Exam 5 - ppt 2 Flashcards
What is ECMO?
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
What are the two most common ECMO’s?
veno-arterial (VA)
veno-venous (VV)
ECMO has been used on ________, but it is seeing more use in ______ with cardiac and respiratory failure
children
adults
ECMO artificially removes the _____________ and ___________ red blood cells.
carbon dioxide
oxygenating
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?
ECMO
_____________ _____ generally used for shorter-term treatment.
cardiopulmonary bypass (CPB) not ECMO
____ ________are typically placed in the ascending aorta and vena cavae, allowing complete bypass.
CPB cannulae
_________________ in ECMO can be placed in the femoral or internal jugular veins, limiting its size and the amount of support.
Venous inflow cannula
________ _______ (if utilized) is placed femorally.
Arterial cannula
___ (intraoperative) can also be converted to ____, in which case right atrial and ascending aortic cannulae will be utilized
CPB
ECMO
Aspirin was first introduced by the drug and dye firm ____ in 1899
Bayer
Aspirin is ___________ acid
Acetylsalicylic
Aspirin is in what class of drugs?
NSAIDS
Aspirin MOA?
Inhibits prostaglandin and thromboxane synthesis
Aspirin inhibits _________ ____ conversion to __________ __.
Arachidonic acid
into Prostaglandin H2
______ ____ of aspirin is required for effective anti-inflammatory action
higher dose
____ _______ of aspirin inhibit platelet generation resulting in an antithrombotic effect
Low doses
What is the typical lose dose ?
typically 75 to 81 mg/day
Intermediate doses of aspirin inhibit ____ and ___, blocking prostaglandin (PG) production
COX1
COX2
What is the typical intermediate dosage for Aspirin?
650 mg to 4 g/day
The anti platelet effect significantly reduces the incidence of ______ and __ in patients at risk .
stroke and MI
Aspirin prolongs ________ ____
bleeding time
How long to the inhibitory effects on platelet aggregation last ?
8 days
What is salicylism?
salicylate poisoning
patients can get what intoxication after repeated administration of high dose ?
mild chronic salicylate
Aspirins ______________ change at higher doses.
pharmacokinetics
What are salicylism symptoms?
Symptoms: headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, nausea, vomiting, and sometimes diarrhea
What type of immediate tx is needed during salicylism ?
Gastric lavage
Activated charcoal to adsorb drug left in the stomach / dialysis
FDA recommends no ASA to those under the age of __?
16
An association between aspirin use and induction of ___________ exists in children
Reye’s syndrome
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).
______ _____ with minimal inflammation and ________ ______ can be signs of Reyes
Fatty liver
cerebral edema
Reyes syndrome effects many organs, especially what?
brain and liver
Reyes syndrome can cause elevated blood ________ level and low _____ _____.
ammonia level ( hepatic encephalopathy )
and
low blood sugar
What are the classic features of Reyes syndrome ?
rash, vomiting and liver damage
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
Heart failure is a syndrome resulting in the inability of the heart to maintain adequate ________ ______ to meet metabolic needs
coronary output
Heartfailure can occur _______ congestion
without
What are some abnormalities that occur with HF?
Myocardial contraction (systolic dysfunction)
Ventricular relaxation (diastolic dysfunction)
or BOTH
What are two common causes of HF?
HTN
CAD
What is the four- staging system that focuses on the symptoms of HF?
American Heart Association (AHA) / American College cardiology (ACC) staging system
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
What staging system and is more popular and used as a tool to assess progress therapy ?
NYHA
Pharmacologic Treatment of Heart Failure is aimed at ____________ the neurohormones that are increased in heart failure (HF).
antagonizing
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.
Pharmacologic Treatment of Heart Failure targets?
a) reduce HF symptoms
b) reduce underlying cause
c) reverse changed body system
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
What is systolic HF?
heart does not pump enough blood
weakening heart muscle cannot squeeze as well
Less blood pumped out of ventricles
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)
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
What is the standard management of SHF?
ACEI + Loop + or - digoxin
What is digoxin?
A cardiac glycoside
What plant is digoxin derived from?
digitalis purpurea
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
Digoxin MOA?
Inhibits NA/K/ATPass Pump
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
The accumulation of intracellular Ca++ binds to _________ which results in increased _____________ of the heart muscle
troponin-C
contractility
How does digoxin work?
increases contraction
prolongs refractory of AV node
decreased conduction through AV and SA nodes
Digoxin is ________ inotrope, which means it?
positive
it increases cardiac output
Digoxin is a ________ chronotrope, which means it ?
negative
it decreases heart rate
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!
How do you treat digoxin toxicity?
Digoxin Immune Fab ( digibind)
Digoxin HF?
Half-life: 36–48 hours, increasing in elderly and with renal impairment.
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)
What does digoxin decrease serum concentrations of?
Aminoglycosides, antimetabolites fibrates antacids bismuth thyroid prep Licorice St. Johns Wort ( high fiber diet) High fibre meal
What does digoxin increase serum concentrations of?
Use of laxatives Use of macrolides ( Z-PAK) Quinidine amiodarone benzodiazepines verapamil
What are contraindications to using Digoxin?
Geriatrics are highly sensitive ( to dig)
AV Blocks and arrhythmias
Hypersensitivities
Patients with hypocalcemia, hypokalemia, hypomagnesemia
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
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.
Digoxin: Geriatrics Special Considerations?
Age-related changes in renal function show dosage must be altered down or else toxicity can occur.
What does the FDA category digoxin for pregnancy?
Category C
What are clinical uses of Antiarrythmic Drugs?
Clinical uses:
Abnormalities in heart rhythm
Fast: tachyarrhythmia
Slow: bradyarrhythmia
Goals with Antiarrythmic Drugs?
Restore normal sinus rhythm
Suppress the initiation of abnormal rhythms
What are class I and what do they do?
Sodium Channel Blockers
Inhibit ventricular automaticity and slow conduction velocity
What are class II and what do they do?
Beta Blockers
Block sympathetic action
What are class III and what do they do?
Potassium Channel Blockers
Prolong action potential duration and refractoriness
What are class IV and what do they do?
Calcium Channel Blockers
Slow AV and SA node conduction velocity
Class I: sodium channel blockers MOA?
Inhibit ventricular automaticity and slow conduction velocity
What do Class IA do?
Lengthen action potential duration
Prolong ventricular refractory period
Increase conduction rate at AV node
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.
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
Class IA: Sodium Channel Blockers examples?
Quinidex
Procainamide
Disopyramide
Clinical uses of Class IA?
treatment of atrial arrhythmias
Class IA has Many side effects and adverse reactions, like?
Cardiovascular
hematologic
neurologic
Drug-induced lupus with procainamide
Given IV
Class IB: Sodium Channel Blockers examples?
Lidocaine (Xylocaine IV)
tocainide (tonocard)
mexiletine ( mexitil)
Clinical uses of Class IB?
Ventricular arrhythmias, especially during an acute myocardial infarction
Digitalis-induced arrhythmias
Class IC: Sodium Channel Blockers examples?
propafenone (Rythmol) flecainide (Tambocor)
Clinical uses of Class IC?
treatment of sustained ventricular tachycardia and paroxysmal supraventricular tachycardia (PSVT)
BBW for Flecainide (Tambocor)?
Use only for life-threatening arrhythmias
Increased risk of mortality when used for non-life-threatening ventricular arrhythmias
Side effects and adverse reactions of class IC?
arrhythmias
Increased QT prolonged with Macrolides ( can progress to Torsades de Pointe)
Class II: Beta Blockers - Beta-1 selective act mainly on?
cardiac muscle
Class II: Beta Blockers - Beta-2 selective act mainly on?
cardiac, lung, arterial, pancreatic, kidney, adipose, liver tissues
Class II: BB MOA?
Decrease heart rate, conduction velocity, and force of contraction
Class II/lll Beta-blocker/ Potassium Channel Blockers combo example?
Sotalol (Betapace)
Class II and Class III drug (Combo)
Sotalol (Betapace) is a non-selective completive ____-___________ receptor blocker that also exhibits Class __ anti arrhythmic properties.
beta-adrenergic
class III
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
Class III: Potassium Channel Blockers examples?
Amiodarone (Cordarone) - Vtach, Vfib, SVT maybe
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
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
What is amiodarone (cordarone) contraindicated with?
many ABS
BBW of Class III: Potassium Channel Blockers?
Hepatotoxicity
Pro-arrhythmic (make worse) - sometimes it can cause other arrhythmias
Pulmonary fibrosis
Examples of Class IV: Calcium Channel Blockers?
verapamil (Calan)
diltiazem (Cardizem)
Class IV: Calcium Channel Blockers give temporary control of rapid ____________ _____ in ____ or ________
ventricular rates
in a-fib and a-flutter ( acute Tx IV)
Class IV: Calcium Channel Blockers achieve conversion of ____ into normal sinus rhythm?
PSVT
Side effects of Class IV: Calcium Channel Blockers ?
Peripheral edema!
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
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
what is angina cause by?
Thought to be caused by the imbalance between oxygen supply and demand
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
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
Short terms treatment for angina ?
Nitrates
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
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
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
Nitroglycerin vaso________
dilates
Does Nitroglycerin work more on veins or arteries?
Greater in the veins than arteries
Because Nitroglycerin works more on the veins, it results in ______ pooling and thereby ___________ left ventricular volume (preload) and ________ ventricular EDV.
venous
decreasing
reducing
Nitroglycerin increases pressure in the _____?
brain
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
Nitroglycerin _________ coronary blood flow by ________ the coronary arteries and improving collateral flow to ischemic regions
Increases
dilating
Nitroglycerin has serious adverse reactions with concurrent use of ________, _________, __________.
sildenafil (Viagra)
tadalafil (Cialis)
vardenafil (Levitra)
PDE5 medications have a ___________ effect that is more significant with nitroglycerin causing ___________
synergistic
Hypotension
Examples of Nitrates for angina?
Isosorbide dinitrate (Isordil) isosorbide mononitrate (Imdur, Monoket)
Clinical uses of Isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur, Monoket)?
prevention of angina
Isosorbide denigrate and Isosorbide mononitrate are not for the treatment of _____ _______.
acute attacks
Dinitrate: undergoes _____ first-pass metabolism
100%
Mononitrate: _______ undergo first-pass metabolism
does not
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
Ranolazine increases efficiency of ___ under _______ conditions.
ATP
under hypoxic
Ranolazine has Antianginal and anti-ischemic effects without ___________ change
hemodynamic
