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ANESTHESIA PRACTICE 3 > VASCULAR DISEASE AND HYPERTENSION > Flashcards

VASCULAR DISEASE AND HYPERTENSION Flashcards

1
Q

how is arterial BP calculated?

A

MAP = SVR x CO

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2
Q

how is cardiac output calculated?

A

CO = SV x HR

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3
Q

how is blood pressure controlled?

A
  • autonomic nervous system (central and peripheral mechanisms)
  • renin-angiotensin-aldosterone system
  • renal changes
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4
Q

how is blood pressure regulated by the autonomic nervous system?

A
  • brainstem control

* baroreceptor reflexes in aortic arch and carotid sinus

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5
Q

how do the brainstem (centrally) and baroreceptors (peripherally) in aortic arch and carotid sinus respond to hypertensive states?

A

decrease HR/ increase vasodilation

    • increase vagal (parasympathetic) tone
    • decrease sympathetic tone
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6
Q

how do the brainstem (centrally) and baroreceptors (peripherally) in aortic arch and carotid sinus respond to hypotensive states?

A

increase HR, vasoconstriction, contractility

    • decrease vagal (parasympathetic) tone
    • increase sympathetic tone
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7
Q

explain how CN IX regulates BP

A

the visceral sensory portion of the glossopharyngeal nerve innervates the baroreceptors of the carotid sinus and the chemoreceptors of the carotid bodies

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8
Q

what nerve innervates the aortic arch baroreceptors?

A

vagus (CN X)

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9
Q

how is the renin-angiotensin-aldosterone system stimulated?

A

the RAAS is activated with hypotension and decreased sympathetic tone (decreased GBF)

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10
Q

how does the RAAS respond to hypotension/decreased sympathetic tone?

A
  • increased vasopressin (ADH) levels

* increased angiotensin II levels

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11
Q

what renal structure initiates the RAAS?

A
  • macula densa senses low fluid flow/low [Na]

* juxtaglomerular cells secrete renin

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12
Q

describe the RAAS

A
  • renin released from juxtaglomerular cells interacts with angiotensinogen from liver to form angiotensin I
  • ACE released from pulmonary blood converts angiotensin I to angiotensin II
  • angiotensin II triggers widespread systemic vasoconstriction and stimulates adrenal cortex to secrete aldosterone
  • aldosterone stimulates Na and H2O reabsorption in the convoluted tubule and collecting ducts
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13
Q

what are the morbidities commonly associated with poorly controlled HTN?

A
  • MI
  • CVA
  • renal failure
  • death
    • leading cause of morbidity and mortality worldwide
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14
Q

what are the general goals for HTN therapy?

A
  • SBP
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15
Q

describe primary hypertension

A
  • essential HTN – not secondary to an underlying disorder

* 90% of all patients with HTN

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16
Q

what are the risk factors for primary HTN?

A
  • age
  • family history
  • obesity
  • insulin resistance
  • diet and lifestyle
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17
Q

describe secondary hypertension

A
  • secondary to underlying medical disorder or therapies

* rare – 10% of all causes of HTN

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18
Q

name 2 renal disorders that are commonly associated with secondary hypertension

A
  • fibromuscular dysplasia

* renal artery stenosis

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19
Q

name 4 endocrine disorders that are commonly associated with secondary hypertension

A
  • pheochromocytoma
  • cushing’s syndrome
  • hyperaldosteronism
  • hyperthyroidism
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20
Q

define autoregulation relative to hypertension

A

ability to maintain constant blood flow during times of changing perfusion pressure

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21
Q

what 3 organ systems autoregulate blood flow?

A
  • brain
  • heart
  • kidneys
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22
Q

define cerebrovascular accident (CVA)/stroke

A
  • sudden death of brain cells due to lack of oxygen when blood flow to brain is impaired by blockage or rupture of an artery to the brain
  • most CVAs are ischemic in etiology
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23
Q

what are the atherosclerotic complications relative to hypertensive end-organ damage?

A
  • myocardial ischemia and systolic disfunction
  • MI, arrhythmias, heart failure
  • death
24
Q

what are the hypertensive complications relative to hypertensive end-organ damage?

A
  • aneurysms
  • left ventricular hypertrophy (LVH) and diastolic dysfunction
  • MI, angina, arrhythmias, heart failure
  • death
25
how does hypertension lead to renal damage?
* glomerular damage leading to protein loss in the urine/albuminuria * ultimately leads to overt renal failure
26
define hypertensive emergency
* severe HTN with evidence of acute end organ damage
27
define hypertensive urgency
* severe HTN without signs of acute end organ damage
28
what are signs of acute end organ damage related to HTN?
* CVA * encephalopathy * LV failure * MI * aortic dissection * renal failure
29
describe treatment for hypertensive emergency vs. urgency
* HTN emergency – IV anti-HTN; BP lowered about 20% in 1st few hrs, and then gradually normalized over days * HTN urgency – managed with PO meds
30
how do HTN treatments differ between general population/diabetes w/o CKD vs CKD w/ or w/o diabetes?
* gen pop/diabetes w/o CKD – thiazide diuretic or CCB (all races) * CKD w/ or w/o diabetes – ACEI or ARB
31
how does race change HTN medication in gen pop/diabetes w/o CKD?
* non-black races add ACEI or ARB | * black races thiazide diuretics or CCB only
32
what is the primary treatment for HTN?
lifestyle modifications * weight loss * reduced salt intake * alcohol and tobacco cessation
33
how do thiazide diuretics such as HCTZ work?
reduce sodium absorption in disal convoluted tubule | * increases water loss
34
how do loop diuretics such as furosemide and torsemide work?
* inhibit Na, Cl reabsorption in LoH * increases water loss * increases prostaglandin levels
35
how do ACE inhibitors such as lisinopril and enalapril work?
inhibit ACE therefore inhibiting conversion of angiotensin I to angiotensin II * vasodilation * vascular smooth muscle relaxation * natriuresis * decreased vasopressin release
36
how do angiotensin receptor blockers (ARBs) such as losartan and valsartan work?
blocks activation of the angiotensin II receptor * vasodilation * vascular smooth muscle relaxation * natriuresis * decreased vasopressin release
37
how do calcium channel blockers (CCBs) such as amlodipine and nicardipine work?
block calcium channels, decreasing intracellular calcium levels * vasodilation * negative inotropy * negative chronotropy * reduced aldosterone production
38
how do beta blockers such as metoprolol and carvedilol work?
block catecholamine action on beta receptors * negative chronotropy * negative inotropy * anti arrhythmic effect * reduced aldosterone production * smooth muscle relaxation * * not 1st line therapy for HTN
39
where are beta-1, -2, and -3 receptors found?
* beta-1 – heart, kidneys * beta-2 – smooth muscle, lungs * beta-3 – adipose tissue
40
what are some postoperative concerns for HTN pts?
* hypoxia * hypercarbia * acute neurologic or cardiac event * medication withdrawal * surgical related
41
what are the three layers of the aortic wall?
(inside – outside) * intima * media * adventitia (or externa)
42
what is the difference between a true aortic aneurysm and a false aortic aneurysm?
* true (fusiform or saccular) aneurysms involve all three layers of aortic tissue * pseudoaneurysms do not involve all three layers of aortic tissue
43
what are some etiologies of aortic aneurysms?
* HTN * atherosclerosis * collagen vascular disease * bicuspid aortic valve * syphilis * hyperlipidemia * mycotic aortic aneurysm * inflammatory
44
describe aortic dissection
intimal tear creating false lumen for blood to enter
45
describe primary aortic dissection
intimal tears on ascending and descending aorta
46
describe secondary aortic dissection
intimal tear on ascending aorta only
47
describe tertiary aortic dissection
intimal tear on descending aorta only
48
what are the common etiologies of aortic dissection?
* HTN * collagen vascular disease * bicuspid aortic valve * inflammatory * trauma * complication from heart surgery
49
describe carotid artery stenosis
* primarily due to atherosclerotic disease * primarily involving internal carotid arteries * intervention indicated for stenosis > 70%
50
what are the risk factors for carotid artery stenosis?
* HTN * hyperlipidemia * DM * PAD * tobacco use
51
what are the treatment options for CAD?
* medical management * risk factor modification * stenting * endarterectomy
52
what kind of receptors are the carotid bodies and carotid sinuses?
* carotid bodies – chemoreceptors | * carotid sinus – baroreceptor
53
what could be expected if the carotid body is damaged surgically?
* carotid body detects hypoxemia in the blood | * if damaged, blunted hypoxic drive and very labile BP
54
describe raynaud's phenomenon
* vasoconstriction in extremities during periods of cold or stress * primarily seen in females * usually does not require intervention – does not lead to ischemic extremities
55
describe venous thromboembolism
* deep venous thrombosis + pulmonary embolism | * DVTS predominantly in lower extremities
56
what are treatment options for DVT/PEs?
* anticoagulation for DVT +/- IVC filter | * possible emergent embolectomy for PE

ANESTHESIA PRACTICE 3 (5 decks)

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