FA Cardio Drugs Flashcards
(180 cards)
1
Q
4 Treatment options for essential (primary) HTN
A
AACD:
- ACE inhibitors
- ATII receptor blockers (ARBs)
- DHP Ca2+ channel blockers
- Thiazide Diuretics
2
Q
4 Treatment options for HTN w/Heart Failure
A
AAB:
- ACE inhibitors/ARBsDiuretics
- Aldosterone antagonists
-
β-blockers (compensated HF)
- C/I in cardiogenic shock
3
Q
when should β-blockers be used carefully?
A
- Caution in decompensated HF
- C/I in cardiogenic shock
4
Q
4 Treatment options for HTN w/diabetes mellitus
A
ABCD:
- ACE inhibitors/ARBs
- β-blockers
- Ca2+ channel blockers
- Thiazide Diuretics
5
Q
Treatment options for HTN in pregnancy
A
HLMN:
- Hydralazine (increases cGMP)
- Labetalol (adrenergic blocker)
- Methyldopa (alpha-2 agonist)
- Nifedipine (Ca2+ channel blocker)
6
Q
Class of drug protective against diabetic nephropathy?
A
ACE inhibitors/ARBs
7
Q
Dihydropyridine Calcium Channel Blocker Drugs
A
- Amlodipine
- Clevidipine
- Nicardipine
- Nifedipine
- Nimodipine
8
Q
DHP Calcium Channel Blocker location of action
A
Vascular smooth mm
9
Q
Non-Dihydropyridine Calcium Channel Blocker Drugs
A
- Diltiazem
- Verapamil
10
Q
Non-DHP Calcium Channel Blocker location of action
A
Heart: SA and AV nodes
11
Q
DHP Calcium Channel Blocker MOA
A
- Block voltage-dependent L-type Ca2+ channels in vasc smooth mm
- Inhibit MLCK
- Arteriodilation
12
Q
DHP Calcium Channel Blocker Clinical Use
A
- HTN
- Angina (incl. Prinzmetal)
- Raynaud phenom
Note: except nimopidine
13
Q
Nimopidine Clinical Use
A
subarachnoid hemorrhage (prevents cerebral vasospasm)
14
Q
Clevidipine Clinical Use
A
HTN urgency or emergency
15
Q
Non-DHP Calcium Channel Blocker Clinical Use
A
- HTN
- Angina
- Afib/Aflutter
16
Q
Calcium Channel Blocker Toxicity
A
- Cardiac depression
- AV block (non-dihydropyridines)
- peripheral edema
- flushing
- dizziness
- hyperprolactinemia (verapamil)
- constipation
- gingival hyperplasia
17
Q
Hydralazine MOA
A
- Increases cGMP
- Causes smooth muscle relaxation
- Vasodilates arterioles > veins
- Reduces afterload
18
Q
Hydralazine Clinical Use
A
- Severe HTN (particularly acute)
- HF (w/organic nitrate)
- Safe to use during pregnancy
- Frequently coadministered w/β-blocker to prevent reflex tachycardia
19
Q
Hydralazine Toxicity
A
- Compensatory tachycardia (C/I in angina/CAD)
- Fluid retention
- headache
- angina
- Lupus-like syndrome.
20
Q
Hydralazine C/I
A
angina/CAD → causes compensatory tachycardia
21
Q
Treatment Options for HTN Emergency
A
- clevidipine
- fenoldopam
- labetalol
- nicardipine
- nitroprusside
22
Q
Nitroprusside Clinical Use
A
HTN emergency
23
Q
Nitroprusside MOA
A
- direct release of NO → increase cGMP
- releases cyanide
24
Q
Nitroprusside Toxicity
A
Cyanide toxicity:
- ETC inhibition → block ATP synth
25
Fenoldopam MOA
* Dopamine D1 receptor agonist → coronary, peripheral, renal, and splanchnic vasodilation
* Decreases BP
* Increases Natriuresis
26
Fenoldopam Clinical Use
HTN emergency
27
Nitrate Drugs
* Nitroglycerin
* isosorbide dinitrate
* isosorbide mononitrate
28
Nitrates MOA
* Increase NO in vascular smooth muscle → increase cGMP → smooth mm relaxation → vasodilation
* Dilate veins \>\> arteries
* Decrease preload
29
Nitrates Clinical Use
* Angina
* Acute coronary syndrome
* Pulmonary edema
30
Nitrates Toxicity
* Reflex tachycardia (treat with β-blockers)
* HypOtension
* Flushing
* Headache
* High doses: Methemoglobinemia
* “Monday disease” in industrial exposure
* develop tolerance for vasodilating action during the work week, loss of tolerance over weekend
* Tachycardia, dizziness, headache upon reexposure
31
Treatment Goals for Angina
Reduction of myocardial O2 consumption (MVO2) by decreasing 1+ of determinants:
* End-diastolic volume (preload)
* BP
* HR
* Contractility
32
Treatment Options for Angina
* Nitrates
* Beta-blockers
* Nitrates + Beta-blockers
33
Effect of Nitrates on:
* EDV
* BP
* Contractility
* HR
* Ejection time
* MVO2
* EDV: decrease
* BP: decrease
* Contractility: no effect
* HR: increase (reflex)
* Ejection time: decrease
* MVO2: decrease
34
Effect of Beta-blockers on:
* EDV
* BP
* Contractility
* HR
* Ejection time
* MVO2
* EDV: no effect or decrease
* BP: decrease
* Contractility: decrease
* HR: decrease
* Ejection time: increase
* MVO2: decrease
35
Effect of Nitrates + Beta-blockers on:
* EDV
* BP
* Contractility
* HR
* Ejection time
* MVO2
* EDV: no effect or decrease
* **BP: decrease**
* Contractility: little/no effect
* HR: no effect or decrease
* Ejection time: little/no effect
* **MVO2: significantly decrease**
36
Beta-blockers C/I in angina
Partial agonists:
* Pindolol
* Acebutolol
37
Cardiac Glycoside Drugs
Digoxin
38
Digoxin MOA
* Direct inhibitor of Na+/K+ ATPase
* binds to same site as K+
* Indirect inhibitor of Na+/Ca2+ exchanger
* Increase intracell [Ca2+] → positive inotropy
* Stimulates Vagus nn → decreases HR
39
Digoxin Clinical Use
* Heart failure (CHF)
* increased contractility
* Afib
* decreased conduction at AV node
* depression of SA node
40
Digoxin Toxicity
* Cholinergic
* blurred/yellow vision
* arrhythmias
* nausea/vomiting/diarrhea
* EKG:
* Increased PR
* Decreased QT
* T-wave inversion
* ST scooping
* AV block
* Hyperkalemia
* indicates poor prognosis
41
Factors predisposing to Digoxin toxicity
* Renal failure → decreased excretion
* HypOkalemia
* permissive for digoxin binding at K+-binding site on Na+/K+ ATPase
* CCBs (Verapamil, Amiodarone)
* Quinidine → decreased clearance
* displaces digoxin from tissue-binding sites
42
Treatment for Digoxin Toxicity
Most often caused by hypOkalemia!
* Slowly normalize K+
* Cardiac pacer
* Anti-digoxin Fab fragments
* Mg2+
43
6 Antiarrhythmic Drug Types
1. Sodium Channel Blockers
2. Beta-blockers
3. Potassium Channel Blockers
4. Calcium Channel Blockers
5. Adenosine
6. Mg2+
44
Class I Antiarrhythmic Drugs
* Fast Sodium Channel Blockers
* Divided into classes IA, IB, & IC
45
Class IA Antiarrhythmic Drugs
**A**bba **P**erformed **D**ancing **Q**ueen:
* Procainamide
* Disopyramide
* Quinidine
46
Class IA Antiarrhythmics MOA
* Increase AP duration
* Increase effective refractory period (ERP) in ventricular action potential
* Increase QT interval
* Decrease slope of Phase 0
47
How does Cardiac AP change w/Class IA Antiarrhythmics?
Moderately decreased slope of Phase 0
48
Class I Antiarrhythmics MOA
* Slow or block conduction (esp in depolarized cells)
* Decrease slope of Phase 0 depolarization
* Increase threshold for firing in abnormal pacemaker cells
* State-dependent (selectively depress tissue that is frequently depolarized [e.g., tachycardia]).
49
Class IA Antiarrhythmics Clinical Use
* Atrial & Ventricular Arrhythmias
* **esp re-entrant and ectopic SVT and VT**
50
Class IA Antiarrhythmics Toxicity
* Cinchonism (headache, tinnitus with quinidine)
* Reversible SLE-like syndrome (procainamide)
* Heart failure (disopyramide)
* Thrombocytopenia
* Torsades de pointes due to increased QT interval
51
Torsades de pointes
* Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG
* Can progress to ventricular fibrillation
* Associated w/prolonged QT interval
* Rx: Magnesium Sulfate
52
Class IB Antiarrhythmic Drugs
Backstreet Boys **P**retty **M**uch **L**ack **T**alent:
* Phenytoin
* Mexiletene
* Lidocaine
* Tocainide
53
Class IB Antiarrhythmics MOA
* Decrease AP duration
* Preferentially affect ischemic tissue:
* Already-depolarized Purkinje fibers/ventricular tissue
* Activated Na+ channels
54
Class IB Antiarrhythmics Clinical Use
* Acute ventricular arrhythmias (esp post-MI)
* I**B** is **B**est Post-MI
* Digitalis-induced arrhythmias
55
How does cardiac AP change w/Class IB Antiarrhythmics?
* Slightly decreased slope of Phase 0
* Shorter AP duration
56
Class IB Antiarrhythmics Toxicity
* CNS stimulation/depression
* Cardiovascular depression
57
Phenytoin S/E
* hirsutism
* gingival hyperplasia
58
Mexiletine S/E
Think Mexican food:
* Oral administration
* Severe GI upset
59
Tocainide S/E
Pulmonary fibrosis (loud S2)
60
What happens to cardiac AP w/Class IC Antiarrhythmics?
* Larger decrease in slope of Phase 0
* No change in AP duration
61
Class IC Antiarrhythmic Drugs
Carly (Rae Jepsen) is **E**xtremely **F**reaking **P**ainful:
* Encainide
* Flecainide
* Propafenone
62
Class IC Antiarrhythmics MOA
* Zero-order kinetics
* No effect on AP length
* Significantly prolongs ERP in AV node and accessory bypass tracts
* No effect on ERP in Purkinje and ventricular tissue
63
Class IC Antiarrhythmics Clinical Use
* SVTs, including Afib
* Only as a last resort in refractory VT
* C/I post-MI
64
Class IC Antiarrhythmics C/I
* post-MI
* structural & ischemic heart disease
65
What makes Propafenone unique?
Blocks Na+ channels AND beta-adrenergic receptors (decreases cAMP)
66
Class IC Antiarrhythmics Toxicity
* Pro-arrhythmic
* C/I post-MI, structural & ischemic heart disease
67
Class II Antiarrhythmic Drugs
* Metoprolol
* propranolol
* esmolol
* atenolol
* timolol
* carvedilol
68
Class II Antiarrhythmics MOA
* Decreases cAMP, Ca2+ currents
* → decreases SA and AV nodal activity
* Decreases slope of nodal AP Phase 4
* → suppresses abnormal pacemakers
* Increases PR interval
* b/c AV node particularly sensitive
69
Longest-acting beta-blocker
Propanolol
70
Shortest-acting beta-blocker
Esmolol
71
3 Beta-blockers safe to give to pts w/asthma, COPD, DM
Partial agonists:
* Acebutolol
* Atenolol
* Pindolol
72
2 Beta-blockers used for HTN emergencies
Also have alpha-1 blocking activity:
* Labetalol
* Carvedilol
73
Beta-blocker than can decrease mortality post-MI or in CHF
Metoprolol
74
Drug that blocks beta-adrenergic receptors and K+ channels
**Sotalol**
* Messing w/K+ → prolonged QT interval → arrhythmia
* Keep pt in hospital and monitor
75
Class II Antiarrhythmics Clinical Use
* SVT
* Ventricular rate control for Afib & Aflutter
76
What happens to cardiac AP w/Class II Antiarrhythmics?
* Decreased slope of Phase 4
* Prolonged repolarization
77
Class II Antiarrhythmics Toxicity
* Impotence
* Exacerbation of COPD/asthma
* CV effects (bradycardia, AV block, HF)
* CNS effects (sedation, sleep alterations)
* May mask signs of hypOglycemia
* Metoprolol can cause dyslipidemia
* Propranolol can exacerbate vasospasm in Prinzmetal angina
* β-blockers cause unopposed α1-agonism if given alone for pheochromocytoma or cocaine toxicity
78
Treatment for β-blocker overdose
* saline
* atropine
* glucagon
79
Class II Antiarrhythmic Drug Type
Beta-blockers
80
Class III Antiarrhythmic Drug Type
Potassium Channel Blockers
81
Class III Antiarrhythmic Drugs
**A**ll **I** **D**o is **S**ing:
* Amiodarone
* Ibutilide
* Dofetilide
* Sotalol
82
Class III Antiarrhythmics MOA
* Increase AP duration
* Increase ERP
* Prolong QT interval
83
Class III Antiarrhythmics Clinical Use
* Ventricular arrhythmias
* Afib/Aflutter
* VTach (Amiodarone, Sotalol)
84
Class III Antiarrhythmics Toxicity
* Sotalol: torsades de pointes, excessive β blockade.\
* Ibutilide: TdP
* Amiodarone:
* pulmonary fibrosis
* hepatotoxicity
* hypothyroidism/ hyperthyroidism
* acts as hapten
* corneal deposits
* blue/ gray skin deposits → photodermatitis
* neurologic effects
* constipation
* CV effects (bradycardia, heart block, HF)
85
Amiodarone S/E
* Iodine effects
* pulmonary fibrosis
* hepatotoxicity
* hypothyroidism/ hyperthyroidism
* Hapten effects
* corneal deposits
* blue/ gray skin deposits
* photodermatitis
* Neurologic effects
* Constipation
* CV effects (bradycardia, heart block, HF)
* Blocks P450 (increases serum levels of certain drugs)
86
Monitor what 3 things with Amiodarone?
* Liver fcn (hepatotoxicity)
* Pulmonary fcn (pulm fibrosis)
* Thyroid fcn (hyper/hypothyroid)
87
What makes Amiodarone unique?
Amiodarone is lipophilic and has antiarrhythmic class I, II, III, and IV effects
88
What happens to cardiac AP w/Class III Antiarrhythmics?
* Markedly prolonged repolarization
* Increased AP duration
89
Class IV Antiarrhythmic Drug Type
Calcium Channel Blockers
90
Class IV Antiarrhythmic Drugs
Cardioselective:
* Verapimil
* Diltiazem
Vasoselective:
* Nimodipine
91
Class IV Antiarrhythmics MOA
* Decrease conduction velocity thru AV node
* Increase ERP
* Increase PR interval
92
Class IV Antiarrhythmics Clinical Use
* Prevention of nodal arrhythmias (e.g., SVT)
* Rate control in Afib
93
Class IV Antiarrhythmics Toxicity
* Constipation
* Gastrin uses Ca2+ as 2nd messenger for motility
* flushing
* edema
* Gingival hyperplasia
* CV effects (HF, AV block, sinus node depression
94
What happens to cardiac AP w/Class IV Antiarrhythmics?
* Slow rise
* prolonged repol @ AV node
* Increased depol threshold
95
Nitrates C/I
Sildenafil (Viagra) -- PDE-5 inhibitor
* Giving concurrently can cause severe hypOtension → death
96
Adenosine MOA
* Increases K+ movement out of cell → hyperpolarization, decreased intracellular Ca2+
* Slows SA and AV node activity
* Prolongs AV node refractory period
97
Adenosine Clinical Use
* Drug of choice for Dx/Rx SVT
* Very short acting
* Effects blunted by theophylline and caffeine (adenosine receptor antagonists)
98
Drug of choice for Dx/Rx SVT
Adenosine
99
Adenosine S/E
* flushing
* hypOtension
* chest pain
* sense of impending doom
* bronchospasm
100
Adenosine blocked by?
* Theophylline
* Caffeine
101
2 Other drugs that act on K+ channels?
**Opiates**:
* Open K+ channels and close Ca2+ channels
* Hyperpol → prevent signal transmission of pain
**Sulfonylurea**:
* Closes K+ channels
* Easier depol → increased insulin release
102
Magnesium MOA
* Gets in the way of Na+
* Blocks depolarization
103
Magnesium clinical use
* torsades de pointes
* digoxin toxicity (arrhythmia)
104
9 Treatment options for CHF
1. **Diuretics**: furosemide, torsemide
2. **Positive inotropes**: digoxin, dobutamine, dopamine
3. **Vasodilators**: nitrates, nitroprusside, nesiritide, hydralazine
4. **ACE Inhibitors**: captopril, enalapril, ramipril
5. **ARBs**: losartan, valsartan
6. **Aldosterone Antagonists**: spironolactone
7. **Beta-blockers**: metoprolol, carvedilol
8. **Calcium Channel Blockers**: diltiazem, verapamil
9. **Morphine** (for acute Rx of assoc pulm edema)
105
Class I Antiarrhythmic Drug Type
Fast Sodium Channel Blockers
106
4 Compensatory Mechanisms in CHF
1. Frank-Starling: increase preload
2. Sympathetic Stim: increase HR & contractility
3. RAA System: sodium & H2O retention → increase blood volume → increase venous return (preload)
4. Hypertrophy: increase ventricular mm mass
107
Cardiac remodeling
* Occurs in chronic heart failure = unrelenting stimulation of heart tissue by NE, ATII, aldosterone + hypertrophy + sustained stress/pressure
* Abnormal changes in gene expression
* Increased cardiac myocyte apoptosis
* Changes in heart shape and performance
108
A failing heart does much worse very quickly when this happens
afterload increases → sharp decline in SV
109
Treatment algorithm for systolic CHF
* fluid retention should be treated before starting ACE inhibitor
* Beta blockers should be started after fluid retention has been treated and/or dose of ACE inhibitor has been titrated
* Pts that remain symptomatic can be given triple therapy: ARB + aldosterone antagonist (e.g. spironolactone) + digoxin
110
Best diuretic for CHF
Loop diuretics (furosemide)
111
3 drug types that reverse cardiac remodeling
* ACE inhibitors or ARBs
* Beta blockers
* Aldosterone antagonists (e.g. spironolactone)
112
Major sites of drug action in CHF
113
This diuretic significantly reduces mortality in CHF
Spironolactone
114
Diastolic vs. Systolic HF
115
Goals for Treatment of Diastolic HF
* Reduce HTN
* Increase diastolic filling → rate control
* Reduce edema
* Reduce myocardial ischemia
* Increase diastolic relaxation
116
Best diuretic for HTN?
Hydrochlorothiazide
117
Drugs C/I in Wolff-Parkinson-White Synd?
* Calcium Channel Blockers (Class IV)
* Digoxin
May cause Vfib
118
Class of antiarrhythmics preferred for rate control in Afib?
Beta-blockers (Class II)
119
preferred Na Channel blocker in Afib?
Flecainide (Class IC)
120
Cardiac drugs that can cause lupus-like syndrome?
* Procainamide
* Hydralazine
121
antiarrhythmic of choice in heart failure?
Amiodarone
122
first-line agent for most cases of Afib requiring rhythm control?
Amiodarone
123
drug of choice for acute paroxysmal SVT?
Adenosine
124
beta-blocker adverse effects
* fatigue
* bronchospasm
* bradycardia
* peripheral vasospasm
* decreased HDL, increased TG
* mask signs of hypoglycemia in diabetics
* insomnia, nightmares
* ED
125
Which drug is contraindicated in variant angina?
Beta-blockers
126
Rx for CCB overdose?
IV calcium gluconate
127
what effect does cimetidine have on CCBs?
increases bioavailability
128
Ranolazine MOA
* Not fully elucidated
* Blocks late Na+ inward current in cardiomyocytes
* Indirectly prevents intracellular Ca2+ overload due to ischemia
* Partial fatty acid oxidation inhibitor
* Shifts ATP production from fatty acid to carb oxidation
129
Ranolazine Clinical Use
provide additional flexibility to existing medical therapies
130
Ranolazine C/I
Preexisting QTc prolongation
131
Ranolazine Interactions
* Inhibitors of CYP3A increase plasma concentration of ranolazine
* Ketoconazole, diltiazem, verapamil, macrolide antibiotics, protease inhibitors, grapefruit juice
* Increases digoxin level 1.5x
132
Class I antiarrhythmic subtype w/longest duration of action?
Class IC
133
Class I antiarrhythmic subtype w/shortest duration of action?
Class IB
134
Which antiarrhythmic is not indicated for SVT?
Class IB
135
Rx Torsades de Pointes
IV magnesium sulfate or isoproterenol
136
Drugs Causing Prolonged QT Interval and/or TdP
* Class Ia antiarrhythmics
* Class III antiarrhythmics
* Azole antifungals
* Fluoroquinolone antibiotics
* Macrolide antibiotics
* Tricyclic antidepressants
* Typical and atypical antipsychotics
* Droperidol
* Indapamide
* Methadone
* Ranolazine
* Tamoxifen
* TMP-SMX
137
preferred drug for mild to moderate hypertension in the absence of comorbidity?
Hydrochlorothiazide
138
Which anti-HTN drug can cause immune hemolytic anemia with positive Coombs test?
Methyldopa
139
sudden withdrawal of alpha-2 blockers can cause what?
rebound HTN
140
Rx for rebound HTN from withdrawal of alpha-2 blockers?
alpha blockers (phentolamine)
141
Venodilators
* Nitrates
* ACE inhibitors
* Alpha-1 antagonists
* Nitroprusside
142
Arteriodilators
* Calcium channel blockers
* Hydralazine
* Minoxidil
143
Rx cyanide toxicity
* sodium thiosulfate
* hydroxocobalamine
144
Which drug can be used to treat hypoglycemia in insulinoma?
Diazoxide (K+ channel activator)
145
Which CCBs reduce heart rate and contractility and block conduction at AV node?
Verapamil and diltiazem
146
Which CCBs cause vasodilation leading to activation of sympathetic reflexes and may lead to increase in heart rate?
Nifedipine
147
Other names for ACE?
* Kininase II
* peptidyl dipeptidase
148
Rx low-renin HTN?
* Diuretic + CCB
* ACE inhibitors and ß-blockers are less effective in pts w/low renin levels when used as single agents
149
This substance may play a key role in resistant HTN
aldosterone
150
Cardiac remodeling mediated by these 3 substances
1. Aldosterone
2. ATII
3. NE (increased symp outflow)
151
Drug that can increase survival in pt w/decompensated HF and edema?
Spironolactone
152
2 drugs usually assoc w/reflex tachycardia
1. Nitrates
2. DHP-CCBs
153
3 drugs usually assoc w/bradycardia and hypotension
* non-DHP CCBs
* alpha-blockers
* beta-blockers
154
Early sign of digoxin toxicity
Stomach upset / nausea / loss of appetite
155
drug that can decrease mortality in MI and/or decrease arrhythmia after MI
Beta-blockers
156
this drug is C/I in heart failure in certain patients (elderly; past MI) b/c of its potent negative inotropic effect
Verapamil (Non-DHP CCB)
157
4 Rx goals for heart failure
1. decrease preload
2. decrease afterload
3. increase contractility
4. decrease remodeling
158
4 Drugs that can decrease preload
1. Diuretics (loop, thiazide)
2. ACE inhibitors
3. ARBs
4. Nitrates (venodilators)
159
3 Drugs that can decrease afterload
1. ACE inhibitors
2. ARBs
3. Hydralazine (arteriodilators)
160
2 Drugs that can increase contractility
1. Digoxin
2. Beta-blockers
161
5 Drugs that can decrease cardiac remodeling
1. ACE inhibitors
2. ARBs
3. Spironolactone
4. Beta-blockers (metoprolol, carvedilol)
5. Hydralazine + nitrates
162
this drug can cause constriction of the afferent arteriole in the kidney
Acetazolamide: blocks carbonic anhydrase → increased NaCl to macula densa → increase in signal for afferent constriction, decrease in renin secretion → decreased GFR
163
Which CCBs are used for arrhythmias?
Non-DHP
164
Which CCBs are used for HTN?
DHP
165
Non-DHP Calcium Channel Blocker MOA
* Block voltage-gated L-type Ca2+ channels in SA and AV nodes
* Increase duration of Phase 0 (nodal depolarization)
* Decrease SA node automaticity
* Slow conduction thru AV node
* Decrease AV node rate of fire
* Decrease contractility
166
Drug type for VTAC?
Class III Antiarrhythmics -- Potassium Channel Blockers
167
What happens in an arrhythmia, how would you go about treating it, and how does each class of antiarrhythmic affect the physiology?
* Problem w/conduction causes irregular beats
* Target either myocyte AP or SA/AV nodal AP
* Class I: Na+ Channel Blockers -- Myocyte AP, decrease Phase 0 slope
* Class II: Beta-blockers -- Nodal AP, decrease Phase 4 slope
* Class III: K+ Channel Blockers -- Myocyte AP, elongate Phase 3 (increase QT)
* Class IV: Non-DHP Ca2+ Channel Blockers -- Nodal AP, increase Phase 0 slope
168
What happens in each type of heart failure?
* Generally: decreased CO → not enough O2 to tissues
* Systolic: decreased **inotropy** (**force** of contaction) (weaker mm)
* Diastolic: **filling** problem (bigger mm)
* Left side: blood backs up into lungs → congestion
* Right side: blood backs up into portal circulation → edema
169
Cardiac myocyte AP
* Phase 0: voltage-gated Na channels open → rapid depol
* Phase 1: Na channels close, K channels open → initial repol
* Phase 2: Ca channels open, balance K efflux → plateau + myocyte contraction
* Phase 3: Ca channels close, voltage-gated K channels open → rapid repol
* Phase 4: High K permeability → resting potential
170
Cardiac Nodal AP
* Phase 4: increased Na conductance → slow spontaneous depol (slope determines HR)
* Phase 0: Ca channels open → rapid depol
* Phase 3: Ca channels close, K channels open → rapid repol
171
Compensation in Heart Failure
* **Increased SV**
* ADH, Aldosterone → increase filling volume → increase preload
* Myocardial hypertrophy → increased force of contraction
* **Increased HR**
* SNS activation → increased rate of contraction
172
Decompensation in Heart Failure
Compensatory mechanisms eventually lead to increased O2 demand, which exacerbates failure:
* SNS overactivation → decreased receptor response
* ADH/Aldosterone-mediated preload increase → increased myocardial O2 demand → cell death
* Myocardial hypertrophy → increased myocardial O2 demand → cell death
173
How would you treat the physiology of early heart failure?
* **Decrease preload (BP)**
* ACE inhibitors/ARBs
* Hydralazine
* Nitrates
* **Decrease SNS activation**
* Beta-blockers
174
How would you treat the physiology of late heart failure?
1. **Aldosterone Antagonist Diuretics**
* Reduced fluid (congestion) and BP
2. **Ca2+ Channel Blockers**
* Arteriodilation + reduced HR (increased filling time)
3. **Digoxin**
* Increased contractility + reduced HR (increased filling time)
4. **ACE Inhibitors + Beta-blockers**
* Decreased BP
175
CCB C/I
* Heart failure (negative inotropic effect)
* WPW (may accelerate conduction down accessory pathway → Vfib)
176
1st line for most cases of Afib requiring rhythm control
Amiodarone (Class III K+ channel blocker)
177
Drug of choice for acute paroxysmal supraventricular tachycardia?
Adenosine
178
ACE inhibitors do this to the kidney
dilate efferent arteriole → reduce GFR → renal failure in pts w/existing problems (diabetics, renal aa stenosis)
179
2 drugs that can decrease GFR
* Acetazolamide (constrict afferent)
* ACE inhibitors (dilate efferent)
180
this beta blocker also acts as a direct vasodilator
Nevibolol → endothelial NO release
