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5230 > Cardiac Drugs > Flashcards

Cardiac Drugs Flashcards

1
Q

Major risk factors for increased perioperative CV risk

A

Unstable Coronary Syndromes
Decompensated Heart Failure
Significant Arrhythmias
Severe Valvular disease

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2
Q

Intermediate risk factors for increased perioperative CV risk

A 
Mild angina
Previous MI
Compensated/previous heart failure
DM (esp insulin dependent)
Renal insufficiency
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3
Q

Minor risk factors for increased perioperative CV risk

A 
Advanced age
Abnormal ECG (LVH, LBBB, ST abnormalities)
Rhythm other than NSR
Low functional capacity
History of smoking
Uncontrolled systemic hypertension
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4
Q

Perioperative cardiac risk reduction strategies

A

Many have conflicting results as to if they are effective or not
Beta blockers show evidence for effectiveness in vascular surgery
Statins show evidence for effectiveness
Preop coronary revascularization shows conflicting evidence
Perioperative monitoring (PA, CVP, TEE) hasn’t shown to be effective

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5
Q

Classes of Antiarrhythmic drugs and what they do

A

I: Block Na channels
II: Beta-adrenergic blocking effects
III: Blocks K channels
IV: Blocks Ca channels

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6
Q

Common class I antiarrhythmic drugs and what they’re used for

A

Lidocaine, procainamide, phenytoin
Used for ventricular arrhythmias
-Blocks Na channels (Na channels cause ventricular depolarization)

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7
Q

Common class III antiarrhythmic drugs and what they’re used for

A

Amiodarone, sotalol
Prolongs repolarization
-Blocks K channels

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8
Q

Common class IV antiarrhythmic drugs and what they’re used for

A

Verapamil, diltiazem
Used for Atrial arrhythmias
-Blocks Ca channels (SA/AV depolarization caused by Ca channels)

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9
Q

1st line therapy for managing A fib

A

Ventricular rate control (<110bpm)

-Use beta blockers or calcium channel blockers

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10
Q

When to avoid beta blocker use

A

COPD or asthma patients

-Cause bronchoconstriction

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11
Q

Where and how does adenosine work

A

Purine (purinergic) receptors
Slows sinoatrial and atrioventricular nodal conduction
Inhibits the AV node
-Opens K channels (hyperpolarize), indirectly inhibits calcium channels from opening

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12
Q

SVT management in the OR

A

Won’t do adenosine (cause asystole)

Calcium channel blockers: Verapamil or diltiazem

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13
Q

V Tach management in the OR

A

Amiodarone or lidocaine

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14
Q

Contraindication for antiarrhythmic drugs

A

Heart block

-Many of the antiarrhythmic drugs slow AV conduction

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15
Q

Hypertensive Urgency vs Emergency

A

Urgency: Isn’t associated with end organ damage, need to get BP down in 24 hours, can use PO meds
Emergency: Presence of acute end organ damage, requires immediate therapy

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16
Q

Mechanism of action of ACEI and ARBs (and normal process)

A

Normal process:
-Catecholamine release, bind to beta 1 receptors in the kidney
-Renin is released, attaches to receptor and converts Angiotensinogen to Angiotensin 1
-ACE converts Angiotensin 1 to 2 (also breaks down bradykinin)
-Angiotensin 2 binds to receptors to conserve Na and cause vasoconstriction (=Increased BP, augments the autonomic nervous system)
ACEI: Stop conversion of Angiotensin 1 to 2, and the breakdown of bradykinin (=cough)
ARBs: Block Angiotensin 2 from binding to receptors (doesn’t cause cough like ACEI but similar effect, more expensive)

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17
Q

Nipride metabolism (and original molecule components)

A

Composed of 5 cyanide molecules (toxic) surrounding a nitric oxide molecule
Metabolism
-By hemoglobin, steels an electron, makes nipride unstable, breaks open
-Some cyanide attaches to hgb to be eliminated later, most goes to cyanide pool
-Cyanide pool reacts with thiosulfate (vitamin B12) in the liver, facilitated by enzyme rhodanese, and is excreted in urine
-If cyanide pool>vit B12 available, excess cyanide blocks cytochrome oxidase which is the enzyme that lets the cells use O2
-Cells then can’t burn O2, patient gets histotoxic hypoxia

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18
Q

Recognizing the signs of nipride toxicity

A

Patients turn pink, their venous blood appears like arterial because they can’t use O2

  • VBGs will show very high O2 levels
  • Patients will be acidotic because they are producing lactic acid
  • Central nervous system dysfunction
  • CV instability
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19
Q

What causes rebound hypertension after stopping nipride

A

Renin release

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20
Q

Labetalol (receptors/effect, onset, half life, dose)

A

Beta blocker with alpha blocking activity
-B1 activity in the heart to decrease contractility and HR but alpha blocking capability in blood vessels causes vasodilation
Onset: 5-10 minutes
Half life: 3-6 hours
Dose: In OR- 5mg increments
Best drug to use when patients are hypertensive and tachycardic

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21
Q

Esmolol (receptors/effect, onset, half life)

A

Beta blocker (Cardioselective per pharmaceutical companies but not really in practice)
-Causes decreased cardiac contractility/HR but vasoconstriction
Onset: 1-2 minutes
Half life: 10-30 minutes (metabolized by nonspecific esterase’s)
Best to use for tachycardia control

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22
Q

Diuretic mechanism of action for use in treating hypertension

A

Not fully understood, thought to work because they open K channels in the blood vessels -> vasodilation

23
Q

Current recommendations per the treatment guidelines for the treatment of hypertension

A

Thiazide-type diuretic, calcium channel blocker, angiotensin-converting enzyme inhibitor, OR angiotensin receptor blocker as initial therapy

24
Q

Calcium channel blocker effect (and ones used in anesthesia)

A

Decreased cardiac contractility and decreased constriction of blood vessels

  • Decreased HR and BP
  • Verapamil, diltiazem
  • ipine
25
Q

ACE inhibitors names vs ARBs

A

ACEI: -pril
ARB: -artan

26
Q

Beta blocker effects on receptors throughout the body

A

Block B1 receptors in heart -> cardiac depression
Block B1 receptors in kidney -> decreased renin release
CNS depressant
Decreased glycogenolysis -> hypoglycemia
Block B2 receptors in vascular -> vasoconstriction
Block B2 receptors in lungs -> bronchoconstriction

27
Q

Which medication causes arterial vasodilation

A

Hydralazine

-Decreases afterload

28
Q

Which medication causes venous vasodilation

A

Nitroglycerin

-Decreases preload

29
Q

Recommendations for patients taking beta blockers who have scheduled surgery, also if noted to have CAD pre-op

A

Continue taking beta blockers (including the day of surgery)
-If found to have CAD preop, should be started on a beta blocker but not on the day of surgery (at least one day and ideally 1 week before scheduled surgery)

30
Q

Recommendations for patients taking ACEI or ARBs scheduled for surgery

A

Very controversial

  • Some research supports not taking the medications the morning of surgery, some supports continuing it
  • If it’s stopped the day of surgery, it should be restarted as soon as possible after
  • If it’s continued the morning of surgery, less propofol should be used for induction and vasoplegia should be treated with vasopressin
31
Q

Alpha blocker effects and treatment for hypertension

A

Causes vasodilation to treat hypertension but have a lot of side effects (tachycardia, orthostatic hypotension)
-Useful for patients with BPH and HTN

32
Q

Central alpha-adrenergic agonists for hypertension

A

Sympatholytic, decreases catecholamine release

  • Used as a last resort medication for patients with hypertension that is refractory to many other medications
  • Patients go through severe withdrawal from this
  • If your patients are on this, they have hard to treat hypertension
  • Ex: Clonidine
33
Q

Direct vasodilators for hypertension

A

Work directly in the blood vessel wall to dilate

  • Nipride and nitroglycerine: Have nitro groups, blood vessel responds to nitric oxide to dilate
  • Hydralazine opens K channels in the blood vessel to dilate them
34
Q

Strongest predictor of perioperative ischemia

A

Tachycardia

  • > 100 but also less for some people
  • Studies have shown greatest protection with HR controlled <70bpm
35
Q

How Beta blockers treat angina (and what type they’re used for)

A

Anyone with CAD/angina should be on a beta blocker

  • Works by decreasing cardiac demand (b/c decreased HR)
  • Also vasoconstricts blood vessels in heart, but decreases the demand so much it doesn’t matter
  • Used for patients with exertional/stable angina
36
Q

How do nitrates treat angina

A

Vasodilation -> decreased heart demand b/c decreased preload
-Decreases venous return (blood pools in LE)
Also dilates blood vessels in heart

37
Q

How calcium channel blockers treat angina (and what type they’re used for)

A

Decreasing demand and increasing supply (decrease spasms)

  • Decrease preload and afterload, increase coronary supply
  • Used for variant angina
38
Q

Angina drug therapy: More effective when it increases supply or decreases demand?

A

Decreases demand

39
Q

Clinical subtypes of angina

A 
Stable (80% of pts)
-Predictable, with exertion
Unstable (15% of pts)
-The worst type
-Occurs at rest and at night
Variant (5% of pts)
-Unpredictable, from spasms (occurs at rest, rarely exercise induced)
-Usually occurs in early AM
40
Q

Beta blockers with ISA (Intrinsic sympathomimetic activity)

A

Beta blockade but also have some intrinsic beta agonist properties
-Get beta blocker effects but not as strong as normal, benefit=less bronchoconstriction, also less resting bradycardia and lipid changes
-Good to use if an asthmatic needs a beta blocker
Ex: Acebutolol, pindolol, penbutolol

41
Q

Beta blockers with MSA (membrane stabilizing activity)

A

Makes them antiarrhythmic

Ex: Propranolol, acebutolol

42
Q

Beta blockers with alpha blocking activity

A

Coreg

Labetalol

43
Q

Mechanism of action of nitrates

A

Nitric group goes into the cell and causes the release of NO, the bodies natural vasodilator

44
Q

Statin use for angina

A 
#1 prescribed drug class in the world
Used to interrupt/stop plaque formation in coronary arteries
45
Q

Bare metal and drug eluding stents: How long to delay elective surgery, what to do with Plavix/aspirin if surgery cant be delayed

A

Bare metal: Delay surgery for 4-6 weeks
Drug eluding: Delay surgery for 12 months
-Most stents are drug eluding now
-If on DAT (dual antiplatelet therapy) and surgery cannot be postponed, recommend to stop Plavix and continue ASA through surgery, restart Plavix ASAP postop

46
Q

Overall anesthetic plan for patients with angina

A
  • Anesthetic gasses have cardioprotective effects (esp sevo or iso)
  • Have patients take prescribed medications including the morning of surgery
  • Keep the HR low (use opioids, beta blockers), if a pts HR/BP stay under their preop HR/BP when they weren’t having angina they shouldn’t be having angina
  • HR is hardest to control during induction/emergence
47
Q

CHF risk to anesthesia

A

Uncontrolled CHF is the highest risk factor for morbidity/mortality with anesthesia

48
Q

“Triple therapy” treatment for CHF

A

ACE Inhibitor
Beta Blocker
Diuretic (If volume overloaded)

49
Q

Anesthetic implications for pts with CHF (2 principle events to control, induction meds, antiarrhythmic meds, inhalation agents)

A

2 principle CV events to control: myocardial depression and vasodilation, changes to these should be minimal

  • Use etomidate or ketamine unless well controlled asymptomatic CHF - can use low dose propofol
  • Many CHF pts are preload dependent and rely on increased sympathetic tone
  • Amiodarone is the best antiarrhythmic - least myocardial depressant effect
  • Inhalation: Sevo or iso both cardioprotective effects similar to ischemic preconditioning, sevo doesn’t cause tachycardia
50
Q

Mechanism of action of digitalis

A

Na/K ATPase inhibition -> Na increase inside the cell

  • Increased Na inside the cell decreases Na/Ca pump so less Ca is pumped out of the cell
  • Increased Ca in the cell -> contraction
51
Q

Relationship between K level and digitalis action

A

Low K = increased digitalis binding - toxicity

-Increasing the K level will cause the digitalis to disengage from the receptor

52
Q

Digitalis and anesthesia: What to know

A 
Why they are taking it
-A fib/flutter or CHF
Efficacy
-Is it working? 
Digitalis level
-Goal= 0.5-0.9
-What dose they take, when they last took it (half life ~36 hours)
Potassium level
53
Q

Digitalis toxicity

A

Most common: Visual disturbances (colored vision, halo vision, flickering lights)
GI/Neurological symptoms
Cardiac arrhythmias (A fib with PVCs most common)

54
Q

Recommendations for anesthesia with patients on antiplatelet medications prescribed for CV events

A

Recommended to continue
The risk of a CV event is higher if antiplatelet meds are stopped preop than the risk of surgical bleeding when they are continued
-Exception=Closed space surgery (intracranial or eye) or surgery associated with massive bleeding/difficult hemostasis (prostate)

5230 (13 decks)

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