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Semester 5 PMCP Exam 2 > Cardio Drugs > Flashcards

Cardio Drugs Flashcards

1
Q

Drugs for Arrhythmia - classification

A

Vaughan Williams Singh Classification

Class 1 -4

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2
Q

Class 1 - drugs for arrhythmia -

A

broken into 1a, 1b, 1c

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3
Q

Examples of Class 1a antiarrhythmic agents

A

quinidine
procainamide
disopyramide

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4
Q

Examples of class 1b antiarrhthmic agents

A

lidocaine

phenytoin

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5
Q

Examples of class 1c antiarrhythmic drugs

A

flecainide

propadenone

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6
Q

Examples of class II antiarrhthmic agens

A

propanolol
metoprolol
BETA BLOCKERS

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7
Q

Examples of class III antiarrhythmic agents

A

amiodarone
sotalol
ibutilide

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8
Q

Examples of class IV antiarr drugs

A

Verapamil
diltiazem
Ca CHANNEL BLOCKERS

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9
Q

Other antiarr drugs

A

Adenosine
Digoxin
Atropine

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10
Q

What is happening during phase 0 with nodal tissue

A

Ca is coming in

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11
Q

What is happening in phase 0 with non-nodal tissue

A

Na is coming in

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12
Q

Using a Ca channel blocker impacts which tissue more (nodal or non-nodal)

A

Nodal!

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13
Q

What happens to AP if you use a K channel blocker

A

Repolarization is slowed so that you have a prolonged AP - this is good so that abnormal impulses come but they might not all be getting depolarized

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14
Q

What happens in phase 4 with nodal tissue

A

Diastolic depolarization

Na and Ca coming in - this is where heart gets automaticity

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15
Q

Effective Refractory Period =

A

Your tissue will not under any circumstance response to external excitation
There is no response to an impulse coming in

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16
Q

Action potential duration

A

the entire duration of AP

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17
Q

ERP/APD ratio

A

The bigger the ratio, the harder it is for abnormal impulses to stimulate your tissue

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18
Q

Class 1 anti arr (generally) agents work by

A

blocking voltage sensitive Na channels

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19
Q 
Class 1 anti arr agents do what to 
Vmax
Automaticity
Conduction
ERP
A

Reduce
Reduce
Delay
Prolong (inc ratio)

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20
Q

Class 1 anti arr agents are good for who

A

varying degrees of ventricular arr

digitalis or MI induced arr

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21
Q

Class 1a anti arr agents - binding is

A

moderate binging to Na channels so moderate effect on phase 0 depolarization

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22
Q

Class 1a anti arr agents - does what to ECG

A

prolonged QRS and QT

Delayed phase 3 repolarization

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23
Q

Class 1a anti arr agents - at high doses can do what

A

Ca channel blocking

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24
Q

Class Ib anti arr - what type of binding

A

weak binding to Na channels so weak effect on phase 0 depolarization

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25
Q

Class Ib anti arr - what does it do to ECG

A

Shortened ADP and QT

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26
Q

Class 1b anti arr - good use in who

A

digitalis or MI induced arr

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27
Q

Class Ic anti arr agents - what type of binding

A

Strongest bidning to Na channels - so has marked effects on pahse 0 depolarization

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28
Q

Class Ic anti arr agents - what will you see on ECG

A 
Lengthened QRS and APD, 
Lengthened PR (depressed AV nodal conduction)
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29
Q

Class II anti arr - comprised of

A

beta adrenergic antagonists

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30
Q

Class II anti arr agents effect what primarily

A

nodal phase 0 depolarization

Depresses SA nodal automaticity (phase 4), AV nodal conduction, and dec ventricular contractility

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31
Q

Class III anti arr agents - how do they work

A

multiplicity of membrane effects at K, Ca, Na, and beta receptors (direct and indirect)

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32
Q

Class III do what to ECG

A

Prolong phase 3 repolarization and inc QT

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33
Q

Class III good for who

A

ventricular re-entry/fibrilliation arr

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34
Q

Class IV anti arr agents - how do they work

A 
Ca channel antagonists
Similar in utility as class II 
Primary effect on nodal phase 0 depolarization
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35
Q

Class IV - impaces include

A

depressed SA nodal automaticity
AV nodal conduction
dec vent contractility

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36
Q

Drugs for bradycardia

A

Atropine
Isoproterenol
Pacemaker

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37
Q

Atropine

A

Produces vagal block to inc HR

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38
Q

Isoproterenol

A

Beta 1 stimulated to inc HR

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39
Q

Pacemaker

A

Morphologic AV nodal block

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40
Q

Sinus Tachycardia drugs

A

Vagal stimulation through carotid sinus massage or vasalva maneuver

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41
Q

Special concerns for PT when tx one with arr

A

Ex might exacerbate or inc potential for arr
HypoTN as side effect of some drugs (orthostatic)
Implantable defib are safe but can limit ROM
External pacemaker - require additional care and monitoring
Antiarr drugs can exacerbate cardiac response to exercise

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42
Q

Positive ionotropic agents - are doing what

A

increasing the contractility of the heart

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43
Q

Heart failure affects how many americans per year

A

more than 3,000,000

44
Q

Heart failure mortality rate per year

A

more than 260,000

45
Q

Heart failure - due to

A

uncontrolled chronic hypertension, CAD, chronic arr, valve disease, cardiomyopathies…

46
Q

Heart failure is characterized as

A

a reduction in SV (and CO) at any given end diastolic volume

47
Q

Frank Starling relationship

A

Ventricular contraction varies directly with muscle fiber length (EDV, preload)

48
Q

Ionotropic influences on cardiac dynamics -

A

+/- ionotropic influences directly alter contractile force for any given EDV

49
Q

Congestive heart failure hemodynamics - low output CHF results from what

A

decreased contractile capacity

50
Q

CHF is charactatized into what three groups of sx

A

Congestive symptoms
Cardiomegaly
Sx of dec CO

51
Q

Clinical tx for CHF

A 
Diet at Na restriction
Exercise
Diuretics, ACEI and VDs
Pos ionotropic agents
other drugs
52
Q

What do you start with for tx of CHF

A

Restrict Na and diet and exercise - relieve load on the heart before you make it work harder with with the diuretics, ACEI, VDs, and pos ionotropic agents

53
Q

Cardiac glycosides include

A

digitalis lanata
digitalis purpurea
(foxglove plant extracts)

54
Q

How does digoxin work

A

Blocks Na/K pump - increasing Na content inside the cell

More Ca in the heart too - leads to more contractility of the heart? SLIDE 25 - ASK

55
Q

Mechanism of action with Digoxin used for CHF

A

Na/K ATPase inhibiiton

56
Q

Mechanism of action with digoxin for Atrial fib

A

vagal stimulation leads to negative dromotropic effect at AV node leading prolonged refraction (inc ERP)

57
Q

Two jobs of digoxing

A

Inc Ca concentration

Slow conduction through AV node

58
Q

How does digoxin slow the ventricular rate

A

dec number of atrial depolarizations that reach the ventricles
Symp stim can override this though

59
Q

Digoxin - adverse effects

A

1 low margin of safety
2 enhanced mortality when combined with diuretics that deplete K
3 Arrhythmia, visual and neuro disturbances, CTZ stimulation inducing anorexia, nausea, vomiting

60
Q

Other drugs used in CHF

A

VDs
Diuretics
Ca channel blockers
Beta blockers

61
Q

VDs used for CHF

A

Ace inhibitors
Alpha 1 antagonists
Nitrates
Other direct acting smooth mm relaxants

62
Q

Diuretics used for CHF

A

Reduced blood volume
Dec preload
Inc edema mobilization

63
Q

Ca channel blockers used for CHF

A

Not widely used for this because of cardiodepressant action

afterload reduction may be beneficial, but produces tachycardia in return

64
Q

Beta blockers for CHF

A

restore number of beta adrenergic receptors

Improve response to circulating catecholamines

65
Q

Special concerns for PT tx patient with CHF

A
  • be alert for signs of digitalis toxicity
  • both disease and drug influence might fatigue or weaken the pt
  • ex tolerance dec
  • diuretics might induce electrolyte depletion
  • VD can cause hypotn and orthostasis
66
Q

Definition of hypertension

A

chronic elevation in arterial pressure above 140/90 (AHA) or above 160/95 (WHO)

67
Q

Non-essential/Secondary Hypertension

A

10%
there is a clinically identifiable cause
primary management is usually surgical

68
Q

Essential/primary Hypertension

A

90%
idiopathic
a genetic basis for incidence most often found in middle aged

69
Q

Pharmacological tx goal for hypertension

A

step care therapy!
Lifestyle mod first 3 months
Continue lifestyle mod and then add pharm

70
Q

How do antihypertensice agents work

A

MAP = CO x TPR
CO = HR x SV
SV = blood volume and cardiac concentration
We want to reduce HR, SV, blood volume, Na content in body

71
Q

Diuretics main location of action

A

nephron tubule

72
Q

Diuretics MOA with hpyertension

A

relatively unknown

appears to be via dec in blood volume and total body Na producing a dec in CO

73
Q

Adverse effects with diruetics

A

Hyperuricemia

Hypokalemia

74
Q

Contraindications for diuretics

A

Diabetes - may induce hyperglycemia

Hyperlipidemia - tend to elevate plasma LDL and TG

75
Q

beta adrenergic antagonists MOA with hypertension

A

blocks beta adrenergic receptors in the heart (dec HR and cont and dec BP) and in the kidneys (dec renin release which dec ang II formation)

76
Q

Adverse effects of beta adrenergic antagonists

A 
1 minor GI and CNS nausea
2 asthma exacerbation
3 Hyperlipidemia
4 Male sexual dysfunction
5 diabetes - masks signs of hypoglycemia
6 may exacerbate CHF
77
Q

Centrally acting sympatholytics include (2)

A

Clonidine

Methyldopa

78
Q

MOA for centrally acting sympatholytics

A

post synaptic alpha 2 agonist in CNS - inhibits sympathetic outflow leading to dec HR
Pre synaptic alpha 2 agonist in periphery - dec NE release from post ganglionic nerve terminals

79
Q

Peripherally acting sympatholytics include (3)

A

Prazosin
Terazosin
Doxazosin

80
Q

MOA for peripherally acting sympatholytics

A

selective antagonist at vascular smooth muscle alpha 1 receptors - by sparing alpha 2 pre synpatic receptors NE release is not induced
You get VD so BP drops

81
Q

Adverse effects to peripherally acting sympatholytics

A

1 mild tolerance
2 mild reflex tachycardia, ortho hypotension
3 sexual dysfunction

82
Q

Ca channel antagonists (2)

A

Verapamil

Diltiazem

83
Q

MOA of Ca channel antagonists for hypertension

A

direct VD activity by inhibiting both Ca entry into vascular smooth mm and Ca release from sarcoplasmic reticulum
Dec Ca so mm will relax and BP goes down

84
Q

Adverse effects to Ca channel antagonists

A

Reflex tachycardia

Cardiodepression

85
Q

Direct acting VDs for hypertension (2)

A

Hydralazine

Minoxidil

86
Q

MOA of direct acting VD (Hydralazine) for hypertension

A

Direct VD via guanylate cyclase stimulation

87
Q

MOA of direct acting VD (Minoxidil) for hypertension

A

direct VD via stimulation of vascular smooth mm K channel opening - leading to membrane hyperpolarization - relaxation

88
Q

Angiotensin converting enzyme inhibitor ex (3)

A

Captopril
Enalapril
Lisinopril

89
Q

MOA of ACEI

A

blocking the mechanisms to make angiotensin II - so you get VD and thus BP dec

90
Q

ACEI adverse effects

A

1 dry, persistent cough
2. proteinuria (nephron tox), angioedema
3 maculopapillary rash and altered tastae
4 PREGNANCY CONTRAINDICATION

91
Q

Angiotensin receptor blockers (ARBs) ex (4)

A

Losartan
Candesartan
Valsartan
Irbesartan

92
Q

Angiotensin receptor blockers (ARBs) MOA

A

specific antagonsists of angiotensin II and AT1 receptors on vascular smooth mm, adrenal cortex, brain, spinal cord, heart..

93
Q

Adverse effects of ARBs

A

relatviiely few

PREGNANCY COTNRAINDICATION

94
Q

Special concerns for PT tx pt with hypertension

A

1 hypotension
2 orthostatic hypotension
MONITOR HR and BP frequently

95
Q

Clinical utility of VDs

A 
Hypertension
PVD
Cerebrovascular insufficiency
Coronary insufficiency 
CHF
Surgical management of BP
96
Q

Angina is characterized b

A

a sense of severe pressure or constricting pain in chest that can radiate through torso, UE, and neck due to cardiac ischemia

97
Q

Cardiac Ischemia is defined by what

A

inadequate blood flow and inadequate oxygen delivery to heart muscle

98
Q

Mechanisms of ischemia - ischemia usually occurs when

A

work load on the myocardium is greater than its oxygen supply

99
Q

Anginal pain comes from what

A

release of bradykinin and adenosine onto nociceptive afferents

100
Q

Angina pain can be counteracted by what

A

procedures that improve myocardial perfusion or dec metabolic demands
Improve oxygen (blood) delivery
Dec work load of myocardium

101
Q

Nitroglycerin is the drug of choice for management of what

A

angina

102
Q

Frequent dosing of nitro can lead to what

A

tachyphylaxis (tolerance development)

103
Q

MOA of nitroglycerin

A

NO is stimulated - stimulates guanylate cyclase and cGMP leading to Ca sequestration and smooth mm relaxation in both arteries (afterload) and veins (pre) so this dec workload of myocardium by dec myocardial wall tension with diastole and systole

104
Q

Nitro adverse effects

A

1 hypotension
2 HA due to cerebral VD
3 flushing of soft tissues (superficial VD)
4 sublingual burning sensation

105
Q

Isosorbide Dinitrate

A

like nitro

used in tx and prophylaxis of angina

106
Q

Isosorbide Dinitrate (ISDN) MOA

A

NO donor

107
Q

Special concerns for PT treating pt with angina pectoris

A

1 hypotension might be present
2 syncope
3 know if taken prophylactically or PRN
If PRN - needs to be readily available with PT
If pro - therapist aware of cardiac limitations with exertion

Semester 5 PMCP Exam 2 (6 decks)

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