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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
Class Ib anti arr - what does it do to ECG
Shortened ADP and QT
26
Class 1b anti arr - good use in who
digitalis or MI induced arr
27
Class Ic anti arr agents - what type of binding
Strongest bidning to Na channels - so has marked effects on pahse 0 depolarization
28
Class Ic anti arr agents - what will you see on ECG
``` Lengthened QRS and APD, Lengthened PR (depressed AV nodal conduction) ```
29
Class II anti arr - comprised of
beta adrenergic antagonists
30
Class II anti arr agents effect what primarily
nodal phase 0 depolarization | Depresses SA nodal automaticity (phase 4), AV nodal conduction, and dec ventricular contractility
31
Class III anti arr agents - how do they work
multiplicity of membrane effects at K, Ca, Na, and beta receptors (direct and indirect)
32
Class III do what to ECG
Prolong phase 3 repolarization and inc QT
33
Class III good for who
ventricular re-entry/fibrilliation arr
34
Class IV anti arr agents - how do they work
``` Ca channel antagonists Similar in utility as class II Primary effect on nodal phase 0 depolarization ```
35
Class IV - impaces include
depressed SA nodal automaticity AV nodal conduction dec vent contractility
36
Drugs for bradycardia
Atropine Isoproterenol Pacemaker
37
Atropine
Produces vagal block to inc HR
38
Isoproterenol
Beta 1 stimulated to inc HR
39
Pacemaker
Morphologic AV nodal block
40
Sinus Tachycardia drugs
Vagal stimulation through carotid sinus massage or vasalva maneuver
41
Special concerns for PT when tx one with arr
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
42
Positive ionotropic agents - are doing what
increasing the contractility of the heart
43
Heart failure affects how many americans per year
more than 3,000,000
44
Heart failure mortality rate per year
more than 260,000
45
Heart failure - due to
uncontrolled chronic hypertension, CAD, chronic arr, valve disease, cardiomyopathies...
46
Heart failure is characterized as
a reduction in SV (and CO) at any given end diastolic volume
47
Frank Starling relationship
Ventricular contraction varies directly with muscle fiber length (EDV, preload)
48
Ionotropic influences on cardiac dynamics -
+/- ionotropic influences directly alter contractile force for any given EDV
49
Congestive heart failure hemodynamics - low output CHF results from what
decreased contractile capacity
50
CHF is charactatized into what three groups of sx
Congestive symptoms Cardiomegaly Sx of dec CO
51
Clinical tx for CHF
``` Diet at Na restriction Exercise Diuretics, ACEI and VDs Pos ionotropic agents other drugs ```
52
What do you start with for tx of CHF
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
Cardiac glycosides include
digitalis lanata digitalis purpurea (foxglove plant extracts)
54
How does digoxin work
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
Mechanism of action with Digoxin used for CHF
Na/K ATPase inhibiiton
56
Mechanism of action with digoxin for Atrial fib
vagal stimulation leads to negative dromotropic effect at AV node leading prolonged refraction (inc ERP)
57
Two jobs of digoxing
Inc Ca concentration | Slow conduction through AV node
58
How does digoxin slow the ventricular rate
dec number of atrial depolarizations that reach the ventricles Symp stim can override this though
59
Digoxin - adverse effects
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
Other drugs used in CHF
VDs Diuretics Ca channel blockers Beta blockers
61
VDs used for CHF
Ace inhibitors Alpha 1 antagonists Nitrates Other direct acting smooth mm relaxants
62
Diuretics used for CHF
Reduced blood volume Dec preload Inc edema mobilization
63
Ca channel blockers used for CHF
Not widely used for this because of cardiodepressant action | afterload reduction may be beneficial, but produces tachycardia in return
64
Beta blockers for CHF
restore number of beta adrenergic receptors | Improve response to circulating catecholamines
65
Special concerns for PT tx patient with CHF
- 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
Definition of hypertension
chronic elevation in arterial pressure above 140/90 (AHA) or above 160/95 (WHO)
67
Non-essential/Secondary Hypertension
10% there is a clinically identifiable cause primary management is usually surgical
68
Essential/primary Hypertension
90% idiopathic a genetic basis for incidence most often found in middle aged
69
Pharmacological tx goal for hypertension
step care therapy! Lifestyle mod first 3 months Continue lifestyle mod and then add pharm
70
How do antihypertensice agents work
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
Diuretics main location of action
nephron tubule
72
Diuretics MOA with hpyertension
relatively unknown | appears to be via dec in blood volume and total body Na producing a dec in CO
73
Adverse effects with diruetics
Hyperuricemia | Hypokalemia
74
Contraindications for diuretics
Diabetes - may induce hyperglycemia | Hyperlipidemia - tend to elevate plasma LDL and TG
75
beta adrenergic antagonists MOA with hypertension
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
Adverse effects of beta adrenergic antagonists
``` 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
Centrally acting sympatholytics include (2)
Clonidine | Methyldopa
78
MOA for centrally acting sympatholytics
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
Peripherally acting sympatholytics include (3)
Prazosin Terazosin Doxazosin
80
MOA for peripherally acting sympatholytics
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
Adverse effects to peripherally acting sympatholytics
1 mild tolerance 2 mild reflex tachycardia, ortho hypotension 3 sexual dysfunction
82
Ca channel antagonists (2)
Verapamil | Diltiazem
83
MOA of Ca channel antagonists for hypertension
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
Adverse effects to Ca channel antagonists
Reflex tachycardia | Cardiodepression
85
Direct acting VDs for hypertension (2)
Hydralazine | Minoxidil
86
MOA of direct acting VD (Hydralazine) for hypertension
Direct VD via guanylate cyclase stimulation
87
MOA of direct acting VD (Minoxidil) for hypertension
direct VD via stimulation of vascular smooth mm K channel opening - leading to membrane hyperpolarization - relaxation
88
Angiotensin converting enzyme inhibitor ex (3)
Captopril Enalapril Lisinopril
89
MOA of ACEI
blocking the mechanisms to make angiotensin II - so you get VD and thus BP dec
90
ACEI adverse effects
1 dry, persistent cough 2. proteinuria (nephron tox), angioedema 3 maculopapillary rash and altered tastae 4 PREGNANCY CONTRAINDICATION
91
Angiotensin receptor blockers (ARBs) ex (4)
Losartan Candesartan Valsartan Irbesartan
92
Angiotensin receptor blockers (ARBs) MOA
specific antagonsists of angiotensin II and AT1 receptors on vascular smooth mm, adrenal cortex, brain, spinal cord, heart..
93
Adverse effects of ARBs
relatviiely few | PREGNANCY COTNRAINDICATION
94
Special concerns for PT tx pt with hypertension
1 hypotension 2 orthostatic hypotension MONITOR HR and BP frequently
95
Clinical utility of VDs
``` Hypertension PVD Cerebrovascular insufficiency Coronary insufficiency CHF Surgical management of BP ```
96
Angina is characterized b
a sense of severe pressure or constricting pain in chest that can radiate through torso, UE, and neck due to cardiac ischemia
97
Cardiac Ischemia is defined by what
inadequate blood flow and inadequate oxygen delivery to heart muscle
98
Mechanisms of ischemia - ischemia usually occurs when
work load on the myocardium is greater than its oxygen supply
99
Anginal pain comes from what
release of bradykinin and adenosine onto nociceptive afferents
100
Angina pain can be counteracted by what
procedures that improve myocardial perfusion or dec metabolic demands Improve oxygen (blood) delivery Dec work load of myocardium
101
Nitroglycerin is the drug of choice for management of what
angina
102
Frequent dosing of nitro can lead to what
tachyphylaxis (tolerance development)
103
MOA of nitroglycerin
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
Nitro adverse effects
1 hypotension 2 HA due to cerebral VD 3 flushing of soft tissues (superficial VD) 4 sublingual burning sensation
105
Isosorbide Dinitrate
like nitro | used in tx and prophylaxis of angina
106
Isosorbide Dinitrate (ISDN) MOA
NO donor
107
Special concerns for PT treating pt with angina pectoris
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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