Drugs in the Treatment of Congestive Heart Failure (CHF) Flashcards
What is Congestive Heart Failure?
- Reduced cardiac output at the expense of cardiac dilatation.
- Systolic ejection fraction is less than 45% of cardiac output (is usually 60%) and diastolic ejection fraction is approximately 30-50%.
–>Leads to cardiac hypertrophy.
What are the common signs and symptoms of CHF?
- Dyspnea (trouble breathing due to exertion or rest)
- Orthopnea (trouble breathing when laying down)
- Fatigue
- Edema reduced renal function
- Enlarged heart
- Echocardiogram (reduced EF)
What are the 2 main factors which contribute to congestive heart failure?
- Increased workload on the heart.
- Decreased muscle contractions
*These factors lead to a decreased CO, decreased BP and an increased TPR.
Responses to CHF include:
-Increased sweating, decreased renal blood flow, increased renin/ ANGII/ ALDO release (RAAS), increased TPR, increased Na+/ H20 retention, increased edema and increased venous pressure.
What is the main goal in drugs for congestive heart failure?
To increase cardiac output and contraction without increasing cardiac energy consumption.
*Digoxin
What are the two compensatory mechanisms of congestive heart failure?
- The sympathetic nervous system (extrinsic control)
- The Frank Stirling Law of the heart (intrinsic control)
*Edema is often associated with congestive heart failure due to increase in RAAS activation/ increased venous pressure (leads to increased capillary filtration)
Furosemide and Spironolactone in the treatment of CHF:
- Furosemide is a loop diuretic, and spironolactone is a K+ Sparing Diuretic, helping with hypokalemia by blocking aldosterone action.
- Spironolactone may cause gynecomastia (adverse effects less prevalent with Eplerenone (new aldosterone antagonist!)
Hydralazine dilates which vessels?
Resistance vessels only (arteries)
Nitrates dilate which vessels?
Veins and arteries!
What is the goal of ACE inhibitors, ARBs and DRIs?
- To decrease the activity of the RAAS.
* Decrease ANGII/ aldosterone and decrease BP.
Enalapril to treat CHF:
- ACE inhibitor
- Decreases sympathetic activity and reduces BP
Digoxin to treat CHF:
- Digoxin inhibits the Na+/ Na+ ATPase pump.
- ->Due to this block, (Na+) intracellular concentrations increase and activate the Ca2+/ Na+ pump, allowing Na+ to exit the cell and Ca2+ to come in, increasing contractility of the heart without an increase in workload in the heart.
–>Leads to a lower threshold for depolarization’s (smaller phase 0), reduced conduction velocity and can cause AV block.
- Digoxin increases BP and vagal tone- causes a decrease in sympathetic activtiy (the increase in vagal tone is responsible for the AV block)
- Adverse Effects include nausea, visual changes, hyperkalemia, vomiting and vagal effect (AB conduction block)
- LOW THERAPEUTIC INDEX (high toxicity)
What is the effect of PDE inhibitors on muscle contraction?
-Prevent hydrolysis of cAMP, and this prolong the action of protein kinase A.
Carvedilol
Beta Blocker
What is most important to monitor when administering Digoxin?
-K+ plasma levels!
If ACE inhibitors and Beta Blockers fail to help reduce BP in CHF, what drugs are used next?
- Furosemide and Spironolactone
2. Digoxin/ Nitrates
