Exam 4: Hypertension Part II Flashcards
1
Q
Encephalopathy and Intracranial HTN:
* Primary agents
* Cautions
* Comments
A
- Primary Agents: Clevidipine, Nirtoprusside, Labetalol, Nicardipine
- Cautions: cerebral ischemia may result from lower BP from altered autoregulation. Risk of Cyanide toxicity with nitroprusside, and increased ICP
- Comments: Lower BP may decrease bleeding in intracranial hemmorhage
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2
Q
Aortic Dissections
* Primary Agents
* Cautions
* Comments
A
- Primary Agents: Clevidipine, nicardipine, esmolol, labetalol
- Cautions: Vasodialators may cause marked drop in BP (end organ ischemia)
- Comments: Goal is decreaseing the pulsatile force of LV contraction
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3
Q
Acute Kidney Injury:
* Primary agents
* cautions
* comments
A
- Primary agents: clevidipine, nicardipin, lebetalol
- Cautions: vasodialators may cause decreased in BP
- Comments: may require emergent hemodialysis if it progresses to renal failure
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4
Q
Preeclampsia and eclampsia
* primary agents
* cautions
* comments
A
- Primary agents: labetalol, nicardipine
- Cautions: beta blockers may reduce uterine blood flow and inhibit labor
- comments: definitive therapy is delivery. ACE and ARBS are teratogenic and contraindicated during preggers
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5
Q
Pheochromocytoma
* Primary agents
* cautions
* comments
A
- Primary agents: phentolamine, phenoxybenzamine, propanolol, labetalol
- Cautions: unopposed alpha adreneric stimulation following beta blockade worsens HTN
- comments: NA
6
Q
Cocain intoxication
* Primary agents
* Cautions
* comments
A
- Primary agents: lebetalol, dexmedetomadine, clevidipine
- Cautions: unopposed alpha adrenergic stimulation following beta blockade worsens HTN
- Comments NA
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7
Q
World Health Organization (WHO) classifications on Pulmonary hypertension
A
- Pulmonary arterial hypertension (PAH)
- PH due to left heart disease
- PH due to lung diseases and/or hypoxia
- Chronic Thromboembolic pulmonary hypertension (CTEPH)
- PH with unclear multifactorial mechanisms
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8
Q
Plumonary HTN
* definition
* S/S
* 3 hemodynamic profiles
A
- Diagnosis is more complex because we can’t monitor on a daily basis like systemic HTN
- The Sixth World Symposium redefined pulmonary HTN as a mean pulmonary artery pressure (mPAP) >20 mmHg she said this will be on test
- S/S: Accentuated S2 & S4 “gallop” heart sounds, LE swelling
- 3 hemodynamic profiles based on PAWP and PVR:
1. isolated precapillary PH
2. isolated postcapillary PH
3. combined pre & postcapillary PH
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9
Q
Precapillary PH definition
A
defined as PVR of ≥3.0 wood units w/o elevated LAP or PAWP (PAWP <15mmHg = normal)
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10
Q
Isolated postcapillary PH definition
A
- results from increased pulmonary venous pressure, usually d/t elevated LAP caused by valve disease or LV dysfunction
- Isolated postcapillary PH is characterized by a PAWP >15mmHg, w/normal PVR
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11
Q
Combined pre- and postcapillary PH definition
A
- (aka reactive PH) reflects chronic pulmonary venous HTN with secondary pulmonary arterial vasoconstriction and remodeling
- Characterized by a PAWP >15mmHg and a PVR > 3.0 WU
- Can be subcategorized as fixed or vasoreactive d/o the response to vasodilators, diuretics, or mechanical assistance
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12
Q
High flow PH definition
A
occurs w/o an elevation in PAWP or PVR and results from increased pulmonary blood flow caused by a systemic-to-pulmonary shunt or high cardiac output
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13
Q
Chart for hemodynamic definitions of PH
A
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14
Q
Pulmonary Artery HTN
* Diagnosis
* 4 mechanisms that increase mPAP
A
- Right heart catheterization is required for a dx, classification and tx plan
- Mechanisms that increase mPAP
1) elevated resistance to blood flow within the arterial circulation
2) increased pulmonary venous pressure from left heart disease
3) chronically increased pulmonary blood flow
4) a combination of these processes
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15
Q
PVR equation:
PH can result from abnormalities in the _ or _ components of the _ _ sometimes both
A
PVR = (mPAP − PAWP)/COP
* PH can result from abnormalities in the arterial or venous components of the lung circulation, sometimes includes contributions from both
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16
Q
Pulmonary Artery HTN
* what does a TEE show?
* Why get an Echo? whats the limitations?
A
- TTE reveals RA & RV enlargement and elevated peak tricuspid-regurgitation velocity
- Echocardiogram is commonly used to estimate pulmonary arterial systolic pressure (PASP) as a screening tool for PH
- Although echocardiographic PASP > 41 mmHg is relatively sensitive and specific for PH, it cannot provide the accurate mPAP for definitive diagnosis
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17
Q
Severity of PH classifications
A
- Once right heart cath is performed, the severity of PH determined:
- Mild PH (mPAP = 20–30 mmHg)
- Moderate PH (mPAP = 31–40 mmHg)
- Severe PH (mPAP >40 mmHg)
- normal pulmonary circulation can accommodate a fourfold increase in COP without a marked change in mPAP
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18
Q
- How many people does PH affect?
- Nearly 1:8 PAH pts have long term improvements with ___
A
- According to the World Health Organization, PAH is classified as a rare disease effecting 15 ppl per million per year
- Idiopathic PAH: no identifiable risk factor
- calcium channel blockers
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19
Q
- 3% of PAH cases are deemed _ , with mutations in __ __ _ receptor type 2 (BMPR2)
- The remaining cases are designated “__ __ ,” since they can be ascribed to manifestations of drugs, toxins, or other diseases
A
- 3% of PAH cases are deemed inheritable, with mutations in 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
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20
Q
- PAH was traditionally a disease of __ __, with median survival rate of 3 yrs, current data shows a demographic shift, now with __ __ and more ____ being diagnosed
- Despite improved diagnosis and therapy, 1-year mortality is ̴____%
A
- PAH was traditionally a disease of young women, with median survival rate of 3 yrs, current data shows a demographic shift, now with older pts and more men being diagnosed
- Despite improved diagnosis and therapy, 1-year mortality is ̴15%
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21
Q
Pulmonary Artery HTN
* development
* 3 main classifications of pulmonary vasodialator drugs
* What kind of therapy is often required?
A
- Development involves multiple events accumulating in addition to genetic predisposition
- Sustained vasoconstriction and remodeling lead to pathologic distortion of the small pulmonary arteries
- There are 3 main classes of pulmonary vasodilator drugs for PAH: Prostanoids, Endothelin receptor antagonists (ERAs), nitric oxide/guanylate cyclase pathways
- Combination therapy is often required for adequate tx of PAH
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22
Q
PAH treatment: Prostanoids and 4 agents
A
- 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
- epoprostenol (IV), iloprost (inhaled), treprostinil (SQ, IV, INH, PO), beraprost(PO)
All provide improvement, but only epoprostenol has been proven to reduce mortality
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23
Q
PAH Treatment: Endothilin receptor antagonists (ERA’s)
A
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
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24
Q
PAH treament: Nitric oxide/guanylate cyclase
A
- 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
- Continuously inhaled nitric oxide has been widely used in both perioperative and critical care settings, and preparations for home use have become available
- Chronic therapy has been directed toward PD-5 inhibitors
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25
PAH preop considerations
* what procedures do we need to pay attention to?
* Consideration should be given to procedures with potential for: **venous embolism, elevations in venous and/or airway pressure, hypoxic pulmonary vasoconstriction, reduction in pulmonary vascular volume, systemic inflammation, and emergency procedures**
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26
PAH preop considerations: S/S
* nonspecific sx of fatigue, dyspnea, and cough
* more advanced s/s: angina and syncope
* On physical exam: may exhibit a parasternal lift, accentuated S2, S3 and/or s4 gallop, JVD, peripheral edema, hepatomegaly, and ascites
* Rarely, compression of a dilated PA may lead to RLN damage and hoarseness
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27
PAH preop considerations:
* what would prompt futher eval?
* For moderate/severe PH, what is recommended prior moderate or high risk surgery?
* What should also be performed because PAWP and LVEDP have potential discrepancies?
* History of PH should prompt further evaluation of functional status, cardiac performance, and pulmonary function tests
* right heart cath prior to moderate-high risk surgery is recommended
* left heart cath should also be performed in pts with coexisting left heart dz because inaccurate LVEDP may lead to misclassification of PH and inappropriate treatment
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28
PAH preop considerations:
* ____testing with ____ is performed during right heart catheterization to determing responsiveness to vasodialator therapy
* ___-___% of PAH pts are unresponsive to inhaled nitric oxide, but those that are responsive to CCB's may benefit from other tageted therapy
* **Vasoreactivity** testing, often with inhaled nitric oxide, is performed during right heart catheterization to determine responsiveness to vasodilator therapy
* **85–90%** PAH pts are nonresponsive to inhaled nitric oxide, but those that are responsive also respond to CCBs and may benefit from other targeted therapy
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29
Look at this card for the heart cath algorithm
## Footnote
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30
Click this slide for a chart for risk factors for morbidity and mortaility in noncardiac surgery with PAH
## Footnote
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31
Perioperative physiology:
* primary intraop goal
* cautions with what interventions
* what added perioperative complexities can have serious consequences? (7 complexities)
* goal is maintaining optimal “mechanical coupling” btw the right ventricle and pulmonary circulation to promote adequate left-sided filling and systemic perfusion
* interventions that may affect RV preload, inotropy, afterload, and oxygen supply/demand relationships
* Serious Consequences with these complexities:
-transient HoTN
-mechanical ventilation
-modest hypercarbia
-small bubbles in IV
-T-burg position
-Pneumoperitoneum
-single-lung ventilation
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32
What is the hallmark of PAH? what does this lead to?
a hallmark of PAH is increased RV afterload, leading to RV dilation, increased wall stress, and RV hypertrophy
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33
* The interaction between the ____ and the ___ ___ is pulsatile and dynamic, involving the compliance and “stiffness” of large & small vessels
* This is relevant during __ __ that occur during surgeries which affect RV pulsatile load
* Ventilator management can have effects on _ _ through the addition of PEEP, hypoventilation, hypercarbia, acidosis, and atelectasis
* The interaction between the **RV** and the **pulmonary circulation** is pulsatile and dynamic, involving the compliance and “stiffness” of large & small vessels
* This is relevant during **acute insults** that occur during surgeries which affect RV pulsatile load
* Ventilator management can have effects on **RV afterload** through the addition of PEEP, hypoventilation, hypercarbia, acidosis, and atelectasis
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34
Myocardial supply and demand:
* What do we worry about with the heart when someone has PH?
* is the RV pressure higher or lower than aortic root pressure under normal circumstances?
* when does RV prefusion occur?
* The thinner-walled RV is subject to **greater wall tension** for the same degree of increase in end-diastolic volume, leading to increased RV myocardial oxygen demand
* RV intramyocardial pressure is lower than the aortic root pressure
* RV coronary perfusion occurs throughout the cardiac cycle
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35
* What does PAH cause in regards to RV pressure?
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
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36
What causes the "lethal combination" and what is the "lethal combination"
* The cause: systemic hypotention, RV ischemia, high afterload
* Lethal combination is: RV dialation, insufficient LV filling, reduced stroke volume, and further systemic hypotension
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37
Procedureal considerations with PAH or PH
* orthopedic considerations
* Laparoscopy considerations
* Orthopedics: studies show a substantial increase in perioperative morbidity and mortality in patients with PH undergoing hip and knee replacement
* Laparoscopy: 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
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38
Procedural considerations for thoracic surgery
* 3 featurs of lung collapse that are relevant
* Thoracic procedures involve nonventilation and atelectasis of the operative lung
* 3 features of lung collapse are particularly relevant:
(1) some centers pressurize the chest to induce atelectasis
(2) 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 vasodilator therapy
* inhaled pulmonary vasodilators are recommended during single-lung ventilation
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39
Key point to read through
* HTN is a significant risk factor for CV disease, stroke, and renal disease. Guidelines define a SBP goal of <130 mmHg, but a high percentage of pts remain poorly controlled
* Preop evaluation of a HTN patients should focus on the adequate BP control, treatment regimen, and the presence of end-organ damage
* **Hemodynamic instability is common during anesthesia and surgery in hypertensive pts**
* PH is defined as a mean PA pressure > 20 mmHg, and can result from a range of processes that directly constrict and remodel arteries, elevate pulmonary venous pressure, or chronically increase blood flow to initiate vascular remodeling
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40
Key points to read through
* PAH represents 1 of 5 PH groups defined by the WHO
* Patients with PAH exhibit endothelial dysfunction, maladaptive arterial remodeling, and in-situ thrombosis
* A right heart cath is required to provide a diagnosis of PAH and guide treatment
* Only a small percentage respond to CCBs
* **Most pulmonary vasodilator treatments consists of prostacyclin analogues, endothelin receptor antagonists, and drugs activating the nitric oxide/guanylate cyclase pathway**
* PAH is the only class of PH found to benefit from pulmonary vasodilators
* Although quality of life and survival have improved with vasodilators, the prognosis for PAH remains poor
* PAH patients on a vasodilators should have them continued intraoperatively and postoperatively, and converted from oral to IV or inhaled when necessary
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