Chronic Heart Failure Practice Flashcards

Definition of Chronic Heart Failure (CHF): A clinical condition in which the heart is unable to pump a sufficient amount of blood to the tissues of the body.
Pathophysiology and Progression: Because the heart is unable to pump blood efficiently, blood begins to build up within the heart itself. This eventually leads to an "overflow" of blood into the lungs.
Clinical Consequences of Fluid Build-up:
- Pulmonary Edema: The presence of fluid in the lungs.
- Peripheral Edema: The presence of fluid in the body, which frequently manifests in the lower extremities.
Associated Symptoms:
- Tiredness.
- Shortness of breath.
- Rapid heart rate.
- Fluid build-up occurring in both the lungs and the extremities.

Ejection Fraction: This term refers to the proportion of blood that is ejected during each contraction of the heart in comparison with the total volume of blood contained within the ventricle of the heart.
Left Ventricular End Diastolic Volume: This is defined as the total amount of blood present in the ventricle immediately before it contracts. This parameter is also formally known as the preload.

Overview: The NYHA system is historically the older of the two common classification systems. Its primary focus is on assessing the severity of the patientɹs symptoms to help clinicians and patients understand the diseaseɹs progression.
Classification Criteria:
- Class I: No limitations on physical activity. Normal physical activity does not cause symptoms.
- Class II: Slight limitations on physical activity. The patient is comfortable when at rest, but ordinary activity causes symptoms.
- Class III: Marked limitation of physical activity. The patient remains comfortable at rest, but less than ordinary activity causes symptoms.
- Class IV: The patient is unable to engage in any physical activity without symptoms, or symptoms are present even while at rest.

Overview: Developed by the American College of Cardiology Foundation and the American Heart Association (ACCF/AHA), this system was more recently developed to assess the stages of heart failure. Its focus is on disease progression as demonstrated by structural changes to the heart.
Stages of Heart Failure:
- Stage A: The patient is at high risk for heart failure but exhibits no symptoms and has no structural heart disease.
- Stage B: Structural heart disease is present, but the patient exhibits no signs or symptoms of heart failure.
- Stage C: Structural heart disease is present with current or past symptoms of heart failure.
- Stage D: Refractory heart failure that requires specialized clinical interventions.

Primary Drugs of Choice:
- ACE-inhibitors.
- Angiotensin II Receptor Blockers (ARBs).
- Certain Beta Blockers.
- Diuretics (primarily used to reduce symptoms; further details provided in the nephrology section).
Escalation of Therapy: As the heart failure condition worsens, aldosterone inhibitors are often added to the treatment regimen.
Late-Stage Addition: Digoxin is typically added only after these other points in the treatment regimen have been established, despite its historical significance.

Drug Class: Digoxin belongs to a unique class known as the cardiac glycosides.
Origin: It was originally obtained from the digitalis plant, also commonly known as foxglove.
Clinical Effect (Mechanism): It is a positive inotrope, which means it increases the force of the heartɹs contraction.
Current Status in Therapy: It has fallen out of clinical favor because it has not been shown to reduce mortality. Additionally, it carries a high risk of toxicity and various drug interactions.
Adverse Events:
- Drop or rise in heart rate.
- Low blood pressure.
- Headache.
- Fatigue.
- Confusion.
- Convulsions.
- Colored vision (specifically green, yellow, or purple tints).
- Anorexia.
- Nausea and vomiting.
- Diarrhea.
Digoxin Toxicity:
- Therapeutic Index: Digoxin has a low therapeutic index, necessitating careful monitoring of drug concentrations, particularly when initiating therapy.
- Signs of Toxicity: Low heart rate, headache, dizziness, confusion, nausea, and visual disturbances (specifically blurred vision or yellow-tinted vision).
- Management: Management strategies range from simply withholding the next scheduled dose to the administration of an antidote therapy for more severe cases.

Rationale for Use: Although beta blockers decrease the workload of the heart (which may seem counterintuitive for a failing heart), they are beneficial because CHF patients often experience tachycardia (increased heart rate) as the heart tries to meet body demands.
Mechanism of Benefit: Because a heart beating too fast is inefficient and cannot meet demands, a beta blocker slows the heart rate. This allows the heart more time to fill with blood and function more efficiently.
Preferred Beta Blockers for CHF:
- Metoprolol.
- Bisoprolol.
- Nebivolol.
- Carvedilol.
Dosing Note: In the context of chronic heart failure, dosages for beta blockers are typically on the lower range.

Status: Both drug classes have become the preferred therapy for managing CHF.
Mechanism of Action: These drugs function by preventing sodium and water from being reabsorbed into the body.
Systemic Effects: By preventing reabsorption, they effectively decrease the overall blood volume and the volume of blood returning to the heart.
Clinical Outcome: This reduction in volume decreases the preload and the subsequent workload required of the heart.