Pharm Week 8 Flashcards
There is no cure for Heart Failure (True of False)
True
Diseases that cause or accelerate HF
mitral stenosis, myocardial infarction (MI), chronic hypertension (HTN), coronary artery disease (CAD), diabetes mellitus
What causes cough and shortness of breath in HF
Blood backs up into the lungs
Cause of left sided HF
excess blood accumulates in the left ventricle, causing it to thicken and enlarge (hypertrophy) in order to compensate for the increased workload
Cause of right sided HF
excess blood backs up into veins, resulting in peripheral edema and engorgement of organs, such as the liver
What should a nurse monitor in HF and diuretic therapy
electrolyte levels, weakness, hypotension, confusion, vital signs, intake and output, blood glucose , blood-urea nitrogen (BUN)
What is the max amount of sodium a heart failure pt should intake
4000mg daily
ACE inhibitors
lisinopril, captopril, zestril
ACE inhibitor side effects
cough, headache, dizziness, orthostatic hypotension, first-dose phenomenon, hyperkalemia; Serious adverse effect-angioedema*
contra-indications of ACE inhibitors
hyperkalemia
Labs to monitor while on ACE inhibitors
BUN, creatinine, K+
Mechanism of action in ACE inhibitors
inhibits conversion of angiotensin I to angiotensin II and decreases aldosterone secretion; BP is decreased and CO is increased
What blocks the action of ACE inhibitors
NSAIDS
Cardiac glycosides
digoxin and lanoxin
MOA of cardiac glycosides
increases contractility of heart and slows conduction which improves cardiac output
Adverse effects of cardiac glycosides (digoxin and lanoxin)
n/v dysrythmia, visual disturbances(halos,yellow-green tinge, blurring)
Serious adverse effect: dysrhythmias especially in the presence of hypokalemia**
Metoprolol side effects
bradycardia, orthostatic hypotension, abnormal sexual function, drowsiness, fatigue
Contra-indications of metoprolol
asthma, COPD
which drug enhances effects of hypoglycemics
metoprolol
Electrical conduction pathway
sinoatrial (SA) node, across both atria>atrioventricular (AV) node> atrioventricular bundle (bundle of His)>to the right and left bundle branches>Purkinje fibers
What is the most common type of dysrthymia
Atrial fibrillation
Types of Dysrhythmias
Premature atrial contraction (PAC)
Premature ventricular contractions (PVC)
Ventricular tachycardia(VT)
Atrial flutter (AF)
Atrial fibrillation (A Fib)
Sinus bradycardia (SB)
Heart block (1st, 2nd, 3rd degree)
When does generation of the action potential
begins when sodium-ion channels open and sodium ions rush in
Depolarization (contraction)
calcium-ion channels open and calcium ions enter the cell, stimulating cardiac-muscle cells, SA and AV cells depolarize in response to calcium-ion influx
Repolarization (resting)
return to a polarized state, sodium pump removes sodium from the cell, potassium-ion channel
Nonpharmacological therapies for dysrhythmias
Cardioversion and defibrillation-(ventricular tachycardia, ventricular fibrillation)electrical shock that stops all electrical impulses in the heart and allows the sinoatrial node to regain control
Catheter ablation- identifies and destroys aberrant cardiac cells that cause dysrhythmias
Cardiac pacemaker-paces the heart at a set rate
Implantable cardioverter defibrillators (ICDs)-combination of pacemaker and defibrillator