HTN Flashcards
Definition of HTN
- BP > 140/90 on at least two occasions
- Reading should be measured at least 1-2 weeks apart
- Prehypertension: 120-130/80-89
- Stage 1 HTN: 140-159/90-99
- Stage 2 HN: ≥160/≥100
Two types of HTN
-
Essential - Unknown etiology (idiopathic)
- 95% of cases
- Strong genetic link (maybe related to inherited biochemical abnormalities)
- Possible Na+ imbalences
- Associated with drinking, smoking, and OSA
-
Secondary - Know etiology
- 5% of cases
- Renal problems is main cause
- Also due to endocrine, pregnancy, neurologic, drug induced, and OSA
Treatment for essential HTN
-
Lifestyle Modification
- Recommended for those without CV disease or end organ damage (Decrease Na intake, take in enough K and Ca exercise, lose weight, stop smokin and drinkin)
-
2nd line treatment: Drug therapy (with lifestyle mod)
- Stage I: diuretic - 1st line
- Stage II: dual therapy
- Stage III: continue adding
- Diabetic: ACE-I are 1st line drugs
Treatment of Secondary HTN
Treat the cause
-
Often times surgical
- pheochromocytoma- adrenalectomy
- renal artery stenosis/primary aldosteronism- angioplasty (HTN d/t activation of RASS because kidneys perceive decreased blood flow
- Drug therapy if not a candidate for surgery
Anesthesia considerations for patients on ß-blockers. Who should they be avoided in?
- Patients who are on them should be take them the morning of surgery to prevent rebound SNS stimulation
- Rebound SNS stimulation is d/t upregulation of receptors
-
AVOID in ß-blockers
- Asthmatics
- COPD
- CHF
- HB
- Sick Sinus Syndrome
Anesthesia considerations for patients on Methyldopa and Clonidine?
- A2 agonist used to treat HTN
- Can cause rebound HTN
- Will DECREASE anesthetic requirements
Anesthesia considerations for patients on Prazosin
- A1 blocker
-
Compensatory vasoconstriction is blocked
- there may be an exaggerated drop in BP during spinal/epidural block
Anesthesia considerations for patients on Hydralazine
- Causes potassium influx and hyperpolarization
- May cause angina in those with ischemic heart disease (not sure the mechanism of action)
Anesthesia considerations for patients on ACE inhibitors
- They are the ‘prils
- Associated with drop in BP and hemodynamic instability.
- tell patients to HOLD THE MORNING OF SURGERY (24-48 hours)
- If they take it they will have very labile blood pressures!!!
- may not respond to phenylephrine of ephedrine - use vasopressin
(BP regulated by three systems - GA knocks out the autonomic, ACE-I take out the RAAS and that leaves the vasopressin system left →they are very likely to be volume dependent (if they take their meds). Hypotension responsive to fluid and sympathomimethic drugs- if they are resistant ususally vasopressin or a vasopressin analough will do the trick!)
Anesthesia considerations for patients on Angiotensin II blockers
- ‘Artans
- Drop in BP with induction
(Patients who take ARBS may be refracitve to convetional vasoconstrictors like phenylephrine and ephedrine → may need to use vasopressin or vasopressin analogue)
Definition of hypertensive crisis
- Acute DBP > 130 mmHg
or
- parturient with a DBP> 109 mmHg
What can a hypertensive crisis cause?
- Encephalopathy
- SAH (Subarachnoid Hemorrhage)
- CHF
- Renal insufficiency
How is a hypertensive crisis treated?
- Goal is to lower BP promptly, but gradually.
- Monitor BP reduction with an a-line. and end organ profusion with a foley
- Decrease MAP by 20% during first 2 hours
- Then even more gradually reduce BP over the next 24-48 hours (160/110 - if no signs of end organ ischemia)
-
Pharmacologic interventions include
-
Sodium Nitroprusside (Nipride): 0.5-10.0 mcg/kg/min
- Immediaate onset and short DOA
- DRUG OF CHOICE
- Nicardipine (dihydropiridine CCB) - says Stoelting
- NTG: 5-200 mcg/min
- Labetolol: 40 - 80 mg q 20 min
- Esomolol: 50-300 mcg/kg/min
-
Sodium Nitroprusside (Nipride): 0.5-10.0 mcg/kg/min
The preoperative evaluation of a person with essential hyperteshion should elicit which things?
- The adequacy of BP controll
- Is it controlled or uncontrolled?
- a DBP of 110-115 should have surgery postponed
- What is their normal Blood Pressure
- What is their medication therapy?
- Do they have evidence of end-organ damage?
- Angina, CHF, LV hypertrophy
- Renal insufficiency
- CVA
- Peripehral Vascular Disease
- Is it controlled or uncontrolled?
Anesthetic management of INDUCTION for patients with HTN
- Minimize SNS stimulation on DVL and intubation (they often have exagerated HTN with this and tachycardia and HTN is a risk for ISCHEMIA)
-
What to do?
- Increasing volatile agent
- Give Esmolol prior to DVL: 10-20 mg
- additional opioids
-
Lidocaine
- IV: 1-1.5 mg/kg
- LTA: 5cc of 2-4%
- Efficient DVL: <15 sec
- NO KETAMINE!!!
Management of MAINTINENCE of anesthesia for patients with HTN
GOAL = to adjust anesthetic depth to minimize wide shifts in hemodynamics
(It is common for patients with HTN to have wide hemodynamic shifts)
- Chose a VA that is easily and quickly titrated
- Low BG coefficient→ des (0.42) or sevo (0.69) - low solubility
- +/- iso (1.4)
-
Rely on multiple agents! = better total coverage
- Use a balanced technique(N2O, opioids, versed)
- Have phenylephrine and ephedrine readily available -
- Consider neo gtt if unable to get adequate depth of anesthesia (i dont get this, but it is in the notes)
Post-op goals for pts with HTN
Minimize SNS stimulation from pain and N/V
opioids, anti-nausea
What are the blood gas coeficients of the volitile agents?
- Nitrous Oxide: 0.47
- Desflurane: 0.42
- Sevoflurane: 0.69
- Isoflurane: 1.4
- Enflurane: 1.8
- Halothane: 2.3
Treatment of intraoperative HYPERtension
- It’s usually due to pain!! →Opioids (if d/t pain)
- Increase volitile anesthetics →will decrease SVR
- ß-Blockers
- NTG and SNP (Nipride) →hang a drip for a longer case or need sustained controll
Treatment of intraoperative HYPOtension
- Reduce anesthetic depth →often caused by being too deep
- Fluids
- Sympathomimetics (neosinephrine and ephedrine)
- Is their rhythm normal? →They may be in a Junctional
- Ephedrine is a good choice →will bring up HR
- Maintain Normocapnea→ HTN in patients with hypercarbia →increases heartrate and BP
- If the rhythm is not normal → AVOID high concentrations of IAs
Bonus ****
What is premissive hypercapnea?
Allowing the PaCO2 to increase up to 55mmHg spontaneously breathing patients to avoid or delay the need for endotracheal intubation
Monitoring used for those with HTN
- 5 Lead EKG
- If the patient has ventricular dysfunction and is having extensive surgery
- →then get a-line, CVP, and/or PA cath
- may want to use a TEE in extreme cases
Anesthesia management of emergence in a patient with HTN
Goal = Nice smooth controlled emergence → these patients will have exagerated responses → if they had labile pressures durring the surgery they will likely have labile pressures at emergence
-
Minimize SNS outflow! When the gasses start to come off the patient will begin to become hypertensive → be ready to treat or pre-treat as anticipated
- Opioids
- Lidocaine
- ß-blockers (esmolol, labetolol)
- NTG
- Deep extubation (if not a difficult airway) →avoids the SNS stimulation of being awake with the ETT
Treatment of potoperative HTN
- If pain is adequately controlled→prompt treament is necessitated to decrease the risk of myocardial ischemia, stroke, dysrhythmias and CHF
- Treat with:
- Labetalol: 5-20 mg IV Q 10 min (ß1 and ß2)
- Hydralazine: 2.5-10 mg IV Q 10-20 min (arterial > venous)
- Sodium Nitroprusside: 0.5-10 mcg/kg/min if an a-line is present
How to treat a intraop junctional rhythm
- decrease anesthetic depth
- maintain normocapnea
(junctional rhythm in a healthy patient is directly realted to anesthetic depth)
Pulmonary arterial HTN
- PAP (mean pulmonary artery pressure) > 25 mm Hg at rest or
- PAP (mean pulmonary artery pressure) > 30 mm Hg with exercise
&
- PAOP (pulmonary artery occlusion pressure) =< of 15 mm Hg or less
- PVR (pulmonary vascular resistance) > 3 Wood units (mm Hg/L/min) - normal 0.2-1.6 woods or 20-130 dyn
Pulm artery HTN treatment
- Oxygen, Anticoagulation, and Diuretics
- Calcium Channel Blockers
- Nifedipine, diltiazem, and amlodipine
- Phosphodiesterase inhibitors
- dilate pulmonary blood vessels and improve cardiac output
- Nitric oxide (NO)
- improves V˙ /Q˙ matching and improves oxygenation by relaxing pulmonary vascular smooth muscle
- Prostacyclins
- epoprostenol, treprostinil, iloprost
- are systemic and pulmonary vasodilators that also have antiplatelet activity.
- Endothelin Receptor Antagonists
- Bosentan
Pulm artery HTN anesthtetic
- Hypoxia, hypercarbia, and acidosis must be aggressively controlled
- they cause increased PVR
- avoid ketamine & etomidate
- may inhibit pulmonary vasorelaxation
- monitor CVP and intra-arterial BP
- maintenance with IA
- Systemic hypotension can be corrected with fluids, phenylephrine, or more potent vasoconstrictors if needed