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Health Assessment > EXAM 4 HTN > Flashcards

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
Q

why is perioperative HTN a concern?

A

Bleeding and CV complications.

26
Q

Why is chronic hypertension such a concern in the OR?

A

Brief periods of hypotension relative to the patient can have profound effects on perfusion dependent organs.

26
Q

LVH goes one of two ways what are they?

A

Reduced contractility or reduced filling.

26
Q

Hypertension leads to what in the heart?

A

LVH

26
Q

What attenuates the hypotension seen during induction?

A

direct laryngoscopy.

27
Q

A quick and easy antihypertensive med to keep near for our severely hypertensive patients?

A

esmolol, very short half life.

28
Q

Another way to attenuate hypotension on induction, something we can do on the floor or in pre op?

A

Tank them up. pay attention to presentation, make sure they are not a heart failure patient or already fluid overloaded.

29
Q

when should we concerned for our OB patients?

A

DBP pressures greater than 100 mmHg. linked to encephalopathy.

30
Q

parturient patients need medical intervention for these parameters?

A

SBP >160 / DBP>110

act immediately

31
Q

Drugs used in a hypertensive crisis?

A

Nitro, Nicardipene, clevidipine, esmolol, labetalol

32
Q

Hypertensive chart for your viewing pleasure

A
33
Q

S2 or s4 heart sound, extremity swelling, PA pressure greater then 20 mmHG, what am i?

A

PAH

34
Q

The classifications of PAH?

A

isolated precapillary PH
isolated postcapillary PH
combined pre & postcapillary PH

35
Q

Precapillary PH is defined as

A

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

36
Q

Isolated postcapillary PH =

A

characterized by a PAWP >15mmHg, w/normal PVR

37
Q

Combined pre- and postcapillary PH (aka reactive PH) =

A

Characterized by a PAWP >15mmHg and a PVR > 3.0 WU

38
Q

High-flow PH is due to?

A

systemic-to-pulmonary shunt or high cardiac output

39
Q

PVR = ?

A

= (mPAP − PAWP)/COP

40
Q

How do we confirm and diagnose PAH?

A

Right heart catheterization

41
Q

Non invasive way to examine if we suspect PAH?

A

TTE

42
Q

Severity of PAH levels

A

Mild PH (mPAP = 20–30 mmHg)
ModeratePH (mPAP = 31–40 mmHg)
SeverePH (mPAP >40 mmHg)

43
Q

The three methods used to treat PAH?

A

Prostanoids, ERAs, and PD-5 Is.

44
Q

PAH preop considerations?

A

venous embolism, elevations in venous and/or airway pressure, hypoxic pulmonary vasoconstriction, reduction in pulmonary vascular volume,systemic inflammation, and emergency procedures

45
Q

How does PAH present?

A

nonspecific symptoms of fatigue, dyspnea, and cough

46
Q

a dilated PA can lead to hoarseness albeit rarely?

A

recurrent laryngeal nerve compression

47
Q

Why is right ventricular hypertrophy such a problem?

A

the right heart is continuously perfused throughout the cardiac cycle in the healthy heart. RVH leads to increased demand that cannot be met.

48
Q

Why would need a left cath of the heart to determine LVEDP?

A

potential discrepancies could lead to mismanagement of our patients.

49
Q

why is a NO test performed on our patients?

A

If they vasodilate appropriately, they are typically responsive to CCBs

50
Q

What is important in dealing with pulmonary hypertensive patients?

A

To maintain the coupling between the Right and left heart.

51
Q

Why do we need to worry about our interventions in pulmonary hypertension?

A

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
Q

What is something that we could see via ultrasound that is a hallmark of PAH?

A

increased RV afterload, leading to RV dilation, increased wall stress, and RV hypertrophy

53
Q

How can we effect right ventricular afterload?

A

Ventilator management can have effects on RV afterload through the addition of PEEP, hypoventilation, hypercarbia, acidosis, and atelectasis

54
Q

What is the lethal combination we can see with pulmonary hypertension?

A

SystemicHoTNalong with RV ischemia and high afterload can result in the “lethalcombination” of RV dilatation, insufficient LV filling, reduced stroke volume, andfurther systemic hypotension

55
Q

concerns of orthopedics?

A

perioperative morbidity and mortality in pts with PH undergoing hip and knee replacement

56
Q

Laparoscopic considerations?

A

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
Q

Thoracic surgery considerations?

A

Intentional atelectasis will increase right ventricular afterload.

58
Q

3 features of lung collapse?

A

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
Q
A

Health Assessment (10 decks)

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