Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is cardiac output calculated?

A

CO = SV x HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is blood pressure controlled?

A
  • autonomic nervous system (central and peripheral mechanisms)
  • renin-angiotensin-aldosterone system
  • renal changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how is blood pressure regulated by the autonomic nervous system?

A
  • brainstem control

* baroreceptor reflexes in aortic arch and carotid sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what nerve innervates the aortic arch baroreceptors?

A

vagus (CN X)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is the renin-angiotensin-aldosterone system stimulated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A
  • increased vasopressin (ADH) levels

* increased angiotensin II levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what renal structure initiates the RAAS?

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

* juxtaglomerular cells secrete renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the general goals for HTN therapy?

A
  • SBP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe primary hypertension

A
  • essential HTN – not secondary to an underlying disorder

* 90% of all patients with HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the risk factors for primary HTN?

A
  • age
  • family history
  • obesity
  • insulin resistance
  • diet and lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

describe secondary hypertension

A
  • secondary to underlying medical disorder or therapies

* rare – 10% of all causes of HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

name 2 renal disorders that are commonly associated with secondary hypertension

A
  • fibromuscular dysplasia

* renal artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

name 4 endocrine disorders that are commonly associated with secondary hypertension

A
  • pheochromocytoma
  • cushing’s syndrome
  • hyperaldosteronism
  • hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

define autoregulation relative to hypertension

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what 3 organ systems autoregulate blood flow?

A
  • brain
  • heart
  • kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

how does hypertension lead to renal damage?

A
  • glomerular damage leading to protein loss in the urine/albuminuria
  • ultimately leads to overt renal failure
26
Q

define hypertensive emergency

A
  • severe HTN with evidence of acute end organ damage
27
Q

define hypertensive urgency

A
  • severe HTN without signs of acute end organ damage
28
Q

what are signs of acute end organ damage related to HTN?

A
  • CVA
  • encephalopathy
  • LV failure
  • MI
  • aortic dissection
  • renal failure
29
Q

describe treatment for hypertensive emergency vs. urgency

A
  • 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
Q

how do HTN treatments differ between general population/diabetes w/o CKD vs CKD w/ or w/o diabetes?

A
  • gen pop/diabetes w/o CKD – thiazide diuretic or CCB (all races)
  • CKD w/ or w/o diabetes – ACEI or ARB
31
Q

how does race change HTN medication in gen pop/diabetes w/o CKD?

A
  • non-black races add ACEI or ARB

* black races thiazide diuretics or CCB only

32
Q

what is the primary treatment for HTN?

A

lifestyle modifications

  • weight loss
  • reduced salt intake
  • alcohol and tobacco cessation
33
Q

how do thiazide diuretics such as HCTZ work?

A

reduce sodium absorption in disal convoluted tubule

* increases water loss

34
Q

how do loop diuretics such as furosemide and torsemide work?

A
  • inhibit Na, Cl reabsorption in LoH
  • increases water loss
  • increases prostaglandin levels
35
Q

how do ACE inhibitors such as lisinopril and enalapril work?

A

inhibit ACE therefore inhibiting conversion of angiotensin I to angiotensin II

  • vasodilation
  • vascular smooth muscle relaxation
  • natriuresis
  • decreased vasopressin release
36
Q

how do angiotensin receptor blockers (ARBs) such as losartan and valsartan work?

A

blocks activation of the angiotensin II receptor

  • vasodilation
  • vascular smooth muscle relaxation
  • natriuresis
  • decreased vasopressin release
37
Q

how do calcium channel blockers (CCBs) such as amlodipine and nicardipine work?

A

block calcium channels, decreasing intracellular calcium levels

  • vasodilation
  • negative inotropy
  • negative chronotropy
  • reduced aldosterone production
38
Q

how do beta blockers such as metoprolol and carvedilol work?

A

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
Q

where are beta-1, -2, and -3 receptors found?

A
  • beta-1 – heart, kidneys
  • beta-2 – smooth muscle, lungs
  • beta-3 – adipose tissue
40
Q

what are some postoperative concerns for HTN pts?

A
  • hypoxia
  • hypercarbia
  • acute neurologic or cardiac event
  • medication withdrawal
  • surgical related
41
Q

what are the three layers of the aortic wall?

A

(inside – outside)

  • intima
  • media
  • adventitia (or externa)
42
Q

what is the difference between a true aortic aneurysm and a false aortic aneurysm?

A
  • true (fusiform or saccular) aneurysms involve all three layers of aortic tissue
  • pseudoaneurysms do not involve all three layers of aortic tissue
43
Q

what are some etiologies of aortic aneurysms?

A
  • HTN
  • atherosclerosis
  • collagen vascular disease
  • bicuspid aortic valve
  • syphilis
  • hyperlipidemia
  • mycotic aortic aneurysm
  • inflammatory
44
Q

describe aortic dissection

A

intimal tear creating false lumen for blood to enter

45
Q

describe primary aortic dissection

A

intimal tears on ascending and descending aorta

46
Q

describe secondary aortic dissection

A

intimal tear on ascending aorta only

47
Q

describe tertiary aortic dissection

A

intimal tear on descending aorta only

48
Q

what are the common etiologies of aortic dissection?

A
  • HTN
  • collagen vascular disease
  • bicuspid aortic valve
  • inflammatory
  • trauma
  • complication from heart surgery
49
Q

describe carotid artery stenosis

A
  • primarily due to atherosclerotic disease
  • primarily involving internal carotid arteries
  • intervention indicated for stenosis > 70%
50
Q

what are the risk factors for carotid artery stenosis?

A
  • HTN
  • hyperlipidemia
  • DM
  • PAD
  • tobacco use
51
Q

what are the treatment options for CAD?

A
  • medical management
  • risk factor modification
  • stenting
  • endarterectomy
52
Q

what kind of receptors are the carotid bodies and carotid sinuses?

A
  • carotid bodies – chemoreceptors

* carotid sinus – baroreceptor

53
Q

what could be expected if the carotid body is damaged surgically?

A
  • carotid body detects hypoxemia in the blood

* if damaged, blunted hypoxic drive and very labile BP

54
Q

describe raynaud’s phenomenon

A
  • 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
Q

describe venous thromboembolism

A
  • deep venous thrombosis + pulmonary embolism

* DVTS predominantly in lower extremities

56
Q

what are treatment options for DVT/PEs?

A
  • anticoagulation for DVT +/- IVC filter

* possible emergent embolectomy for PE

ANESTHESIA PRACTICE 3 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions