Exam 5 - ppt 2 Flashcards
1
Q
What is ECMO?
A
Extracorporeal membrane oxygenation
providing both cardiac and respiratory support to persons whose heart and lungs are unable to provide an adequate amount of gas exchange
2
Q
What are the two most common ECMO’s?
A
veno-arterial (VA)
veno-venous (VV)
3
Q
ECMO has been used on ________, but it is seeing more use in ______ with cardiac and respiratory failure
A
children
adults
4
Q
ECMO artificially removes the _____________ and ___________ red blood cells.
A
carbon dioxide
oxygenating
5
Q
Generally it is only used in the later treatment of a person with heart or lung failure as it is solely a life-sustaining intervention.
What is it?
A
ECMO
6
Q
_____________ _____ generally used for shorter-term treatment.
A
cardiopulmonary bypass (CPB) not ECMO
7
Q
____ ________are typically placed in the ascending aorta and vena cavae, allowing complete bypass.
A
CPB cannulae
8
Q
_________________ in ECMO can be placed in the femoral or internal jugular veins, limiting its size and the amount of support.
A
Venous inflow cannula
9
Q
________ _______ (if utilized) is placed femorally.
A
Arterial cannula
10
Q
___ (intraoperative) can also be converted to ____, in which case right atrial and ascending aortic cannulae will be utilized
A
CPB
ECMO
11
Q
Aspirin was first introduced by the drug and dye firm ____ in 1899
A
Bayer
12
Q
Aspirin is ___________ acid
A
Acetylsalicylic
13
Q
Aspirin is in what class of drugs?
A
NSAIDS
14
Q
Aspirin MOA?
A
Inhibits prostaglandin and thromboxane synthesis
15
Q
Aspirin inhibits _________ ____ conversion to __________ __.
A
Arachidonic acid
into Prostaglandin H2
16
Q
______ ____ of aspirin is required for effective anti-inflammatory action
A
higher dose
17
Q
____ _______ of aspirin inhibit platelet generation resulting in an antithrombotic effect
A
Low doses
18
Q
What is the typical lose dose ?
A
typically 75 to 81 mg/day
19
Q
Intermediate doses of aspirin inhibit ____ and ___, blocking prostaglandin (PG) production
A
COX1
COX2
20
Q
What is the typical intermediate dosage for Aspirin?
A
650 mg to 4 g/day
21
Q
The anti platelet effect significantly reduces the incidence of ______ and __ in patients at risk .
A
stroke and MI
22
Q
Aspirin prolongs ________ ____
A
bleeding time
23
Q
How long to the inhibitory effects on platelet aggregation last ?
A
8 days
24
Q
What is salicylism?
A
salicylate poisoning
25
patients can get what intoxication after repeated administration of high dose ?
mild chronic salicylate
26
Aspirins ______________ change at higher doses.
pharmacokinetics
27
What are salicylism symptoms?
Symptoms: headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, nausea, vomiting, and sometimes diarrhea
28
What type of immediate tx is needed during salicylism ?
Gastric lavage
Activated charcoal to adsorb drug left in the stomach / dialysis
29
FDA recommends no ASA to those under the age of __?
16
30
An association between aspirin use and induction of ___________ exists in children
Reye’s syndrome
31
Reye's syndrome is a rapidly progressive ____________ which usually begins shortly after recovery from an acute viral illness, especially _________ & _________ (chickenpox)
encephalopathy
influenza and varicella (chickenpox).
32
______ _____ with minimal inflammation and ________ ______ can be signs of Reyes
Fatty liver
cerebral edema
33
Reyes syndrome effects many organs, especially what?
brain and liver
34
Reyes syndrome can cause elevated blood ________ level and low _____ _____.
ammonia level ( hepatic encephalopathy )
and
low blood sugar
35
What are the classic features of Reyes syndrome ?
rash, vomiting and liver damage
36
What are complications and precautions with ASA?
GI bleeding - b/c it is a cyclooxyrgenase drug
coagulation disorder
G6PD deficiency
influenza, varicella, or febrile viral infection (pts <20 yo think reyes)
caution in pts 80 yo and older - liver metabolism is narrow
37
Heart failure is a syndrome resulting in the inability of the heart to maintain adequate ________ ______ to meet metabolic needs
coronary output
38
Heartfailure can occur _______ congestion
without
39
What are some abnormalities that occur with HF?
Myocardial contraction (systolic dysfunction)
Ventricular relaxation (diastolic dysfunction)
or BOTH
40
What are two common causes of HF?
HTN
CAD
41
What is the four- staging system that focuses on the symptoms of HF?
American Heart Association (AHA) / American College cardiology (ACC) staging system
42
What is the staging system that has categories based on how heart failure affects a person's ability to function?
New York Heart Association (NYHA) staging system
43
What staging system and is more popular and used as a tool to assess progress therapy ?
NYHA
44
Pharmacologic Treatment of Heart Failure is aimed at ____________ the neurohormones that are increased in heart failure (HF).
antagonizing
45
What are the drugs used most to treat HF?
Drugs used most are beta blockers, vasodilators, nitrates, diuretics, and digitalis (cardiac glycoside).
Patients are often on a multidrug regimen to prolong life and control symptoms.
46
Pharmacologic Treatment of Heart Failure targets?
a) reduce HF symptoms
b) reduce underlying cause
c) reverse changed body system
47
What is diastolic HF?
heart does not fully relax so it does not fill with blood
stiff heart muscle can't relax normally
less blood fills the ventricles
48
What is systolic HF?
heart does not pump enough blood
weakening heart muscle cannot squeeze as well
Less blood pumped out of ventricles
49
Management of Diastolic HF ?
Angiotensin converting enzyme inhibitors (ACEI)
Beta blockers
Diuretics
Calcium channel blockers (CCB)
Negative inotrope (flecainide) CCB, BB, Class Ia, Ic)
Angiotensin receptor blockers (ARB)
50
Management of Systolic HF?
Digoxin
Diuretics (esp Loop)
Nitrates
ACEI’s
B-adrenergic amine (Dobutamine) (sympathometic)
PDE3 (phosphodiesterase): Amrinone, Milrinone
Standard therapy = ACEI + Loop ± Digoxin
51
What is the standard management of SHF?
ACEI + Loop + or - digoxin
52
What is digoxin?
A cardiac glycoside
53
What plant is digoxin derived from?
digitalis purpurea
54
What are the actions of digoxin that meet the goals for SHF treatment?
Strengthen the heartbeat
Slow the heart rate
Convert irregular cardiac/sinus rhythms
Maintain ventricular rate between 70 and 80 beats/minute
55
Digoxin MOA?
Inhibits NA/K/ATPass Pump
56
When cardiac glycosides like ________ inhibit the Na/K ATPase pump on cardiac cells, it increases Na that is exchanged for ___ by the ___/__ exchanger.
digoxin
exchanges for Ca
by the Na+/Ca++ exchanger
57
The accumulation of intracellular Ca++ binds to _________ which results in increased _____________ of the heart muscle
troponin-C
contractility
58
How does digoxin work?
increases contraction
prolongs refractory of AV node
decreased conduction through AV and SA nodes
59
Digoxin is ________ inotrope, which means it?
positive
it increases cardiac output
60
Digoxin is a ________ chronotrope, which means it ?
negative
it decreases heart rate
61
What are clinical considerations with digoxin ?
There is systemic, coronary arterial, and venous vasoconstriction (especially when given by injection ... over 15–20 min).
There is some diuretic effect as it inhibits reabsorption of Na+.
Digoxin use is recommended in concert with diuretics, ACEI’s, and beta blockers to alleviate CHF symptoms.
Many interactions and contraindications!
Monitor for electrolyte imbalances!
Watch aldosterone blockers (Potassium sparing diuretics) worsening renal failure
Monitor for narrow therapeutic index which can lead to digitalis toxicity!
62
How do you treat digoxin toxicity?
Digoxin Immune Fab ( digibind)
63
Digoxin HF?
Half-life: 36–48 hours, increasing in elderly and with renal impairment.
64
Digoxin adverse reactions EENT, META, NEURO?
EENT: blurry vision “yellow, green halo’s”
META: electrolyte imbalance (K+) , increase in K+
NEURO: headache, weakness, disorientation, hallucinations ( get a dig level, ASA level)
65
What does digoxin decrease serum concentrations of?
```
Aminoglycosides, antimetabolites
fibrates
antacids
bismuth
thyroid prep
Licorice
St. Johns Wort ( high fiber diet)
High fibre meal
```
66
What does digoxin increase serum concentrations of?
```
Use of laxatives
Use of macrolides ( Z-PAK)
Quinidine
amiodarone
benzodiazepines
verapamil
```
67
What are contraindications to using Digoxin?
Geriatrics are highly sensitive ( to dig)
AV Blocks and arrhythmias
Hypersensitivities
Patients with hypocalcemia, hypokalemia, hypomagnesemia
68
Patient education of digoxin?
Instruct patient on how to take pulse and HR
Review signs and symptoms of toxicity
Advise patient to keep away from excess sunlight
Advise patient to use original Rx container
Warn of diminished effect with high fiber meal
Advise patient to wear MedicAlert bracelet
Advise patient to increase intake of potassium
Warn that antacids and antidiarrheals diminish effect
Advise missed doses need to be taken within 12 hours of next dose
69
Digoxin: Pregnancy Special Considerations?
Experience shows it can be used on a case-by-case situation when risk of not using it is high to mother.
70
Digoxin: Geriatrics Special Considerations?
Age-related changes in renal function show dosage must be altered down or else toxicity can occur.
71
What does the FDA category digoxin for pregnancy?
Category C
72
What are clinical uses of Antiarrythmic Drugs?
Clinical uses:
Abnormalities in heart rhythm
Fast: tachyarrhythmia
Slow: bradyarrhythmia
73
Goals with Antiarrythmic Drugs?
Restore normal sinus rhythm
Suppress the initiation of abnormal rhythms
74
What are class I and what do they do?
Sodium Channel Blockers
Inhibit ventricular automaticity and slow conduction velocity
75
What are class II and what do they do?
Beta Blockers
Block sympathetic action
76
What are class III and what do they do?
Potassium Channel Blockers
Prolong action potential duration and refractoriness
77
What are class IV and what do they do?
Calcium Channel Blockers
Slow AV and SA node conduction velocity
78
Class I: sodium channel blockers MOA?
Inhibit ventricular automaticity and slow conduction velocity
79
What do Class IA do?
Lengthen action potential duration
Prolong ventricular refractory period
Increase conduction rate at AV node
80
What do Class IB MOA?
Slow conduction and shorten action potential duration in healthy cardiac tissue ( healthy tissues doing the work )
Alters signal conduction in neurons by blocking the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for signal propagation.
81
What do Class IC MOA?
Acts in the refractory period of Purkinje fibers without altering the refractory period of the adjacent myocardium
Works by slowing the influx of sodium ions into the cardiac muscle cells, causing a decrease in excitability of the cells.
Propafenone is more selective for cells with a high rate
82
Class IA: Sodium Channel Blockers examples?
Quinidex
Procainamide
Disopyramide
83
Clinical uses of Class IA?
treatment of atrial arrhythmias
84
Class IA has Many side effects and adverse reactions, like?
Cardiovascular
hematologic
neurologic
Drug-induced lupus with procainamide
Given IV
85
Class IB: Sodium Channel Blockers examples?
Lidocaine (Xylocaine IV)
tocainide (tonocard)
mexiletine ( mexitil)
86
Clinical uses of Class IB?
Ventricular arrhythmias, especially during an acute myocardial infarction
Digitalis-induced arrhythmias
87
Class IC: Sodium Channel Blockers examples?
propafenone (Rythmol) flecainide (Tambocor)
88
Clinical uses of Class IC?
treatment of sustained ventricular tachycardia and paroxysmal supraventricular tachycardia (PSVT)
89
BBW for Flecainide (Tambocor)?
Use only for life-threatening arrhythmias
Increased risk of mortality when used for non-life-threatening ventricular arrhythmias
90
Side effects and adverse reactions of class IC?
arrhythmias
Increased QT prolonged with Macrolides ( can progress to Torsades de Pointe)
91
Class II: Beta Blockers - Beta-1 selective act mainly on?
cardiac muscle
92
Class II: Beta Blockers - Beta-2 selective act mainly on?
cardiac, lung, arterial, pancreatic, kidney, adipose, liver tissues
93
Class II: BB MOA?
Decrease heart rate, conduction velocity, and force of contraction
94
Class II/lll Beta-blocker/ Potassium Channel Blockers combo example?
Sotalol (Betapace)
Class II and Class III drug (Combo)
95
Sotalol (Betapace) is a non-selective completive ____-___________ receptor blocker that also exhibits Class __ anti arrhythmic properties.
beta-adrenergic
class III
96
Due to the dual action of sotalol, it is often used preferentially to other beta blockers as treatment for both ventricular ____________ and ventricular ___________.
fibrillation
tachycardia
97
Class III: Potassium Channel Blockers examples?
Amiodarone (Cordarone) - Vtach, Vfib, SVT maybe
98
Clinical uses of Class III: Potassium Channel Blockers PO?
PO: Management of supraventricular tachyarrhythmias
Restricted for life-threatening arrhythmias because of potential for drug toxicity
99
Clinical uses of Class III: Potassium Channel Blockers IV?
IV: ACLS/PALS management of ventricular fibrillation and pulseless ventricular tachycardia
Restricted for life-threatening arrhythmias because of potential for drug toxicity
100
What is amiodarone (cordarone) contraindicated with?
many ABS
101
BBW of Class III: Potassium Channel Blockers?
Hepatotoxicity
Pro-arrhythmic (make worse) - sometimes it can cause other arrhythmias
Pulmonary fibrosis
102
Examples of Class IV: Calcium Channel Blockers?
verapamil (Calan)
| diltiazem (Cardizem)
103
Class IV: Calcium Channel Blockers give temporary control of rapid ____________ _____ in ____ or ________
ventricular rates
in a-fib and a-flutter ( acute Tx IV)
104
Class IV: Calcium Channel Blockers achieve conversion of ____ into normal sinus rhythm?
PSVT
105
Side effects of Class IV: Calcium Channel Blockers ?
Peripheral edema!
106
Conscientious Prescribing of Antiarrhythmics?
Need thorough medication history
Monitor serum electrolytes
Refer to cardiologist for initial outpatient therapy
Monitor potassium levels
Monitor renal and hepatic function
Monitor serum levels after reaching steady state
Monitor with 12 lead electrocardiogram
107
Patient/Family Education of Antiarrhythmics?
Instruct patient on how to take a pulse and BP
Advise to wear Medic Alert bracelet as ID for drugs
Advise to seek help if hypotensive (Buy a BO Cuff)
Advise to seek help if patient develops fever, chills, sore throat, bruising
Advise to keep follow-up appointments
Advise of side effects, especially dizziness
Caution to be careful when driving or activity that requires alertness
108
what is angina cause by?
Thought to be caused by the imbalance between oxygen supply and demand
109
Chronic stable angina symptoms and signs?
deep pressure or pain in the sternum that usually radiates elsewhere
Brought on by exertion
Relieved by rest or
nitroglycerine
Lasts less than 10 minutes
110
Treatment goals for angina?
Reducing myocardial oxygen demand
Improving oxygen supply to myocardial tissue
Treating cardiac risk factors
Controlling any factors that could lead to ischemia
111
Short terms treatment for angina ?
Nitrates
112
Long terms treatment for angina ?
ABCDE
A: aspirin and anticoagulation
B: beta blockers and blood pressure control - reduce activity of myocardium
C: cholesterol-lowering agents and smoking cessation
D: diet
E: exercise ? make sure cardiologist screened them to make sure they can exercise and to what extent
113
What is nitrates MOA?
Frank-Starling mechanism
Increases coronary blood flow by dilating the coronary arteries and improving collateral flow to ischemic regions
Reduces myocardial oxygen demand by decreasing preload and to a lesser extent decreasing afterload
114
What is Frank-Starling mechanism?
Larger volume of blood flows into the ventricle
The blood will stretch the walls of the heart, causing a greater expansion during diastole
In turn this increases the force of the contraction and thus the quantity of blood that is pumped into the aorta during systole
115
Nitroglycerin vaso________
dilates
116
Does Nitroglycerin work more on veins or arteries?
Greater in the veins than arteries
117
Because Nitroglycerin works more on the veins, it results in ______ pooling and thereby ___________ left ventricular volume (preload) and ________ ventricular EDV.
venous
decreasing
reducing
118
Nitroglycerin increases pressure in the _____?
brain
119
Clinical uses of Nitroglycerin?
Acute angina (sublingual dosage forms)
Long-term prophylaxis of angina pectoris (oral, buccal, and transdermal forms)
Adjunct in the treatment of acute myocardial infarction and acute heart failure (IV form)
inferior wall MI exception of treating chest pain with NITRO - do not give them nitro - their pressure will tank and you will kill them
120
Nitroglycerin _________ coronary blood flow by ________ the coronary arteries and improving collateral flow to ischemic regions
Increases
dilating
121
Nitroglycerin has serious adverse reactions with concurrent use of ________, _________, __________.
sildenafil (Viagra)
tadalafil (Cialis)
vardenafil (Levitra)
122
PDE5 medications have a ___________ effect that is more significant with nitroglycerin causing ___________
synergistic
Hypotension
123
Examples of Nitrates for angina?
Isosorbide dinitrate (Isordil) isosorbide mononitrate (Imdur, Monoket)
124
Clinical uses of Isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur, Monoket)?
prevention of angina
125
Isosorbide denigrate and Isosorbide mononitrate are not for the treatment of _____ _______.
acute attacks
126
Dinitrate: undergoes _____ first-pass metabolism
100%
127
Mononitrate: _______ undergo first-pass metabolism
does not
128
Clinical uses of Ranolazine (Ranexa)?
chronic angina
New 2006
Can be used in conjunction with other BP medications
nitrate for chronic use and does not react with a lot of the drugs but it does reactive with the PDE5’s
129
Ranolazine increases efficiency of ___ under _______ conditions.
ATP
under hypoxic
130
Ranolazine has Antianginal and anti-ischemic effects without ___________ change
hemodynamic
