Test 2 content Flashcards
1
Q
Negative effects of angiotensin on kidneys
A
Increased glomerular pressure and fibrosis
Protein leak
Increased Na reabsorption
2
Q
-ACE-I use benefits HF patients, prevents the following so failing heart doesn’t haven’t to work hard:
A
- angiotensin increased in HF since low CO
- baroreceptors send signals to kidneys or blood vessels to increase blood volume/flow
- preload increases
- NE released
- endothelin-modifies blood vessels to constrict
3
Q
Negative effects of angiotensin on heart, primarily what side?
A
LV
4
Q
Esmolol MOA and Dosing
A
MOA: Agent is cardioselective B-adrenergic blocker
Dose: 500mcg/kg over 1min then 50mcg/kg/min with max 300mcg/kg/min (titrate every 5 min)
Esmolol has very short duration of action which is commonly desired in ICU
Lack of intrinsic sympathomimetic and membrane-stabilizing activity
KEY: If desired effect not observed bolus administration repeated before infusion rate is increased
5
Q
Esmolol vs Labetalol Effect on Myocardial oxygen
A
Increased
6
Q
Esmolol vs Labetalol onset of drugs?
A
Rapid
7
Q
Labetalol has about____ the active B effects as propranolol
A
1/5
8
Q
Esmolol vs Labetalol Duration of Effect HR
A
Esmolol: Rapid
Labetalol: Slower
9
Q
PANS is _____activity.
A
Cholinergic
10
Q
Beta-blocker comparision esmolol vs labetalol
A
Onset-Rapid for both
Duration of effect HR-
Esmolol (Rapid) Labetalol (slower)
11
Q
a-adrenergic blockers
A
Vasodilator activity on the peripheral vasculature
Side effects -
o-Orthostatic hypotension (hypotension (blood pressure drop from sitting to standing is too much for patient’s body to compensate for and pt can have syncope)
o- Reflex tachycardia - compensate for severe drop in B- this drop can be sensed by brain and drive sympathetic response
12
Q
Spironolactone is specifically an _____ ______ and is the ______ ______ ______.
A
aldosterone antagonist
Most common one
13
Q
SANS is ______ with alpha, B receptors
A
Adrengeric (EPI NE)
14
Q
HTN is high ____. This causes ____ in the vasculature. The goal is to _____ the vasculature.
A
BP
constriction
dilate
15
Q
Beta blockers can be helpful because they can decrease
A
Renin
16
Q
Esmolol Absorption, Metabolism, and Excretion:
A
- Onset of action is seconds and duration of action up to 10-20 min after cessation
- Metabolism occurs in erythrocytes by esterases and has metabolite (1/500 activity) eliminated in urine
- Do not need to adjust in hepatic or renal failure
- Useful in patients with acute myocardial infarction
17
Q
Central factors in HTN? 4 physiologic causes of HTN?
A
1) adrenergic drive = Increased HR & CO
2) High aldosterone - Increased Na+ and Ca2+ -> increased SVR
3) Low renin: Increased Na+ and Ca2+ -> increased SVR
4) High renin -> increased AII -> increased SVR
18
Q
Postoperative HTN Requires rapid control of BP (3 things)
A
Control bleeding at suture sites
Neurology checks (patient used to x BP, now receiving y)
Myocardial ischemia develops due to increased oxygen needs
19
Q
Low BP → ↓ PANS → ↑ HR ↑ SANS → ↑ CO ↑ SVR goal or end result?
A
Increase BP
20
Q
Hydralazine on HTN
A
- Initially slower onset of 5-15min then precipitous fall in BP lasting up to 12 hours
- Circulating half-life is about 3 hours, however effect on BP can last up to 100 hours
- Agent has unpredictable effects on BP and is difficult to titrate
21
Q
Labetalol Absorption, Metabolism, Excretion
A
- Onset of action is 5-15min and lasts up to 2-12 hours after cessation
- Extensive first pass metabolism therefore oral form is only about 20-40% bioavailable
- Minute amount of unchanged drug excreted in urine
- Bolus doses of 1-2mg/kg have produced precipitous drops in BP
22
Q
Esmolol vs Labetalol Effect on SVR
A
Esmolol: None
Labetalol: decreased SVR
23
Q
Labetalol MOA & Dosing
A
MOA: Agent is a selective alpha and non-selective B-adrenergic receptor blocker with a to B ratio of 1:7
Dose: 20mg bolus then 1-2mg/min with max 5mg/min
a-Receptor blocking is responsible for vasodilation of arterial smooth muscle and B-blocking effects the smooth muscle as well as sympathetic stimulation
24
Q
5 classes of treatment for HTN.
A
vasodilators:
- Calcium Channel Blockers
- Nitrovasodilators
- Dopamine agonists
- ACE inhibitors
Affect CO
- Beta-Blockers (especially selective ones)
25
barorecptors sense changes in pressure and flow to _____. Baroreceptors also sense ____ rises and drops (ex: due to dehydration)- baroreceptors can also cause signal to
brain
acute
increase blood volume
26
Catecholamines can increase HR and cause .
Vasoconstriction
27
BP Tracing- Pulse Pressure
(SBP-DBP)
- HR
- BP
28
ACE inhibitors and AT-1 blockers cause ____ in SVR by?
decrease
reducing Angiotensin II
29
Etiology of HTN perioperative
Vasoconstriction (catacholamines/baroreceptor) combined with intravascular hypovolemia
30
Angiotensin inhibition for HTN 3 ways to inhibit angiotension:
ACEi
ARB
Parasympathetic stimulation
31
Postoperative HTN Generally lasts about _____ Higher association with _____
2 to 6 hours
ICU admissions and mortality
32
Nicardipine Absorption, Metabolism, and Excretion:
- Onset of action is with 1-5 min and duration of action is 2-6 hours after cessation
- Agent is about >95% bound
- Metabolism occurs through CYP 3A4 system substrate therefore monitor for potential drug interactions
- Cardiac sparing effect, therefore no contractility suppression
33
Rapid changes in peripheral circulation (ie high or low) are addressed via
signal transmission to CNS
34
Baroreceptors provide the CNS with information regarding BP changes. Most common place is
Carotid arteries
35
High BP → ↑PANS → ↓ HR ↓ SANS → ↓ CO ↓ SVR goal or end result?
decrease BP
36
Low blood volume- sends message to kidney to
cause water retention through ADH (but the kidney mechanisms take longer than that of catecholamines)
37
Nitroglycerin on HTN
- Only effective at higher doses
- Concern for hypotension and tachycardia
- Compromised cerebral and renal perfusion due to preload and caridac output
- Difficult agent to titrate (often given as bolus instead of continuously)
- vasodilator
- Useful in ACS
38
objectives of Anti-HTN
▪ Overview of therapeutic targets for HTN management
▪ Describe the CV benefits of HTN control
▪ Describe the mechanism of action of each drug class for the management of HTN
▪ Describe the mechanism of action of intravenous therapies used to manage acute HTN
39
Indications of ACE-I therapy:
HTN -Lower BP
HF - Management of hypertrophy
Post-MI - Prevent additional hypertrophy
DM - Prevention of nephropathy (serum creatinine reflects kidney function, which declines -protein leaks into urine)
40
Aldosterone normally causes _____
sodium retention
-drugs will prevent that by maintaining sodium within tubule which water follows leading to decreased tension/volume overload
41
Aldosterone has what physiological effects?
- Increases Na retention -> Water retention
- Increased vascular hypertrophy
- Ability to mediate cardiac injury
- Decreases release of NE
- Monitor serum K for patients on aldosterone antagonist therapy*****
42
Class 3: Amiodarone Toxicity effects
Pulmonary fibrosis
Photodermatitis:
Corneal microdeposits:
Hepatic: necrosis and failure (IV and oral)
Thyroid dysfunction (hyperthyroidism/ hypothyroidism )
43
Esmolol vs Labetalol Duration of Effect HR
Esmolol: Rapid
Labetalol: Slower
44
Anti-Arrythmia objectives
▪ Overview of the classifications for antiarrhythmic agents
Describe the mechanism of action of each drug class for the management of arrhythmias
Describe the unique side effects from Amiodarone therapy
Describe the goals of therapy for antiarrhythmics
45
Therapeutic targets for HTN
- Aldo blockers
- Diuretics
- Catecholamine inhibitors
- vasodilators
- ARBs
- ACE-i
46
What are the two classes for rate control? Rhythm control?
Rate: Classes 2 and 4 (BBs and CCBs)
Rhythm: Classes 1 and 3 (Na channel blockers and Potassium channel blockers)
47
Low BP → ↓ PANS → ↑ HR ↑ SANS → ↑ CO ↑ SVR goal or end result?
increase BP
48
which non-DHP is more cardioselective for AA:
diltiazem Not as cardioselective as verapamil
49
MOAs of Beta Blocker AAs
Prevents activation of ß receptors
Decrease the phase 4 slope of pacemaker
↓SA node activation and AV node conduction
By blocking beta receptors, it can decrease the slope of the face takes more time to reach to potential
50
Perioperative HTN: Systolic BP (SBP) is what?
SBP 20% >perioperative reading >15min, or increase of >50% original value
Incidence is almost 50% depending on the surgery
51
abnormal systole and diastole
blood pools and goes to brain and clots
52
AA Suppression of IKr drugs? what class? These drugs can be ____-arrythmia
class 3
can be pro-arrythmia
Ibutilide -However a higher rate of conversion for atrial fibrillation or flutter
Sotalol -QT interval increases of 25-80 msec, dosage dependent
Dofetilide -Initiation of therapy via pharmaceutical monitored program
53
Acute AP drop: send message to ANS and causes
endogenous catecholamine production and release (EPI and NE) and in the kidneys
54
Clinical benefits of HTN management
- Decreased pressure on the aortic arch
- Improvements in patients with Sleep Apnea
- Reduced incidence of Stroke
-Improved kidney function
Longevity (High blood pressure is detrimental to kidney function)
55
What are the 2 most common segments of the EKG?
ST segment
| QT interval
56
Rapid changes in peripheral circulation (ie high or low) are addressed via
signal transmission to CNS
57
Esmolol vs Labetalol Effect on SVR
Esmolol: None
Labetalol: decreased SVR
58
Toxicities of lidocaine?
Hypotension when given in large doses (reduced contractility)
Neurologic (tremor, Nausea, slurred speech, and seizures)
Higher incidence in patients with plasma concentrations greater than 9 mcg/ml
59
Labetalol MOA & Dosing
MOA: Agent is a selective alpha and non-selective B-adrenergic receptor blocker with a to B ratio of 1:7
Dose: 20mg bolus then 1-2mg/min with max 5mg/min
a-Receptor blocking is responsible for vasodilation of arterial smooth muscle and B-blocking effects the smooth muscle as well as sympathetic stimulation
60
Amiodarone Complex t1/2?
short term 3-10 days and chronic of several weeks to months
61
Esmolol MOA and Dosing
MOA: Agent is cardioselective B-adrenergic blocker
Dose: 500mcg/kg over 1min then 50mcg/kg/min with max 300mcg/kg/min (titrate every 5 min)
Esmolol has very short duration of action which is commonly desired in ICU
Lack of intrinsic sympathomimetic and membrane-stabilizing activity
KEY: If desired effect not observed bolus administration repeated before infusion rate is increased
62
Rate control AA Classes?
2 and 4 (BBs and CCBs)
63
Vaughan Williams Classification of AAs
Class I: Na channel blockers
Class 2: Beta blockers - excluding sotalol that also has class III effects
Class 3: blockade of IKr (Potassium Channel Blocking)
Class 4: CCB
64
what kind of treatment do HF patients get for Anti-Arrythmia?
ICD, can shut off
65
Adenosine Therapeutic use and dosing
Conversion of PSVT or diagnostic for EKG
Dose: 6 mg IVP followed by rapid saline flush - T1/2 in bloodstream is approx 10 sec
Can administer a second dose of 12 mg if needed
66
provides the driving force for organ perfusion & depends on ____ and ____
Art Pressure (AP)
CO and SVR
67
Lidocaine is what class AA? When do you use it?
Treatment of ventricular tachycardia & fibrillation when amiodarone is unavailable
Prevention of VF after cardioversion in Acute M
I
Prophylactic use for the prevention of VF after acute MI is NOT recommended → increased mortality
68
Class 3: Amiodarone is given for how long to a patient?
For life
69
Esmolol vs Labetalol onset of drugs?
Rapid
70
Class 4 CCB Therapeutic use:
Acute and chronic Paroxysmal Supraventricular Tachycardia (PSVT)
Rate control for atrial fibrillation
71
Esmolol vs Labetalol Effect on Myocardial oxygen
Increased
72
Adenosine is ___ effective in presence of theophylline and caffeine
less effective
73
Perioperative HTN: Systolic BP (SBP) is what?
SBP 20% >perioperative reading >15min, or increase of >50% original value
Incidence is almost 50% depending on the surgery
74
Class 4: Ca2+ Channel Blockers MOA
Block slow cardiac Ca-channels
↓ phase 0, ↓ phase IV of (automaticity phase) nodal tissues and enhances ERP
Suppress Ca dependent tissues activation or depolarization - ↓ SA activity & ↓ AV conduction (enhance ERP, more effect)
75
Class 3: Amiodarone Toxicity effects
Pulmonary fibrosis (in 45% of patients) (most important & fatal): inflammatory response to Iodine, regular x-ray monitoring required. Dose realted
Photodermatitis: Blue/Grey skin pigmentation “smurf skin”
Corneal microdeposits: optic neuritis (blindness)
Hepatic: necrosis and failure (IV and oral)
Thyroid dysfunction (hyperthyroidism/ hypothyroidism ), monitor thyroid function tests prior/during treatment (prevents conversion of T4 → T3)
76
Catecholamines can increase HR and cause
Vasoconstriction
77
Perioperative, Antihypertensive treatment reduces how are the drugs given?
myocardial ischemia,
neurological deficits
mortality
IV push or infusion
78
BP Tracing- Pulse Pressure
(SBP-DBP)
- HR
- BP
79
AA Classes 1 and 3
(Na channel blockers and Potassium channel blockers)
80
Lidocaine is metabolized where? How many metabolites?
Liver
| 2
81
Class 3: Ibutilide MOA
Slows repolarization via blockade of rapid component of potassium current (IKr)
82
Protein in urine: microalbuminurea is a consequence:
of poor BP management for a long period of time.
83
High sodium intake: retention of water and increased ____ _____ which will keep______
blood volume which will keep blood pressure high. This is why low sodium intake is important in HTN
84
What are the common clinical etiologies of Arrythmias?
- Ischemia
- Hypoxia
- Excessive catecholamine exposure - Infusion of EPI, NE, or DA
- Drug toxicity - ie digoxin
- Overstretch of cardiac fibers - ie HF
- Presence of scarred tissue
85
Arythmiasare an abnormality in the site of origin of the
impulse,
rate or regularity,
or its conduction
86
Are AA Class 2 BBs selective or nonselective and for which receptors?
Selective B1 receptor
87
5 classes of treatment for HTN.
vasodilators:
- Calcium Channel Blockers
- Nitrovasodilators
- Dopamine agonists
- ACE inhibitors
Affect CO
- Beta-Blockers (especially selective ones)
88
Digoxin MOA? involves both ____ and ____? lower dose involves? higher dose involves?
sensitization of baroreceptors, central vagal stimulation, and facilitation of muscarinic activity
Increased DADs and PVCs
-Involve both the SANS and PANS
Lower dose range: PANS predominate
Higher dose range: SANS predominate
89
Adenosine MOA
Purine base adenine attached to ribose sugar (nucleoside)
Activate adenosine receptor in nodal tissues
Activate Gi protein - decrease in cAMP
Activation of K+ channels/current (inward rectifier) and suppression of Ca2+ current
Hyperpolarization and suppression Ca dependent action potentials
Suppress AV nodal conduction & increase the refractory period
Lesser effects on SA Node
90
Acute AP drop: send message to ANS and causes
endogenous catecholamine production and release (EPI and NE) and in the kidneys
91
Class 3: Amiodarone Toxicities caused by?
Iodine
92
provides the driving force for organ perfusion & depends on ____ and ____
Art Pressure (AP)
CO and SVR
93
Repolarization time is aka?
relaxation
94
Digoxin dosing and admin
Administration both IV and oral tablets
Dose: 500 mcg IV x1 dose, then 250 mcg x2 doses total 1 mg
Monitor: level next day and at steady state (approx 5 days)
95
what are cardiac depolarizations aka?
contractions
96
Diuretics : decrease ____-> decrease ____
BV -> BP
97
Adenosine has ____ effect in the presence of dipyridamole? Should give ____ dose if given via central line
increased
reduced. start at 3mg
98
Class 3: K channel blockers MOA
Block K-channels (↓IK delayed rectifier current) slowing phase 3 (repolarization) of AP
↑APD and ERP
Lower incidence of prolonged QT-prolongation and torsades de pointes
99
Therapeutic targets for HTN
- Aldo blockers
- Diuretics
- Catecholamine inhibitors
- vasodilators
- ARBs
- ACE-i
100
Cardiac effects of Lidocaine?
Uses – always administered by IV infusion (since low F)
Blockade of activated and inactivated Na channels
Effects on cells with longer potentials (ie ventricles) in comparison to atria
101
ACE inhibitors and AT-1 blockers cause ____ in SVR by?
decrease
reducing Angiotensin II
102
Goals of Therapy
Rate control
Rhythm control - both it and rate have Pharmacologic and Electrical
Stroke Prevention - anticoagulation
Prevention of Sudden Cardiac Death - ICD
103
Chronically, HTP causes thickening of
LVH- this will compromise EF.
104
Arrythmias consist of cardiac depolarizations that _____ ____ ____ the prior mentioned pathways for conduction
Do not follow
105
Low blood volume- sends message to kidney to
cause water retention through ADH (but the kidney mechanisms take longer than that of catecholamines)
106
after the atram signal travels via _____ system and ____
His-Purkinje system
ventricles.
Generally in synchrony, therefore hemodynamically effective
107
Pharmacologic Management for (Anti hypertensives)
- Sodium Nitroprusside
- Esmolol
- Labetalol
- Fenoldopam
- Nicardipine
- Misc(nifedipine, NTG, and hydralazine)
108
What's the least pro-arrythmia drug?
Amioderone
109
_____ mechanisms regulate CV function are under control of receptors in the arteries and veins (ie baroreceptors)
Neural and hormonal (neurohormonal)
110
Electrolytes are affected by AA in what ways?
2 most common are
Hypokalemia - Serum K less than 4 mEq/L can intensify IKr drug block
Hypocalcemia-Severe levels measured via ionized Ca
Hypomagnesemia- Serum Mg level less than 2 mg/dl
Intracellular depletion with diuretic therapy- Slow Vd during replacement phase
Repletion of electrolytes will shorten QT interval
111
Chronically, HTP causes thickening of
LVH- this will compromise EF.
112
Inhibitors of renal cation exchange can prolong effect (ie cimetidine, HCTZ, etc) of what drug?
Class 3: Dofetilide
113
Rhythm control AA classes?
Classes 1 and 3 (Na channel blockers and Potassium channel blockers)
114
Nicardipine MOA & Dose
MOA: Agent is 2nd generation dihydropyridine CCB which is particularly selective for cerebral and coronary vessels
Dose: 5mg/hr titrate to max of 15mg/hr every
5 min by 2.5mg and bolus dosing is NOT FDA approved
Primary mechanism of action on the L-type calcium channels
PO and IV formulation available, since 100 times more hydrophilic than nifedipine
115
Antiarrhythmic Class 1c agents
Flecanide
| Propafenone
116
Postoperative HTN Generally lasts about _____ Higher association with _____
2 to 6 hours
ICU admissions and mortality
117
catheter ablation is not the 1st treatment. why? when can it be a first treatment?
arrythmia isnt localized to one specific area.
Can be first when flutter because Arrythmia is localized
118
Central factors in HTN? 4 physiologic causes of HTN?
stress
1) adrenergic drive = Increased HR & CO
2) High aldosterone - Increased Na+ and Ca2+ -> increased SVR
3) Low renin: Increased Na+ and Ca2+ -> increased SVR
4) High renin -> increased AII -> increased SVR
119
Etiology of HTN perioperative
Vasoconstriction (catacholamines/baroreceptor) combined with intravascular hypovolemia
120
AntiArrythmia Beta BLocker Therapeutic uses:
Prophylaxis in post-MI - To prevent arrhythmias
Supraventricular tachyarrhythmias (SVTs)- Atrial flutter & atrial fibrillation -Slows AV nodal conduction & reduce the ventricular response
Esmolol (IV) is used in acute SVT & intraoperative arrhythmias
121
Class 4 AAs are CCB. What type of CCBs? Where does it slow conduction?
nonDHPs;
Slows conduction in areas more Ca dependent (ie SA and AV nodes)
122
Therapeutic targets for HTN
- Diuretics - Decrease volume
- Beta-blockers- Decrease heart rate and sympathetic drive
- Calcium channel blockers- vasodilation (decrease in SVR
)
- Angiotensin inhibitors -
Vasodilation, Aldosterone inhibition, Decrease hypertrophy
123
Signal transmission flows from ____ to ____ via _____
atria to ventricles via AV node
124
Labetalol Absorption, Metabolism, Excretion
- Onset of action is 5-15min and lasts up to 2-12 hours after cessation
- Extensive first pass metabolism therefore oral form is only about 20-40% bioavailable
- Minute amount of unchanged drug excreted in urine
- Bolus doses of 1-2mg/kg have produced precipitous drops in BP
125
Normal impulse generating cardiac contraction originates at the _____ with what bpm?
SA node;
| 60-100 bpm
126
_____ mechanisms regulate CV function are under control of receptors in the arteries and veins (ie baroreceptors)
Neural and hormonal (neurohormonal)
127
Class 3: Ibutilide Administration via IV for
acute conversion of atrial fibrillation or atrial flutter
128
What are AA classes 2 and 4?
2 and 4 (BBs and CCBs)
129
Nicardipine Absorption, Metabolism, and Excretion:
- Onset of action is with 1-5 min and duration of action is 2-6 hours after cessation
- Agent is about >95% bound
- Metabolism occurs through CYP 3A4 system substrate therefore monitor for potential drug interactions
- Cardiac sparing effect, therefore no contractility suppression
130
Class 4: Ca2+ Channel Blockers - Verapamil dosing, metabolism, admin, and side effects?
IV administration for acute use and oral therapy for chronic
Dose: 2.5 to 5 mg IV as bolus
Extensive hepatic metabolism
Side effects: constipation, hypotension (vasodilatation), AV block
Drug interactions: CYP 3A4 inhibitor
131
As a whole, beta blockers decrease SV and HR so they They help decrease _____ by working together with ACE-Inhibitors
decrease CO.
renin secretion
132
Class 3: Amiodarone is drug of choice for ____
wide array of arrhythmias
133
objectives of Anti-HTN
▪ Overview of therapeutic targets for HTN management
▪ Describe the CV benefits of HTN control
▪ Describe the mechanism of action of each drug class for the management of HTN
▪ Describe the mechanism of action of intravenous therapies used to manage acute HTN
134
Net effect of amiodarone conversion from atrial fibrillation in 24 hr*
```
Intravenous= ?
Oral= ?
```
```
Intravenous= 28%
Oral= 52%
```
135
Angiotensin inhibition for HTN 3 ways to inhibit angiotension:
ACEi
ARB
Parasympathetic stimulation
136
Overall, HTN will cause
HF
137
Class 3: Dofetilide MOA
Acts by blockade of the rapid component of the delayed rectifier potassium current (IKr)
Increase APD & ERP
Used to maintain sinus rhythm in Atrial fibrillation
Bioavailability is 100%, initiate in hospital - QTc > 500 msec can be fatal
Renal elimination accounts for 80% unchanged
Inhibitors of renal cation exchange can prolong effect (ie cimetidine, HCTZ, etc)
138
Postoperative HTN Requires rapid control of BP (3 things)
Control bleeding at suture sites
Neurology checks (patient used to x BP, now receiving y)
Myocardial ischemia develops due to increased oxygen needs
139
Extracardiac effects of Class 3: Amiodarone
Hypotension, secondary to IV administration due to the diluent, polysorbate 80
Resolve hypotension by slowing the rate of infusion
140
Nitroglycerin on HTN
- Only effective at higher doses
- Concern for hypotension and tachycardia
- Compromised cerebral and renal perfusion due to preload and caridac output
- Difficult agent to titrate (often given as bolus instead of continuously)
- vasodilator
- Useful in ACS
141
what are the classes of Arrythmias?
Suprventricular
ventricular
142
Non-pharmacologic methods for management
Ablation - catheter fries cardiac muscle to prevent Arrythmia
Implantation of ICD
Electrical cardioversion
143
a-adrenergic blockers
Vasodilator activity on the peripheral vasculature
Side effects -
o-Orthostatic hypotension (hypotension (blood pressure drop from sitting to standing is too much for patient's body to compensate for and pt can have syncope)
o- Reflex tachycardia - compensate for severe drop in B- this drop can be sensed by brain and drive sympathetic response
144
Esmolol Absorption, Metabolism, and Excretion:
- Onset of action is seconds and duration of action up to 10-20 min after cessation
- Metabolism occurs in erythrocytes by esterases and has metabolite (1/500 activity) eliminated in urine
- Do not need to adjust in hepatic or renal failure
- Useful in patients with acute myocardial infarction
145
Class 4: Ca2+ Channel Blockers - Diltiazem admin, dosing, side effects,
IV administration for acute use and oral therapy for chronic
Dose: 20 mg IVP, then infusion of 2.5 mg/hr
Not as cardioselective as verapamil
Side effects: hypotension and bradycardia
Drug interactions: CYP 3A4 inhibitor
146
Acutely (IMMEDIATELY) reducing BP can be bad too because your body has been used to this
high pressure, and now the brain isnt going to get enough perfusion, neither is the kidneys, etc.
147
8 Risk Factors of AAs
Electrolyte abnormalities (ie K, Mg, Ca)
ECG findings (Bradycardia, Ion channel mutations)
Female - have longer Q-T intervals by 5-10
CAD
Recent electrical cardioconversion - toward rhythm control
Overdose of QT-prolongation medications
Drug-Drug interactions
Medications -Antiarrhythmic’s and Non-antiarrhythmics
148
Hydralazine on HTN
- Initially slower onset of 5-15min then precipitous fall in BP lasting up to 12 hours
- Circulating half-life is about 3 hours, however effect on BP can last up to 100 hours
- Agent has unpredictable effects on BP and is difficult to titrate
149
what are the supraventricular Arrythmias?
atrial and AV node
150
Clinical benefits of HTN management
- Decreased pressure on the aortic arch
- Improvements in patients with Sleep Apnea
- Reduced incidence of Stroke
-Improved kidney function
Longevity (High blood pressure is detrimental to kidney function)
151
Conduction via the AV node is_____ than SA
slower
152
Baroreceptors provide the CNS with information regarding BP changes. Most common place is
carotid arteries
153
Net effect of conversion of Class 3: Ibutilide Atrial fibrillation ?
Dose: ?
within 90 minutes for 44% of patients*
1 mg over 10 minutes
Metabolism via liver and metabolite clearance via kidney
Adverse event: Torsades de pointes
Monitor QTc 4 hours after dose given
154
Amiodarone Advanced Cardiac Life Support (ACLS) 1st line for ?
Acute VT
155
Class 3: Amiodarone Cardiac Effects of what classes?
1, 2, 3, and 4
Chronic administration IKs
Weak Class 2 and Class 4 effects with IV administration
156
As a whole, beta blockers decrease SV and HR so they? They help decrease _____ by working together with ACE-Inhibitors
decrease CO.
renin secretion
157
Why is it important to do eye exams on patients on amiodarone?
see what kind of corneal microdeposits they have to prevent blindness
158
Nicardipine MOA & Dose
MOA: Agent is 2nd generation dihydropyridine CCB which is particularly selective for cerebral and coronary vessels
Dose: 5mg/hr titrate to max of 15mg/hr every
5 min by 2.5mg and bolus dosing is NOT FDA approved
Primary mechanism of action on the L-type calcium channels
PO and IV formulation available, since 100 times more hydrophilic than nifedipine
159
What kind of depolarizations are AA Class 2 BBs effective for?
Efficacy against ventricular ectopic depolarizations
Direct membrane effects are not fully characterized
160
Therapeutic targets for HTN
- Diuretics - Decrease volume
- Beta-blockers- Decrease heart rate and sympathetic drive
- Calcium channel blockers- vasodilation (decrease in SVR)
- Angiotensin inhibitors -
Vasodilation, Aldosterone inhibition, Decrease hypertrophy
161
Perioperative, Antihypertensive treatment reduces? how are the drugs given?
myocardial ischemia,
neurological deficits
mortality
IV push or infusion
162
-Absorption, metabolism, and excretion are the_____ for all catecholamines
same
163
Isoproterenol MOA & dosing
MOA: Non-selective B-receptor agonist with B1= B2 activity
Dosing: 0.01 mcg/kg/min then titration
-Lowers peripheral vascular resistance
-Shortens AV nodal conduction
-Increase in CO secondary to HR rather than SV
-Useful for patients to increase HR (ie. torsades de pointes)
164
High perfusion and low congestion is what class?
Dry-Warm
165
Catecholamine Therapies for HF
NE-primarily B1 and alpha
Epi-Beta1=Beta2, alpha
-depends on dose
-higher dose causes beta 1(increases HR) and alpha 1(increases BP)
Dobutamine(synthetic)-beta 1 more than beta 2 activity(3:1 ratio)
-increase contractility with minor drop in BP
-can have minor alpha activity
Dopamine-beta 1 and beta 2, not beneficial for patients
-dilates renal vasculature for increase blood flow BUT negative electrophysiological response
166
Phosphodiesterase (PDE) III Inhibitors MOA and drugs
cAMP triggers calcium increase
Rememeber milrinone as main PDE-I
-commonly combined with dobutamine(beta1)
-milrinone works inside cell while dobutamine works outside cell
Amrinone causes thrombocytopenia(low platelet levels)
-not available
167
Low Perfusion and high congestion is what class?
Wet-Cold
168
Catecholamines in general have
very short half life
169
RV send what kind of blood to lungs? What happens if RV isnt working?
deoxygenated blood
| -if not working, deoxygenated blood won’t be oxygenated
170
Chronic HF therapies (patients ready for discharge, at home, taking the meds for years to come)
```
ACE-I/ARBs
BB
Aldosterone antagonists
Diuretics
Digoxin
Hydralazine/Isosorbide dinitrate
```
171
Nitroprusside is metabolized by ____ and causes _____
blood vessels to nitric oxide leading to cGMP and vasodilation
causes vasodilation (can decrease preload and afterload)
Tolerance generally does not develop as with NTG
Little effect on renal blood flow and myocardial oxygen demand
172
Adrenergic effects of NE in HF
NE can act on alpha 1vasoconstriction
Epi at high dose can act on alpha 1vasoconstriction
-low dose refers to EPI PEN(0.3mg) compared to IV(1mg)
-epi works more on beta receptors and low dose will activate them
-EPI PEN used for Beta 2 to open lungs
-adrenergic effect not always advantageous so anti-adrenergic drugs used
-too much will imbalance systole/diastole
173
Congestion & Perfusion are what for the classification?
fluid build-up & blood flow to vital organs/extremities
Grid is specific for different infusion choices for therapy
WET-diuretic needed because fluid build-up
174
RV failure can lead to ____
pulmonary hypertension
- hypertrophy of RV
- blood vessels constrict because hungry for oxygen but there is none so constrict even more
- therapies to dilate that vasculature exist
175
Vasopressin and Acute HF
Vasopressin is endogenous
- triggered when blood volume low
- brain releases signal
- travels to kidney to reabsorb water(V2 receptor) to increase blood volume and BP
- V1 receptor activated causing vasoconstriction(IV infusion used for this mechanism)
When too much volume
- vasopressin antagonists used
- V-2 blockage prevents water reabsorption
176
De-compensation and hospitalization?
occur in a cycle over and over
decompensation means to get worse
177
2 Types of heart failure
Acute and chronic
178
Low perfusion and low congestion is what class?
Dry-Cold
179
Chronic-can be managed _____
At home with infusions
180
-nitroprusside has better vasodilation capabilities than _____ but very toxic
Nitroglycerin
181
Dopamine MOA
-only during high doses will dopamine affect alpha and beta receptors because secondary to NE
182
High Perfusion and high congestion is what class?
Wet-Warm
183
Chronic HF therapies
*Drugs listed on top reduce mortality
RAAS-renin angiotensin aldosterone system
Spironolactone-aldosterone antagonist, potassium sparing diuretic
-prevents sodium reabsorption and water follows
-K increases because Na and K not exchanged
Beta blockade helps during hyper-adronergic states
ACE inhibitor-angiodema side effect, inibite ACE1ACE2 conversion, potassium sparing diuretic
ARB(angiotensin receptor blockers)-prevents angiotensin 2 binding to receptor preventing aldosterone release, potassium sparing diuretic
Nitrate-Hydralazine-combination which reduce preload(nitrate) and afterload(hydralazine)
*Don’t worry about novel therapies
184
Mechanism of Action: Cellular Level of HF drugs
```
MYOCARDIUM
Beta agonist(dobutamine)
-acts on beta receptor
-increases cAMP
-increases inotropic effect
PDE breaks down cAMP-milrinone is PDE-I which increase cAMP
```
VESSEL WALL
- Alpha agonist-phenylephrine
- Acts on alpha receptor
- intracellular mechanism leadings to vasoconstriction
185
Sodium Nitroprusside Toxicity/Precautions:
- Hypotension being most observed side effect
- Accumulation of cyanide can lead to lactic acidosis
- Thiocyanate is 100 times less toxic than cyanide
- Infusion >4mcg/kg/min for >24 hours can lead to toxicity
- Cyanide toxicity: cardiac arrest, coma, encephalopathy, and seizures
- usually change in mental status
- longer infusion duration, high doses, or both are problematic
186
PAH Therapies
```
PAH-pulmonary hypertension-focus on bold, main drugs used in pulmonary hypertension
LEFT side
-All oral
-used only chronically
RIGHT side
-used acutely
```
- nitric oxide, not nitrous oxide(laughing gas)
- inhaled
- increase cGMP
- dilates pulmonary vasculature to alleviate Right heart failure
- sildenafil(tablet)-phosphodiesterase 5 inhibitors
- prevent breakdown of cGMP, increasing it
- used in patients with elevated pulmonary arterial pressures
- prostacyclins-increase cAMP
- dilates vasculature
- epoprostenol(IV or inhaled)
