EXAM 4 HTN Flashcards

under pressure

1
Q

Hypertension is defined by what SBP and DBP?

A

sustained SBP > 130 mmHg and/or a DBP > 80 mmHg

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2
Q

Risk of Hypertension in the US?

A

90%

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3
Q

Stage 2 hypertension parameters

A

> 140 mmHg and/or >90 DBP

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4
Q

Like DM, HTN can lead to what?

A

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

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5
Q

What parameters do we keep our patients in regards to hemodynamics, especially BP?

A

20%. HTN patients have a shift to the right of their autoregulation curve.

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6
Q

Why is a wide pulse pressure a concern?

A

suggest arterial stiffness, or reduced compliance.

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7
Q

contributing factors to primary hypertension?

A

no clear cause per se.

Linked to SNS, RAAS, endothelial vasodilator dysfunction.

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8
Q

Drugs that can increase BP
(chart from class)

A
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9
Q

common cause of HTN in the youth?

A

coarctation of the aorta

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10
Q

whats more treatable, primary or secondary HTN

A

secondary, as the BP is typically linked to another disorder.

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11
Q

Quick noninvasive way to determine if your patient has had long term hypertension.

A

Look at their EKG, pay attention to axis shift suggesting hypertrophy

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12
Q

Resistant HTN medical presentation?

A

above-goal BP despite 3+ antihypertensive drugs @ max dose

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13
Q

controlled resistant presentation?

A

controlled BP requiring 4+medications

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14
Q

Refractory HTN presentation?

A

5+ drugs and still hypertensive.

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15
Q

What can cause psuedoresistant hypertension?

A

white coat syndrome. (some people freak themselves)

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16
Q

Best treatment for HTN?

A

lifestyle modifications

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17
Q

For every Kg lost we can roughly expect to see what decrease in BP?

A

about 1 mmHg. (this is not set in stone)

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18
Q

How are K+ and Ca++ linked to HTN?

A

Inversely, correct dietary amounts of these electrolytes are associated with lower BPs.

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19
Q

An easy dietary measure to keep BP low?

A

salt restriction

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20
Q

AHA guidelines.

A
  1. Out-of-office BP’s are recommended for diagnosis and titration of antihypertensive meds
  2. Evidence supports treating pts with ischemic heart dz, cerebrovascular dz, CKD, or atherosclerotic cardiovascular dz w/ BP meds if SBP >130 mmHg
  3. There is limited data to support treating pts w/o cardiovascular or cerebrovascular dz with nonpharmacologic therapy if SBP >130 or DBP >80
  4. The same goals are recommended for HTN pts w/DM or CKD as for the general HTN population
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21
Q

AHA guidelines continued

A
  1. ACE-I’s,ARBs, CCBs, or thiazide diuretics are useful and effective in nonblack HTN pts,including those with diabetes
  2. In black adult HTN pts w/o heart failure or CKD, including those with DM, there ismoderate evidence to support initial antihypertensive therapy with a CCB or thiazidediuretics
  3. There is moderate evidence to support antihypertensive therapy with an ACE-I or ARB in those with CKD to improve kidney outcomes
  4. Nonpharmacologic interventions are important components to a comprehensive BPmanagement approach
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22
Q

Treatment of secondary HTN includes?

A

surgical correction of renal artery stenosis, adrenal adenoma or pheochromocytoma

can use meds as well

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23
Q

should you delay surgery due to hypertension?

A

Not really, unless you expect end organ damage. Try and reduce your patients anxiety, and determine if the HTN is transient.

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24
Q

which anti-htn med classes are typically held on day of surgery?

A

ARBs and ACE-Is

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25
why is perioperative HTN a concern?
Bleeding and CV complications.
26
Why is chronic hypertension such a concern in the OR?
Brief periods of hypotension relative to the patient can have profound effects on perfusion dependent organs.
26
LVH goes one of two ways what are they?
Reduced contractility or reduced filling.
26
Hypertension leads to what in the heart?
LVH
26
What attenuates the hypotension seen during induction?
direct laryngoscopy.
27
A quick and easy antihypertensive med to keep near for our severely hypertensive patients?
esmolol, very short half life.
28
Another way to attenuate hypotension on induction, something we can do on the floor or in pre op?
Tank them up. pay attention to presentation, make sure they are not a heart failure patient or already fluid overloaded.
29
when should we concerned for our OB patients?
DBP pressures greater than 100 mmHg. linked to encephalopathy.
30
parturient patients need medical intervention for these parameters?
SBP >160 / DBP>110 act immediately
31
Drugs used in a hypertensive crisis?
Nitro, Nicardipene, clevidipine, esmolol, labetalol
32
Hypertensive chart for your viewing pleasure
33
S2 or s4 heart sound, extremity swelling, PA pressure greater then 20 mmHG, what am i?
PAH
34
The classifications of PAH?
isolated precapillary PH isolated postcapillary PH combined pre & postcapillary PH
35
Precapillary PH is defined as
PVR of ≥3.0 wood units w/o elevated LAP or PAWP (PAWP <15mmHg = normal)
36
Isolated postcapillary PH =
characterized by a PAWP >15mmHg, w/normal PVR
37
Combined pre- and postcapillary PH (aka reactive PH) =
Characterized by a PAWP >15mmHg and a PVR > 3.0 WU
38
High-flow PH is due to?
systemic-to-pulmonary shunt or high cardiac output
39
PVR = ?
= (mPAP − PAWP)/COP
40
How do we confirm and diagnose PAH?
Right heart catheterization
41
Non invasive way to examine if we suspect PAH?
TTE
42
Severity of PAH levels
Mild PH (mPAP = 20–30 mmHg) Moderate PH (mPAP = 31–40 mmHg) Severe PH (mPAP >40 mmHg)
43
The three methods used to treat PAH?
Prostanoids, ERAs, and PD-5 Is.
44
PAH preop considerations?
venous embolism, elevations in venous and/or airway pressure, hypoxic pulmonary vasoconstriction, reduction in pulmonary vascular volume, systemic inflammation, and emergency procedures
45
How does PAH present?
nonspecific symptoms of fatigue, dyspnea, and cough
46
a dilated PA can lead to hoarseness albeit rarely?
recurrent laryngeal nerve compression
47
Why is right ventricular hypertrophy such a problem?
the right heart is continuously perfused throughout the cardiac cycle in the healthy heart. RVH leads to increased demand that cannot be met.
48
Why would need a left cath of the heart to determine LVEDP?
potential discrepancies could lead to mismanagement of our patients.
49
why is a NO test performed on our patients?
If they vasodilate appropriately, they are typically responsive to CCBs
50
What is important in dealing with pulmonary hypertensive patients?
To maintain the coupling between the Right and left heart.
51
Why do we need to worry about our interventions in pulmonary hypertension?
preload, inotropy, afterload, and oxygen supply/demand can all be effected. Think about too much of a recruitment maneuver or too much PEEP. reducing venous return.
52
What is something that we could see via ultrasound that is a hallmark of PAH?
increased RV afterload, leading to RV dilation, increased wall stress, and RV hypertrophy
53
How can we effect right ventricular afterload?
Ventilator management can have effects on RV afterload through the addition of PEEP, hypoventilation, hypercarbia, acidosis, and atelectasis
54
What is the lethal combination we can see with pulmonary hypertension?
Systemic HoTN along with RV ischemia and high afterload can result in the “lethal combination” of RV dilatation, insufficient LV filling, reduced stroke volume, and further systemic hypotension
55
concerns of orthopedics?
perioperative morbidity and mortality in pts with PH undergoing hip and knee replacement
56
Laparoscopic considerations?
C02 pneumoperitoneum has an acute impact on biventricular load and pump function. The combination of pneumoperitoneum, head-down position, and increased inspiratory pressure affects RV pressures and afterload
57
Thoracic surgery considerations?
Intentional atelectasis will increase right ventricular afterload.
58
3 features of lung collapse?
some centers transiently pressurize the chest to induce atelectasis (2) there is a potential for systemic hypoxia (3) hypoxic pulmonary vasoconstriction (HPV) will further increase RV afterload
59