Hypertension- (Final, Mordecai) Flashcards

1
Q

What defines hypertension (HTN)?

A

Sustained SBP > 130 mmHg and/or DBP > 80 mmHg.

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2
Q

What percentage of adults in the US have hypertension?

A

Nearly 50%, affecting over 100 million people.

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3
Q

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

A

90%.

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4
Q

What are the three subtypes of hypertension?

A

Isolated systolic HTN, isolated diastolic HTN, and combined systolic-diastolic HTN.

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5
Q

What causes HTN pathophysiologically?

A

Increased cardiac output, increased vascular resistance, or both.

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6
Q

What are key contributors to primary HTN?

A

SNS hyperactivity, RAAS dysregulation, and deficient vasodilators.

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7
Q

Name three modifiable risk factors for primary HTN.

A

Obesity, alcohol use, and tobacco.

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8
Q

What are common causes of secondary HTN in adults?

A

Hyperaldosteronism, thyroid dysfunction, OSA, Cushing’s, pheochromocytoma.

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9
Q

What should be suspected in a child with HTN?

A

Secondary HTN, commonly due to renal disease or aortic coarctation.

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10
Q

What are some complications of chronic HTN?

A

Ischemic heart disease, LVH, CHF, stroke, PVD, nephropathy, retinopathy.

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11
Q

How is early vasculopathy detected?

A

Ultrasound (intimal-to-medial thickness) and pulse-wave velocity.

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12
Q

What is the general BP goal in HTN treatment?

A

<130/<80 mmHg.

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13
Q

What defines resistant hypertension?

A

BP above goal despite 3+ antihypertensives at max doses.

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14
Q

What is pseudo-resistant HTN?

A

Apparent resistance due to measurement errors or noncompliance.

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15
Q

How much does BP reduce per 1 kg of weight loss?

A

~1 mmHg.

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16
Q

Which minerals are inversely related to BP?

A

Potassium and calcium.

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17
Q

What first-line antihypertensives are recommended for non-Black patients?

A

ACE-I, ARBs, CCBs, or thiazide diuretics.

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18
Q

What are β-blockers reserved for?

A

CAD, tachydysrhythmia, or part of multidrug therapy in resistant HTN.

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19
Q

When should surgery be delayed for HTN?

A

If SBP >180 mmHg or DBP >110 mmHg with end-organ damage.

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20
Q

Which antihypertensives should not be stopped pre-op?

A

β-blockers and clonidine.

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21
Q

Why are HTN patients vulnerable at induction?

A

Prone to hypotension from drugs and hypertension from DL/intubation.

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22
Q

What helps stabilize BP in hypertensive patients before induction?

A

Modest fluid loading and pre-induction β-blockers (e.g., esmolol).

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23
Q

What defines hypertensive urgency vs emergency?

A

Presence of end-organ damage.

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24
Q

What are first-line drugs for acute HTN control?

A

Labetalol, SNP, clevidipine, nicardipine.

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25
What defines pulmonary hypertension (PH)?
Mean pulmonary artery pressure (mPAP) > 20 mmHg.
26
What are the three classifications of PH?
Precapillary, postcapillary, and combined.
27
What is the gold standard for PH diagnosis?
Right heart catheterization.
28
What is idiopathic pulmonary arterial hypertension (PAH)?
PAH without an identifiable cause.
29
What are the three main PAH drug classes?
Prostanoids, endothelin receptor antagonists, and nitric oxide pathway enhancers.
30
Which PAH drug reduces mortality?
Epoprostenol (IV prostanoid).
31
What is the primary intraop goal in PAH patients?
Maintain RV-pulmonary artery coupling to ensure LV filling and systemic perfusion.
32
What factors increase RV afterload during surgery?
PEEP, hypercarbia, acidosis, hypoxia, T-burg position, and pneumoperitoneum.
33
Why is the RV at higher ischemic risk in PAH?
Elevated wall tension increases O2 demand, and systemic hypotension impairs coronary perfusion.
34
What diagnostic test is required for definitive diagnosis and classification of PH?
Right heart catheterization.
35
What does the pulmonary vascular resistance (PVR) equation look like?
PVR = (mPAP − PAWP) / Cardiac Output.
36
What can transthoracic echocardiogram (TTE) show in PH?
RA & RV enlargement, elevated tricuspid-regurgitation velocity, and estimated PASP.
37
How is the severity of PH graded by mPAP?
Mild: 20–30 mmHg Moderate: 31–40 mmHg Severe: >40 mmHg
38
What is a normal physiologic response of pulmonary circulation to increased CO?
It accommodates a fourfold increase in cardiac output without a major rise in mPAP.
39
What are common causes of PAH?
Genetic mutations (e.g., BMPR2), connective tissue disease, toxins/drugs, idiopathic cases.
40
What is the prognosis for PAH despite treatment?
1-year mortality remains ~15%, with generally poor long-term outcomes.
41
What are the three main classes of drugs used to treat PAH?
Prostanoids Endothelin receptor antagonists (ERAs) Nitric oxide/guanylate cyclase pathway drugs
42
What do prostanoids do in PAH?
Mimic prostacyclin to vasodilate, inhibit platelet aggregation, reduce inflammation, and limit vascular remodeling.
43
Which prostanoid has been shown to reduce mortality in PAH?
Epoprostenol (IV).
44
How does nitric oxide cause pulmonary vasodilation?
By activating guanylate cyclase and increasing cGMP in smooth muscle cells.
45
Why is the effect of inhaled nitric oxide short-lived?
It is rapidly bound by hemoglobin and degraded by phosphodiesterase type 5 (PDE5).
46
What drugs prolong nitric oxide's effect in PAH treatment?
PDE5 inhibitors.
47
What clinical symptoms raise suspicion for PAH preoperatively?
Fatigue, dyspnea, angina, syncope, accentuated S2, parasternal lift, JVD, and peripheral edema.
48
What test is recommended before moderate-high risk surgery in PAH patients?
Right heart catheterization.
49
What is the purpose of vasoreactivity testing during right heart cath?
To determine responsiveness to vasodilator therapy like inhaled nitric oxide or CCBs.
50
What is the main intraoperative goal in PAH patients?
Maintain mechanical coupling between RV and pulmonary circulation.
51
What factors increase RV afterload during surgery?
PEEP, hypoventilation, hypercarbia, hypoxia, acidosis, surgical stimulation.
52
Why is the RV more vulnerable to ischemia in PAH?
Increased wall tension and pressure demand compromise coronary perfusion during hypotension.
53
Why is orthopedic surgery high risk for patients with PH?
Studies show increased perioperative morbidity and mortality, particularly with hip and knee replacements.
54
What are the main concerns with laparoscopy in PH patients?
Pneumoperitoneum, increased airway pressure, and head-down position increase RV pressure and afterload.
55
What makes thoracic surgery particularly risky in PH?
It often involves lung collapse, systemic hypoxia, and hypoxic pulmonary vasoconstriction, all of which increase RV afterload.
56
What inhaled therapy is often initiated during thoracic surgery in PAH patients?
Inhaled pulmonary vasodilators.
57
What is the primary anesthetic concern for patients with PAH?
Preserving right ventricular function and preventing increases in pulmonary vascular resistance.
58
Why are small air bubbles in IV lines dangerous for PAH patients?
They can travel to the pulmonary circulation and exacerbate pulmonary hypertension or cause embolic complications.
59
What ventilation strategies should be avoided in PAH patients?
High PEEP, hypoventilation, hypercarbia, and acidosis, as they all increase PVR and RV strain.
60
What is the consequence of systemic hypotension in PAH?
It reduces coronary perfusion pressure, worsening RV ischemia and potentially causing cardiovascular collapse.
61
What positioning should be used cautiously in PAH patients?
Trendelenburg position, due to effects on venous return and RV afterload.
62
Should PAH medications be continued perioperatively?
Yes — especially vasodilators. Oral drugs may need conversion to IV or inhaled forms intraoperatively.
63
What anesthetic technique may help with pulmonary vasodilation in PAH?
Inhaled nitric oxide or prostacyclin analogs during periods of increased PVR.