

What should be done before you leave the OR and head to PACU?

Manage airway, move all extremities as before, follow commands

Adequate neuro exam before leaving the OR

Neurological compromise is a reason to reexplore!!

What kind of regional block for CEA?

What are the 3 Risks?

Deep and superficial cervical plexus blocks (C1-C4 is cervical plexus)

**Need to block C2-C4**

What is the advantage of Regional for CEA patient?

What are some patient considerations that may make regional more difficult than general?

Patient can be awake and is considered the best monitor for neuro changes.

Considerations:

Patient preference, language barriers, difficult anatomy, claustrophobia, phrenic nerve block in COPD- can result in diaphragmatic dysfunction

Consider:

1) having surgeon inject local at the end of case

2) converting to general during case

3) inadequate access to airway

4) Seizure or loss of consciousness during clamping

5) skill of person performing block

Carotid Cross Clamp

Risk loss of blood flow to brain

Should heparinize before clamping

Shunt may be done but risk CVA from emboli

when unclamp: reflex vasodilation hypotensiona and bradycardia??

Neurologic dysfunction

Hemodynamic instability

Respiratory insufficiency

Hemodynamic instability postop CEA

What do you treat HTN with?

Usually HTN > HoTN

HTN can lead to myocarial ischemia, cerebral edema

Esmolol, labetalol, nitroprusside

Rule out causes (full bladder, pain, hypoxia, hypercarbia)

HoTN may be from re-exposure of baroreceptors

-coexistent bradycardia

TREAT only if neuro deficits with fluids and vasopressors

Recurrent laryngeal or hypoglossal nerve injury

Hematoma

Deficient carotid body function (respiratory drive in response to hypoxia not working)

MAC (dexmedetomidine)

on antiplatelet meds for 1 month

Aortic surgies are complicated by what?

Main goals are to preserve?

Need to cross-clamp and potential for large blood loss

Myocardium

Renal system

Pulmonary system

CNS
Visceral organs

1) Coronary Arteries

2) Aortic Arch Branches

     -Innominate artery

         (Branches into right carotid and right subclavian)

     -Left Carotid artery

     -Left Subclavian artery

Celiac Trunk (first branch of aorta below the diaphragm)

3 branches

1) Common hepatic artery

2) Left gastric artery

3) Splenic artery

Superior mesenteric (pancreas, duodenum, jejunum, ileum, colon)

Renal (kidneys and adrenal glands)

Inferior mesenteric (transverse and descending colon, sigmoid colon, and rectum)

What is the most likely aortic pathology?

Risk factors?

Aneurysmal

Chronic inflammation: atherosclerosis

Most likely: abdominal aorta

May also include dissections of the aorta

Age, smoking, HTN, Low HDL, HLD, Male, Low fibrinogen, platelets

Aortic Layers

In an aneurysm, the vessel wall becomes disrupted. Mostly happens in what layers?

Have degredation and remodeling of aortic wall

Intima/medial

Foam cells, thrombosis, rupture of layers

Proteolysis of medial layer in aneurysms

Intima/medial disruption in dissection

What is the biggest risk from a diseased aorta?

What are the risk levels?

Rupture and exsangination

< 4cm, rupture risk is 1%

 4-4.9 cm, risk is 2%

>5 cm, rupture risk increases to 20% (usually intervention when > 5 cm)

Mortality for ruptured AAA is 50%

HTN

Congenital connective tissue disorders (Marfan, Ehlers-Danlos)

Trauma

Pregnancy

Iatrogenic

Aneurysm: Maybe be incidental, asymptomatic pulsatile mass, CT or MRI

Dissection: Pain, severe HTN from vasoconstriction, reduced peripheral pulses, ischemic extremities, CVA (HTN, emboli, decreased blood flow)

Widened mediastinum on CXR

Tracheal deviation

Hemoptysis

Compression of left recurrent layrngeal nerve

SVC syndrome

Acute aortic regurgitation

MI (coronary artery anatomy, increase afterload)

Cardiac tamponade

CT/MRI

Reduce SBP to 100 mmHg

Cardiac depression

pain control

surgery

Emergency Case- so RSI

Stable vs. unstable

RSI

resuscitate through induction phase

1) volume

2) preserve renal function

3) Several large bore IVs

4) O negative blood

5) Immediate surgical control is a priority

6) Warm patient (fluids, forced air ABOVE defect)

1) Aortic proximal pressure increases ( increased ICP)

2) Shift of blood volume to the brain (increases ICP)

3) Decreased distal aortic pressure

4) The combination of decreased distal aortic pressure (MAP) and increased ICP

     -Decreased spinal cord perfusion

     -Spinal cord perfusion = MAP- ICP or CSF pressure

2 Posterior spinal cord arteries

Sensory or motor?

Supply how much of spinal column?

Sensory tract supply

Branch from posterior and inferior cerebellar arteries, vertebral arteries and radicular arteries

Supply 25% of spinal column

Anterior spinal cord artery

Branches from??

Supplies how much to spinal cord?

Major circulation to spinal cord

Branch from vertebral arteries and anastamose with radicular arteries in the lumber/thoracic region

Largest radicular arter is Artery of Adamkiewicz (arteria radicularis magna)

Origin variable, usually T9-12 (also T5-L5)

What is anterior spinal artery syndrome caused by?

Symptoms?

What increases your risk?

Loss of perfusion of arter of adamkiewicz

-paraplegia

-rectal/urinary incontinence

-loss of pain and temperature sense (proprioception preserved)

Risk: cross clamp time, clamp location, increased body temp, poor collateral flow, poor reperfusion

What are methods to decrease anterior spinal artery syndrome?

Hypothermia

Partial bypass

     -increased blood loss risk due to increased 

      heparinization, heparin coated shunts help

Avoid glucose-containing solutions

     -Worsen neuro outcome in the face of ischemia

Lumbar drain

     -Aortic clamp increases CSF pressure by 10-15

       mmHg

Mannitol

Adequate BP

Drugs with varied success (barbs, steriods, Ca channel blockers, Mg, naloxone, papaverine)

Renal concerns with cross clamp?

What is the strongest predictor of mortality in these patients?

Postop renal failure is strongest predictor (4-5 fold)

Renal flow may be compromised

Level of clamp is most important factor

     -5% incidence in infrarenal surgeries

     -13% in suprarenal

Blood flow redistributed in kidney

     -toward cortical and juxtamedullary regions

     -away from medulla

Renal vascular resistance increases 70%

     -persists after cross clamp removed ( up to 30 mins)

Renal protection in cross clamping

Drugs used?

Does it help with need for dialysis?

What is the best factor?

Dopamine 2-3 mcg/kg/min

Fenaldopam, ACE inhib, PGs, thoracic epidurals, vasodilators, furosemide, mannitol

Mannitol functions as a free-radical scavenger

     -Improve cortical blood flow, decreases renal cell  

      edema, vascular congestion

     -reduces renin, increases PG synthesis

None of above have warded off dialysis

Best factor is hydration

Compromise of distal perfusion

-Decreased total body O2 consumption/extraction

-increased mixed venous O2 saturation

-increased catecholamine levels

-decreased CO2 production

-respiratory alkalosis

-metabolic acidosis