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Health Assessment Exam 4 > Exam 4 - HTN - Organized > Flashcards

Exam 4 - HTN - Organized Flashcards

1
Q

what is normal classification of HTN?

A

SBP < 120
DBP < 80

s2

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2
Q

what are clinical consequences of chronically elevated BP assoc w?

s3

A

ischemic heart disease, stroke, renal failure, retinopathy, PVD, and overall mortality

s3

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3
Q

what is considered isolated systolic HTN?
isolated diastolic HTN?
combined sys and diastolic HTN?

s3

A
  • isolated systolic HTN - SBP >130 mm Hg and DBP <80 mm Hg
  • isolated diastolic HTN - SBP <130 mm Hg with DBP >80 mm Hg
  • combined systolic and diastolic HTN - SBP >130 mm Hg and DBP >80 mm Hg

s3

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4
Q

what are (3) genetic and lifestyle risk factors for HTN?

s4

A

obesity, alcoholism and tobacco

s4

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5
Q

what is also a risk factor for cardiovascular morbitity (in addition to SBP and DBP elevation)?
and why?

s3

A

widened pulse pressure because it correlates w/vascular remodeling and “stiffness”

s3

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6
Q

what herbals elevate BP?

s4

A

ephedra, ginseng, ma huang

s4

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7
Q

What are contributing factors for primary HTN?

s4

A
  • SNS activity
  • dysregulation of the RAAS
  • deficiency in endogenous vasodilators

Actual cause of primary HTN is unclear!

s4

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8
Q

What are (5) common causes of secondary HTN in middle-aged adults?

s4

A

hyperaldosteronism, thyroid dysfunction, OSA, Cushings, and pheochromocytoma

s4

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9
Q

What are 2 causes for children w/ secondary HTN?

s4

A

renal parenchymal disease or coarctation of the aorta

s4

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10
Q

what are correlations seen in this image?

A
  • Top L: Correlation btw SBP and Ischemic heart dz mortality across 5 age groups
  • Top R: Correlation btw DBP and Ischemic heart dz mortality across 5 age groups
  • Bottom L:Correlation btw SBP and Stroke mortality across 5 age groups
  • Bottom R: Correlation btw DBP and stroke mortality across 5 age groups

s5

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11
Q

what is an Anti-infective that elevates BP?

s6

A

Ketoconazole

s6

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12
Q

what are the 2 anti-inflammatory classes that elevate BP?

s6

A

NSAIDs and COX-2 inhibitors (-coxib’s)

s6

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13
Q

what 2 illicit drugs elevate BP?

A

amphetamines and cocaine

s6

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14
Q

list 3 immunosuppresive agents that may elevate BP

A

cyclosporine, sirolimus, tacrolimus

s6

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15
Q

what 2 steroids may elevate BP?

A

methylprednisolone and prednisone

s6

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16
Q

what 2 random sympathomimetics elevate BP?

s6

A

decongestant and diet pills

s6

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17
Q

list hormones and psych meds that may elevate BP

A
  • hormones: oral contraceptives (estrogen and progesterone), androgens
  • psych: buspar, carbamazepine, lithium, clozapine, MAO-Is, SSRIs, TCAs

s6

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18
Q

Per ACC/AHA guidelines, there is a moderate evidence to support antihypertensive therapy with which medications in those w/ CKD to improve kidney outcomes?

A

ACE-I or ARB

S7

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19
Q

what are 3 causes of secondary HTN in older adults (>65 yo)?

s7

A

atherosclerotic renal artery stenosis, renal failure, hypothyroidism

s7

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20
Q

What does chronic HTN lead to? (vascularly..)

A

remodeling of small & large arteries, endothelial dysfunction, and potentially irreversible end-organ damage

s8

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21
Q

What plays a major role in ischemic heart dz, LVH, CHF, CVA, PAD, aortic aneurysm, and nephropathy?

A

Disseminated vasculopathy

s8

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22
Q

what 2 ultrasound measurements can provide an early dx of vasculopathy?

A
  1. common carotid intimal to medial thickness
  2. arterial pulse-wave velocity
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23
Q

what tests can track progression of LV hypertrophy?

A

Echocardiographic and electrocardiographic indexes

s8

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24
Q

what imaging can be used to identify cerebrovascular damage?

A

MRI - to follow microangiopathic changes

s8

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25
Q

What are the 4 examples of end-organ damage due to HTN?

A

Vasculopathy
Cerebrovascular damage
Heart disease
Nephropathy

S9

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26
Q

What is the therapeutic goal for HTN treatment?

A

<130/<80

S10

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27
Q

How many people in the US have untreated HTN? How many patients have their BP above their goal?

A

28 million people in US have untreated HTN
29 million treated pts are above their BP goal

S10

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28
Q

What is resistant HTN? What is the treatment for resistant HTN?

A

Above-goal BP despite 3+ antihypertensive drugs at max dose.
Tx usually includes a LA CCB, an ACI-I or ARB + a diuretic

S10

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29
Q

How would you define the controlled resistant HTN?

A

Controlled BP requiring 4+medications

S10

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30
Q

What is refractory HTN? How many patients present w/ refractory HTN?

A

Uncontrolled BP on 5+ drugs, present in 0.5% of pts

S10

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31
Q

What is pseudo-resistant HTN? What are the causes of pseudo-resistant HTN?

A

Intolerance to drugs that can result from BP inaccuracies (including white-coat syndrome) or medication noncompliance

S10

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32
Q

What are some lifystyle modifications recommended for patients w/ HTN?

A

Weight loss,↓ETOH, exercise, and smoking cessation

There is a continuous relationship btw ↑BMI and HTN.

S11

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33
Q

What is the most effective nopharmacological intervention for HTN?

A

Weight loss
(expect a 1 mmHg reduction in BP for every 1 kg of weight loss)

- weight loss can synergistically enhance the drug efficacy.

S11

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34
Q

What other factors can increase or decrease the BP?

A

Increase BP:
- Increase in physical activity
- Excessive alcohol use

Decrease BP:
- Dietary potassium and calcium intake
- Salt restriction

S12

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35
Q

Per ACC/AHA guidelines, what is recommended for diagnosis and titration of antihypertensive meds?

A

Out-of-office BPs

S13

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36
Q

Per ACC/AHA guidelines, the evidence supports treating pts w/ CKD, CAD, ischemic heart dz with SBP____ ?

A

SBP >130 mmHgrequires treatment with BP meds

S13

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37
Q

Per ACC/AHA guidelines, do you need to treat pts w/o cardiovascular or cerebrovascular dz with nonpharmacological therapy if SBP>130 or DBP >80?

A

There is limited data to support treatment of these patients.

S13

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38
Q

Per ACC/AHA guidelines, do patients with DM and CKD have a different BP goal?

A

No, same goal for DM/CKD population as well as HTN population.

S13

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39
Q

Per ACC/AHA guidelines, which medications are recommended for nonblack HTN pts, including those with DM?

A

ACE-I’s,ARBs, CCBs, or thiazide diuretics

S14

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40
Q

Per ACC/AHA guideline #8, what is the important component to comprehensive BP management?

A

Nonpharmacologic intervention

S14

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41
Q

Which drug is reserved as the 1st line therapy for pts w/ hx of CAD or tachydysrhythmia or those w/ resistant HTN?

A

β blockers

S15

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42
Q

How many drug classes have been approved for HTN?

A

15

S15

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43
Q

What is the treatment of secondary HTN?

A

often interventional, including surgical correction of:
- renal artery stenosis
- adrenal adenoma
- pheochromocytoma

treat the underlying issue

S16

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44
Q

When are ACE-I’s, ARBs, and direct renin inhibitors are not recommended to use for Secondary HTN intervention?

A

in bilateral renal artery stenosis
as they can accelerate renal failure

S16

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45
Q

What certain disease processes require a combined pharmacologic and surgical approach?

Secondary HTN

A

Pheochromocytoma

S16

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46
Q

What can Primary hyperaldosteronism be treated with?

A

Aldosterone Antagonist
(Ex: Spironolactone)

S16

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47
Q

What medications of Secondary HTN patients are instructed to be paused on the day of surgery?

A

ACE-I’s and Diuretics

S17

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48
Q

Preop BP assessment is often complicated by ____ (white-coat HTN)

Assessing BP in a single moment in time does not give an ____ picture of overall BP trends

Current guidelines state that multiple elevated BP readings ____ are necessary for a diagnosis of HTN

A
  • anxiety
  • accurate
  • over time

PCP have the pt trend their BP at home

S17

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49
Q

When should surgery NOT be delayed for patients with elevated BP?

A
  • in asymptomatic pt w/oother risk factors
  • pt. experiencing extreme HTN or end-organ injury that could bereversed w/BP control

S18

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50
Q

If BP elevated, a pressure on what side of the arm should be obtained?

A

contralateral side
(of first arm)

S18

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51
Q

What is necessary to carefully review to gain an overall picture of CV health of Secondary HTN?

A
  • clinic data
  • homeBP’s
  • thorough history

S18

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52
Q

What symptoms suggests Pheochromocytoma is the cause of Secondary HTN?

A
  • flushing
  • sweating
  • palpitations

S19

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53
Q

What symptom suggests Renal Artery Stenosis is the cause of Secondary HTN?

A

Renal bruit

S19

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54
Q

What symptom suggests Hyperaldosteronism is the cause of Secondary HTN?

A

hypokalemia

S19

55
Q

What is the risk of stopping Beta Blockers or Clonidine before surgery of pt’s with Secondary HTN?

A

can cause rebound effects

So, have patient take BBs or Clonidine before surgery

S19

56
Q

What is the risk of stopping Calcium Channel Blockers before surgery of pt’s with Secondary HTN?

A

increased perioperative cardiovascular events

So, have patient take CCBs before surgery

S19

57
Q

What are hypertensive pts prone to and why?

A

hemodynamic volatility

d/t physiologic factors along with the BP meds on-board

S20

58
Q

What can brief periods of hypotension cause on pts with organ damage from chronic HTN?

A
  • acute kidney injury
  • myocardial injury
  • death

Clinicians need to consider acute intraoperative BP changes in the context of end-organ functional reserve

S20

59
Q

What are the factors of Left Ventriucular Hypertension (LVH) and what does LVH cause ?

A

see chart

21

60
Q

When are HTN pts hemodynamically vulnerable during anesthesia and why?

A

during induction of GA

Induction drugs produce HoTN whileDirect Laryngoscopy & intubation elicit HTN & tachycardia

S22

61
Q

Poorly controlled hypertension is often accompanied by what volume status and how can you fix it?

A

-volume deficit, especially if pt is on diuretic!
-volume loading prior to induction might provide hemodynamic stability however careful in left ventricular hypertrophy and diastilic dysfunction

22

62
Q

When considering vasoactive drugs, consider what 4 factors?

A

Pt’s age, functional reserve, medications and the planned surgery

22

63
Q

Induction causes what 3 changes in vital signs ?

Which drug may be use after induction?

A

hypotension, direct laryngoscopy and intubation elicit hypertension and tachycardia

-esmolol! and consider a pre induction a line

23

64
Q

Women with pregnancy induced hypertension show evidence of organ damage dysfunction, especially encepalopathy at which diastolic value?
In peripartum HTN, when should you intervene?

A

DBP >100

Intervene immediatly for SBP >160/ DBP >110!

23

65
Q

Hypertensive crisis is categorized either urgent or emergent, and is based on organ damage. Which organ injuries is the patient at risk for?

A

CNS injury, kidney injury , and cardiovascular insult!

Pt w/ chronic HTN may tolerate higher SBP than normal pt

23

66
Q

For rapid arterial dilation, which drug is gold standard?

which other 2 drugs have become available as well?

A

-sodium nitroprosside! fast & easily titratable
-clevidipine (CCB, short DOA ~ 1 min half life) has selevtive vasoarterial but it’s expensive!
-nicardipine (CCB, 1/2 life 30 min) less easy to titrate

24

67
Q

When treating HTN r/t aortic dissection, what can vasodilators cause?
What is the treatment goal

A

Vasodilators may cause hypotension–> end organ ischemia :(

treatment goal is lessening pulsatile force of LV conraction

25

68
Q

When treating preeclampsia and eclamsia, BB may cause what 2 things?

What 2 groups of drugs are teratogenic so contraindicarted w pregnancy?

A

uterine blood flow and they might inhibit labor!

ACE inhibitors and ARBS!
delivery is the only ultimate treatment :(

25

69
Q

When treating pheo and cocaine intoxication for, what do you watch for when giving beta blockers?

A

unopposed alpa adrenergic stimulation after BB makes HTN worse!

25

70
Q

3% of PAH cases are deemed inheritable, with mutations in which gene?

A

bone morphogenetic protein receptor type 2 (BMPR2)

The remaining cases are designated “associated PAH,” since they can be ascribed to manifestations of drugs, toxins, or other diseases.

S26

71
Q

What are 3 main classes of pulmonary vasodilator drugs for Pulmonary artery HTN?

A

1) Prostanoids
2) endothelin receptor antagonists (ERAs)
3) those working through nitric oxide/guanylate cyclase pathways

Combination therapy is often required for adequate tx of PAH

S26

72
Q

What diagnostic intervention is recommended for patients with suspected PAH?

A

Right heart cath

S26

73
Q

What is MOA of Prostanoids?

A

mimic the effect of prostacyclin to produce vasodilation while inhibiting platelet aggregation. They also have anti-inflammatory effects and may reduce proliferation of vascular smooth muscle cells

S26

74
Q

What medication has been proven to reduce mortality among PAH pts?

A

Epoprostenol

Prostanoid

S26

75
Q

What is MOA of Endothilin Receptor antagonists (ERAs)?

A

The vascular endothelial dysfunction associated with PAH involves an imbalance btw vasodilating (nitric oxide) and vasoconstricting (endothelin) substances.

ERAs have been shown to improve hemodynamics and exercise capacity.

S27

76
Q

What is MOA of Nitric oxide/guanylate cyclase?

A

Nitric oxide produces pulmonary vasodilation by stimulating guanylate cyclase and cGMP formation in smooth muscle cells.
This effect is transient because nitric oxide is quickly bound by hgb and degraded by phosphodiesterase type 5.

S27

77
Q

What signs are most likely be exhibited by patients with PAH?

A

parasternal lift, S3 gallop, JVD, peripheral edema, hepatomegaly, and ascites.

compression of a dilated PA may lead to RLN damage and hoarseness

S27

78
Q

Due to potential discrepancies btw PAWP and LVEDP, what diagnostic intervention should also be performed in pts with coexisting left heart dz?

A

Left heart cath

because inaccurate LVEDP may lead to misclassification of PH and inappropriate treatment

S27

79
Q

Which gas is used in vasoreactivity testing to determine responsiveness to vasodilator therapy?

A

inhaled nitric oxide

S27

80
Q

85–90% PAH pts are nonresponsive to inhaled nitric oxide, but those that are responsive will most likely benefit from which drug therapy?

A

CCB

S27

81
Q

What defines pulmonary HTN accorting to 6th world symposium?
What are the s/s?

A

mPAP >20 mmHG!

S/S: S2 and S4 gallop hear sounds, LE swelling

28

82
Q

Pulm HTN is divided into 3 profiles based on PAWP and PVR. What are the classifications?

A

isolated precapillary PH
isolated postcapillary PH
combined pre and post capillary PH

28

83
Q

What is the definition of isolated postcapillary pulmonary hypertension?

A
  • increased pulmonary venous pressure
  • usually determined by elevated LAP cause by valve disease or LV dysfunction

Slide 29

84
Q

Isolated postcapillary pulmonary hypertension is characterized by?

A
  • PAWP >15mmHg with a normal PVR

Slide 29

85
Q

Describe combined pre and postcapillary pulmonary hypertension?

A
  • (aka reactive PH) reflects chronic pulmonary venous HTN with secondary pulmonary arterial vasoconstriction and remodeling

Slide 29

86
Q

What are the characteristics of combined pre and postcapilliary pulmonary hypertension ?

A
  • PAWP >15mmHg and a PVR > 3.0 WU
  • subcategorized as fixed or vasoreactive do to the response to vasodilators, diuretics, or mechanical assistance

Slide 29

87
Q

Describe high- flow pulmonary hypertension?

A

occurs without an elevation in PAWP or PVR and results from increased pulmonary blood flow cause by a systemic-to-pulmonary shunt or high cardiac output

Slide 29

88
Q

What are the
mPAP, PAWP, PVR and Groups of isolated postcapillary pulomnary hypertension.

A

Slide 30

89
Q

What are the
mPAP, PAWP, PVR and Groups of combined pre and post capillary pulomnary hypertension.

A

Slide 30

90
Q

What is the formula for Pulmonary Vascular Resistance?

A

PVR=(mPAP - PAWP)/ CO

.schmidt…

31

91
Q

What procedure is done to diagnose, classify and devlop treatment for Pulmonary Artery HTN?

A

Right Heart Catheterization

31

92
Q

mPAP can be increased by what four mechanisms?

A
  1. Elevated resistance to blood flow within arterial circulation
  2. Increased pulmonary venous pressure from Left heart disease
  3. Chronically increased pulmonary blood flow
  4. A combination of these processes

31

93
Q

PH can result from abnormalities in the __________________ or ________________ components of the lung circulation, sometimes includes contributions from ____________.

A

PH can result from abnormalities in the arterial or venous components of the lung circulation, sometimes includes contributions from both

31

94
Q

After Right heart catheterization the severity of the PH can be determined to be:
Mild PH (mPAP = ________________)
Moderate PH (mPAP = ____________)
Severe PH (mPAP= ________________)

A

Mild PH (mPAP = 20-30mmHg)
Moderate PH (mPAP = 31-40mmHg)
Severe PH (mPAP= >40mmHg)

32

95
Q

Which diagnostic test or screening tool can be done to estimate pulmonary arterial systolic pressure (PSAP)?

A

Echocardiogram

32

96
Q

Can a echocardiographic Pulmonary arterial systolic pressure of >41mmHg provide a definitive diagnosis for Pulmonary Hypertention?

A

**No

Although echocardiographic
PASP > 41 mmHg is relatively sensitive and specific for PH,* it cannot provide the accurate mPAP for definitive diagnosis*

32

97
Q

How much volume can a normal Pulmonary circulation accomodate without a marked change in mean pulmonary artery pressure (mPAP)?

A

Normal pulmonary circulation can accommodate a fourfold increase in COP without a marked change in mPAP

32

98
Q

What three things can a TTE reveal to help diagnose Pulmonary Artery HTN?

A
  1. RA enlargement
  2. RV enlargement
  3. Elevated Peak tricuspid-regurgitation

32

99
Q

According to the World Health Organization, PAH is classified as a __________ disease. It affects ________ people per million per year

A

According to the World Health Organization, PAH is classified as a rare disease effecting15 ppl per million per year

33

100
Q

Does idopathic PAH have any identifiable risk factors?

A

NOPE

33

101
Q

What medication has shown long-term improvements in 1 in 8 patients with PAH?

A

Calcium channel blockers

33

102
Q

What percent of patients have the inherited genetic protein mutation (BMPR2) that can cause PAH?

What is BMPR2?

A

3% of PAH cases are deemed inheritable.

BMPR2 - bone morphogenetic protein receptor type 2

33

103
Q

Remaining cases of PAH that are not genetic mutations are caused by:
a. drugs
b. toxins
c. various diseases
d. all of the above

A

d. all the above

The remaining cases are designated “associated PAH,” since they can be ascribed to manifestations of drugs, toxins, or other diseases

33

104
Q

Current data shows PAH develops in this age range and population.

A

Current data shows a demographic shift, now with older pts and more men being diagnosed

PAH was traditionally a disease of young women, with median survival rate of 3 yrs

33

105
Q

Even with improved diagnosis of PAH and therapies the 1 year mortality rate is:
a. 10%
b. 15%
c. 25%
d. 5%

A

b. 15%

Despite improved diagnosis and therapy, 1-year mortality is** ̴15%**

33

106
Q

What medication has shown long-term improvements in 1 in 8 patients with PAH?

A

Calcium channel blockers

33

107
Q

What PAH treatment mimics the effect of prostacyclin to produce vasodilation while inhibiting platelet aggregation.

A

Prostanoids!

35

108
Q

What are the four examples of Prostanoids medications and their routes of administration?

A

epoprostenol (IV)
iloprost (inhaled)
treprostinil (SQ, IV, INH, PO)
beraprost(PO)
*

35

109
Q

Which Prostanoid medication has been PROVEN to reduce mortality?

A

Epoprostenol IV

35

110
Q

What is the MOA of Postanoids, when using it to treat pulmonary artery hypertenision?

A
  • mimic the effect of prostacyclin to produce vasodilation while inhibiting platelet aggregation.
  • They also have anti-inflammatory effects and may reduce proliferation of vascular smooth muscle cells

slide 36

111
Q

How does Endothilin Receptor antagonists (ERAs) improve pulmonary arterial hypertenion

A

hemodynamics and exercise capacity

The vascular endothelial dysfunction associated with PAH involves an imbalance between vasodilating (nitric oxide) and vasoconstricting (endothelin) substances. ERAs have been shown to improve hemodynamics and exercise capacity

Slide 37

112
Q

How does nitric oxide/ guanylate cycase improve pulmonary arterial hypertenion?

A

nitric oxide produces pulmonary vasodilation by stimulating guanylate cyclase and cGMP formation in smooth muscle cells.
*
This effect is transient because nitric oxide is quickly bound by hgb and degraded by phosphodiesterase type 5*

Slide 37

113
Q

What are the areas that nitric oxide has been widely used?

A

perioperative
critical care
preparpations for home

slide 37

114
Q

True or False: Chronic therapy has been directed toward PD-5 inhibitors

A

True

Slide 37

115
Q

What are the nonspecific signs of pulmonary arterial hypertension for preop consideration?

A
  • fatigue
  • dyspnea
  • cough

Slide 38

116
Q

What consideration should be given to pulmonary arterial hypertension procedure with pre-op?

A
  • venous embolism
  • elevations in venous and/or airway
  • pressure hypoxic pulmonary

Slide 38

117
Q

What are the more advance signs to take in consideration for preop for patients with pulmonary arterial hypertnsion?

A

**angina and syncope **

occur with exercise if coronary blood flow cannot meet demand of a hypertrophied RV

Slide 38

118
Q

Patient with pulmonary arterial hypertension may exhibit____ on physical exam

list

A
  • parasternal lift
  • accentuated S2, S3 and/or s4 gallop
  • JVD
  • peripheral edema
  • hepatomegaly
  • ascites

Slide 38

119
Q

PAH Preop Considerations

What is recommended prior to mod-high risk surgery in pts with mod-severe PH?

A

Right Heart Cath

S39

120
Q

PAH Preop Considerations

  • Due to potential discrepancies btw PAWP and LVEDP, a _____ _____ ____ is done with coexisting left heart dz bc may lead to ____ of PH
  • Vasoreactivity testing, often with inhaled _____ ______ , during right heart cath to determine responsiveness to ______ therapy
    o __-__ % PAH pts are nonresponsive to inhaled nitric oxide, but those that are responsive also respond to ____ ***
A
  • left heart cath
  • misclassification
  • nitric oxide
  • vasodilator
  • 85-90%
  • CCB’s

S39

121
Q

Precapillary PH is defined as PVR of ____ wood units w/o elevated ____ or ____ (PAWP < 15mmHg = normal)

A

Precapillary PH is defined as PVR of ≥ 3.0 wood units w/o elevated LAP or PAWP (PAWP < 15mmHg = normal)

S41

122
Q

Isolated postcapillary PH results from increased ____ venous pressure, usually d/t elevated ____ c/b valve disease or LV dysfunction

Isolated postcapillary PH is characterized by a PAWP ____mmHg , w/ ____ PVR

A

Isolated postcapillary PH results from increased pulmonary venous pressure, usually d/t elevated LAP c/b valve disease or LV dysfunction

Isolated postcapillary PH is characterized by a PAWP >15mmHg, w/ normal PVR

S41

123
Q

What reflects chronic pulmonary venous HTN with secondary pulmonary arterial vasoconstriction and remodeling?

A

Combined pre- and postcapillary PH
(aka reactive PH)

S41

124
Q

Combined pre- and postcapillary PH (aka reactive PH) is characterized by a PAWP ____ mmHg and a PVR ____ WU

Can be subcategorized as fixed or ____ d/o the response to vasodilators, diuretics, or mechanical assistance

A

**Combined pre- and postcapillary PH **(aka reactive PH) is characterized by a PAWP >15 mmHg and a PVR **> 3.0 **WU

Can be subcategorized as fixed or vasoreactive d/o the response to vasodilators, diuretics, or mechanical assistance

S41

125
Q

High-flow PH occurs ____ an elevation in PAWP or PVR and results from ____ pulmonary blood flow c/b a systemic-to-pulmonary shunt or high cardiac output

A

High-flow PH occurs w/o an elevation in PAWP or PVR and results from increased pulmonary blood flow c/b a systemic-to-pulmonary shunt or high cardiac output

S41

126
Q

Perioperative Phsyiology

* Primary intraoperative goal is maintaining optimal “______ ______” btw the RV + pulmonary circulation to promote adequate left-sided filling and systemic perfusion
* Any intervention that may affect ____ , ____ , ___ , _______ needs to be considered

A
  • mechanical coupling
    *RV preload, inotropy, afterload, and oxygen supply/demand

42

127
Q

Perioperative Phsyiology

What added perioperative complexities can have potentially serious consequences? (7)

A

HoTN ,, mechanical ventilation ,, hypercarbia ,, bubbles in IV ,, Trendelenburg ,, Pneumoperitoneum ,, single-lung ventilation

42

128
Q

Periop :: RV Afterload

  • Increased RV afterload leads to? (3)
  • Interaction bw RV + pulm circulation is ____ + _____ and involves the compliance of the pulm vessels
  • How does ventilator management effect RV afterload? (5)
A
  • RV dilation, increased wall stress, and RV hypertrophy
  • pulsatile + dynamic
  • PEEP , hypoventilation , hypercarbia , acidosis , atelectasis

43

129
Q

Periop :: Myocardial Supply + Demand

  • RV is thinner walled which leads to greater wall tension and can cause increased _____ _____ ____
  • In PAH, elevated RV pressures cause increased ______ __ which makes RV vulnerable to ____ ____ and worsens the O2 supply/demand mismatch
  • HTN + RV ischemia/afterload causes the “LETHAL COMBINATION” which consists of what factors?
A
  • myocardial oxygen demand
  • coronary flow
  • systemic htn
  • RV dilatation, insufficient LV filling, reduced stroke volume, and further systemic hypotension

44

130
Q

Procedural Considerations

  • Ortho : Increase M+M with PH + what 2 surgeries?
  • Laparoscopy : combination of what 3 things affects RV pressures?
  • Thoracic : involve _____ and ____ of operative lung
  • What are the 3 features of lung collapse?
A
  • Hip + Knee
  • pneumoperitoneum (insufflation) ,, head-down position ,, increased inspiratory pressure
  • nonventilation + atelectasis
  • (1) pressurize the chest to induce atelectasis&raquo_space; increase pressure on pulm
    o (2) potential for systemic hypoxia
    o (3) hypoxic pulmonary vasoconstriction (HPV)&raquo_space; increase RV afterload

45

131
Q

Key Points

__________ _________ is common during anesthesia and surgery in hypertensive pts
* PH = MPAP > ____ mmHg, and can result from a range of processes that directly constrict and remodel ______, elevate pulmonary venous ______, or chronically increase blood flow to initiate _____ ______

A
  • Hemodynamic Instability
  • 20
  • arteries
  • pressure
  • vascular remodeling

46

132
Q

Key Points

  • PAH represents group #___ of the 5 PH groups defined by WHO
    • Pts with PAH exhibit ________ dysfunction, maladaptive arterial ________, and in-situ ________
  • A ______ _____ ______ is required to provide a dx of PAH and guide tx
A
  • 1
  • endothelial
  • remodeling
  • thrombosis
  • R heart cath

47

133
Q

Key points

  • What are the 3 primary pulm vasodilator treatments?
  • Only a small percentage respond to ____.
  • What is the prognosis for PAH?
A
  • prostacyclin analogues, endothelin receptor antagonists, and drugs activating the nitric oxide/guanylate cyclase pathway
  • CCBs
  • poor
    *

47

134
Q

Key Points

PAH pts on vasodilators should have them continued ____ + _____ and they should be converted from oral to ______ or ______

A
  • intraop + postop
  • IV or inhalation

47

Health Assessment Exam 4 (7 decks)

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