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Assessment '24 - Mordecai > T4 - HTN Assessment > Flashcards

T4 - HTN Assessment Flashcards

1
Q

What are the 2017 ACC/AHA thresholds for hypertension?

A

SBP > 130 mmHg or DBP > 80 mmHg.

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2
Q

How many people in the US are affected by hypertension?

A

Over 100 million.

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3
Q

Which race has the highest prevalence of hypertension in the US?

A

African Americans at 40%.

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4
Q

Which countries have higher hypertension rates?

A

Low- to middle-income countries.

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5
Q

What is the lifetime risk of developing hypertension in the US?

A

90%.

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6
Q

What are the blood pressure parameters in the classification of systemic blood pressure in adults? (i.e. normal, elevated, stage 1, stage 2)

A
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7
Q

What conditions are associated with chronic hypertension?

A

Ischemic heart disease, stroke, renal failure, retinopathy, peripheral vascular disease (PVD), and increased overall mortality.

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8
Q

Why is hypertension a concern in the surgical population?

A

It’s a common risk factor for perioperative morbidity and mortality, especially if untreated.

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9
Q

What does the spectrum of chronic hypertension include?

A

It ranges from elevated BP to severe disease.

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10
Q

Name the three subtypes of hypertension based on blood pressure readings.

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)

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11
Q

Do risk associations and treatment goals vary among hypertension subtypes?

A

Yes, they can vary among the subtypes.

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12
Q

What does a widened pulse pressure indicate?

A

It correlates with vascular remodeling and stiffness, posing a risk for cardiovascular morbidity.

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13
Q

What distinguishes primary from secondary hypertension?

A

Primary HTN has unclear causes but includes factors like SNS activity and RAAS dysregulation, while secondary HTN has specific, often correctable, causes.

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14
Q

What are contributing factors to primary hypertension?

A

Increased sympathetic nervous system (SNS) activity, dysregulation of the renin-angiotensin-aldosterone system (RAAS), and a deficiency in endogenous vasodilators.

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15
Q

What are some genetic and lifestyle risk factors associated with hypertension?

A

Obesity, alcoholism, and tobacco use.

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16
Q

What are common causes of secondary hypertension in middle-aged adults?

A

Hyperaldosteronism, thyroid dysfunction, obstructive sleep apnea (OSA), Cushing’s syndrome, and pheochromocytoma.

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17
Q

What are common causes of secondary hypertension in children?

A

Renal parenchymal disease and coarctation of the aorta.

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18
Q

Correlation Graphs

A

Top L: Correlation btw SBP and Ischemic heart dz mortality across 5 age groups

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19
Q

Correlation Graphs

A

Top R: Correlation btw DBP and Ischemic heart dz mortality across 5 age groups

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20
Q

Correlation Graphs

A

Bottom L:Correlation btw SBP and Stroke mortality across 5 age groups

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21
Q

Correlation Graphs

A

Bottom R: Correlation btw DBP and stroke mortality across 5 age groups

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22
Q

Drugs that might raise BP

A
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23
Q

Secondary HTN Causes

A
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24
Q

What structural changes does chronic hypertension induce in arteries?

A

Chronic hypertension leads to the remodeling of small and large arteries and endothelial dysfunction, which can cause irreversible end-organ damage.

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25
Q

What role does disseminated vasculopathy play in chronic hypertensive patients?

A

It contributes significantly to ischemic heart disease, left ventricular hypertrophy (LVH), congestive heart failure (CHF), cerebrovascular accidents (CVAs), peripheral arterial disease (PAD), aortic aneurysm, and nephropathy.

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26
Q

Which ultrasound measurement can provide an early diagnosis of vasculopathy?

A

Measurement of the common carotid intimal-to-medial thickness and arterial pulse-wave velocity.

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27
Q

What diagnostic trends may track the progression of left ventricular hypertrophy (LVH)?

A

Trends on an EKG and echocardiogram.

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28
Q

Which imaging modality can be used to follow microangiopathic changes indicative of cerebrovascular damage?

A

MRI (Magnetic Resonance Imaging).

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29
Q

What is the general therapeutic blood pressure goal for treating hypertension?

A

The goal is to achieve a blood pressure reading below 130/80 mmHg.

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30
Q

How many people in the US have untreated hypertension?

A

Approximately 28 million.

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31
Q

How many treated hypertension patients are above their blood pressure goal?

A

Around 29 million.

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32
Q

What is considered resistant hypertension?

A

Blood pressure that remains above goal despite using three or more antihypertensive medications at maximum doses.

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33
Q

What does treatment for resistant hypertension typically include?

A

A long-acting calcium channel blocker (LA CCB), an ACE inhibitor (ACI-I) or angiotensin receptor blocker (ARB), and a diuretic.

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34
Q

What is controlled resistant hypertension?

A

Blood pressure that is controlled but requires four or more medications.

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35
Q

What percentage of patients have refractory hypertension?

A

Approximately 0.5%, which is characterized by uncontrolled blood pressure on five or more drugs.

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36
Q

What can cause pseudo-resistant hypertension?

A

Pseudo-resistant hypertension can be due to inaccuracies in blood pressure measurement (like white-coat syndrome) or medication noncompliance.

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37
Q

What lifestyle modifications can help manage hypertension?

A

Weight loss, reducing alcohol consumption (↓ETOH), regular exercise, and smoking cessation.

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38
Q

How does body mass index (BMI) relate to hypertension?

A

There is a continuous relationship between increased BMI and higher blood pressure.

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39
Q

What benefits does weight loss offer to hypertensive patients?

A

Weight loss is an effective nonpharmacologic intervention that can directly reduce blood pressure and enhance the efficacy of antihypertensive drugs.

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40
Q

What blood pressure improvement can overweight adults expect with weight loss?

A

They can expect a 1 mmHg reduction in blood pressure for every 1 kg of weight loss.

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41
Q

What is the effect of increasing physical activity on blood pressure?

A

Even modest increases in physical activity are associated with decreases in blood pressure.

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42
Q

How does excessive alcohol use affect hypertension?

A

It is associated with increased hypertension and can also lead to resistance to antihypertensive drugs.

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43
Q

What is the relationship between dietary potassium and calcium intake and hypertension?

A

Potassium and calcium intake are inversely related to hypertension and cerebrovascular disease.

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44
Q

What is the impact of salt restriction on blood pressure?

A

Salt restriction is associated with small but consistent decreases in blood pressure.

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45
Q

What do the ACC/AHA guidelines recommend for the diagnosis and management of hypertension?

A

They recommend out-of-office blood pressure measurements for the diagnosis and titration of antihypertensive medications.

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46
Q

When should patients with ischemic heart disease or other cardiovascular conditions be treated with blood pressure medications?

A

Treatment is recommended if their systolic blood pressure (SBP) is over 130 mmHg.

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47
Q

Is there evidence to support treating patients without cardiovascular diseases with nonpharmacologic therapy if their SBP is over 130 mmHg or DBP is over 80 mmHg?

A

The data to support such treatment is limited.

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48
Q

Are the blood pressure goals different for patients with hypertension who also have diabetes or chronic kidney disease (CKD)?

A

No, the same goals are recommended for these patients as for the general hypertension population.

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49
Q

Which medications are effective for non-black hypertension patients, including those with diabetes?

A

ACE inhibitors (ACE-Is), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), and thiazide diuretics.

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50
Q

What is recommended for initial antihypertensive therapy in black adults without heart failure or chronic kidney disease, including those with diabetes?

A

Moderate evidence supports the use of calcium channel blockers (CCBs) or thiazide diuretics.

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51
Q

For patients with chronic kidney disease (CKD), what does moderate evidence suggest for antihypertensive therapy?

A

It supports the use of ACE inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) to improve kidney outcomes.

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52
Q

Notably absent from 1st line therapy are ________________, which are reserved for pts w/ CAD or tachydysrhythmia, or as a component of multidrug tx in resistant HTN

A

β blockers

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53
Q

15 different drug classes have been approved for HTN

A
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54
Q

What can complicate preoperative blood pressure assessment?

A

Anxiety can lead to white-coat hypertension, affecting the accuracy of preoperative blood pressure assessment.

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55
Q

What is often instructed regarding antihypertensive medications on the day of surgery?

A

Patients are often instructed to pause blood pressure medications, such as ACE inhibitors and diuretics, on the day of surgery.

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56
Q

Why might assessing blood pressure at a single moment be misleading?

A

A single blood pressure measurement does not provide an accurate picture of overall blood pressure trends.

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57
Q

What do current guidelines state about the diagnosis of hypertension?

A

Multiple elevated blood pressure readings over time are necessary to diagnose hypertension.

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58
Q

What should be done if a patient has elevated blood pressure preoperatively?

A

If blood pressure is elevated, a measurement should be taken on the contralateral arm for confirmation.

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59
Q

How can a comprehensive picture of a patient’s cardiovascular health be obtained?

A

By reviewing clinic data, home blood pressure readings, and a thorough patient history.

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60
Q

Should surgery be delayed for asymptomatic patients with elevated blood pressure but no risk factors?

A

Elevated blood pressure is not a direct indication to delay surgery in asymptomatic patients without risk factors.

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61
Q

When should surgery be considered for delay in patients with hypertension?

A

Surgery should not be delayed due to transient hypertension, unless the patient has extreme hypertension (SBP >180 or DBP >110) or evidence of end-organ injury that could be reversed with blood pressure control.

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62
Q

What symptoms may suggest a pheochromocytoma as the cause of secondary hypertension?

A

Flushing, sweating, and palpitations.

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63
Q

What clinical sign might suggest renal artery stenosis in a patient with hypertension?

A

A renal bruit.

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64
Q

What laboratory finding might suggest hyperaldosteronism in a hypertensive patient?

A

Hypokalemia.

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65
Q

Once the decision is made to proceed with surgery, which antihypertensive medications might be paused?

A

Angiotensin receptor blockers (ARBs) and ACE inhibitors (ACE-Is) might be excluded.

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66
Q

What is the risk associated with stopping beta-blockers (BBs) or clonidine abruptly before surgery?

A

Stopping these medications can be associated with rebound hypertension.

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67
Q

What is the risk associated with discontinuing calcium channel blockers (CCBs) preoperatively?

A

Stopping CCBs is associated with an increased risk of perioperative cardiovascular events.

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68
Q

What are the consequences of perioperative hypertension?

A

Perioperative hypertension increases blood loss and the incidence of myocardial infarction (MI) and cerebrovascular accidents (CVA).

69
Q

Why are hypertensive patients prone to intraoperative hemodynamic volatility?

A

Physiological factors and the medications they are taking for blood pressure contribute to intraoperative hemodynamic instability.

70
Q

What are the consequences of hypotension, especially in hypertensive patients with existing organ damage?

A

Even brief periods of hypotension can lead to acute kidney injury, myocardial injury, and death, especially when superimposed on organ damage from chronic hypertension.

71
Q

What are the consequences of perioperative hypertension?

A

Perioperative hypertension increases blood loss and the incidence of myocardial infarction (MI) and cerebrovascular accidents (CVA).

72
Q

Why are hypertensive patients prone to intraoperative hemodynamic volatility?

A

Physiological factors and the medications they are taking for blood pressure contribute to intraoperative hemodynamic instability.

73
Q

What are the consequences of hypotension, especially in hypertensive patients with existing organ damage?

A

Even brief periods of hypotension can lead to acute kidney injury, myocardial injury, and death, especially when superimposed on organ damage from chronic hypertension.

74
Q

How should clinicians interpret acute intraoperative blood pressure changes?

A

They should consider these changes in the context of the patient’s end-organ functional reserve.

75
Q

Hemodynamic load picture

A
76
Q

How are hypertensive patients vulnerable during induction of general anesthesia?

A

Hypertensive patients are hemodynamically vulnerable to induction due to the potential for hypotension from induction drugs and subsequent hypertension and tachycardia during laryngoscopy and intubation.

77
Q

What effects do induction drugs have on blood pressure?

A

Induction drugs typically produce hypotension, while laryngoscopy and intubation can elicit hypertension and tachycardia.

78
Q

What approach may be beneficial for hypertensive patients during induction?

A

A multimodal induction approach that includes a pre-induction arterial line and selective beta-blockade (such as Esmolol) may be beneficial.

79
Q

What should be considered regarding volume status in hypertensive patients, especially those on diuretics?

A

Poorly controlled hypertension is often accompanied by volume depletion, so modest volume loading prior to induction may provide better hemodynamic stability.

80
Q

Why should caution be exercised with volume loading in some hypertensive patients?

A

This approach may be counterproductive in patients with left ventricular hypertrophy (LVH) and diastolic dysfunction.

81
Q

What factors should be considered when choosing vasoactive drugs for hypertensive patients?

A

Age, functional reserve, medications, and the planned operation should be taken into account when selecting vasoactive drugs.

82
Q

How are hypertensive crises categorized, and what distinguishes them?

A

Hypertensive crises are categorized as either urgent or emergent based on the presence of progressive organ damage.

83
Q

How do patients with chronic hypertension typically tolerate higher blood pressure levels compared to normotensive individuals?

A

Patients with chronic hypertension tend to tolerate a higher systolic blood pressure (SBP) than normotensive individuals.

84
Q

What are some examples of perioperative emergencies related to hypertension?

A

Perioperative emergencies may include CNS injury, kidney injury, and cardiovascular insult.

85
Q

How might women with pregnancy-induced hypertension (PIH) present with end-organ dysfunction?

A

Women with PIH may exhibit evidence of end-organ dysfunction, particularly encephalopathy, with a diastolic blood pressure (DBP) greater than 100 mmHg.

86
Q

What do current guidelines recommend for intervention in peripartum hypertension?

A

Immediate intervention is recommended for systolic blood pressure (SBP) above 160 mmHg or diastolic blood pressure (DBP) above 110 mmHg.

87
Q

How can arterial line (A-line) monitoring facilitate blood pressure management?

A

A-line monitoring allows for continuous and accurate blood pressure measurements, facilitating the titration process.

88
Q

What is the first-line medication for peripartum hypertension?

A

Labetalol is considered a first-line drug for peripartum hypertension.

89
Q

What is considered the gold standard for rapid arterial dilation?

A

Sodium nitroprusside (SNP) infusion is considered the gold standard due to its fast onset and titratability.

90
Q

What is Clevidipine, and what are its properties?

A

Clevidipine is a third-generation dihydropyridine calcium channel blocker (CCB) with an ultrashort duration of action (approximately 1-minute half-life) and selective arteriolar vasodilating properties.

91
Q

What is an alternative to Clevidipine for blood pressure management?

A

Nicardipine, a second-generation dihydropyridine CCB, can also be used, although it has a longer half-life (approximately 30 minutes), making it less titratable than Clevidipine.

92
Q

Treatment for Hypertensive Emergencies

A
93
Q

Classification of Pulmonary Hypertension table:

A
94
Q

How does the diagnosis and treatment of pulmonary hypertension (PH) differ from systemic hypertension?

A

Unlike systemic hypertension, which can be diagnosed based on blood pressure and monitored daily, the diagnosis and treatment of PH are more complex.

95
Q

How was pulmonary hypertension redefined by the Sixth World Symposium?

A

Pulmonary hypertension is defined as a mean pulmonary artery pressure (mPAP) greater than 20 mmHg.

96
Q

What are some symptoms of pulmonary hypertension?

A

Symptoms may include accentuated S2 and S4 heart sounds (“gallop”), as well as lower extremity swelling.

97
Q

How is pulmonary hypertension classified based on hemodynamic profiles?

A

Pulmonary hypertension is classified into three hemodynamic profiles based on pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance (PVR):

Isolated precapillary PH
Isolated postcapillary PH
Combined pre and postcapillary PH

98
Q

How is precapillary pulmonary hypertension (PH) defined?

A

Precapillary PH is defined as a pulmonary vascular resistance (PVR) of ≥3.0 Wood units without elevated left atrial pressure (LAP) or pulmonary artery wedge pressure (PAWP), where PAWP is <15 mmHg (considered normal).

99
Q

What typically causes isolated postcapillary PH

A

Isolated postcapillary PH results from increased pulmonary venous pressure, usually due to elevated left atrial pressure (LAP) caused by valve disease or left ventricular (LV) dysfunction.

100
Q

How is isolated postcapillary PH characterized hemodynamically?

A

Isolated postcapillary PH is characterized by a pulmonary artery wedge pressure (PAWP) >15 mmHg with normal pulmonary vascular resistance (PVR).

101
Q

What does combined pre- and postcapillary PH (reactive PH) reflect?

A

Combined pre- and postcapillary PH reflects chronic pulmonary venous hypertension with secondary pulmonary arterial vasoconstriction and remodeling.

102
Q

How is combined pre- and postcapillary PH characterized hemodynamically?

A

It is characterized by a pulmonary artery wedge pressure (PAWP) >15 mmHg and a pulmonary vascular resistance (PVR) >3.0 Wood units.

103
Q

How can combined pre- and postcapillary PH be further subcategorized?

A

It can be subcategorized as fixed or vasoreactive based on the response to vasodilators, diuretics, or mechanical assistance.

104
Q

What characterizes high-flow pulmonary hypertension (PH)?

A

High-flow PH occurs without an elevation in pulmonary artery wedge pressure (PAWP) or pulmonary vascular resistance (PVR) and results from increased pulmonary blood flow due to a systemic-to-pulmonary shunt or high cardiac output.

105
Q

Precapillary PH Definition

A

Precapillary PH: PVR ≥3.0 Wood units, PAWP <15 mmHg

106
Q

Isolated Postcapillary PH Causes

A

Increased pulmonary venous pressure (PVP), often due to valve disease or LV dysfunction.

107
Q

Characteristics of Isolated Postcapillary PH

A

PH: PAWP >15 mmHg, normal PVR.

108
Q

Combined Pre- and Postcapillary PH

A

Chronic pulmonary venous HTN with PAWP >15 mmHg and PVR >3.0 WU.

109
Q

Characteristics of Combined Pre- and Postcapillary PH

A

Reflects chronic pulmonary venous HTN, PAWP >15 mmHg, PVR >3.0 WU.

110
Q

Subcategories of Combined Pre- and Postcapillary PH

A

Fixed or vasoreactive, based on response to treatment to vasodilators, diuretics, or mechanical assistance

111
Q

High-Flow PH Characteristics

A

No elevation in PAWP or PVR, caused by increased pulmonary blood flow c/b a shunt or high cardiac output.

112
Q

What is required for a dx, classification, and tx plan for PA HTN?

A

Right heart catherization

113
Q

Hemodynamic Definitions of PH table:

A
114
Q

What can cause an increase in mPAP?

A
  • Elevated resistance within arterial circulation
  • Increased pulmonary venous pressure from left heart disease
  • Chronically increased pulmonary blood flow
  • A combination of these processes.
115
Q

What is the formula for PVR?

A

PVR = (mPAP − PAWP)/CO

116
Q

What can PH result from?

A

Abnormalities in the arterial or venous components of lung circulation, sometimes includes contributions from both

117
Q

What does TTE reveal that can indicate PH?

A

RA & RV enlargement and elevated peak tricuspid-regurgitation velocity

118
Q

What is echocardiogram’s role in PH screening?

A

It’s used to estimate pulmonary arterial systolic pressure (PASP).

119
Q

Why can’t echocardiographic PASP > 41 mmHg provide an accurate mPAP for definitive diagnosis of PH?

A

While it’s relatively sensitive and specific for PH, it cannot provide the accurate mPAP required for definitive diagnosis.

120
Q

How is the severity of PH determined after right heart catheterization?

A
  • Mild PH: mPAP = 20–30 mmHg
  • Moderate PH: mPAP = 31–40 mmHg
  • Severe PH: mPAP >40 mmHg
121
Q

How does normal pulmonary circulation respond to a fourfold increase in COP?

A

It can accommodate the increase without a marked change in mPAP.

122
Q

How is PAH classified according to the World Health Organization?

A

PAH is classified as a rare disease affecting 15 people per million per year.

123
Q

What is idiopathic PAH?

A

PAH has no identifiable risk factor.

124
Q

What proportion of PAH patients show long-term improvements with calcium channel blockers (CCBs)?

A

Nearly 1 in 8 PAH patients.

125
Q

What percentage of PAH cases are inheritable and which gene is often mutated?

A

3% of PAH cases are inheritable, often with mutations in BMPR2

126
Q

What are “associated PAH” cases?

A

They are cases that can be ascribed to manifestations of drugs, toxins, or other diseases.

127
Q

How has the demographic of PAH changed in terms of age and gender?

A

There’s a shift to older patients and more men being diagnosed.

128
Q

What was the median survival rate for PAH and how has it changed?

A

It was traditionally 3 years for young women, but current data shows a demographic shift.

129
Q

What is the approximate 1-year mortality rate for PAH despite improvements in diagnosis and therapy?

A

Approximately 15%.

130
Q

What factors contribute to the development of PAH?

A

A combination of genetic predisposition and multiple accumulating events

131
Q

What leads to pathologic distortion of the small pulmonary arteries in PAH?

A

Sustained vasoconstriction and remodeling processes.

132
Q

What are the three main classes of pulmonary vasodilator drugs for PAH?

A
  • Prostanoids
  • Endothelin receptor antagonists (ERAs)
  • Drugs working through nitric oxide/guanylate cyclase pathways
133
Q

Is combination therapy needed for PAH?

A

Yes, combination therapy is often required for adequate treatment of PAH.

134
Q

PAH diagnosis video link:

A

https://www.youtube.com/watch?v=O2jX0ZGrtc8

135
Q

What is the effect of prostanoids in the treatment of PAH?

A
  • Mimic prostacyclin to produce vasodilation
  • Inhibit platelet aggregation
  • Have anti-inflammatory effects
  • May reduce vascular smooth muscle cell proliferation.
136
Q

List the forms and routes of administration for prostanoids used in PAH treatment.

A
  • Epoprostenol (IV)
  • Iloprost (inhaled)
  • Treprostinil (subcutaneous [SQ], IV, inhaled [INH], oral [PO])
  • Beraprost (PO)
137
Q

Which prostanoid has been proven to reduce mortality in PAH patients?

A

Epoprostenol

138
Q

What role do endothelin receptor antagonists (ERAs) play in PAH treatment?

A

Counteract vascular endothelial dysfunction by addressing the imbalance between vasodilating (nitric oxide) and vasoconstricting (endothelin) substances, improving hemodynamics and exercise capacity.

139
Q

How does nitric oxide produce pulmonary vasodilation in the context of PAH?

A

Nitric oxide stimulates guanylate cyclase, leading to cGMP formation in smooth muscle cells, causing vasodilation.

This effect is transient due to rapid binding by hemoglobin and degradation by phosphodiesterase type 5.

140
Q

What is the use of continuously inhaled nitric oxide in PAH treatment?

A

It’s widely used in perioperative and critical care settings, and preparations for home use are available.

141
Q

What is the direction of chronic therapy for PAH?

A

It is directed toward phosphodiesterase type 5 (PD-5) inhibitors.

142
Q

What are the pre-op considerations for patients with PAH?

A
  • Procedures with potential for venous embolism
  • elevations in venous/airway pressure
  • hypoxic pulmonary vasoconstriction
  • reduction in pulmonary vascular volume
  • Systemic inflammation
  • Emergency procedures
143
Q

What are common nonspecific symptoms of PAH?

A

Fatigue, dyspnea, and cough.

144
Q

What advanced symptoms may indicate coronary blood flow cannot meet the demands of a hypertrophied RV?

A

Angina and syncope, particularly with exercise.

145
Q

What might you find on physical exam in PAH patients?

A

Parasternal lift, accentuated S2, S3/S4 gallop, jugular venous distention (JVD), peripheral edema, hepatomegaly, and ascites.

146
Q

What is a rare complication of PAH that can lead to hoarseness?

A

Compression of a dilated pulmonary artery may lead to recurrent laryngeal nerve damage and hoarseness.

147
Q

What should be evaluated in patients with a history of PH?

A

Functional status, cardiac performance, and pulmonary function tests.

148
Q

When is a right heart catheterization recommended preoperatively?

A

For patients with moderate or severe PH before moderate to high-risk surgery.

149
Q

Why should a left heart catheterization be performed in patients with coexisting left heart disease?

A

To avoid discrepancies between pulmonary artery wedge pressure (PAWP) and left ventricular end-diastolic pressure (LVEDP), which can lead to misclassification of PH and inappropriate treatment.

150
Q

What is vasoreactivity testing and when is it performed?

A

It is often done with inhaled nitric oxide during right heart catheterization to determine responsiveness to vasodilator therapy.

151
Q

What percentage of PAH patients are nonresponsive to inhaled nitric oxide and how does responsiveness affect treatment?

A

85–90% of PAH patients are nonresponsive. Those who are responsive may also respond to calcium channel blockers (CCBs) and may benefit from other targeted therapies.

152
Q

Righ heart catherization flow chart

A
153
Q

Risk factors for morbidity and mortality in noncardiac surgery in patients with PAH chart:

A
154
Q

What is the primary intraoperative goal for patients with PH?

A

Maintaining optimal mechanical coupling between the right ventricle and pulmonary circulation to promote left-sided filling and systemic perfusion.

155
Q

What intraoperative interventions should be considered for patients with PH?

A

Those that may affect RV preload, inotropy, afterload, and oxygen supply/demand relationships.

156
Q

What are some added perioperative complexities for patients with PH?

A
  • Transient hypotension (HoTN)
  • Mechanical ventilation
  • Modest hypercarbia
  • Small bubbles in intravenous fluid
  • Trendelenburg position
  • Pneumoperitoneum
  • Single-lung ventilation
157
Q

What effect does increased RV afterload have in PAH?

A

It leads to RV dilation, increased wall stress, and RV hypertrophy.

158
Q

Describe the interaction between the RV and pulmonary circulation in PAH.

A

It is pulsatile and dynamic, involving the compliance and stiffness of large and small vessels.

159
Q

Why is the interaction between the RV and pulmonary circulation relevant during surgery?

A

Acute insults during surgeries can affect the RV pulsatile load.

160
Q

How can ventilator management affect RV afterload?

A

Through the addition of positive end-expiratory pressure (PEEP), hypoventilation, hypercarbia, acidosis, and atelectasis.

161
Q

How does increased end-diastolic volume affect the RV compared to the LV?

A

The RV, being thinner-walled, is subject to greater wall tension for the same increase in volume, leading to increased myocardial oxygen demand.

162
Q

When does RV coronary perfusion normally occur?

A

RV coronary perfusion occurs throughout the cardiac cycle because RV intramyocardial pressure is lower than aortic root pressure.

163
Q

What is the “lethal combination” in PAH that can lead to systemic hypotension?

A

RV dilatation, insufficient LV filling, reduced stroke volume, alongside systemic hypotension, which can result in myocardial ischemia and worsen RV performance.

164
Q

How does PAH affect RV coronary flow and myocardial oxygen demand?

A

PAH causes elevated RV pressure, leading to increased diastolic coronary flow and making the RV more vulnerable to systemic hypotension, exacerbating the oxygen supply/demand mismatch and potentially causing ischemia.

165
Q

What is the perioperative risk for patients with PH undergoing hip and knee replacement?

A

There is a substantial increase in perioperative morbidity and mortality.

166
Q

What impact does CO2 pneumoperitoneum have in laparoscopic procedures on patients with PH?

A

It acutely impacts biventricular load and pump function, affecting RV pressures and afterload, especially when combined with the head-down position and increased inspiratory pressures.

167
Q

What are the concerns for patients with PH undergoing thoracic surgery?

A
  • Thoracic procedures involve
  • Nonventilation and atelectasis of the operative lung
  • Transient pressurization to induce atelectasis
  • Systemic hypoxia
  • Hypoxic pulmonary vasoconstriction (HPV).
168
Q

What type of pulmonary vasodilators are recommended during single-lung ventilation in PAH patients?

A

Inhaled pulmonary vasodilators

169
Q

What are the 3 features of lung collapse relevant to thoracic surgery in PH patients?

A
  • Some centers transiently pressurize the chest to induce atelectasis.
  • There is a potential for systemic hypoxia.
  • Hypoxic pulmonary vasoconstriction (HPV) will further increase RV afterload.

Assessment '24 - Mordecai (10 decks)

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