Cardio 2 Flashcards
(385 cards)
1
Q
Cardiovascular infections
A
Rheumatic fever
Infective endocarditis
Pericarditis
2
Q
Rheumatic fever
A
Autoimmune reaction to infection with group A strep
Group A strep URI progresses to ARF and potentially rheumatic heart disease
Kids 5-14
Molecular mimicry-immune response targets both bacteria and human tissue
-can lead to lysis of endothelial cells on heart valve
3
Q
Heart and ARF
A
Valvular damage
Mitral valve almost always affected
4
Q
Joint pain ARF
A
Knees, ankles, hips, elbows (asymmetric
5
Q
Factors associated with increase risk of ARF
A
Multiple previous attacks of ARF
Short intervals between attacks of acute rheumatic fever
Increased risk of exposure to strep infections
-kids and adolescents, parents of young kids, teachers, physicians, nurses, day care workers, military recruits, individuals living in crowded situations
Young
High risk patient having poor adherence to secondary prophylaxis
6
Q
Empiric treatment ARF
A
Penicillin G and gentamicin
7
Q
Treat ARF if penicillin allergy or hypersensitive to beta lactams
A
Erythromycin, azithromycin, clarithromycin, clindamycin
8
Q
Concern for recurrent acute rheumatic fever in a patient hypersensitive to beta lactams
A
Erythromycin, azithromycin, clarithromycin
9
Q
Clindamycin
A
Not used for prophylaxis of recurrent acute rheumatic fever due to the chance of clindamycin eliciting the opportunistic infection of the GI tract C diff
10
Q
How manage joint pain and fever with ARF
A
NSAIDS like asprin or naproxen
11
Q
Macrolides
A
Erythromycin
Azithromycin
Clarithromycin
12
Q
NSAIDS
A
Asprin (acetylsalicylic acid)
Naproxen
13
Q
Aminoglycosides
A
Gentamicin
14
Q
Infective endocarditis
A
Prototypic lesion=vegetation
Oral-viridans strep
Skin-staph
URI-HACEK
15
Q
Empiric treatment for infective endocarditis
A
Vancomycin (IV) and ceftriaxone
16
Q
Penicillin and strep viridans
A
Great
17
Q
Ceftriaxone and strep viridans
A
Highly penicillin susceptible
Mid penicillin allergy
18
Q
Strep viridans gentamicin and penicillin g
A
Shorter course, no renal disease
19
Q
Gentamicin and ceftriaxone strep viridans
A
Shorter drug course no renal disease
Mid penicillin allergy
20
Q
Vancomycin strep viridans
A
Severe penicillin allergy
21
Q
Penicillin desensitization strep viridans
A
Severe penicillin allergy
22
Q
Strep viridans
A
Highly penicillin G susceptible
-penicillin G or ceftriaxone
No preexisting renal disease, uncomplicated native valve infective endocarditis, shorter drug course
-gentamicin+ penicillin or ceftriaxone
Mid beta lactam sensitivity
-ceftriaxone
Severe beta lactam hypersensitivity (history of anaphylaxis)
-preferred: penicilllin G desensitization
Alternat_vancomycin
23
Q
Penicillin desensitization
A
Small dose of drug that is gradually increased until the therapeutic dose is acheived
-1 unit of drug is given IV and the patient observed for 15-30 min
No reaction=dose gradually increased every 15-30 min
-tenfold or doubling
Cove 2 million units reached, the remainer of dose can be given
24
Q
What kind of reaction is penicillin desensitization
A
IgE mediated allergic
Drug must be physically present to maintainability desensitization
25
S aureus methicillin susceptible
Nafcillin
Oxacillin
26
A aureus MRSA
Daptomycin (Alt)
Vancomycin
27
S aureus mild penicillin allergy
Cefazolin
28
S aureus severe penicillin allergy
Daptomycin
Vancomycin
29
S aureus brain abscess accompanying infective endocarditis
Nafcillin
30
Daptomycin
Similar spectrum of activity as vancomycin
| -gram positive, including MRSA
31
MOA daptomycin
Not known
Binds to the cell membrane via calcium dependent insertion of its lipid tail leading to depolarization, K efflux, and rapid cell death
32
Treat S epidermis and other coagulates negative staphylococci
Vancomycin
33
HACEK treat
Ceftriaxone
34
Enterococci (E faecalis)
Penicillin G or ampicillin or vancomycin)+gentamicin
35
Aminoglycosides
Gentamicin
36
1st class cephalosporins
Cefazolin
37
Aminopenicillin
Ampicillin
38
3rd gen cephalosporin
Ceftriaxone
39
Glycopeptide
Vancomycin
40
Penicillinase resistant penicillins
Nafcillin
| Oxacillin
41
Pericarditis
Inflammation of the pericardial sac
42
Treat pericarditis in immunocompetent patients
NSAIDS (asprin or naproxen)+colchicine
-important to order CRP to track treatment
Corticosteroids (prednisone) are used in severe or refractory cases
-risk prolong illness or to increase the chance of relapse
43
Colchicine pharmacodynamics
Anti-inflammatory action mediated by binding to tubulin
- prevents tubulin polymerization into microtubules
- leads to inhibiton of leukocyte migration and phagocytosis
44
AE colchicine
Diarrhea and occasional nausea, vomiting and abdominal pain
Hair los, bone marrow depression, peripheral neuritis, myopathy
-more likely seen with IV colchicine versus oral colchicine
45
A 42 yo has fever and unintentional weight loss. A diagnosis of IE is made and blood cultures are positive for s epidermidis
Ok
46
A 54 male fever, joint pain, night sweats. Past history of rheumatic fever at the age of 9 and for dental surgery 1 month ago. Symptoms started 2 weeks after dental procedure. PE shows mitral regurgitation. The blood cultures were ordered and an empiric therapy was started
Ok
47
32 females heroin addict was admitted with 2 day fever, shaking, chills, Rigors, and night sweats. Her vitals 100/60, pulse 120, respiration’s 24 , fever. 3 small vegetations tricuspid valve (echo). Three blood cultures drawn and empiric therapy was initiated
Ok
48
Fast action potential
Ventricular contractile cardiomyocytes
Atrial cardiomyocytes
Purkinje fibers
Deconvolution of cationic fluxes of the cardiac AP
49
Slow action potential
SA node
AV node
50
Pacemaker AP phase 4
Slow spontaneous depolarization
- poorly selective ionic influx (NA K) known as pacemaker current (funny current If)-activated by hyperpolarization
- slow Ca influx (T type (transient) Chanel’s)
51
Pacemaker AP phase 0
Upstroke of action potential
Ca influx through the relatively slow L type (long acting ) Ca channels
52
Pacemaker AP phase 3
Repolarization
Inactivation of calcium channels with increased K efflux
53
Factors that determine the rate of firing or automaticity of pacemaker AP
Rate of spontaneous depolarization in phase 4
-decreased slope-decreased rate (need more time to reach threshold potential)
Threshold potential
-the potential at which action potential is triggered
Resting potential
-if potential is less negative, less time is needed to reach the threshold-firing rate increases
54
Class 1 antiarrhythmic drugs
Na channel blocking drugs
55
Antiarrhythmic drugs 1A
Quinidine
Procainamide
Disopyramide
56
1B drugs
Lidocaine
Mexiletine
57
1C drugs
Flecainide
Propafenone
58
Class 2 antiarrhythmic
Beta beta blockers
- esmolol
- propranolol
59
Class 3 antiarrhythmic
K channel blocking
- amiodarone
- sotalol
- dofetilide
- ibutilide
60
Class 4 antiarrhythmic
Cardioactive CCB
- verampamil
- dilitazem
61
Miscellaneous antiarrhythmic
Adenosine
62
Class 1 function of the sodium channel
When sodium channel is activated, Na current occurs down electric and concentration gradients
63
Resting state
The channel is closed but ready to generated AP
64
Activated state
Depolarization to threshold opens m gates greatly increasing Na permeability
65
Inactivated state
H gates are closed, inward Na flux is inhibited , the channel is not available for reactivation-this state is responsible for the refractory period
66
State dependent block
Drugs have different affinities toward the ion channel protein while it shutttles through different states of the cycle
-most therapeutically useful drugs block activated or inactivated Na channels, with very little affinity towards channels in a resting state
67
The role of the ___ form of class 1 drugs in binding to a channel
Cationic
Lidocaine! Bind pka 7.8
68
Kinetics and dissociation na channel blockers
Determines how quickly drugs dissociate fromt he channel
| -fast, intermediate or slow kinetics
69
Class 1A effects
Block Na channels, slow impulse conduction, reduce automatism of latent (ectopic) pacemakers
State dependent block-preferential bind to open sodium chennsle
-ectopic pacemaker cells with faster rhythms will be preferentially targeted
Dissociated from channel with intermediate kinetics
Block K channels
Prolong action potential duration
Prolong QRS and QT intervals of the ECG
70
Class 1B
Block Na channels
State dependent block-bind to inactivated Na channels
-preferentially bind to depolarize cells
Dissociate from channel with fast kinetics-no effect on conduction in normal tissue
May shorten AP
More specific action on Na channels-do not block K channels, do not prolong AP or QT duration on ECG
71
Class 1C
Block Na channels, slow impulse conduction
State dependent block-preferentially bind to open (activated Na channels
Dissociate from channel with slow kinetics
Block certain K channels
Do not prolong AP duration and QT interval duration of the ecg
Prolong QRS interval duration
72
Class 2 drugs
Beta blockers
73
Sympathetic effect on SA nodal cells
Role of cAMP
Effect on the funny current-If
Effect on Ca channels-lower the threshold
Increased slope due to effects of If and T type Ca channels
Reduce threshold due to effect on L type ca channels
74
What drugs class 2
Propranolol
Esmolol
75
How b blockers work
SA node
Decreased HR
AV node
Decreased AV conductance (increase PR interval)
Decreased slope due to effects on If and T type Ca channels
Increased threshold due to effect on L type Ca channels
76
Type 3
K channel blockers
77
Types of K channels
Calcium activated
Inwardly rectifying
Tandem pore domain
Voltage gated
78
K channel blockers regulation of resting potential
Inward (electric) gradient is in equilibrium with the outward (concentration) gradient in the resting cell
Inwardly rectifying k channels are open int he resting state
No current occurs in these channels in a steady state bc of this equilibrium
If extracellular K concentration changes, membrane potential will have to readjust to reach a new equilibrium
79
K channel blockers regulation of action potential
Voltage gated K channels contribute to the regulation of AP
Repolarization of cell membrane during AP
Limit the frequency of AP (regulate the duration of refractory period)
80
Class 3 drugs MOA
Block K channels
Prolong AP duration
Prolong QT interval on ECG
Prolong refractory period
81
Class 4 drugs
Block both activated and inactivated L type calcium channels
Active in slow response cells
- decrease the slope of phase 0 depolarization
- increase L type Ca channel threshold potential
- prolong refractory period in AV node
Decrease the slope of phase 0, increase the threshold of potential at SA node
82
Name class 4 drugs
Verampamil, dilitazem
83
MOA class 4
Slow SA node depolarization, cause bradycardia
Prolong AP and conduction in AV duration and conduction time in AV node
84
Adenosine
Activates K current and inhibtiors Ca and funny currents, causing marked hyperpolarization and suppression of AP in slow cells
Inhibits AV conduction and increases nodal refractory period
Turns on AC increase cAMO and activated protein kinase to open If and ca into cell
K out
85
Clinical use adenosine
Conversion to sinus rhythm in paroxysmal SVT
86
AE adenosine
```
SOB
Bronchoconstriction (both a1 and a2b adenosine receptors cause bronchoconstriction)
```
Chest burning
AV block
Hypotension
87
Phase 0 fast action potential in cardiac muscle
Voltage dependent fast Na channels open as a result of depolarization; Na enters the cells down its electrochemical gradient
88
Phase 1 fast action potential in cardiac muscle
K exits cells down its gradient, while fast Na channels close, resulting in some repolarization
89
Phase 2 fast action potential inc radial muscle
Plateau phase results from K exiting cells offset by and Ca entering through slow voltage dependent Ca channels
90
Phase 3 fast action potential in cardiac muscle
Ca channels close and K begins to exit more rapidly resulting in repolarization
91
Phase 4 fast action potential inc radial muscle
Resting membrane potential is gradually restored by Na/K atpase and Na/Ca exchanger
92
Deconvolutoin of cationic fluxes of the cardiac action potential
Inward Na
Inward Ca
Outward K
93
Phase 4
Slow spontaneous depolarization
- poorly selective ionic influx (na K) known as pacemaker current (funny current If)-activated by hyperpolarization
- slow Ca influx (via t type (transient ) channels)
94
Phase ) upstroke of action potential
Ca influx through the relatively slow L type (long acting) Ca channels
95
Phase 3 repolarization pacemaker action potential
Inactivation of Ca channels with increased K efflux
96
Factors tha determine the firing rate of pacemaker AP
Rate of spontaneous depolarization in phase 4
(Slope): decreased slope-decreased rate (need more time to reach threshold potential)
Threshold potential-the potential at which AP is triggered
Resting potential -if potential is less negative, less time is needed to reach the threshold-firing rate increases
97
Procainamide
Class 1a
98
What is procainamide used to treat
Sustained ventricular tachycardia, may be used in arrhythmias associated with myocardial
99
MOA procainamide
Directly depresses the activities of SA and AV nodes
Possesses antimuscarinic activity
Has ganglion blocking properties, reduces peripheral vascular resistance-may cause hypotension
100
Pharmacokinetics procainamide
Active metabolite N acetylprocainamide has class 3 activity, has longer half life, accumulates in renal dysfunction-measurements of both parent drug and metabolite are necessary in pharmacokinetics studies
101
AE procainamide
Cardiac
- QT interval prolongation
- induction of torsades de pointes arrhythmias and syncope
- excessive inhibition of conduction
Extracardiac
- lupus erythematosus syndrome with arthritis, pleuritis, pulmonary disease , hepatitis fever
- nausea, diarrhea
- agranulocytosis
102
Quinidine
Natural alkaloid from cinchona bark
103
Pharmacodynamics and clinical use
Used occasionally for restoring rhythm in atrial flutter/fibrillation patients with normal (but arrhymic) hearts
Sustained ventricular arrhythmia
In clinical trials patients on quinidine twice as likely have normal sinus rhythm, but the risk of death is increased two to three fold
Affords antimuscarinic effect ont he heart-may enhance AV conductance-consequences for AF treatment
Exhibits beta-blocking activity (effect on PR interval is variable)
May cause hypotension->tachycardia
104
AE quinidine
Cardiac: QT interval prolongation
- Induction of torsades de pointes arrhymia and syncope
- Excessive slowing of conduction throughout the heart
Extracardiac
- GI side effects (diarrhea, nausea, vomiting)
- HA, dizziness, tinnitus (cinchoism)
- thrombocytopenia, hepatitis, fever
105
Disopyramide use
Recurrent ventricular arrhythmias
Affords potent antimuscarinic effect on the heart
106
AE disopyramide
Cardiac-QT interval prolongation, induction of torsades de pointes arrhythmia and syncope, negative inotropy effect-may precipitate heart failure, excessive depression of cardiac conduction
Extracardiac
-atropine like symptoms-urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma
107
Lidocaine MOA
Blocks inactivated sodium channels
| Selectively blocks conduction in depolarized tissue, making damaged tissue electrically silent
108
AE cardiac lidocaine
Rapid kinetics results in recovery form block between AP, with no effect on cardiac conductivity in normal tissue
109
Use lidocaine
Mono and polymorphic ventricular tachycardia
| -very efficient in arrhythmias associated with acute MI
110
Pharmacokinetics lidocaine
Extensive first pass metabolism-used only by the intravenous route
111
AE lidocaine
The least toxic of all class 1 drugs
Cardio-may cause hypotension in patients with heart failure by inhibiting cardiac contractility, proarrhythmic effects are uncommon
Neurological effects: paresthesia, tremor, slurred speech, convulsions
112
Mexiletine
Orally active drug
Electrophysiological and antiarrhythmic effects are similar to lidocaine
113
Clinical use mexiletine
Ventricular arrhythmias
To relieve chronic pain, espicially pain due to diabetic neuropathy and nerve injury
114
AE mexiletine
Tremor, blurred vision, nausea, lethargy
115
Flecainide
1C
Blocks sodium and potassium channels
Has no antimuscarinic effects
116
Clinical use flecainide
In patients with normal hearts
Treating supraventricular arrhythmias including AF, paroxysmal SVT (AVNRT, AVRT)
Life threatening ventricular arrhythmias, such as sustained ventricular tachycardia
117
AE flecainide
May be effective in suppressing premature ventricular arrhythmias when administered to
- patients with preexisting ventricular tachyarrhythmias
- patientswith a previous myocardial infarction
- patients with ventricular ectopic rhythms
118
Propafenone
Class 1C possesses weak b blocking activity
119
Use propafenone
Prevent paroxysmal AF and SVT in patients with structural disease
In sustained ventricular arrhythmias
120
AE propafenone
Exacerbation of ventricular arrhythmias
A metabolic tase
Constipation
Do not combine with the CYP2D6 and CYP3A4 inhibtiors as the risk of proarrhythmia may be increased
121
Clinical indications for the propranolol use in cardiac arrhythmias (class 2 drugs)
Arrhythmias associated with stress
Re-entrant arrhythmias that involve AV node
- AV nodal recent rant tachycardia (AVNRT)
- AV recent rant tachycardia (AVRT)
A fib and flutter
Arrhythmias associated with MI
-decreased mortality in patients with acute MI
122
Asmolol
Short acting selective beta 1 blocker
123
HL esmolol
10 min bc of hydrolysis by blood esterases
124
How is esmolol given
Uses as continuous iv infusion, with rapid onset and termination of its actions
125
Clinical use esmolol
Supraventricular arrhythmias
Arrhythmias associated with thyrotoxicosis
Myocardial ischemia or acute myocardial infarction with arrhythmias
As an adjunct drug in general anesthesia to control arrhythmias in perioperative period
126
AE beta blockers (class 2)
Reduced cardiac output
Bronchoconstriction
Impaired liver glucose mobilization
Produce an unfavorable blood lipoprotein profile (increase VLDL and decrease HDL)
Sedation, depression
Withdrawal syndrome associated with sympathetic hyperresponsiveness
127
Contraindications beta blockers
Asthma
Peripheral vascular disease
Raynaud syndrome
Type 1 diabetics on insulin
Brady arrhythmias and AV conduction abnormalities
Severe depression of cardiac function
128
Amiodarone
Class 3 blocks K channels
129
MOA amiodarone
Prolongs QT interval and APD uniformly over a wide range of heart rates
Blocks inactivated sodium channels
Possesses adrenoleukodystrophy activity
Has calcium channel blocking activities
Causes bradycardia and slows AV conduction
Causes peripheral vasodilation (effect may be related to the action of the vehicle)
130
Clinical use amiodarone
Treatment of ventricular arrhythmias
A fib
131
Pharmacokinetics amiodarone
CYP3A4-its half life is affected by drugs that inhibit CYP3A4 (cimetidine), or induce it (rifampin)
Major metabolite is active, with very long elimination half life (weeks-months)
Effects are maintained 1 to 3 months after discontinuation, and metabolites are found in the tissues 1 year after discontinuation
Inhibits many CYP enzymes-may affect the metabolism the metabolism of many other drugs
All medications should be carefully reviewed in patients on amiodarone-dose adjustments may be necessary
132
AE amiodarone
Cardiac
- AV block and bradycardia
- incidence of torsades de pointes is low as compared to other class 3 drugs
Extracardiac
- fatal pulmonary fibrosis
- hepatitis
- photodermatitis, deposits in the skin, give blue grey skin discoloration in sub exposed areas
- deposits of drug in cornea and other eye tissues, optical neuritis
- blocks the peripheral conversion of thyroxine to tiiodothyronine, also a source of inorganic iodine in the body-may cause hypo or hyperthyroidism
133
Sotalol
Class 2 (non selective beta blocker) and class 3 agent (prolongs APD)
134
Clinical use sotalol
Treatment of life threatening ventricular arrhythmias
Maintenance of sinus rhythm in patients with a fib
135
AE sotalol
Depression of cardiac function
Provokes torsades de pointes
136
Dofetilide
Class 3
137
MOA dofetilide
Specifically blocks rapid component of the delayed rectifier potassium current-effect is more pronounced at lower heart rates
138
Pharmacokinetics dofetilide
Eliminated by kidneys, has very narrow therapeutic window-dose has to be adjusted based on creatinine clearance
139
Use dofetilide
Convert AF to the sinus rhythm and maintain the sinus rhythm after cardioversion
140
AE dofetilide
QT interval prolongation and increased risk of ventricular arrhythmias
141
Ibutilide
Similar to dofetilide, slows cardiac repolarization by blockade of the rapid component of the delayed rectified potassium current
142
How give ibutilide
IV and rapidly cleared by hepatic metabolism
143
Use ibutilide
Convert a flutter and a fib to sinus rhythm
144
AE ibutilide
QT interval prolongation and increased risk of ventricular arrhythmias
Patients require continuous ECG monitoring until QT returns to baseline
145
Clinical use verampamil, dilitiazem
Prevention of paroxysmal SVT
Rate control in AF and a flutter
146
AE verampamil, dilitazem
Cardiac
- negative inotropy
- AV block
- SA node arrest
- bradyarrhythmias
- hypotension
Extracardiac
-constipation (verampamil)
147
Clinical use adenosine
Conversion to sinus rhythm in paroxysmal SVT
148
AE adenosin
SOB
Bronchoconstriction (both a1 and a2b adenosine receptors cause bronchoconstriction)
Chest burning
AV block
Hypotension
149
MOA adenosin
Activates K current and inhibits Ca and funny currents, causing marked hyperpolarization and suppression of action potentials in slow cells
Inhibits AV conduction and increases nodal refractory period
150
Proarrhythmia
Drug induced significant new arrhythmia or worsening of an existing arrhythmia
151
Torsades de pointes (TdP, twisting the pointe)
Rapid form of polymorphic VT associated with the evidence of prolonged ventricular repolarization (long QT syndrome)
152
What is long qt and torsades de pointes associated with
Often associated with the impaired function of K channels leading to a prolonged period of repolarization
153
What exacerbates long qt and torsades de pointes
Factors that prolong action potential duration
- slow heart rates
- electrolyte abnormalities (hypokalemia, hypomagnesemia)
154
Drugs causing long qt syndrome and torsades de pointes arrhythmias
Antiarrhymic drugs-groups 1A and 3 (amiodarone very rarely induces TdP)
Antipsychotics
Antihistamines
Antibiotics
Antidepressants
155
Long qt syndrome and torsades de pointes
TdP
156
Mechanism of TdP arrhythmias:
A type of a triggered activity resulting from early afterdepolarizations
157
Triggered activity
Depolarizing oscillations in the membrane potential induced by the preceding AP
158
Early afterdepolarizations
Often associated with the impaired function of K channels leading to a prolonged period of repolarization
Abnormal depolarizations that occur during phase 2 or phase 3 of AP are due to the opening of Ca or Na channels, respectively
159
To prevent TdP, monitoring what is necessary
QTc (QT corrected for heart rate)
160
Do not give TdP inducing drugs if QTis
>450 ms
161
What drugs cause long QT
Many
FDA ordered cardiotoxicity studies
- a number of long QT inducing drugs have been removed from the market
- requirement to test the effect of new drugs on QT interval before they are approved
162
Termination of TdPs if drug induced
Discontinuation of the potentially causative agent
163
Termination of TdPs if hemodynamically unstable
Immediate synchronized direct current cardioversoin
Correction of electrolyte abnormalities, such as hypokalemia and hypomagnesemia
Magnesium sulfate iv irrespective of whether the patient is hypomagnesemia or not
Transvenous temporary pacemaker for overdrive pacing or isoproterenol iv
164
Flecainide and other 1C drugs
Cause ventricular arrhythmias, such as PVCs, sustained VT and VF
165
Flecainide
Was included in cardiac arrhythmia suppression trial (CAST), a. Long term multi center, randomized double blind study in patients with asymptomatic non life threatening ventricular arrhythmias who had a MI
An excessive mortality or non fatal cardiac arrest rate was seen in patients treated with flecainide compared with that seen in a carefully matched placebo treated group
166
Why was CAST terminated prematurely
Bc flecainide and other class 1C drugs increased the mortality by 2.5 fold
167
MOA of digoxin induced arrhythmias
Tachyarrhymias and ectopic rhythms
- a type of a triggered activity resulting from delayed afterdepolarization
- occur during phase 4 as a result of increased cytosolic Ca due to Ca overload
- spontaneous Ca release from SR activated 3 Na/Ca exchange leading to a net depolarizing current
168
Bradyarrhythmias and AV blocks digoxin
Central parasympathetic activity accentuation of vagal effects on the heart
169
Treatment of digoxin induced arrhythmias
Cancel digoxin
Anti-digoxin antibodies
K supplementation to upper normal levels
170
A fibrillation
Ventricular Rate Control (see the scheme on the next slide)
- ca channel blockers
- beta blockers
- digoxin
- amiodarone
171
What do with paroxysmal or persistent AF
Assess LV function
-no HF, LVEF >40%->CCB or B block->CCB and digoxin or b blocker and dogoxin->amiodarone
HF with LVEF<40%->B blocker->B blocker and digoxin->amiodarone
Decision algorithm for long term ventricular rate control therapy. Goal less than 100 bpm or 20% reduction rate reduction with symptom relief. If goal is not met, move to the next step in algorithm
172
Stroke prevention in patients with a fib
Most patients require therapy with oral anticoagulants
In patients with no risk factors for stroke, anticoagulation may not be necessary
173
CHADS score
```
CHF 1 point
HTN 1 point
Age greater than or equal to 75 1 point
Diabetes 1 point
Stroke TIA history 2 points
```
174
CHADs score 0
Low degree of risk for a fib
Antithrombotic therapy is not recommended. For patients who choose antithrombin therapy: asprin 75-325 mg daily
175
CHADs >1
Moderate high risk for a fib
Give oral anticoagulation with warfarin or DOAC
176
A fib treat
Rhythm control (conversion to sinus rhythm)
Maintence of sinus rhythm after conversion to sinus rhythm
177
Rhythm control
Cardioversion using direct current cardioversion
Pharmacological (chemical) cardioversion
- amiodarone
- flecainide
- dofetilide
- ibutilide
- propafenone
178
Maintenance of sinus rhythm after the conversion to sinus rhythm
```
Dronedarone
Flecainide
Propafenone
Sotalol
Amiodarone
Dofetilide
Catheter ablation
```
179
AF-> consider DCC-> if DCC is unreadable to undesirable or unsuccessful, consider what
- no HF, LVEF>40%->amiodarone, dofetilide, flecainide, ibutilide, propafenone
- HF with LVEF <40->amiodarone, dofetilide ibutilide
Decision algorithm for conversion of hemodynamically stable AF to sinus rhythm
180
Termination paroxysmal supraventricular tachycardia
Adenosine
Verampamil or dilitazem
Beta blockers
Digoxin
Amiodarone
181
Prevention paroxysmal supraventricular tachycardia
Verapamil
Digoxin
Catheter ablation
182
PSVT_>vagal maneuvers->adenosine
- LVEF>40% or no history of HF->dilitazem or verampamil->b blocker->digoxin
- LVEF<40% or history of HF->digoxin->amiodarone->dilitazem
183
Treat AV block
Rarely necessary; patients should be monitored
184
Acute high grade AV block that is symptomatic
Atropine
If ineffective, dopamine or epinephrine
-transvernous cardiac pacing can be initiated
185
Long standing AV second or third degree block
If patients take medications that may cause AV block, the drugs should be discontinued
-if AV block persists, or discontinuation of drugs causing AV block is undesirable, implantation of a permanent pacemaker is indicated
186
Drugs for heart failure
ACE inhibitors
ARBC
Carvedilol
Spironolactone
Diuretics
Direct vasodilators
Digoxin
Dobutamine, dopamine, milrinone
187
Name ACE inhibitors
Prils
188
Name ARDS
Losartan
Vallarta’s
Sacubitril
189
Name diuretics
Loop, thiazide, k sparing
190
Name direct vasodilators
Nitroglycerin/isosorbide, dinitrate, nitroprusside, hydralazine
191
What is Cor pulmonale
Right sided heart failrue due to increased pressure transferred back through lungs bc of left side HF
Causes include COPD, interstitial lung disease, pulmonary HTN, thromboembolic disease, obstructive sleep apnea
192
High output heart failure
Body’s need for cardiac output is abnormally elevated to a point beyond the hearts capabilityy
Causes include hyperthyroidism, preg, anemia, arteriovenous fistula, wet beri
193
Major causes of HF
Coronary artery disease/MI
Chronic HTN
Diabetes
194
Systolic failure
Decrease ESPVR slope
Increase ESV and EDV
Decrease SV and EF
195
Diasolic failure
Increase EDPVR
Decrease EDV
Increase end diastolic pressure
196
Systolic HF characteristics
Reduced LVEF
-usually 60-70%
With SHF, LVEF<50%=HFrEF
Progressice chamber dilation ith eccentric remodeling
197
Characteristics of DHF
Prevelance now estimated at 40-69% of HF; espicially common finding in elderly women
Preserved HFpEF
198
What does CHF cause
Poor tolerance of a fib since loss of atrial contraction-> decreased ventricular filling
-poor tolerance of tachycardia since shorter duration of diastole limited time for relaxation and filling
Worsened by increase MAP, espicially if abrupt or severe
Worsening of DHF by ischemia raises left atrial pressure->angina pain with wheezing, SOB, flash pulmonary edema
199
Digitalis
Decreased hospitalization
Did not prolong life
People felt better right up until the moment they would have otherwise dies and then died typically due to a fatal arrhythmia
200
Consequences of vascular remodeling
High pressure in the ventricle during systole and diastole heightens myocardial oxygen consumption, a situation that promotes further hypertrophy and activates neurohormonal systems
- reduction in ejection fraction
- reduced ventricular erformance
- morbid and mortality
And incrase in CO is transient and never enough so cycle repeats continuously with diminishing returns
201
Adaptive mechanisms in HF from a drop in CO
Increase renin
Increase aldosterone
Increase sympathetic discharge
Increase in preload and afterload of the heart
Increase in release of Natiuretic peptides (effects are overwhelmed
Increase INR emodeling of the heart..deleterious, leads to cycle of worsening heart function
202
MI remodeling
Fibrous scar tissue , spherical ventricular dilation with hypertrophy of adjacent myocytes surround by increased levels of collagen
203
What are the thee patterns of remodeling after an MI
Concentric
Eccentric hypertrophy
Concentric hypertrophy
204
Heart failure treatment objectives
Remove the precipitating cause
Correct the underlying cause
Prevent deterioration of cardiac function
-ACI/ARB/BB/spironolactone/eplerenone
Control the CHF state
-diet, diuretics, vasodilators to Reduce cardiac work, dogixin to increase contractility
205
RAAS inhibtors
Aliskiren
ACEI
ARB
Spironolactone
206
Aliskiren
Block angiotensinogen to angiotensin I
Renin inhibitor
207
ACE_
Block angiotensin I to II
Kinase I
208
ARB
Block angiotensin II action on kidney and adrenal gland (which reduced aldosterone)
AT1 receptos
209
Spironolactone
Stops aldosterone action on the kidney to reabsorbed NaCl and water
210
How do ACE and ARB work-major drugs for heart failure! Have been shown to increase survival in heart failure patients (high doses required)
Prils and Spartans
Less angiotensin II leads to
- less vasoconstriction (decreased afterload
- less aldosterone secretion and less Na/water retention (decrease preload)
- decrease cell proliferationa and remodeling
211
MOA captopril (ACE)
Competitive inhibitor of angiotensin converting enzyme ACE
212
Effects captopril
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor and nitrogen for cardiovascular remodeling
Lowers levels of angiotensin II-> increase plasma renin activity and decrease aldosterone secretion
Lowers BP
213
Clinical captopril
HTN, add thiazide or loop diuretic if additional lowering is needed at max recommended dose
Acute HTN
HF with reduced ejection fraction (HFrEF)
LV dysfunction following MI
Diabetic nephropathy
O
214
Pharmacokinetics captopril
Rapidly absorbed
CYP2D6
Excreted primarily in uring 40-50% as unchanged drug
HL 1.7 hours
215
AE captopril
Cough
Hypotension
Angioedema
216
Enalapril
Another early ACEI, a prodrug with active form
217
Benazepril
Now widely used ACE inhibitor, longer HL permitting 1 day dosing
218
Lisonopril
Now widely used ACE inhibtors, longer HL permitting once day dosing
219
Losartan MOA
Competitive nonpeptide angiotensin II receptor antagonist with 1000x greater selectivity for AT1 than AT2 receptor
220
Effects losartan
Blocks vasoconstrictor and aldosterone secreting effects of angiotensin II
Induces a more complete inhibition of the renin angiotensin system than ACE inhibtiors
Dose not affect the response to bradykinin
221
Clinical losartan
Heart failure if intolerant to ACEI
Off label Marian
HT
222
Pharmacokinetics losartan
CYP2C9 and 3A4
1/2 is 6-9 hours
223
AE losartan
With diabetic nephropathy
Fatigue, dizzy, fever
Hypoglycemia, hyperkalemia,
Cough
Anemia, weaknesss
224
Vallarta’s
6-10 hours
Not a prodrug requiring activation
225
Candesartan
5-9 hours
Irreversible binding
226
Valsartan/sacubitril MOA
Prodrug that inhibits neprilysin through the active metabolites LBQ657
Valsartan ARB
Drugs are co-crystallized
227
Effects valsartan/sacubitril
Block leads to increased levels of peptides, including netriuretic peptides
Valsartan antagonizes AT1 receptors
228
Clinical valsartan/sacubitril
HF to reduce risk of cardiovascular death and hospitalization
229
Pharmacokinetics valsartan/sacubitril
Twice daily dosing
LBQ657 11 hours
Valsartan 9 hours
230
AE valsartan/sacubitril
Common
Hypotension
Hyperkalemia
Increased serum creatinine
231
When secrete natriuretic peptide
Atrial distention
Sympathetic stimulation
Angiotensin II
Endothelin1
232
Blocks neurologic endopeptidase by valsartan/sacubitril
Blocks degradation of ANP
233
Effects of ANP
Increase GFR, decrease renin, decrease aldosterone, decrease Na and water reabsorption in collecting duct
Decrease ADH secretion and ADH effects in collecting duct
234
ACE or ARB better
Same
235
Who gets ACE ARB
```
All patients with LV systolic failure or LV dysfunction without heart failure unless:
Not tolerated
-pregnant
-hypotensive
-serum creatinine >3
-hyperkalemia
```
236
HF increases sympathetic activity
Increase HR, myocardial contractility, vascular resistance
237
What beta blockers use in HF
Metoprolol
Bisoprolol
Carvedilol* best
Not all beneficial!
238
Carvedilol MOA
A racemic mixture is a nonselective beta and alpha adrenergic blocker with no intrinsic sympathomimetic activity
239
Effects carvedilol
In HT, reduction of cardiac output, exercise or beta agonist induced tachycardia, reflec orthostatic tachycardia
Increased ANP
In CHF, decreased pulmonary capillary wedge pressure, pulmonary artery pressure, heart rate, systemic vascular resistance, right atrial pressure
-increased stroke volume index
240
Linical carvedilol
If clinically stable,
Recent or remote history of MI or ACS and reduced ejection fraction (rEF;<40)
REF to prevent symptomatic HF
Reduced morbidity and mortality
241
Pharmacokinetics carvedilol
Rapid and extensive absorption
CYP2D6, 2C9, 2D6, 3A4, 2C10, 1A2, 2E1
242
AE carvedilol
Hypotension, bradycardia, syncope, edema, angina, AV block
Impotence
Blurred vision
Cough, anemia
243
Labetalol
Another alpha/beta blocker used primarily for severe HTN, treatment of hypertensive emergencies
244
Carvedilol
Prevent down regulation of B1 adrenergic receptors in the heart as a result of excessive sympathetic stimulation
245
What does carvedilol do
Keeps heart responsive to sympathetic drive
Protects against dysrhthmias
Reduce renin secretion
Reduces myocardial oxygen consumption
Limits heart msucle remodeling and reduces necrosis and apoptosis of myocardial cells
246
How give carvedilol
Low dose initially with caution in patients that is stable
ONLY GIVE TO CLINCIALLY STABLE
247
Who give carvedilol
Patients with diastolic heart failure will benefit from a lower heart rate
B blockers should be given to all patients with symptomatic CHF and LVEF<40% unless contraindication
- bronchospasm is disease
- symptomatic bradycardia or heart block
With ACE I to all patients with left ventricular systolic dysfunction caused by myocardial infarction to reduce mortality
248
AE carvedilol
Allergy
Chest pain, discomfort, tightness, or heaviness
Dizziness, lightheaded ness, or fainting
Generalized swelling or swelling of the feet, ankles or lower legs
Pain
SOB
Bradycardia
Weight gain
Angina/heart attack if abruptly iscontinued
249
Ivabradine MOA
Selective and specific inhibition of the hyperpolarization
| -activated cyclic nucleotide gated (HCN) channels (f channels) within the SA node of cardiac tissue
250
Effects ivabradine
Disrupts If (funny current) to prolong diastole and slow HR
251
Clinical ivabradine
Treatment of resting HR >70 bpm in patients with stable , symptomatic chronic heart failure <45% who are in sinus rhythm with
- max tolerated dose of beta blockers
- contraindication to use beta blocker use
252
Pharmacokinetics ivabradine
PO 40% bioavailability due to intestinal and hepatic CYP3A4
6 hours
253
AR ivabradine
Bradycardia, HTN, increase risk of a fib , heart block, SA arrest
254
Spironolactone MOA
Competitive antagonist of aldosterone receptors, decreases aldosterone stimulated gene expression
Side effects due in part to it being a partial agonist at androgen receptors
255
Effects spironolactone
K sparing diuretic, blunts ability of aldosterone to promote NaK exchange in collecting duct
256
Clinical spironolactone
Counteracts K loss induced by other diuretics in the treatment of HTN, heart failure, ascitestreatment of primar hyperaldosteronism
Reduce fibrosis post MI
257
Pharmacokinetics spironolactone
Drug has active metabolites including canrenone with 20 hour 1.2
Steroid effects are slow on and slow off....single dose give effects 2-3 days
258
AE spironlactone
Hyperkalemia
Amenorrhea hirstiutism
Gynecomastia
Impotence
Tumorigen inchronic animal toxicity studies
259
Eplerenone
More selective aldosterone antagonist, approved for use in post MI heart failure and alone or in combo for treatment of HTN
260
Spironolactone and ep
Competitive inhibtiors of the mineralocorticoid, aldosterone
| -increases plasma K, decreases plasma Na and volume by opposing the effects of aldosterone on kidney
261
Beneficial heart effects of spironolactone after MI
Decrease myocardial fibrosis
Reduces early morning rise in heart rate
Reduces mortality and morbidity in patients with severe HF
Prevent Na and water retention, k loss, mg los, reduced baroreceptor reflex, cardiac fibrosis, ischemia, sympathetic activation
262
After damaged heart vasculature synthesizes aldosterone after MI...
Locally produced aldosterone contributes to cardiac fibrosis
263
Clinical use spironolactone
Cardioprotective, antifibrotic and antiarrhythmic effects have been proven in animal experiments
Effects on morbidity and mortality have been demonstrated in RCT
Approved for treatment of symptomatic HF with reduced systolic function but...
-most underutilized of all classes of medications for HF< primarily bc of feat of hyperkalemia
264
Sarcomere length vs strength
Cardiac has longer length than skeletal but similar tension?
265
Furosemide MOA
Directly inhibits reabsorption of Na and Cl in the thick ascending limb of the TAL by blocking Na K 2Cl
Indirectly inhibits paracellular reabsorption of Ca and Mg by the TAL due to loss of K backleak responsible for lumen +transepithelial potential
266
Effects furosemide
Causes increased excretion of water, Na, K, Cl, mg and Ca
267
Clinical furosemide
Edema
-HF, hepatic, renal
Acute pulmonary edema by decreasing preload
- decreases EC col
- rapid dyspnea
Treatment of HTN
Works if low GFR
268
Pharmacokinetics furosemide
IV-5 min onset
PO-30-60 min
IM-30 min
269
AE furosemide
Hypok, na, ca, mg,
Hypochloremic met alkalosis
Hyperglycemia
Hyperuricemia
Ototoxicity
Sulfonamides, so risk hypersensitivity
270
Torsemide
Sulfonamide similar to furosemide with longer t1/2 better oral absorption and some evidence that is works better in heart failure
271
Bumetanide
Sulfonamide similar to furosemide, but more predictable oral absorption
272
Ethacrynic acid
Non sulfonamide loop diuretic reserved for those with sulfa
273
Hydrochlorothiazide MOA
Inhibits Na reabsorption in the distal tubules cia blockade of Na Cl cotransporter
274
Effects hydrochlorothiazide
Increases urinary excretion of Na and H2O
Also increases urinary excretion of K and Mg
K losing
275
Clinical hydrochlorothiazide
HTN
Not ok if GFR low
Edema
Calcium nephropathy Asia
276
AE hydrochlorothiazide
Sulfonamide-hypersensitivity
Hypok, mg, na,
Hypochloremic metabolic alkalosis
277
Chlorothiazide
Similar to HCTZ but poor oral absorption
278
Chlorthalidone
Similar to HCTZ but half life of 40-60 hrs...prolonged stable response with proven benefits is reason it is preferred
279
Metolazone
Another long acting thiazide diuretic , favorite of cardiologists for use as an adjunct diuretic int he treatment of CHF
280
What do diuretics help with in HF
Relieve congestion
| -must get rid of excess volume to relieve the congestion and return ventricular fiber length to more optimal range
281
Which diuretics try first
1. Loop
Add K sparing if needed
If still need more diuresis give thiazide
282
Causes of diuretic failure during heart failure treatment
Noncompliance
Excess dietary Na
Decreased renal perfusion and GFR from
-excessive volume depletion and hypotension due to aggressive diuretic or vasodilator therapy
-decline in CO due to worsening HF, arrhythmias or other primary cardiac causes
-selective reduction in glomerular perfusion pressure following initiation or dose increase of ACEI therapy
NSAID
Renal
Reduced or impaired diuretic absorption due to gut wall edema and reduced splanchnic blood flow
283
Vasodilators for chronic HF
Isosorbide dinitrate (to dilate veins, decrease preload) plus hydralazine (dilate arteries, decrease afterload)
- packaged as BiDil
- espicially in african Americans
- new frontier of personalized medicine, the first drug even intended for one racial group
- the reason why whites fail to respond is unknown
Can consider in patients who cant tolerate ACE I
284
Nitroglycerin MOA
Forms free radical NO, which in SM activates soluble granulated cyclase to increase cGMP->dephosphorylation of myosin light chains and smooth muscle relaxation
285
Effects ntiroglycerin
Produces a vasodilator effect on the peripheral veins and arteries with more prominent effects ont he veins
Primarily reduces cardiac oxygen demand by decreasing preload
May modestly reduce afterload
Dilated coronary arteries/improves collateral flow
286
Clinical nitroglycerin
Treatment or prevention of angina pectoris
Acute decompensated HF (specially when associated with acute MI)
Perioperative HTN
287
AE nitroglycerin
Reflex tachycardia
Flushing
Hypotension
288
Isosorbide dinitrate
Slower onset of action, administered orally for prevention of angina and for HF with reduced ejection fraction
289
Hydralazine MOA
Not understood
Endothelium dependent
Hyperpolarized
Requires COX
Mediated by PGI2
290
Effects hydralazine
Direct vasodilation of arterioles_>decreased systemic resistance
291
Clinical hydralazine
HTN(not Initial)
HF with reduced ejection fraction if intolerance to ACE or ARB
HF with reduced ejection fraction NYHA class III IV (self identified african American)
Hypertensive emergency in pregnancy
Post op htn
292
pharmacokinetics hydralazine
Ordeal or IV
Hepatically acetylated with extensive first pass effect
293
AE hydralazine
Angina pectoris flushing peripheral edema, tachycardia
Drug induced lupus like syndrome
Pruritis
294
Digoxin MOA
Inhibits Na K ATPase pump in myocardial cels
295
Effects digoxin
Increased contractility
Direct suppression of AV node conduction
Positive inotropic effect, enhanced vagal tone and decreased ventricular rate to fast atrial arrhythmias
296
Clinical digoxin
Control of ventricular response rate in adults with chronic a fib ...
Treatment of mild to moderate Herat failure in adults and pediatric patients to increase myocardial contractility
297
Pharmacokinetics digoxin
Administered orally
1/2 is 36-48 hours
-needs a loading dose
Crosses the placenta but long history of safe in preg with supraventricular tachycardia
298
AE dogixin
Accelerated junctional rhythm, asystole, a tachycardia with or without block , AV dissociation, first second or third block, PVC(bigeminy or tri), ST depression, ventricular fib,
Mental disturbances, rash, laryngeal edema
299
Digitalis
Naturally occurring
Increases myocardial contractility
-increase cardiac output, decrease sympathetic tone, increase vagal tone
300
AE digitalis
Severe dysrhythmias
301
MOA digitalis
Blocks Na K atpase
302
Why get digitalis toxicity
Myocytes become overloaded with Ca and spontaneous oscillatory uptake and release from the SR causes delayed afterdepolarizations and aftercontractions contributing to arrhythmias...excess free radicals
303
Cardiac effects digoxin
Positive inotropic action on the heart
Increases the force of ventricular contraction
304
How tell if too little or too much dogixin
K!
305
Hemodynamically benefits dogoxin
Increased CO
-decreased sympathetic tone
Increased urine production
Decreased renin release
306
Electrical effects digoxin
Increases the firing rate of vagal fibers
Alters the electrical properties of the heart
-increases the responsiveness of the SA node to acetylcholine
307
Automaticity digoxin
Increase or decrease SA
Increase purkinje
308
Duration of refractory period digitalis
Increase AV node
Decrease ventricular myocardium
Incrase purkinje fibers
309
Excitability digoxin
Increase atrial myocardium
Increase purkinje fibers
Increase ventricular myocardium
310
Conduction velocity digoxin
Increase atrial myocytes
Decrease AV node
Increase ventricular myocardium
311
Overall digoxin
Uncouple atria from ventricles while making regular cardiomyocytes more twitchy/prone to arrhythmias
312
Effects of digoxin ecg
Depression of ST and longer PR
Toxic effect of digitalis on AV conduction involves AV dissociation
-lack of relationship between P and QRS
Toxic effect of digitalis on purkinje automaticity and ventricular refractory perior results one ctopic ventricular beats
-arrow shows example of bigeminy (ectopi beat alternating with normal beat)
313
What must be normal before giving digoxin
HR
314
Non cardiac effects digoxin
Anorexia, nausea, vomiting, salivation
Excessive urination
Fatigue, visual disturbances (blurred vision, halos, yellowish or greening tinge to objects)
315
Digoxin treatment for too much
KCI
Lidocaine
Phenytoin
Antidigitalis antibodies
316
Drug interactions digoxin
Diuretics cause hypokalemia, which leads to increased digoxin binding, which leads to increased digoxin toxicity
ACE and ARB cau increase K levels decreasing digoxin effect
Sympathomimetics
Quinidine ,spironolactone, verampamil, propafenone and alprazolam are among a range of drugs that interfere with clearance of digozin
317
Clinical digoxin
Used in patiets with left ventricular systolic heart failure in combinations ith diuretics, b blockers and ACE inhibits
Espicially useful in patients with a fib...benefit comes from prolongation of the effective refractory period at the AV node
318
Pharmacokinetics digoxin
Readily absorbed but affected by disease states , other drugs, bioavailability can be inconsistent dissolution of oral formations
Cross placenta
Eliminated by renal
HL 1.5 days...loading dose is required to get beneficial effects immediately
319
Loading dose digoxin
For when u need that therapeutic concentration now
320
ACC/AHA A HF
At high risk HF but without structural heart disease or symptoms of HF
321
ACC/AH B HF
Asymptomatic
322
ACC/AHA structural heart disease with prior or current symptoms of HF
Symptomatic with moderate exertion
Symptomatic with minimal exertion
323
ACC/AHA D HF
Advanced structural heart disease with marked symptoms of HF at rest despite maximal medical therapy. Specialized interventions required
Symptomatic at rest
324
Drug to reduce fluid volume
Thiazide and loop diuretics
325
Drug to reduce synthesis of angiotensin II to prevents remodeling
ACEI
326
Drug to reduce effect of angiotensin II at receptor preventing remodeling
Angiotensin II receptor blockers
327
Inhibits effects of aldosterone
Spironolactone
328
Direct cardiotonic effect
Digitalis
329
Reduce sympathetic effect
Prevent remodeling
Prevent arrhythmia
B blockers
330
Reduce afterload and preload
Vasodilators
331
Drug choice overview for HFpEF (diastolic failrue)
Neutral results from clinical trials so must direct therapy at symptoms and associated conditions Cush as
-HTN, lung disease, CAD, a fib, obesity anemia, DM, kidney disease, sleep disordered breathing
Exercise is beneficial and need but avoid: tachycardia, abruptin increase in bp, ischemia, a fib
Use judicially: loop diuretics to treat edema....but decrease preload too much, decrease CO, hypotension, death
Spironolactone...mixed benefit
If justified symptoms-bb, ACEI.ARB, CCB
No evidence of benefit-nitrates, digoxin, PDE5 inhibtiors
332
Adherence causes of acute decompensated HF
Dietary
Nonadherance to meds
Iatrogenic volume overload
Significant drug interactions/side effects associated with new drug addition
333
Cardiac causes of ADHF
Myocardial infarction and myocardial ischemia
Valvular disease
A fib
Progression of underlying cardiac dysfunction
Stress
Toxic agents
334
Non cardiac cause of ADHF
HTN
Renal fail
Pulmonary emboli
335
Symptoms of ADHF
Acute dyspnea, orthopnea, tachypnea, tachycardia, and HTN
Hypotension reflects severe disease and arrest may be imminent; assess for inadequate peripheral or end organ perfusion
Accessory msucles used to breathe
Diffusion pulmonary crackles are common ; wheezing (cardiac asthma0 may be present
S3 is specific sign but may not be audible; elevated jugular venous pressure and/or peripheral edema may be present
336
ECG ADHF
Looks for evidence of ischemia, infarction, arrhythmia, and left ventricular hypertrophy
337
Obtain portable chest radiograph ADHF
Look for signs of pulmonary edema, cardiomegaly, alternative diagnosis; normal radiograph does not rule out ADHF
338
Blood ADHF
CBC, troponin, electrolytes, BUN and cr, arterial blood gas, liver functions ests, BNP or NT proBNP if diagnosis is uncertain
339
Echo ADHF
If cardiac or valvular function is not known
340
ADHF now hat
Place in seated position
All need continuous pulse oximetry and supplemental oxygen and assisted ventilation to ensure adequate ventilation and oxygenation
Assess blood pressure noting if HTN or hypotensive set up for continuous cardiac monitoring
Monitor urine output
Give 2 IV lines
341
All patients with ADHF ate volume overloaded
Must get rid of excess volume to relieve the congestion and return ventricular fiber length to more optimal range
-differs from cardiogenic shock, where volume needs to be checked first
Initiate diuretic therapy
342
Purpose of diureticsin ADHF
Use loop fits
Add k if needed
If need more add thiazide
343
Vasodilators for ADHF
Nitroprusside:dilates both arterial and venous
Nitroglycerin: dilates venous..decrease preload
344
HTN ADHF
Diuretic and vasodilator (nitroglycerin, nitroprusside)
345
Normotensive ADHF
Diuretic and vasodilator (nitroglycerin)
346
Hypotensive ADHF
Diuretic
347
Nitroprusside MOA
Forms free radical NO which in MS activeate cGMP and dephosphorylates myosin light chains...SM relax
348
Effects nitroprusside
Peripheral vasodilation by direct action on venous and arteriolar smooth muscle
Reduces peripheral resistance
Will increase cardiac output by decreasing afterload
Reduces aorta and left ventricular impedance
349
Clinical nitroprusside
HTN crises
ADHF
Controlled hypotension to reduce bleeding during surgery
Acute ischemic stroke
350
Pharmacokinetics nitroprusside
IV 1/2 is 2 min
Metabolism generates cyanide
Eliminated in urine as thiocyanate
351
AE nitroprusside
Tachycardia, ecg changes, flushing, hypotension, palpitation, substernal distress, increased intracranial pressure
Metabolic acidosis from cylinder toxicity
Tinnitus(thiocyanate toxicity)
352
Nesiritide MOA
Synthetic B natiuretic peptide
Binds to guanylate cyclase receptor on vascular smooth muscle and endothelial cells surface to increase intracellular cGMP
353
Effects nesiritide
Increases intracellular cGMP resulting in smooth muscle cell relaxation
Produces dose dependent reductions in pulmonary capillary wedge pressure and systemic arterial pressure
354
Clinical nesiritide
Treatment of acutely decompensated HF with dyspnea at rest or with minimal activity
355
Pharmacokinetics nesiritide
Proteolytic cleavage by vascular endopeptidase
Proteolysis following binding to the membrane bound natiuretic peptide ND CELLULAR INTERNALIZATION
1/2 IS EIGHT MINUTES
356
AE NESIRITIDE
HYPOTENSION
Increased serum creatinine
Vent tachycardia
Ventricular extrasystoles, angina, tachycardia, a fib, AV node conduction abnormalities, pruritis, rash,
Amblyopia
Apnea, cough increased, hemoptysis
357
What do catecholamines do
B-AR increase cAMP and PKA and msucle contraction
358
Discontinue carvedilol
Kind of hard to stimulate adrenergic receptors when they’re blocked
359
Inotropic agents
Short term rescue therapy in ED/ICU
Indicated if symptomatic hypotension with end organ dysfunction despite adequate filling pressure
360
Sympathomimetics
Dobutamine
Dopamine
361
Dobutamine
Synthetic catecholamines
Selectively activates B1 adrenergic receptors, preferred
362
Dopamine
A catecholamines, activates B1 adrenergic receptors in the heart to increase HR and contractility
Also stimulates a adrenergic receptors at higher doses
363
Phosphodiesterase inhibitors
Block the degradation of cAMP in heart and blood vessels
Prototype: milrinone
Restyling increases in cAMP lead to increased contractility in heart, vasodilation
Must be given IV , so genereally not suitable for outpatient use..can be combined with sympathomimetics
Have been shown to decrease survival in some studies
But may help if patient is not responding
364
Dobutamine MOA
B1 and b2 adrenergic receptors
365
Effects dobutamine
Increased contractility and heart rate
Lowers central venous pressure and wedge pressure, little effect pulmonary vascular resistance
366
Clinical dobutamine
Short term management of patients with cardiac decompensation
367
Pharmacokinetics dobutamine
IV
| Metabolized by liver
368
AE dobutamine
Tachycardia, ventricular premature contractions, angina, palpitations, HTN
Headache, paresthesia
Local pain
Dyspnea
Fever
369
Dopamine MOA
Activates B1 adrenergic receptors at low doses and stimulates a adrenergic receptors at high doses
370
Effects dopamine
Increases HR and contractility
Does not selectively presence renal function
371
Clinical dopamine
Adjunct int he treatment of shock
MI
Open heart surgery
Renal failure
Cardiac decompensation
372
Pharmacokinetics dopamine
IV 2 min half life
COMT and MAO
373
AE dopamine
Angina, a fib, bradycardia, ectopic beats, HTN, hypotension, palpitations, tachy, wide QRS
Increase IOP
374
Milrinone MOA
Selective phosphodiesterase 3 inhibitor
375
Effects milrinone
Inhibitors in cardiac and vascular tissue, resulting in vasodilation and inotropic effects with little chronotropy activity
376
Clinical milrinone
Inotropic therapy for patients unresponsive to other acute heart failure therapies
Outpatient for heart transplant candidates
Palliation of symptoms in end stage heart failure patients who cant otherwise be discharged form the hospital and are not transplant candidates
Perioperative inotropic support for heart transplant recipients
377
Pharmacokinetics milrinone
IV
| 2.5 hours half life
378
AE milrinone
>10% incidence of ventricular arrhythmia
Also causes supraventricular arrhythmia, hypotension, angina/chest pain
HA
379
Inamrinonr
Similar drug albeit less safe, withdrawn from market in 2011 but still shows up in drug lists
380
Dobutamine
Direct cardiotonic
381
Dopamine
Direct cardiotonic
382
PDE III inhibitors
Reduce preload and afterload direct cardiotonic effect
383
Nesiritide
Reduces preload and afterload
384
Nitroglycerin nitroprusside
Reduce preload and afterload
385
Drugs to avoid
Class I Antiarrhythmics ...some are negative inotropes all can cause arrhythmias in heart failure patients
-consider amiodarone
CCB...directly suppress myocardial contractility
NSAIDS..impair renal salt and water excretion which can exacerbate HF
