Heart Failure Flashcards
How does ACE inhibitors improve HF
Angiotensin-Converting Enzyme (ACE) Inhibitors are central to managing heart failure due to their ability to disrupt the cycle of neurohumoral activation—a hallmark of heart failure. Here’s how they work:
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Inhibition of Angiotensin I to Angiotensin II Conversion: ACE inhibitors block the enzyme responsible for converting angiotensin I into angiotensin II. Angiotensin II is a potent vasoconstrictor and a key player in heart failure progression. By reducing its levels, ACE inhibitors:
- Decrease Peripheral Vasoconstriction: This lowers the resistance against which the heart must pump, thereby reducing the workload on the heart.
- Reduce Sympathetic Nervous System Activation: High levels of angiotensin II can lead to increased sympathetic activity, which exacerbates heart failure. By lowering angiotensin II, ACE inhibitors help calm this overactive system.
- Decrease Aldosterone Release: Aldosterone promotes sodium and water retention, leading to increased blood volume and worsening heart failure. By reducing its levels, ACE inhibitors help mitigate fluid overload.
- Mitigate the Renin-Angiotensin System Activation by Diuretics: Diuretics often increase renin release as a compensatory mechanism, but ACE inhibitors can prevent this, making them particularly effective when used together with diuretics.
Clinical Impact:
- Improvement in Effort Tolerance: In moderate to severe heart failure, ACE inhibitors significantly enhance a patient’s ability to perform physical activities without discomfort.
- Reduction in Mortality: Long-term use of ACE inhibitors has been shown to decrease the risk of death in heart failure patients.
- Prevention of Overt Heart Failure Post-MI: In patients with poor left ventricular function after a myocardial infarction (MI), ACE inhibitors help prevent the progression to symptomatic heart failure.
While ACE inhibitors are beneficial, they do come with potential side effects:
- Symptomatic Hypotension: Due to their blood pressure-lowering effects, ACE inhibitors can cause significant hypotension, especially in patients who are volume-depleted or have low baseline blood pressure.
- Renal Impairment: ACE inhibitors can worsen kidney function, particularly in patients with bilateral renal artery stenosis or pre-existing renal disease.
- Hyperkalemia: An increase in serum potassium levels can occur, which may be beneficial by counteracting hypokalemia from loop diuretics but can also lead to dangerous levels of potassium in some patients.
- Marked Blood Pressure Drops with Short-Acting ACE Inhibitors: Especially in the elderly or those with pre-existing hypotension, ACE inhibitors can cause significant drops in blood pressure.
Starting Therapy:
- In patients with stable blood pressure (systolic BP >100 mmHg), ACE inhibitors can usually be started safely in an outpatient setting.
- For higher-risk patients, such as those with hypotension, hypovolemia, or hyponatremia, it is advisable to withhold diuretics for 24 hours before starting ACE inhibitors at a low dose, preferably at night. Monitoring renal function and potassium levels 1–2 weeks after initiation is crucial.
How does ARBs improve HF
ARBs work by blocking the action of angiotensin II on its receptors in the heart, blood vessels, and kidneys.
- Mechanism: While ACE inhibitors prevent the formation of angiotensin II, ARBs block its effects directly at the receptor level. This leads to similar beneficial effects on blood pressure and heart function.
- Tolerability: ARBs are often better tolerated than ACE inhibitors, particularly because they are less likely to cause the persistent cough associated with ACE inhibitors.
- Comparable Benefits: ARBs offer similar improvements in mortality and heart failure symptoms as ACE inhibitors.
Adverse Effects:
- ARBs share the more serious side effects of ACE inhibitors, including the risk of renal dysfunction and hyperkalemia.
Usage:
- ARBs are typically used as an alternative for patients who cannot tolerate ACE inhibitors.
- In some cases of resistant or recurrent heart failure, ARBs may be combined with ACE inhibitors for added benefit.
Conclusion: ACE inhibitors and ARBs are cornerstone therapies in managing heart failure due to their ability to interfere with the renin-angiotensin-aldosterone system (RAAS). Their use improves symptoms, enhances quality of life, and reduces mortality. However, careful monitoring and individualized dosing are essential to minimize the risk of adverse effects.
How does Vasodialators help a AF patient and it’s limitations
Vasodilators are crucial in managing chronic heart failure, especially when ACE inhibitors or ARBs are contraindicated. Their primary function is to reduce the workload on the heart by dilating blood vessels, which can be achieved in two ways:
- Venodilators: These drugs, such as nitrates, primarily dilate the veins, which leads to a reduction in preload (the amount of blood returning to the heart). By decreasing preload, venodilators lower the volume of blood that the heart must pump with each beat, thereby reducing the strain on the heart.
- Arterial Dilators: Drugs like hydralazine target the arteries, reducing afterload (the resistance the heart must overcome to eject blood). By lowering afterload, arterial dilators make it easier for the heart to pump blood into the circulation, which helps in improving cardiac output.
Limitations:
- Pharmacological Tolerance: Over time, the body may develop a tolerance to vasodilators, particularly nitrates, which can reduce their effectiveness. This often necessitates either dosage adjustments or the introduction of drug-free intervals.
- Hypotension: A common side effect of vasodilators is hypotension (low blood pressure), which can be problematic, especially in patients who already have low baseline blood pressure. This requires careful monitoring and dose titration to balance the benefits with the risk of adverse effects.
How does beta blockers benefit a HF patient
Beta-adrenoceptor blockers, commonly known as beta-blockers, play a significant role in the management of chronic heart failure due to their ability to mitigate the harmful effects of enhanced sympathetic nervous system stimulation. In heart failure, the body often compensates for poor cardiac function by increasing sympathetic activity, which leads to an increased heart rate, higher blood pressure, and a greater risk of arrhythmias (irregular heartbeats). While initially compensatory, these effects can become detrimental over time, worsening heart failure.
Mechanism of Action:
- Reduction of Sympathetic Overactivity: Beta-blockers work by blocking the effects of adrenaline and other stress hormones on the heart. This reduces the heart rate, lowers blood pressure, and decreases the heart’s oxygen demand.
- Reduction in Arrhythmias: By stabilizing the heart’s electrical activity, beta-blockers help prevent potentially life-threatening arrhythmias and reduce the risk of sudden cardiac death.
Clinical Benefits:
- Improvement in Ejection Fraction: When started at low doses and gradually increased, beta-blockers can improve the heart’s ejection fraction (the percentage of blood the left ventricle pumps out with each contraction), which is often reduced in heart failure patients.
- Symptom Relief: Patients may experience less shortness of breath and fatigue, leading to a better quality of life.
- Reduction in Hospitalizations and Mortality: Beta-blockers significantly reduce the frequency of hospital admissions due to heart failure exacerbations and lower overall mortality rates in chronic heart failure patients.
Dosage and Administration:
- Initiation and Titration: Beta-blockers should be started at a very low dose to avoid precipitating acute-on-chronic heart failure. For example, bisoprolol typically starts at 1.25 mg daily and is gradually increased over a 12-week period to a target dose of 10 mg daily. This slow titration is crucial to allow the heart to adapt to the reduced sympathetic stimulation without decompensating.
- Comparison with ACE Inhibitors: While both beta-blockers and ACE inhibitors are beneficial in heart failure, beta-blockers have been shown to have a greater impact on reducing mortality. In clinical studies, beta-blockers reduced the relative risk of death by 33%, compared to a 20% reduction with ACE inhibitors.
Conclusion: Vasodilators and beta-blockers are essential components in the treatment of chronic heart failure. Vasodilators reduce the heart’s workload by lowering preload and afterload, while beta-blockers counteract the harmful effects of sympathetic overactivity, improve heart function, and reduce mortality. The careful initiation and titration of these medications are key to maximizing their benefits while minimizing risks.
What are the other medications that can be used in HF?
Mechanism of Action:
- Ivabradine specifically targets the If (funny) current in the sinoatrial (SA) node, the natural pacemaker of the heart. By inhibiting this current, ivabradine reduces the heart rate without affecting the strength of heart contractions.
Clinical Benefits:
- Ivabradine has been shown to reduce hospital admissions and lower mortality rates in patients with heart failure, particularly those with moderate to severe left ventricular systolic dysfunction.
- The drug’s effects are most significant in patients with a resting heart rate above 77 beats per minute, making it particularly useful for those who cannot tolerate beta-blockers or whose heart rate remains elevated despite beta-blockade.
Limitations:
- Ineffective in Atrial Fibrillation: Ivabradine does not work in patients with atrial fibrillation (AF) because its action depends on a regular heart rhythm originating from the SA node.
Mechanism of Action:
- Digoxin is primarily used to control the heart rate in patients with atrial fibrillation and heart failure. It works by increasing the force of heart muscle contractions (positive inotropic effect) and slowing the heart rate by enhancing vagal (parasympathetic) activity.
Clinical Benefits:
- Digoxin is particularly useful in rate control for patients with heart failure and atrial fibrillation, where it helps to manage the irregular and often rapid heartbeat associated with AF.
- In patients with severe heart failure (New York Heart Association [NYHA] class III-IV), digoxin can reduce the likelihood of hospitalizations due to heart failure exacerbations, though it does not improve long-term survival.
Limitations:
- Digoxin does not affect long-term survival rates in heart failure, so its use is mainly focused on symptom management and reducing hospital admissions.
Mechanism of Action:
- Amiodarone is a potent anti-arrhythmic drug that has minimal impact on the force of heart contractions (negative inotropic effect), making it suitable for patients with poor left ventricular function.
- It works by stabilizing the heart’s electrical activity and is effective in treating various types of arrhythmias, including both atrial and ventricular arrhythmias.
Clinical Benefits:
- Amiodarone is effective in the treatment of symptomatic arrhythmias, such as atrial fibrillation or ventricular arrhythmias, particularly in patients who have not responded to other treatments.
- It is often used when other pharmacological options have been exhausted, providing a last line of defense against symptomatic arrhythmias.
Limitations:
- Not for Preventative Use: Amiodarone should not be used as a preventive medication in asymptomatic patients due to its potential side effects and the risk of unnecessary exposure to the drug’s toxicities.
Ivabradine, Digoxin, and Amiodarone are important medications in the management of heart failure, each with distinct roles:
- Ivabradine is best suited for reducing heart rate in patients with sinus rhythm and high heart rates, especially when beta-blockers are not an option.
- Digoxin is particularly useful for controlling the heart rate in patients with atrial fibrillation and heart failure, focusing on reducing hospitalizations.
- Amiodarone is a valuable anti-arrhythmic agent for managing symptomatic arrhythmias in patients with heart failure, especially when other treatments have failed.
Each of these medications has specific indications, benefits, and limitations, requiring careful consideration by clinicians to optimize heart failure management and improve patient outcomes.
What are the causes of HF
- Myocardium
Dilated cardiomyopathy
Restrictive cardiomyopathy
Preparrum cardiomyopathy
Ischemic heart dxs
Infective myocarditis
Toxic myocarditis
Nutritional def. HF - endocardium
Ventricular septal dxs
Congenital valvular dxs
Senile valvular dxs
Infective endocarditis
Rheumatic valvular dxs - Extra cardial
Thyro toxicosis
Beri beri
Drugs
HTN
Hyper thyroidism
IV fluid overload
What are the clinical presentation of acute heart failure
udden onset of dyspnoea at rest that rapidly progresses to acute respiratory distress,orthopnoea and prostration. Often there is a clear precipitating factor, such as an acute MI, which may be apparent from the
history.
The patient appears agitated, pale and clammy.
The peripheries are cool to the touch and the pulse is rapid, but in some cases there may be an inappropriate bradycardia that may contribute to the acute episode of heart failure. The BP is usually high because of SNS activation, but may be normal or low if the patient is in cardiogenic shock.
The jugular venous pressure (JVP) is usually elevated, particularly with associated fluid overload or right heart failure.
In acute heart failure, there has been no time for ventricular
A ‘gallop’ rhythm, with
a third heart sound, is heard quite early in the development of acute left-sided heart failure
Differentiate between L & R side hear failure
LHF
- reduced systole
- gallop rhythm heart sound
- Bilateral reduction in air entry
- Oliguria
- reduction in vital capacity
- pulmonary edema
- cardiomegaly
RHF
- +Hepatojugular reflexe
- Tender hepatomegaly
- increase JVP
- bilateral pitting edema
- kussmal sign
Ascitis
What are the complications bod HF?
Weight loss
HypoK
HyperK
Renal Failure
Thromboembolism
Impaired liver function
Arrhythmias (ventricular tachycardia)
Sudden death
What are the investigations you will do in a heart failure pt
X Ray:
A: Alveolar Edema
B: Kelly B Line
C: cardiomegaly
D: Dilated pulmonary (arteries)vessels
E: Pleura Effusion
E/U/Cr
Thyroid function test
BNP
is elevated in heart failure and is a prognostic marker, as well
as being useful in differentiating heart failure from other causes
of breathlessness or peripheral oedema.
- Describe the pathophysiology of heart failure and how it progresses.
Heart failure (HF) is a condition in which the heart is unable to pump enough blood to meet the body’s demands. The pathophysiology involves multiple processes:
- Decreased Cardiac Output: The failing heart has a reduced ability to pump blood, leading to a decrease in cardiac output. This triggers compensatory mechanisms to maintain perfusion.
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Compensatory Mechanisms:
- Sympathetic Nervous System (SNS) Activation: When cardiac output drops, the body activates the SNS, increasing heart rate and vasoconstriction. However, over time, this increases the heart’s workload and exacerbates heart failure.
- Renin-Angiotensin-Aldosterone System (RAAS): Reduced perfusion to the kidneys stimulates the RAAS, leading to vasoconstriction and fluid retention. This raises blood pressure and increases preload (the volume of blood in the ventricles before contraction), worsening heart failure.
- Ventricular Remodeling: In response to increased workload, the ventricles undergo structural changes. Hypertrophy (increased muscle mass) or dilation (stretching of the heart chambers) occurs, further reducing the heart’s efficiency.
- Progression: Over time, the heart cannot maintain compensatory mechanisms. This leads to symptoms such as fluid overload, pulmonary edema, and organ perfusion deficits. The disease progresses through stages, from mild (NYHA Class I) to severe symptoms (NYHA Class IV).
- Differentiate between systolic and diastolic heart failure in terms of etiology, pathophysiology, and clinical features.
Systolic Heart Failure (HFrEF):
- Etiology: Most commonly caused by ischemic heart disease, myocardial infarction, or dilated cardiomyopathy. It is characterized by a reduced ejection fraction (EF < 40%).
- Pathophysiology: The heart’s contractile ability is weakened, resulting in impaired ejection of blood during systole. This leads to increased end-systolic volume and decreased stroke volume, lowering cardiac output.
- Clinical Features: Patients present with signs of fluid overload (e.g., peripheral edema, pulmonary congestion) and reduced organ perfusion (e.g., fatigue, exercise intolerance).
Diastolic Heart Failure (HFpEF):
- Etiology: Commonly associated with conditions like hypertension, hypertrophic cardiomyopathy, and aging. It is characterized by a preserved ejection fraction (EF > 50%).
- Pathophysiology: The heart’s ability to relax and fill during diastole is impaired. This causes elevated filling pressures, leading to pulmonary congestion despite a normal ejection fraction.
- Clinical Features: Similar to systolic heart failure, patients present with dyspnea, exercise intolerance, and fluid retention, but their heart’s pumping function remains relatively normal.
- Explain the compensatory mechanisms in heart failure and how they can become maladaptive over time.
In response to decreased cardiac output, several compensatory mechanisms are activated:
- Sympathetic Nervous System (SNS) Activation: The SNS increases heart rate and contractility to maintain cardiac output. However, chronic SNS activation leads to increased afterload, arrhythmias, and myocardial ischemia, worsening heart failure.
- Renin-Angiotensin-Aldosterone System (RAAS): Activation of the RAAS increases blood volume and vasoconstriction to maintain blood pressure. However, chronic RAAS activation results in fluid retention (leading to pulmonary and systemic congestion) and increased afterload, placing further strain on the heart.
- Ventricular Remodeling: In response to chronic pressure and volume overload, the heart undergoes hypertrophy and dilation to maintain cardiac output. However, this remodeling leads to increased wall stress, reduced contractility, and eventually heart failure progression.
Over time, these compensatory mechanisms, initially protective, become maladaptive and contribute to the progression of heart failure by increasing the heart’s workload and promoting further structural and functional deterioration.
- Discuss the clinical presentation of heart failure, including the major signs and symptoms.
The clinical presentation of heart failure can vary depending on the severity of the disease but typically includes:
- Dyspnea (shortness of breath): Often worse with exertion or when lying down (orthopnea). This occurs due to pulmonary congestion from fluid buildup.
- Fatigue and weakness: Due to reduced cardiac output and poor tissue perfusion, especially during physical activity.
- Edema: Fluid retention in heart failure leads to swelling in the legs, ankles, and abdomen (peripheral edema). Pulmonary edema may also develop, causing a productive cough with frothy sputum.
- Paroxysmal nocturnal dyspnea (PND): Waking up suddenly at night with shortness of breath due to redistribution of fluids into the lungs when lying flat.
- Jugular venous distension (JVD): Increased pressure in the right atrium leads to distended neck veins.
- Weight gain: Rapid weight gain may indicate fluid retention, a common feature in decompensated heart failure.
- S3 heart sound (gallop rhythm): This is often present in systolic heart failure due to increased filling pressures and a dilated ventricle.
