Drugs used in heart failure CIS (Linger) Flashcards
58 year old Caucasian male cc- increasing SOB recent 17 lb weight gain dyspnea on exertion ankle edema orthopnea episodes of nocturnal dyspnea productive cough nocturia mild dependent edema
PMH:
HTN
depression
osteoarthritis managed with NSAIDs***
PE: dyspnea, cyanosis, tachy BP 160/100 S3 gallop hepatomegaly neck venous distention RR 28
3+ pitting edema
inspiratory rales and rhonci bilaterally
Current meds-
HCTZ- thiazide diuretic
Ibuprofen-> blocks prostaglandin synthesis which reduces vasodilation of the renal afferent arteries and the body retains sodium and water
Ranitidine - H2 histamine receptor blocker
Citalopram
which class of diuretics are most efficacious for reducing volume overload and are appropriate choice for this patient ?
Heart failure:
occurs when CO is inadequate to provide O2 needed by the body
Diuretics most appropriate?
Loop diuretic –> powerful alleviators of the congestive part of heart failure but don’t reduce mortality
Prototypes-Furosemide, ethacrynic acid
Results of loop: decrease intracellular K+ in TAL decrease back diffusion of K+ and positive potential Decrease reabsorption of Ca and Mg increase diuresis Cause hypokalemia and alkalosis
patient in heart failure is given furosemide and an additional agent to control his BP and edema
he develops a swollen tongue and nagging cough. what is the additional agent?
what is an appropriate replacement therapy in this situation to control BP and edema in combination with furosemide?
ACE inhibitor –> cause angioedema, cough, swollen face
why do these cause these adverse effects?
-ACE inhibitors 1) less ANG II production 2) no longer have break down of bradykinin by ACE so you have more bradykinin –> vasodilation
Substitute? ARB
-act at ang I receptor - block effects of angiotensin but have no effects on bradykinin so they don’t cause cough, but in very rare cases they can cause angioedema
patient with HF is now stable of furosemide and losartan
a third drug is give that has been shown to reduce symptoms and improve survival in patients with HF
you inform the patient that his symptoms may temporarily get worse upon initiation of this drug but improvement should be apparent 3-6 months of therapy….
what drug was most likely prescribed?
Metoprolol –> B-blocker
why? this is a negative inotropic agent
start stable patients on low doses of B-blockers and this has been shown to improve survival in patients with HF
overtime in HF the chronic sympathetic activation is detrimental to the heart –> cardiac muscle becomes less responsive to catecholamines b/c there are less b-receptors and reduces the responsiveness of the myocardium
the heart responds to b-blockers by expressing more beta receptors again, can increase ejection fraction, slow heart rate, etc.
patient in HF develops palpitations
develops S3 heart sound
patient is given a drug that may cause paroxysmal atrial tachycardia with block at toxic concentrations … which agent is given?
Digoxin
cardiac glycoside
indications –> HF, afib and shock
improves symptoms and reduces hospitalizations, but there is no net effect on mortality
MOA–> inhibits Na/K ATPase and increases myocardial contractility –> increases Ca in sarcoplasmic reticulum
NARROW THERAPEUTIC index - but Na/K ATPase is all over the body…. so this is scary
what are the therapeutic effects of digoxin
brief prolongation of AP followed by AP shortening
increases intracellular Ca
increases cardiac contractility
increases parasympathetic tone and reduces sympathetic tone ***
slows things down at the AV node by increasing the refractory period
Toxic levels of digoxin and its effects
premature depolarizations- if these reach threshold they can cause PVC –> if allowed to progress, it can lead to ventricular fibrillation –> fatal
RMP is increased due to buildup of intracellular sodium
AP is dramatically shortened
Most common cardiac manifestation is arrhythmia - most commonly it reduces the refractory period of the AV node
sympathetic outflow is increased by digoxin
which of the patients current medications might be expected to potentiate the toxic effects of digoxin?
losartan ibuprofen furosemide ranitidine citalopram
furosemide–> hypokalemia can potentiate the toxic effects of digoxin. loop diuretic can cause hypokalemia. potassium and digoxin compete for binding at the Na/K ATPase
PDE
phosphodiasterase which degrades cAMP
