Exam 4 - HTN - Organized Flashcards
1
Q
what is normal classification of HTN?
A
SBP < 120
DBP < 80
s2
2
Q
what are clinical consequences of chronically elevated BP?
s3
A
ischemic heart disease, stroke, renal failure, retinopathy, PVD, and overall mortality
s3
3
Q
What is the range for :
isolated systolic HTN?
isolated diastolic HTN?
combined sys and diastolic HTN?
s3
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
s3
4
Q
what are (3) genetic and lifestyle risk factors for HTN?
s4
A
obesity, alcoholism and tobacco
s4
5
Q
what is also a risk factor for cardiovascular morbitity (in addition to SBP and DBP elevation)?
and why?
s3
A
widened pulse pressure because it correlates w/vascular remodeling and “stiffness”
s3
6
Q
what herbals elevate BP?
s4
A
ephedra, ginseng, ma huang
s4
7
Q
What are contributing factors for primary HTN?
s4
A
- SNS activity
- dysregulation of the RAAS
- deficiency in endogenous vasodilators
Actual cause of primary HTN is unclear!
s4
8
Q
What are (5) common causes of secondary HTN in middle-aged adults?
s4
A
hyperaldosteronism, thyroid dysfunction, OSA, Cushings, and pheochromocytoma
s4
9
Q
What are 2 causes for children w/ secondary HTN?
s4
A
renal parenchymal disease or coarctation of the aorta
s4
10
Q
what is an Anti-infective that elevates BP?
s6
A
Ketoconazole
s6
11
Q
what are the 2 anti-inflammatory classes that elevate BP?
s6
A
NSAIDs and COX-2 inhibitors (-coxib’s)
s6
12
Q
what 2 illicit drugs elevate BP?
A
amphetamines and cocaine
s6
13
Q
list 3 immunosuppresive agents that may elevate BP
A
cyclosporine, sirolimus, tacrolimus
s6
14
Q
what 2 steroids may elevate BP?
A
methylprednisolone and prednisone
s6
15
Q
what 2 random sympathomimetics elevate BP?
s6
A
decongestant and diet pills
s6
16
Q
list hormones and psych meds that may elevate BP
A
- hormones: oral contraceptives (estrogen and progesterone), androgens
- psych: buspar, carbamazepine, lithium, clozapine, MAO-Is, SSRIs, TCAs
s6
17
Q
Per ACC/AHA guidelines, there is a moderate evidence to support antihypertensive therapy with which medications in those w/ CKD to improve kidney outcomes?
A
ACE-I or ARB
S7
18
Q
what are 3 causes of secondary HTN in older adults (>65 yo)?
s7
A
atherosclerotic renal artery stenosis, renal failure, hypothyroidism
s7
19
Q
What does chronic HTN lead to? (vascularly..)
A
remodeling of small & large arteries, endothelial dysfunction, and potentially irreversible end-organ damage
s8
20
Q
What plays a major role in ischemic heart dz, LVH, CHF, CVA, PAD, aortic aneurysm, and nephropathy?
A
Disseminated vasculopathy
s8
21
Q
what 2 ultrasound measurements can provide an early dx of vasculopathy?
A
- common carotid intimal to medial thickness
- arterial pulse-wave velocity
22
Q
what tests can track progression of LV hypertrophy?
A
Echocardiographic and electrocardiographic indexes
s8
23
Q
what imaging can be used to identify cerebrovascular damage?
A
MRI - to follow microangiopathic changes
s8
24
Q
What are the 4 examples of end-organ damage due to HTN?
A
Vasculopathy
Cerebrovascular damage
Heart disease
Nephropathy
S9
25
What is the therapeutic goal for HTN treatment?
<130/<80
## Footnote
S10
26
How many people in the US have untreated HTN? How many patients have their BP above their goal?
28 million people in US have untreated HTN
29 million treated pts are above their BP goal
## Footnote
S10
27
What is resistant HTN? What is the treatment for resistant HTN?
Above-goal BP despite 3+ antihypertensive drugs at max dose.
Tx usually includes a LA CCB, an ACI-I or ARB + a diuretic
## Footnote
S10
28
How would you define the controlled resistant HTN?
Controlled BP requiring 4+ medications
## Footnote
S10
29
What is refractory HTN? How many patients present w/ refractory HTN?
Uncontrolled BP on 5+ drugs, present in 0.5% of pts
## Footnote
S10
30
What is pseudo-resistant HTN? What are the causes of pseudo-resistant HTN?
Intolerance to drugs that can result from BP inaccuracies (including white-coat syndrome) or medication noncompliance
## Footnote
S10
31
What are some lifystyle modifications recommended for patients w/ HTN?
Weight loss,↓ETOH, exercise, and smoking cessation
There is a continuous relationship btw ↑BMI and HTN.
## Footnote
S11
32
What is the most effective nopharmacological intervention for HTN?
Weight loss
(expect a 1 mmHg reduction in BP for every 1 kg of weight loss)
*- weight loss can synergistically enhance the drug efficacy.*
## Footnote
S11
33
What other factors can increase or decrease the BP?
Increase BP:
- Increase in physical activity
- Excessive alcohol use
Decrease BP:
- Dietary potassium and calcium intake
- Salt restriction
## Footnote
S12
34
Per ACC/AHA guidelines, what is recommended for diagnosis and titration of antihypertensive meds?
Out-of-office BPs
## Footnote
S13
35
Per ACC/AHA guidelines, the evidence supports treating pts w/ CKD, CAD, ischemic heart dz with SBP____ ?
SBP >130 mmHg requires treatment with BP meds
## Footnote
S13
36
Per ACC/AHA guidelines, do you need to treat pts w/o cardiovascular or cerebrovascular dz with nonpharmacological therapy if SBP>130 or DBP >80?
There is limited data to support treatment of these patients.
## Footnote
S13
37
Per ACC/AHA guidelines, do patients with DM and CKD have a different BP goal?
No, same goal for DM/CKD population as well as HTN population.
## Footnote
S13
38
Per ACC/AHA guidelines, which medications are recommended for nonblack HTN pts, including those with DM?
ACE-I’s, ARBs, CCBs, or thiazide diuretics
## Footnote
S14
39
Per ACC/AHA guideline #8, what is the important component to comprehensive BP management?
Nonpharmacologic intervention
## Footnote
S14
40
Which drug is reserved as the 1st line therapy for pts w/ hx of CAD or tachydysrhythmia or those w/ resistant HTN?
β blockers
## Footnote
S15
41
How many drug classes have been approved for HTN?
15
## Footnote
S15
42
What is the treatment of secondary HTN?
often interventional, including surgical correction of:
- renal artery stenosis
- adrenal adenoma
- pheochromocytoma
| treat the underlying issue
## Footnote
S16
43
When are ACE-I’s, ARBs, and direct renin inhibitors are *not recommended* to use for Secondary HTN intervention?
in **bilateral renal artery stenosis**
as they can accelerate renal failure
## Footnote
S16
44
What certain disease processes require a combined pharmacologic and surgical approach?
| Secondary HTN
Pheochromocytoma
## Footnote
S16
45
What can Primary hyperaldosteronism be treated with?
Aldosterone Antagonist
(Ex: Spironolactone)
## Footnote
S16
46
What medications of Secondary HTN patients are instructed to be *paused* on the day of surgery?
ACE-I's and Diuretics
## Footnote
S17
47
Preop BP assessment is often complicated by ____ (white-coat HTN)
Assessing BP in a *single moment* in time does not give an ____ picture of overall BP trends
Current guidelines state that multiple elevated BP readings ____ are necessary for a diagnosis of HTN
* anxiety
* accurate
* over time
| PCP have the pt trend their BP at home
## Footnote
S17
48
When should surgery NOT be delayed for patients with elevated BP?
* in **asymptomatic pt w/o other risk factors**
* pt. experiencing extreme HTN or end-organ injury **that could be reversed w/BP control**
## Footnote
S18
49
If BP elevated, a pressure on what side of the arm should be obtained?
contralateral side
(of first arm)
## Footnote
S18
50
What is necessary to carefully review to gain an overall picture of CV health of Secondary HTN?
* clinic data
* home BP’s
* thorough history
## Footnote
S18
51
What symptoms suggests Pheochromocytoma is the cause of Secondary HTN?
* flushing
* sweating
* palpitations
## Footnote
S19
52
What symptom suggests Renal Artery Stenosis is the cause of Secondary HTN?
Renal bruit
## Footnote
S19
53
What symptom suggests Hyperaldosteronism is the cause of Secondary HTN?
hypokalemia
## Footnote
S19
54
What is the risk of stopping Beta Blockers or Clonidine before surgery of pt's with Secondary HTN?
can cause rebound effects
| So, have patient take BBs or Clonidine before surgery
## Footnote
S19
55
What is the risk of stopping Calcium Channel Blockers before surgery of pt's with Secondary HTN?
increased perioperative cardiovascular events
| So, have patient take CCBs before surgery
## Footnote
S19
56
What are hypertensive pts prone to and why?
hemodynamic volatility
d/t physiologic factors along with the BP meds on-board
## Footnote
S20
57
What can brief *periods of hypotension* cause on pts with organ damage from chronic HTN?
* acute kidney injury
* myocardial injury
* death
*Clinicians need to consider acute intraoperative BP changes in the context of end-organ functional reserve*
## Footnote
S20
58
What are the factors of Left Ventriucular Hypertension (LVH) and what does LVH cause ?
see chart
## Footnote
21
59
When are HTN pts hemodynamically vulnerable during anesthesia and why?
during induction of GA
Induction drugs produce HoTN while Direct Laryngoscopy & intubation elicit HTN & tachycardia
## Footnote
S22
60
Poorly controlled hypertension is often accompanied by what volume status and how can you fix it?
-volume deficit, especially if pt is on diuretic!
*-volume loading prior to induction might provide hemodynamic stability however careful in left ventricular hypertrophy and diastilic dysfunction*
## Footnote
22
61
When considering vasoactive drugs, consider what 4 factors?
Pt's age, functional reserve, medications and the planned surgery
## Footnote
22
62
Induction causes what 3 changes in vital signs ?
Which drug may be use after induction?
hypotension, direct laryngoscopy and intubation elicit hypertension and tachycardia
-esmolol! and consider a pre induction a line
## Footnote
23
63
Women with pregnancy induced hypertension show evidence of organ damage dysfunction, especially encepalopathy at which diastolic value?
In peripartum HTN, when should you intervene?
DBP >100
Intervene immediatly for SBP >160/ DBP >110!
## Footnote
23
64
Hypertensive crisis is categorized either urgent or emergent, and is based on organ damage. Which organ injuries is the patient at risk for?
CNS injury, kidney injury , and cardiovascular insult!
| Pt w/ chronic HTN may tolerate higher SBP than normal pt
## Footnote
23
65
For rapid arterial dilation, which drug is **gold standard?**
which other 2 drugs have become available as well?
-**sodium nitroprosside**! fast & easily titratable
**-clevidipine** (CCB, short DOA ~ 1 min half life) has selevtive vasoarterial but it's expensive!
**-nicardipine** (CCB, 1/2 life 30 min) less easy to titrate
| 24
66
When treating HTN r/t aortic dissection, what can vasodilators cause?
What is the treatment goal
Vasodilators may cause hypotension--> end organ ischemia :(
*treatment goal is lessening pulsatile force of LV conraction*
## Footnote
25
67
When treating preeclampsia and eclamsia, BB may cause what 2 things?
What 2 groups of drugs are teratogenic so contraindicarted w pregnancy?
uterine blood flow and they might inhibit labor!
ACE inhibitors and ARBS!
*delivery is the only ultimate treatment :(*
## Footnote
25
68
When treating pheo and cocaine intoxication for, what do you watch for when giving beta blockers?
unopposed alpa adrenergic stimulation after BB makes HTN worse!
## Footnote
25
69
3% of PAH cases are deemed inheritable, with mutations in which gene?
bone morphogenetic protein receptor type 2 (**BMPR2**)
*The remaining cases are designated “**associated PAH**,” since they can be ascribed to manifestations of drugs, toxins, or other diseases.*
## Footnote
S26
70
What are 3 main classes of pulmonary vasodilator drugs for Pulmonary artery HTN?
1) Prostanoids
2) endothelin receptor antagonists (ERAs)
3) those working through nitric oxide/guanylate cyclase pathways
| *Combination therapy is often required for adequate tx of PAH*
## Footnote
S26
71
What diagnostic intervention is recommended for patients with suspected PAH?
Right heart cath
## Footnote
S26
72
What is MOA of Prostanoids?
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
## Footnote
S26
73
What medication has been proven to reduce mortality among PAH pts?
Epoprostenol
| *Prostanoid*
## Footnote
S26
74
What is MOA of Endothilin Receptor antagonists (ERAs)?
The vascular endothelial dysfunction associated with PAH involves an imbalance btw vasodilating (nitric oxide) and vasoconstricting (endothelin) substances.
ERAs have been shown to improve hemodynamics and exercise capacity.
## Footnote
S27
75
What is MOA of Nitric oxide/guanylate cyclase?
Nitric oxide produces **pulmonary vasodilation** by **stimulating guanylate cyclase and cGMP formation** in smooth muscle cells.
This effect is **transient** because nitric oxide is quickly bound by hgb and degraded by **phosphodiesterase type 5.**
## Footnote
S27
76
What signs are most likely be exhibited by patients with PAH?
parasternal lift, S3 gallop, JVD, peripheral edema, hepatomegaly, and ascites.
compression of a dilated PA may lead to RLN damage and hoarseness
## Footnote
S27
77
Due to potential discrepancies btw PAWP and LVEDP, what diagnostic intervention should also be performed in pts with coexisting left heart dz?
Left heart cath
*because inaccurate LVEDP may lead to misclassification of PH and inappropriate treatment*
## Footnote
S27
78
Which gas is used in vasoreactivity testing to determine responsiveness to vasodilator therapy?
inhaled nitric oxide
## Footnote
S27
79
85–90% PAH pts are nonresponsive to inhaled nitric oxide, but those that are responsive will most likely benefit from which drug therapy?
CCB
## Footnote
S27
80
What defines pulmonary HTN accorting to 6th world symposium?
What are the s/s?
mPAP >20 mmHG!
S/S: S2 and S4 gallop hear sounds, LE swelling
## Footnote
28
81
Pulm HTN is divided into 3 profiles based on PAWP and PVR. What are the classifications?
isolated precapillary PH
isolated postcapillary PH
combined pre and post capillary PH
## Footnote
28
82
What is the definition of isolated postcapillary pulmonary hypertension?
* increased pulmonary venous pressure
* usually determined by elevated LAP cause by valve disease or LV dysfunction
## Footnote
Slide 29
83
Isolated postcapillary pulmonary hypertension is characterized by?
* PAWP >15mmHg with a normal PVR
## Footnote
Slide 29
84
Describe combined pre and postcapillary pulmonary hypertension?
* (aka reactive PH) reflects chronic pulmonary venous HTN with secondary pulmonary arterial vasoconstriction and remodeling
## Footnote
Slide 29
85
What are the characteristics of combined pre and postcapilliary pulmonary hypertension ?
* PAWP >15mmHg and a PVR > 3.0 WU
* subcategorized as fixed or vasoreactive do to the response to vasodilators, diuretics, or mechanical assistance
## Footnote
Slide 29
86
Describe high- flow pulmonary hypertension?
occurs without an elevation in PAWP or PVR and results from increased pulmonary blood flow cause by a systemic-to-pulmonary shunt or high cardiac output
## Footnote
Slide 29
87
What are the
mPAP, PAWP, PVR and Groups of isolated postcapillary pulomnary hypertension.
## Footnote
Slide 30
88
What are the
mPAP, PAWP, PVR and Groups of combined pre and post capillary pulomnary hypertension.
## Footnote
Slide 30
89
What is the formula for Pulmonary Vascular Resistance?
PVR=(mPAP - PAWP)/ CO
| .schmidt...
## Footnote
31
90
What procedure is done to diagnose, classify and devlop treatment for Pulmonary Artery HTN?
Right Heart Catheterization
## Footnote
31
91
mPAP can be increased by what four mechanisms?
1. *Elevated resistance* to blood flow within arterial circulation
2. Increased pulmonary venous pressure from *Left* heart disease
3. Chronically increased pulmonary blood flow
4. A combination of these processes
## Footnote
31
92
PH can result from abnormalities in the __________________ or ________________ components of the lung circulation, sometimes includes contributions from ____________.
PH can result from abnormalities in the arterial or venous components of the lung circulation, sometimes includes contributions from both
## Footnote
31
93
After Right heart catheterization the severity of the PH can be determined to be:
Mild PH (mPAP = ________________)
Moderate PH (mPAP = ____________)
Severe PH (mPAP= ________________)
Mild PH (mPAP = 20-30mmHg)
Moderate PH (mPAP = 31-40mmHg)
Severe PH (mPAP= >40mmHg)
## Footnote
32
94
Which diagnostic test or screening tool can be done to estimate pulmonary arterial systolic pressure (PSAP)?
Echocardiogram
## Footnote
32
95
Can a echocardiographic Pulmonary arterial systolic pressure of >41mmHg provide a definitive diagnosis for Pulmonary Hypertention?
****No
Although echocardiographic
PASP > 41 mmHg is relatively sensitive and specific for PH,* it cannot provide the accurate mPAP for definitive diagnosis*
## Footnote
32
96
How much volume can a normal Pulmonary circulation accomodate without a marked change in mean pulmonary artery pressure (mPAP)?
Normal pulmonary circulation can accommodate a **fourfold increase** in COP without a marked change in mPAP
## Footnote
32
97
What three things can a TTE reveal to help diagnose Pulmonary Artery HTN?
1. RA enlargement
2. RV enlargement
3. Elevated Peak tricuspid-regurgitation
## Footnote
32
98
According to the World Health Organization, PAH is classified as a __________ disease. It affects ________ people per million per year
According to the World Health Organization, PAH is classified as a rare disease effecting 15 ppl per million per year
## Footnote
33
99
Does idopathic PAH have any identifiable risk factors?
NOPE
## Footnote
33
100
What medication has shown long-term improvements in 1 in 8 patients with PAH?
Calcium channel blockers
## Footnote
33
101
What percent of patients have the inherited genetic protein mutation (BMPR2) that can cause PAH?
What is BMPR2?
3% of PAH cases are deemed inheritable.
BMPR2 - bone morphogenetic protein receptor type 2
## Footnote
33
102
Remaining cases of PAH that are not genetic mutations are caused by:
a. drugs
b. toxins
c. various diseases
d. all of the above
d. all the above
The remaining cases are designated “associated PAH,” since they can be ascribed to manifestations of drugs, toxins, or other diseases
## Footnote
33
103
Current data shows PAH develops in this age range and population.
Current data shows a demographic shift, now with **older pts and more men** being diagnosed
*PAH was traditionally a disease of young women, with median survival rate of 3 yrs*
## Footnote
33
104
Even with improved diagnosis of PAH and therapies the 1 year mortality rate is:
a. 10%
b. 15%
c. 25%
d. 5%
b. 15%
Despite improved diagnosis and therapy, 1-year mortality is** ̴15%**
## Footnote
33
105
What medication has shown long-term improvements in 1 in 8 patients with PAH?
Calcium channel blockers
## Footnote
33
106
What PAH treatment mimics the effect of prostacyclin to produce vasodilation while inhibiting platelet aggregation.
Prostanoids!
## Footnote
35
107
What are the four examples of Prostanoids medications and their routes of administration?
epoprostenol (IV)
iloprost (inhaled)
treprostinil (SQ, IV, INH, PO)
beraprost(PO)
*
## Footnote
35
108
Which Prostanoid medication has been PROVEN to reduce mortality?
Epoprostenol IV
## Footnote
35
109
What is the MOA of Postanoids, when using it to treat pulmonary artery hypertenision?
* 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
## Footnote
slide 36
110
How does Endothilin Receptor antagonists (ERAs) improve pulmonary arterial hypertenion
**hemodynamics and exercise capacity**
*The vascular endothelial dysfunction associated with PAH involves an imbalance between vasodilating (nitric oxide) and vasoconstricting (endothelin) substances. ERAs have been shown to improve hemodynamics and exercise capacity*
## Footnote
Slide 37
111
How does nitric oxide/ guanylate cycase improve pulmonary arterial hypertenion?
**nitric oxide produces pulmonary vasodilation by stimulating guanylate cyclase and cGMP formation in smooth muscle cells.**
*
This effect is transient because nitric oxide is quickly bound by hgb and degraded by phosphodiesterase type 5*
## Footnote
Slide 37
112
What are the areas that nitric oxide has been widely used?
perioperative
critical care
preparpations for home
## Footnote
slide 37
113
True or False: Chronic therapy has been directed toward PD-5 inhibitors
True
## Footnote
Slide 37
114
What are the nonspecific signs of pulmonary arterial hypertension for preop consideration?
* fatigue
* dyspnea
* cough
## Footnote
Slide 38
115
What consideration should be given to pulmonary arterial hypertension procedure with pre-op?
* venous embolism
* elevations in venous and/or airway
* pressure hypoxic pulmonary
## Footnote
Slide 38
116
What are the more advance signs to take in consideration for preop for patients with pulmonary arterial hypertnsion?
**angina and syncope **
*occur with exercise if coronary blood flow cannot meet demand of a hypertrophied RV*
## Footnote
Slide 38
117
Patient with pulmonary arterial hypertension may exhibit____ on physical exam
## Footnote
*list*
* parasternal lift
* accentuated S2, S3 and/or s4 gallop
* JVD
* peripheral edema
* hepatomegaly
* ascites
## Footnote
Slide 38
118
# PAH Preop Considerations
What is recommended prior to mod-high risk surgery in pts with mod-severe PH?
Right Heart Cath
## Footnote
S39
119
# PAH Preop Considerations
* Due to potential discrepancies btw PAWP and LVEDP, a _____ _____ ____ is done with coexisting left heart dz bc may lead to ____ of PH
* Vasoreactivity testing, often with inhaled _____ ______ , during right heart cath to determine responsiveness to ______ therapy
o __-__ % PAH pts are nonresponsive to inhaled nitric oxide, but those that are responsive also respond to ____ ***
* left heart cath
* misclassification
* nitric oxide
* vasodilator
* 85-90%
* CCB's
## Footnote
S39
120
**Precapillary PH** is defined as PVR of ____ wood units w/o elevated ____ or ____ (PAWP < 15mmHg = normal)
**Precapillary PH** is defined as PVR of **≥ 3.0** wood units w/o elevated **LAP** or **PAWP** (PAWP < 15mmHg = normal)
## Footnote
S41
121
**Isolated postcapillary PH** results from increased ____ venous pressure, usually d/t elevated ____ c/b valve disease or LV dysfunction
**Isolated postcapillary PH** is characterized by a PAWP ____mmHg , w/ ____ PVR
**Isolated postcapillary PH** results from increased **pulmonary** venous pressure, usually d/t elevated **LAP** c/b valve disease or LV dysfunction
**Isolated postcapillary PH** is characterized by a PAWP **>15mmHg**, w/ **normal** PVR
## Footnote
S41
122
What reflects chronic pulmonary venous HTN with secondary pulmonary arterial vasoconstriction and remodeling?
Combined pre- and postcapillary PH
(aka reactive PH)
## Footnote
S41
123
**Combined pre- and postcapillary PH** (aka reactive PH) is characterized by a PAWP ____ mmHg and a PVR ____ WU
Can be subcategorized as fixed or ____ d/o the response to vasodilators, diuretics, or mechanical assistance
**Combined pre- and postcapillary PH **(aka reactive PH) is characterized by a PAWP **>15** mmHg and a PVR **> 3.0 **WU
Can be subcategorized as fixed or **vasoreactive** d/o the response to vasodilators, diuretics, or mechanical assistance
## Footnote
S41
124
**High-flow PH** occurs ____ an elevation in PAWP or PVR and results from ____ pulmonary blood flow c/b a systemic-to-pulmonary shunt or high cardiac output
**High-flow PH** occurs **w/o** an elevation in PAWP or PVR and results from **increased** pulmonary blood flow c/b a systemic-to-pulmonary shunt or high cardiac output
## Footnote
S41
125
# Perioperative Phsyiology
*** Primary** intraoperative goal is maintaining optimal “______ ______” btw the RV + pulmonary circulation to promote adequate left-sided filling and systemic perfusion
* Any intervention that may affect ____ , ____ , ___ , _______ needs to be considered
* mechanical coupling
*RV preload, inotropy, afterload, and oxygen supply/demand
## Footnote
42
126
# Perioperative Phsyiology
What added perioperative complexities can have potentially serious consequences? (7)
HoTN ,, mechanical ventilation ,, hypercarbia ,, bubbles in IV ,, Trendelenburg ,, Pneumoperitoneum ,, single-lung ventilation
## Footnote
42
127
# Periop :: RV Afterload
* Increased RV afterload leads to? (3)
* Interaction bw RV + pulm circulation is ____ + _____ and involves the compliance of the pulm vessels
* How does ventilator management effect RV afterload? (5)
* RV dilation, increased wall stress, and RV hypertrophy
* pulsatile + dynamic
* PEEP , hypoventilation , hypercarbia , acidosis , atelectasis
## Footnote
43
128
# Periop :: Myocardial Supply + Demand
* RV is thinner walled which leads to greater wall tension and can cause increased _____ _____ ____
* In PAH, elevated RV pressures cause increased ______ __ which makes RV vulnerable to ____ ____ and worsens the O2 supply/demand mismatch
* HTN + RV ischemia/afterload causes the "LETHAL COMBINATION" which consists of what factors?
* myocardial oxygen demand
* coronary flow
* systemic htn
* RV dilatation, insufficient LV filling, reduced stroke volume, and further systemic hypotension
## Footnote
44
129
# Procedural Considerations
* Ortho : Increase M+M with PH + what 2 surgeries?
* Laparoscopy : combination of what 3 things affects RV pressures?
* Thoracic : involve _____ and ____ of operative lung
* What are the 3 features of lung collapse?
* Hip + Knee
* pneumoperitoneum (insufflation) ,, head-down position ,, increased inspiratory pressure
* nonventilation + atelectasis
* (1) pressurize the chest to induce atelectasis >> increase pressure on pulm
o (2) potential for systemic hypoxia
o (3) hypoxic pulmonary vasoconstriction (HPV) >> increase RV afterload
## Footnote
45
130
# Key Points
__________ _________ is common during anesthesia and surgery in hypertensive pts
* PH = MPAP > ____ mmHg, and can result from a range of processes that directly constrict and remodel ______, elevate pulmonary venous ______, or chronically increase blood flow to initiate _____ ______
* Hemodynamic Instability
* 20
* arteries
* pressure
* vascular remodeling
## Footnote
46
131
# Key Points
* PAH represents group #___ of the 5 PH groups defined by WHO
* * Pts with PAH exhibit ________ dysfunction, maladaptive arterial ________, and in-situ ________
* A ______ _____ ______ is required to provide a dx of PAH and guide tx
* 1
* endothelial
* remodeling
* thrombosis
* R heart cath
## Footnote
47
132
# Key points
* What are the 3 primary pulm vasodilator treatments?
* Only a small percentage respond to ____.
* What is the prognosis for PAH?
* prostacyclin analogues, endothelin receptor antagonists, and drugs activating the nitric oxide/guanylate cyclase pathway
* CCBs
* poor
*
## Footnote
47
133
# Key Points
PAH pts on vasodilators should have them continued ____ + _____ and they should be converted from oral to ______ or ______
* intraop + postop
* IV or inhalation
## Footnote
47
