1
Q
Idiopathic HTN
A
- overactivity of the ANS and an interaction with RASS and factors related to Na homeostasis and intravascular volume
2
Q
causes of perioperative HTN
A
- hypercarbia
- hypoxia
- aortic cross clamp
- hypervolemia
- hypothermia
- pain
- airway manipulation
3
Q
primary cause of peri-op HTN
A
- increased sympathetic discharge with sympathetic vasoconstriction
4
Q
prevalence of peri-op HTN
A
~ 80% of cardiac surgery patients
~ 25% of non-cardiac surgery patients
- does not have to be a diagnosis of HTN
5
Q
vasodilators MOA
A
- direct smooth muscle dilation (production of smooth muscle NO)
6
Q
types of vasodilators
A
- alpha 1 antagonists (prazosin and labetalol)
- alpha 2 agonists (clonidine, alpha methyldopa)
- ACE inhibitors (captopril, enalapril)
7
Q
how vasodilators are classified according to their predominate site of action
A
- arterial dilators
- venodilators
- balanced vasodilators
8
Q
hemodynamic effects of vasodilators
A
- pure arteriole dilators cause minimal effects of preload
- pure venodilators do not exist
- balanced vasodilators decrease afterload and preload
9
Q
reflex response to vasodilators
A
- reflex increase in HR (baroreceptors)
- redistribution of coronary blood flow (may improve or cause coronary steal)
10
Q
coronary steal
A
- narrowed coronaries are already max dilated. Dilating other arteries may cause blood to be shunted away from the coronary vessels
11
Q
SNP effect on coronary steal
A
- dilates both epicardial conductance and intramyocardial resistance vessels and in the presence of CAD, shunts blood away from the ischemic zone
12
Q
NGT and coronary steal
A
- preferentially dilates conductance vessels and directs more blood toward ischemic zones
13
Q
hydralazine effects and reflex response
A
- direct acting arterial vasodilator (alters Ca movement and metabolism)
- has its own receptor
- decreases BP (diastolic > systolic) and SVR
- reflex = (increase HR, contractility, renin activity, fluid retention, CO, SV)
14
Q
who to avoid hydralazine in
A
- avoid with CAD, increased ICP, lupus
- increases myocardial O2 demand leading to ischemia (from reflex tachycardia)
15
Q
side effects of hydralazine
A
- 5-10% of patients on hydralazine will have a positive ANA (lupus) titer (butterfly rash, joint pain)
- headache, dizziness, tremor, angina, tachycardia, flushing, palpitations, anorexia, agranulocytosis congestion, muscle cramps, edema
16
Q
pharmacokinetics of hydralazine
A
- metabolized in the liver
- excreted in kidney
- highly protein bound
- onset 30 min
17
Q
how nitroglycerine works and what it does to the body
A
- causes a release of nitric oxide for non-specific relaxation of the vascular smooth muscle
- dilates veins > arteries
- decreases PVR, venous return, myocardial O2 consumption
- relaxes coronary vessels and relieves spasms
18
Q
nitroglycerin non-cardiac effects
A
- dilates meningeal vessels (caution with ICP) (causes headaches)
- decreases renal blood flow with decreased BP
- dilates pulmonary vessels
19
Q
pharmacokinetics of nitroglycerine
A
- onset 1 min
- duration 3-5 min
20
Q
nitroglycerine metabolism
A
- metabolized by glutathione nitrate reductase in the liver
- nitrite ion oxidizes Hgb to methemoglobin
- arterial vessels can build tolerance but not venous vessels
21
Q
nitroglycerin warnings/ contraindications
A
- PDE 5 inhibitors (Viagra, Cialis) (usually end in “fil”)
- narrow angle glaucoma
- head trauma / cerebral hemorrhage
- severe anemia
- hypotension
22
Q
advantages of nitroglycerine
A
- rapid onset
- coronary vasodilator
- dec myocardial O2 consumption
- no toxicities
- no coronary steal
- reduced PVR
23
Q
disadvantages of nitroglycerin
A
- decreased diastolic BP
- reflex tachycardia
- possible hypotension
- tachyphylaxis
- methemoglobinemia
- intrapulmonary shunting
- prolonged bleeding time
24
Q
sodium nitroprusside actions and effects on the body
A
- directly vasodilates arteries and veins
- decease BP and HR
- inc cerebral blood flow and ICP
- renal blood flow maintains
- overall reduction in myocardial O2 demand
- with abrupt discontinuation = reflex tachycardia and hypertension
25
warnings / contraindications w/ sodium nitroprusside
- congenital optic atrophy
- hypovolemia
- compensatory HTN (AV shunting, aortic coarctation)
- increased ICP
- severe renal/ hepatic impairment
26
presentation of cyanide toxicity w/ sodium nitroprusside
- hypotension, blurred vision, fatigue
- metabolic acidosis
- pink skin
- absence of reflexes
- faint heart sounds
27
toxic thiocyanide and cyanide levels
- thiocyanate (toxic >30)
- cyanide (toxic >2) (normal 0.2 smoker 0.4)
28
treatment of cyanide toxicity
- 100% O2
- correct acidosis
- 3% Na nitrate 4-6 mg/kg slow
- sodium thiosulfate
- hydroxocobalamin
29
phenoxybenzamine (dibenzyline) binding and uses
- nonselective alpha antagonist
- irreversibly binds to receptor (must wait for new receptors to be made)
- long-term preop control of pheochromocytoma
- relieve ischemia in PVD
- BPH to improve flow
30
phenoxybenzamine (dibenzyline) effects on body
- reduced PVR to reduce BP
- secondary increases in NE due to alpha 2 blockade can increase HR and CO
- crosses the BBB
31
oral alpha 1 antagonists
- prazosin
- terazosin
- doxazosin
- tamsulosin
- silodosin
- alfuzosin
32
clonidine receptor and effects
- central acting alpha 2 agonist
- decreases release of sympathetic neurotransmitters
- inhibits renin
33
clonidine actions
- decrease HR, BP, CO, SVR
- abrupt cessation may lead to rebound HTN
34
clonidine withdraw
- from sudden discontinuation, due to NE
- manifests with sudden HTN, tachycardia, restlessness, insomnia, headache, nausea
- at risk after 6 days of use
35
caution with clonidine
- severe coronary insufficiency, conduction disturbances, recent MI/CVA, CKD
36
clonidine and anesthesia
- reduced propofol and thiopental requirements
- alternative to N2O for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia
37
methyldopa (aldomet)
- acts as a false neurotransmitter in the periphery (alpha-methyl-NE is almost as potent as NE)
- in the CNS its metabolized to alpha-methylepinephrine (acts at alpha-2 to decrease sympathetic outflow)
- treats HTN during pregnancy
38
why hyperkalemia from ACE inhibitors
- prevents angiotensin II from causing K+ excretion
39
RASS pathway
- angiotensinogen from the liver forms with renin from the kidney to make angiotensin 1 which forms with ACE from the lungs to make angiotensin II
40
ACE inhibitors primary function and use
- predominantly arterial vasodilators
- treat CHF and MR by afterload reduction
- used post MI
- improves outcomes in DM
41
renal function and ACE inhibitors
- with HTN: decreased renal vascular resistance improves RBF and GFR
- with hypotension: if BP is decreased renal function may deteriorate b/c compensatory constriction is blocked
- avoid in pts with significant renal dysfunction or renal artery stenosis
42
side effects of ACE inhibitors
- cough, congestion, rhinorrhea
- angioedema from increased bradykinin
- do not use in pregnancy
43
peri-op issues with ACE inhibitors
- prolonged hypotension can occur
- risk of ARF
44
ACE inhibitor med interactions
- increased hypotensive effects with diuretics, vasodilators and anesthetics
- NSAIDs and ASA interaction: reduce antihypertensive effect, increased risk of hyperK and ARF
45
primary action of CCB
- negative inotropic effect
- negative dromotropic effect (AV conduction block)
- vasodilation of systemic, splanchnic, coronary and pulmonary beds
46
dihydropyridines
- nifedipine
- nicardipine
- amlodipine
- pure arterial dilators, minimal reflex tachycardia
- minimal negative inotropic and dromotropic effects
47
nicardipine
- potent vasodilator of systemic, coronary, and cerebral circulations
- arteriole specific vasodilator
- no coronary steal, favorable myocardial O2 supply/ demand
- onset < 5 min
48
clevidipine
- IV CCB (dihydropyridine)
- vasodilation reduces PVR, arteriole specific
- onset <5min, half life 1 min
- reduces gastric emptying
49
verapamil
- phenylalkylamine
- potent negative inotrope, dromotrope, and vasodilator
- for aortic stenosis, conversion of atrial re-entry tacyarrhythmias, coronary artery vasospasms
50
diltiazem
- benzothiazine
- used for rate control in a-fib and atrial tach
- moderate CYP3A4 inhibitor, weak CYP2D6 inhibitor, weak P-gp inhibitor (tons of drug interactions)
51
verapamil and diltiazem effect on myocardial O2 balance
- enhance myocardial O2 balance (decrease myocardial O2 consumption by afterload reduction and or negative inotrope effect and increased o2 delivery through coronary vasodilation
52
dihydropyridine vasodilators effect on myocardial O2 balance
- may worsen MvO2 by causing diastolic hypotension and reflex tachycardia (except nicardipine)
- decrease reperfusion injury after ischemia
53
CCB effect on renal perfusion
- increase RBF and GFR and induce naturesis
- benefits reversed in they induce hypotension
- reflex catecholamine release and angiotensin activation lead to decreased RBF and GFR
54
recommendations with CCB
- continue up to surgery without risk of significant drug interactions
- may potentiate NMB
- primarily block L type Ca channels in CV system (causing NDNMB to bind to P-type channels that effect Ach release)
55
BB actions
- decrease CO (HR and contractility)
- decrease renin release
- do not vasodilate
56
BB advantages over vasodilators
- no reflex tachycardia or widening pulse pressure
- improve MvO2
- antiarrhythmic activity
57
beta 1 selective BB
- metoprolol
- atenolol
- acebutolol
- bisoprolol
- esmolol
- decrease velocity of A-V conduction, HR, contractility, renin release, lipolysis
58
non-selective BB
- propranolol
- nadolol
- timolol
- pindolol
- carteolol
- block beta 1 and beta 2 (bronchoconstriction, peripheral vasoconstriction)
59
combined alpha 1 and non selective beta
- carvedilol
- labetalol
60
short acting BB elimination
- red cell esterases (esmolol)
61
adverse effects of BB
- non-selective blockade of beta 2 = vasoconstriction and worsening PVD, bronchospasm
- myocardial depression
- life threatening bradycardia asystole
- hyperkalemia in renal failure
62
BB contraindications and cautions
- bradycardia, heart block
- cardiogenic shock
- raynauds disease
- caution with asthma, COPD, diabetes, HF
63
propranolol
- non-selective BB
- lipid soluble (can penetrate CNS)
- undergoes 1st pass (70%)
64
esmolol
- beta 1 selective
- blunts cardiovascular response to intubation
- control SVT a-fib
- rapid onset and off
- red cell esterase metabolism
65
metoprolol
- beta 1 selective
- approved for treatment of angina and acute MI
- antihypertensive
- longer DOA
66
Labetalol
- combines a weak alpha blockade with weak non-selective beta blockade
- negative inotrope and chronotrope with vasodilation, providing antihypertensive action
- for aortic dissection
- treatment of tachyphylaxis with SNP
- intercranial HTN (does not increase ICP)
67
adverse effects of labetalol
- unwanted negative inotropy
- prolonged DOA with higher dose
- bronchospasm in high doses
- hyperkalemia in renal failure
- caution in hypothermic pt ( may exacerbate rewarming hypotension)
68
BB warnings
- negative inotropic effects and conduction delays are potentiated by general anesthetics
- rebound HTN and tachycardia with abrupt cessation
- mask hypoglycemia and hyperthyroidism
- anticholinesterases may increase bradycardia
69
treatment of BB overdose
- glucagon
- atropine
- beta 1 agonists
- high dose insulin
- IV lipids
- ca and bicarb
70
antihypertensives and pregnancy
- alpha-methyldopa is favored
- labetalol can be used in 2nd and 3rd trimester
- hydralazine during delivery
- nifedipine PO
