Hypertension - Exam V Flashcards
1
Q
Hypertension defined as:
A
Defined as a sustained SBP > 130 mmHg and/or a DBP > 80 mmHg
2
Q
How many people affect by HTN:
A
Effects >100 million ppl in US
3
Q
How many adults deal with HTN:
A
Nearly ½ adults
4
Q
Race most suspectable to HTN?
A
40% of African Americans, 30% of Whites, 29% of Asians, 27% of Hispanics
5
Q
Risk of developing HTN in USA?
A
The lifetime rx of developing HTN in the United States is 90%
6
Q
Categories of HTN?
A
7
Q
What can chronic HTN lead to?
A
Chronic HTN leads to ischemic heart disease, stroke, renal failure, retinopathy, PVD, and an overall increased mortality
8
Q
What is the most common risk factor for perioperative morbidity & mortality, particularly if undiagnosed/untreated?
A
HTN, in the surgical population.
9
Q
_____ pulse pressure is alsoa risk factor for cardiovascular morbidity as it correlates withvascular remodeling and “stiffness”
A
Widened
10
Q
Chronic HTN represents a spectrum of elevated BP to severe disease: 3 of them?
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
11
Q
What hemodynamic factors can result in HTN?
A
Increased cardiac output, increased vascular resistance, or both.
12
Q
What is the cause of Primary HTN?
A
unclear, but contributing factors include SNS hyperactivity, dysregulation of the RAAS, anda deficiency in endogenous vasodilators
13
Q
What risk factors are associated with HTN?
A
Genetic and lifestyle risk; including: obesity, alcoholism, and tobacco.
14
Q
What is secondary HTN?
A
More rare, but the cause is potentially correctable.
15
Q
What are common causes of HTN in adults?
A
Hyperaldosteronism, thyroid dysfunction, OSA, Cushings, and pheochromocytoma.
16
Q
What do you suspect with children with HTN?
A
usually will have secondary HTN d/t renal disease or coarctation of the aorta.
17
Q
Drugs that increase BP? Slide 6 table
A
18
Q
Secondary HTN causes by age? slide 7 table
A
19
Q
How does chronic HTN affect your CV system?
A
remodeling of small & large arteries, endothelial dysfunction, and potentially irreversible end-organ damage
20
Q
What does disseminated vasculopathy plays a major role in?
A
in ischemic heart dz, LVH, CHF, CVA, PAD, aortic aneurysm, and nephropathy
21
Q
What can we use to track progression of LVH?
A
EKG & cardiac Echo
22
Q
What study can we use to track the microvascular changes associated with cerebrovascular damage?
A
MRI
23
Q
What does vasculopathy on ultrasound detect?
A
Vasculopathy can be detected early on ultrasound with measurement of the common carotid intimal-to-medial thickness and arterial pulse-wave velocity
24
Q
A
25
What is the main treatment goal for HTN patients?
Treatment: general therapeutic goal is <130/<80
26
How many people with HTN have untreated HTN and are the ones that are on treatment, are still above their BP goal?
- 28 million people in US have untreated HTN
- 29 million people treated pts are above their BP goal
27
How many meds are needed to control resistant HTN?
Controlled resistant HTN: controlled BP requiring 4+ medications
28
What is resistant HTN?
What does treatment usually consist of for these patients?
Resistant HTN: above-goal BP despite 3+ antihypertensive drugs @ max dose
Tx usually includes a LA CCB, an ACI-I or ARB + a diuretic
29
What is refractory HTN:
Refractory HTN: uncontrolled BP on 5+ drugs, present in 0.5% of pts
30
What is pseudo-resistant HTN?
Pseudo-resistant HTN (appears resistant to drugs): often d/t BP inaccuracies (i.e. white-coat syndrome) or medication noncompliance
31
Lifestyle modifications for HTN?
weight loss, ↓ETOH, exercise, and smoking cessation
32
There is a continuous relationship btw ___ and ____
There is a continuous relationship btw ↑BMI and HTN
33
_______ is an effective nonpharmacologic intervention, through direct BP reduction and synergistic enhancement of drug efficacy.
Weight loss is an effective nonpharmacologic intervention, through direct BP reduction and synergistic enhancement of drug efficacy
34
How much reduction of mmHg in BP is there with every kg of weight loss?
1 mmHg reduction in BP for every 1 kg of weight loss
**Overweight adults should aim for ideal body weight
35
What is something else that is associated with BP decrease? lifestyle modification.
Even modest increases in physical activity are associated with BP decrease.
36
What dietary intake are inversely related to HTN and cerebrovascular disease?
Dietary potassium and calcium intake.
37
How does salt reduction in diet affect BP?
Salt restriction is assoc w/small but consistent BP decreases
38
How does excessive ETOH use affect your HTN treatment?
Excessive alcohol use is assoc w/HTN as well as resistance to antihypertensive drugs
39
ACC/AHA Guidelines: 1 to 4 conclusions:
1. Out-of-office BP's are recommended for dx and titration of BP 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 nonpharmacologically 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
40
ACC/AHA Guidelines: 5 to 8 conclusion:
5. ACE-I’s, ARBs, CCBs, or thiazide diuretics are effective in nonblack HTN pts
6. In black adult HTN pts w/o heart failure or CKD, there is moderate evidence to support initial therapy with a CCB or thiazide diuretics
7. Moderate evidence supports antihypertensive therapy with an ACE-I or ARB in those with CKD to improve kidney outcomes
8. Nonpharmacologic interventions are important components of comprehensive BP management
41
15 different drug classes have been approved for HTN
42
When is beta blockers used as 1st line therapy for HTN patients?
Notably absent from 1st line therapy are β blockers, which are reserved for pts w/ CAD or tachydysrhythmia, or as a component of multidrug tx in resistant HTN
43
Secondary HTN treatment?
-interventional, including surgical correction of renal artery stenosis, adrenal adenoma or pheochromocytoma
44
Treatment for 2nd HTN without the possibility renal artery repair?
If renal artery repair not possible, BP can be controlled w/ACE-I’s +/- diuretics
ACE-I’s, ARBs, and direct renin inhibitors are not recommended in bilateral renal artery stenosis as they can accelerate renal failure
45
How do we treat primary hyperaldosteronism?
- an aldosterone antagonist such as spironolactone
46
Which disease processes that require combined pharmacologic and surgical approach?
Pheochromocytoma
47
What is white-coat HTN?
pre-op BP assessment is often complicated by anxiety.
48
What does BP assessment in a single moment in time?
does no give an accurate picture of overall BP trends.
**Current guidelines state that multiple elevated BP readings over time are necessary for a diagnosis of HTN
49
2nd HTN are instructed to do what on the day of surgery?
to pause BP meds
50
If BP is elevated in 2nd HTN patients, what can you do to further assess BP?
pressure on the contralateral arm should be obtained.
51
When should surgery be delayed with 2nd HTN?
pt is experiencing extreme HTN (SBP >180 or DBP >110) or end-organ injury that could be reversed w/BP control.
52
When should we *not* delay surgery with 2nd HTN patients?
-Surgery should not be delayed d/t a transient HTN
-Elevated BP is not a direct prompt to delay surgery in asymptomatic pts w/o risk factors.
53
symptoms of secondary HTN?
- flushing, sweating & palpitations suggestive of pheochromocytoma
- renal bruit may suggest renal artery stenosis
-hypokalemia may suggest hyperaldosteronism
54
Once the decision is made to proceed with surgery, it is common practice to continue antihypertensive meds, with the possible exclusion of ____ and ___ meds.
ARBs and ACE-I’s
55
Stopping what medications is associated with rebound HTN?
Stopping BBs or clonidine
56
Stopping what medications is associated with increased perioperative cardiovascular events?
stopping CCBs
57
perioperative HTN increases ____ and the incidence of ___ & ___
perioperative HTN increases *blood loss* and the incidence of *MI & CVA*
58
Hypertensive pts are prone to intraop hemodynamic volatility d/t what?
physiologic factors along with the various BP meds on-board
59
what to consider in the context of end-organ functional reserve?
Acute intraoperative BP changes need to be considered in the context of end-organ functional reserve
60
PT w/organ damage from chronic HTN, what considerations?
PT w/organ damage from chronic HTN, are less resilient to periods of hypotension and have increased rx of acute kidney and myocardial injury
61
Hemodynamic Load Table
62
HTN and induction expectations?
- HTN pt's are hemodynamically vulnerable to induction medications
- induction drugs produce hypotension; while DL & intubation elicit HTN & tachycardia
63
What can be beneficial in pre-induction for HTN patients?
- A pre-induction A-Line
- Multimodal induction that includes SA BB (esmolol)
64
What do you expect HTN that are poorly controlled and on a diuretic?
Hypovolemia.
65
What should be things to consider when giving a vasoactive drug?
Pt's age, functional reserve, medications, and the planned surgery
66
What intervention can provided a better hemodynamic stability to HTN patients?
Modest volume loading before induction, although this may be counterproductive in pts with LVH and diastolic dysfunction
67
What categories is HTN based on presence of organ damange?
either urgent or emergent, b/o the presence of organ damage.
68
What do pts with chronic HTN tolerate better than normotensive patients?
- tolerate higher SBP
69
What are some peri-operative emergencies may include? ( in the context of HTN crisis)
CNS injury, kidney injury, and cardiovascular injury.
70
What are the current guidelines for peripartum HTN recommendation?
immediate intervention for SBP > 160 / DBP > 110.
71
What can women with PIH experience with a DBP > 100?
end-organ dysfunction (such as encephalopathy)
72
As an anesthesia provider, how can you avoid overshooting BP in the OR? what equipment can help?
BP must be titrated down slowly to avoid overshooting.
A-line monitoring can facilitate this process.
73
What is the 1st line drug for peripartum HTN?
labetalol
74
What drug to use and why for rapid dilation?
SNP infusion is the gold standard d/t fast onset and titratability.
75
Clevidipine (Cleviprex)
Class:
Duration of action:
provider consideration?
- 3rd generation dihydropyridine CCB
- ultrashort duration of action (~1 min half time)
- expensive medication, more titratable than nicardipine
76
Nicardipine (Cardene)
Class:
1/2 time:
provider consideration?
- 2nd generation dihydropyridine CCB
- longer half-life (~30 mins)
- making it less titratable than clevidipine.
77
How does pulmonary HTN and systemic HTN differ?
- systemic HTN can be diagnosed and monitored daily via BP trends.
- pulmonary HTN is more complex.
78
How is pulmonary HTN defined as?
Mean PA pressures (mPAP) = **> 20 mmHg**
79
# Pulmonary HTN
symptoms?
* LE swelling
* Accentuated S2 & S4 "gallop" heart sounds
80
# Pulmonary HTN
Subdivided into 3 hemodynamic profiles based on what?
| Its a measurement.
* PA wedge pressure (PAWP)
* Pulmonary Vascular Resistance (PVR)
81
# Pulmonary HTN
What are the 3 classificaitons?
* Isolated **pre**capillary pulmonary HTN
* Isolated **post**capillary pulmonary HTN
* Combined pre & postcapillary pulmonary HTN
82
Define **Pre**capillary Pulmonary HTN
| Values of PVR, LAP, and PAWP?
* Primary issue lies in the pulmonary arterial circulation
* Pulmonary vascular resistance (PVR) ≥ 3.0 wood units w/ normal LAP
* or PAWP: <15 mmHg
83
Define **Post**capillary pulmonary HTN
| PAWP? PVR? LAP?
* increased pulmonary venous pressure d/t elevated LAP usually c/b left heart disease
* elevated PAWP (>15 mmHg)
* normal PVR
## Footnote
Note that pulm venous pressure is elevated, not pulm vascular resistance.
84
Defline Combined pre & postcapillary pulmonary HTN
| PVR? PAWP?
* Chronic pulmonary venous HTN with secondary pulm art vasoconstriction and remodeling
* PVR > 3.0 wood units
* PAWP > 15 mmHg
| This can be subcategorized as fixed and vasoreactive.
85
# Combined pre & postcapillary pulmonary HTN
How is this disease further subcategorized?
* Fixed or vasoreactive
* depending on the response to vasodilators, diuretics, or mechanical assistance
86
Define High-flow pulmonary HTN
| PAWP? PVR?
* occurs without an elevation in PAWP or PVR
* results from increased pulmonary blood flow complicated by **systemic-to-pulmonary shunt** or **high cardiac output states**.
87
# Pulmonary **artery** HTN
How is this disease diagnoised?
Right heart cath
| diagnosis, classification and Tx plan is determined by this procedure.
88
# mPAP
What mechanisms increase mPAP?
| 4 mechanisms.
1. elevated resistenace to blood flow within the art circulation
2. increased pulmonary venous pressure form left heart disease
3. chronically increased pulmonary blood flow
4. a combination of these processes
89
What is the formula for PVR?
PVR = (mPAP - PAWP) / C.O.
90
What abnormalities can cause pulm HTN?
Art or venous components of pulmonary circulation, sometimes inclusing contributions from both.
91
# Pulmonary **Artery **HTN
What can TTE show?
* enlargement of right atrium & ventricle
* elevated tricuspid-regurgitation velocity
92
What is commonly used as a screening tool for pulmonary HTN?
Echocardiogram used to estimate pulmonary arterial systolic pressure (PASP)
93
# Pulm HTN
* PASP from an echo provides what?
* Can you use an echo to diagnose pulm HTN?
| PASP = pulm artery systolic pressure
* PASP > 41 mmHg on echo is relatively sensitive and specific for PH; it can not provide an accurate mPAP for definitive Pulm HTN diagnosis.
| mPAP is needed for diagnosis, not PASP.
94
# mPAP values for each severity of pulm HTN?
* Mild Pulm HTN
* Moderate Pulm HTN
* Severe Pulm HTN
* Mild Pulm HTN: mPAP = 20 - 30 mmHg
* Moderate Pulm HTN: mPAP = 31 - 40 mmHg
* Severe Pulm HTN: mPAP = >40 mmHg
95
# CO and mPAP
How much can CO increase without a marked change in mPAP?
Pulmonary circulation can accommodate a **four-fold increase** in CO perfusion without marked change in mPAP.
96
What is idopathic Pulm artery HTN?
no identifiable risk factors
97
# Genetics and Pulm Art HTN
What % of Pulm Art HTN is genetic? What receptor mutation is to blame?
* 3%
* mutations in bone morphogenetic protein receptor type 2 **(BMPR2) **
98
What is historically known about Pulm art HTN?
* a disease of young women with median survival rate of 3 years.
## Footnote
Now, we see older pts and more men being diagnosed.
99
# Pulm Artery HTN
What medication is shown to have long term improvements?
* Nearly **1:8** Pulm patients have long-term improvements with **CCBs**
| Only a small percentage respond to CCBs
100
What is the 1 year mortality % in Pulm Art HTN?
~15%
101
# Pulmonary artery hypertension
What does sustained vasoconstriction and remodeling lead to?
leads to pathologic distortion of the pulmonary arteries
102
# Pulmonary Artery HTN
What are the 3 main classes of pulmonary vasodilator drugs?
* Prostanoids
* Endothelin receptor antagonists (ERAs)
* drugs that enhance nitric oxide/guanylate cyclase pathway
| combo therapy is often required for adequate tx of Pulm Art HTN.
103
# Pulm Artery treatment
Prostanoids: MOA
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.
104
# Pulm Art HTN tx
Prostanoids: Meds
* Epoprostenol (IV)
* iloprost (Inh)
* treprostinil (SQ, IV, INH, PO)
* beraprost (PO)
| All provide improvement, but only epoprostenol is proven to reduce mort
105
# Pulm Art HTN tx:
Endothilin Receptor Antagonist (ERAs)
vascular endothelial dysfunction associated with PAH involves an imbalance btw vasodilating (nitric oxide) and vasoconstricting (endothelin) substances. ERAs improve hemodynamics and exercise capacity.
106
# Pulm Art HTN tx:
Nitric oxide/guanylate cyclase: MOA
nitric oxide produces pulmonary vasodilation by stimulating guanylate cyclase and cGMP in smooth muscle cells. The effect is transient because nitric oxide is quickly bound by hgb and degraded by phosphodiesterase type 5
* Continuous inhaled nitric oxide is used in perioperative and critical care settings
* Chronic therapy has been directed toward PD-5 inhibitors to prolong the half-life of nitric oxide
107
# Pulmonary Art HTN
What procedures should be given consideration?
| Pre-Op Considerations
* Procedures with potential for venous embolism
* Elevation in venous and/or airway pressure
* hypoxic pulmonary vasoconstriction
* reduction in pulm vascular volume
* systemic inflammation
* emergency procedure
108
# Pulmonary Art HTN
What are some non-specific sx?
| Pre-Op Considerations
Fatigue, dyspnea, and cough
109
# Pulmonary Art HTN
What is severe sx?
| Pre-Op Considerations
* angina
* syncope
Which can occur with exercise if coronary blood flow doesn't meet the demands of hypertrophied RV
110
# Pulm Art HTN
What are some assessment factors noted in these patients?
| Pre-Op Considerations
* Parasternal lift
* accentuated S2,S3or S4 gallop
* JVD
* peripheral edema
* hepatomegaly
* ascites
111
# Pulm Art HTN
What is a rare sx seen in Pulm Art HTN?
| Pre-op consideration
Compression of a dilated PA may lead to RLN damage and hoarseness
112
# Pulm Art HTN
What is recommended for pts with moderate/severe pulm HTN?
| Pre-Op Considerations
A right heart cath recommended prior to moderate-high risk surgery
113
What does the discrepancies btw PAWP and LVEDP mean?
| Pre-Op Consideration
a left heart cath is indicated in pts with left heart dz, because inaccurate LVEDP may lead to misclassification of PH and inappropriate treatment.
114
What is done during a right heart cath?
Vasoreactivity testing with inhaled nitric oxide, is performed to determine responsiveness to vasodilator therapy.
115
What % of Pulm Art HTN patients are nonresponsive to inhaled nitric oxide?
| Pre-Op consideration
85-90%
116
# Pulm Art HTN
What if these patients are responsive to inhaled nitric oxide?
| pre-op consideration
- also respond to CCBs and may benefit from other targeted therapy
117
Table on slide 40
118
Table on slide 41
| Risk factors for morbidity and mortality in non-cardiac surgery in pts
119
# Peri-Op Physiology
What is the primary intaoperative goal?
to maintain optimal "mechanical coupling" btw the right vent. and pulm circulation to promote adequate left-sided filling and systemic perfusion.
120
What interventions shoudl be considered during surgery?
any intervention that may affect RV preload, inotropy, afterload, and O2 supply/demand needs to be considered
121
What added perioperative cokmplexities can increase risk of complications?
* transient HoTN
* mechanical ventilation
* modest hypercarbia
* small bubbles in IV
* T-burg position
* Pneumoperitoneum
* single-lung ventilation
122
# Right ventricular afterload:
What is a hallmark of Pulm Art HTN?
Increased RV afterload, leading to RV dilation, increased wall stress, and RV hypertrophy.
123
# Right ventricular afterload:
what is the interaction btw the RV and pulm circulation?
Pulsatile and dynamic, involving the compliance and "stiffness" of Ig & small vessels.
124
# Right ventricular afterload:
What can affect RV pulsatile load?
This is exacerbated during surgerical stimulation, which affect RV pulsatile load
125
# Right ventricular afterload:
Vent settings that affect RV afterload?
Vent settings such as PEEP, hypoventilation, hypercarbia, acidosis, and atelectasis can affect RV afterload.
126
# Myocardial supply & demand:
What leads to an increased RV O2 demand?
In contrast to the LV, the thinner-walled RV is subject to greater wall tension for the same degree of end-diastolic volume.
127
# Myocardial supply & demand:
Under normal circumstances; RV intramyocardial pressure is?
RV intramyocardial pressure is lower than the aortic root pressure, and RV coronary perfusion occurs throughout the cardiac cycle.
128
# Myocardial supply & demand:
How does elevated RV pressure ultimately causing myocardial ischemia?
In Pulm Art HTN, the elevated RV pressure leads to increased coronary flow during diastole, making the RV more vulnerable to systemic HoTN, worsening the 02 supply/demand mismatch and potentially causing myocardial ischemia
129
# Myocardial supply & demand:
What combo is considered lethal that leads to RV ischemia?
The "lethal combination of RV dilatation, insufficient LV filling, reduced stroke vol. and systemic hypotension can lead to RV ischemia.
130
Orthopedics:
| Procedural Considerations
studies show increased perioperative morbidity and mortality in pts with PH undergoing hip and knee replacement
131
Laparoscopy:
| Procedural Considerations
Pneumoperitoneum impacts biventricular load and pump function. The combination of pneumoperitoneum, head-down position, and increased AW pressure invreases RV pressures and afterload
132
Thoracic surgery:
| Procedural Considerations
Thoracic procedures involve nonventilation and atelectasis of the operative lung
133
3 features of lung collapse are particularly relevant:
| procedural considerations
1. 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
* PAH pts are often converted from oral to inhaled or pulmonary vasodilators
* inhaled pulmonary vasodilators are recommended during single-lung ventilation
134
# Key Points/Recap
What is HTN a risk factor for?
HTN is a significant risk factor for CV dz, stroke, and renal dz
135
# Key Points/Recap
Guidelines define a SBP goal is?
SBP goal of <130 mmHg, but many pts remain poorly controlled
136
# Key Points/Recap
Preop evaluation of a HTN pts should focus on?
adequate BP control, tx regimen, and the presence of end-organ damage
137
What is common with HTN pts under anesthesia?
Hemodynamic instability is common during anesthesia in hypertensive pts
138
# Key points/recap
What is Pulm HTN defined as?
Pulm HTN is defined as a mean PA pressure > 20 mmHg, and can result from processes that constrict arteries, elevate pulmonary venous pressure, or chronically increase blood flow, leading to vascular remodeling
139
Pulmonary vasodilators include:
* prostacyclin analogues
* endothelin receptor antagonists
* drugs activating the nitric oxide/guanylate cyclase pathway
140
Prognosis for Pulm Art HTN?
Poor prognosis even with improved survival and quality of life from vasodilators.
141
Pulm Art HTN pts on a vasodilators: should hold or continue medicaitons during surgery?
Pulm Art HTN pts on a vasodilators should have them continued intraoperatively and postoperatively, and converted from oral to IV or inhaled when necessary.
