​Kembara Xtra - Medicine - Chronic Heart Failure

​Kembara Xtra - Medicine - Chronic Heart Failure 
Introduction
Heart failure (HF) is caused by the heart's inability to fill and/or pump blood effectively enough to meet tissue metabolic needs. When a sufficient cardiac output can only be achieved at the cost of increased filling pressures, HF may result. It is the primary side effect of cardiac disease.
HF is preferable over congestive HF since individuals aren't always fluid-overloaded (congested). HF can affect either the left or right heart, or it can be biventricular.
It is a progressive condition that manifests as remodeling (a changed heart's geometry).

● A patient's functional state is categorized using a subjective grading system called the New York Heart Association (NYHA) classification: Asymptomatic in NYHA class I, symptomatic with moderate activity in NYHA class II, symptomatic with modest exertion in NYHA class III, and symptomatic at rest in NYHA class IV.

The stages established by the American Heart Association (AHA) and American College of Cardiology (ACC) serve to outline how HF progresses: Stage A: at risk for HF; stage B: structural disease; stage C: structural disease with HF symptoms; stage D: end-stage disease. Stage A: at risk for HF; stage B: structural disease.

Nearly 1 million hospital admissions every year are caused by idiopathic HF, with a readmission rate of 25% after 30 days. In the US, HF has an annual direct and indirect cost of $34.4 billion.
Incidence
550,000 new cases are identified each year in the US, and there are over 250,000 deaths annually.
Worldwide, there are an estimated 23 million people with HF.
HF affects 6.5 million people in the United States; it affects 1% of those under 50 and 10% of those over 80. It is mostly a disease of the elderly; 75% of HF hospital admissions include those over 65.

Pathophysiology and Etiology 
Most clinical HF observations are explained by two physiologic factors, which can be divided into four broad groups.
Systolic hypertension (SH) with reduced ejection fraction (HFrEF) is an inotropic condition that frequently results from myocardial infarction (MI) or dilated cardiomyopathy (CM) and causes impaired systolic emptying (EF 40%).
- HF with preserved EF (HFpEF) or diastolic HF: a compliance disorder in which the ventricular relaxation is compromised (EF 50%), frequently brought on by hypertensive CM
- Borderline HFpEF (EF 41-49%): moderate systolic dysfunction that exhibits clinical characteristics of HFpEF
The two most common etiologies are coronary artery disease (CAD)/MI and hypertension (HTN). - Improved HFpEF (EF > 40%): Previously HFrEF, with improvement in systolic function. Others:
Alcoholism, viruses, medications, muscular dystrophy, infiltrative diseases (such as amyloidosis and sarcoidosis), postpartum conditions (such as Chagas disease and HIV), hypertrophic CM (HCM), and hereditary familial dilated CM are all associated with myocarditis.
- Valvular and vascular abnormalities, including renal artery stenosis, which is typically bilateral and can lead to recurrent "flash" pulmonary edema, valvular stenosis or regurgitation, and rheumatic heart.
- Pulmonary HTN and chronic pulmonary disease
- Arrhythmias (high-grade heart block, frequent PVCs, atrial fibrillation [AF] and other tachyarrhythmias)
– Other high-output conditions include anemia, hyperthyroidism, cardiac depressants (overdose on beta-blockers), stress-related conditions, iatrogenic volume overload (severe overload in persons with healthy hearts and kidneys), and idiopathic conditions.
20% to 50% of familial dilated CM cases are idiopathic.
Genetics
Numerous genetic anomalies that cause various phenotypes have been discovered. For first-degree relatives who have HCM or arrhythmogenic RV dysplasia, think about genetic testing.

Risk factors include CAD/MI, high blood pressure, valvular heart disease, diabetes, cardiotoxic drugs, obesity, and advanced age.

Controlling HTN and other risk factors is prevention.

Dyspnea upon exertion: the hallmark of left-sided HF.
Deteriorating exercise capacity: general weakness, easy weariness, and nocturnal nonproductive cough with orthopnea; occasionally, frothy or pink sputum. breathing difficulty, especially at night, without a history of asthma or an illness (cardiac asthma); the Cheyne- Stokes respirations
Anorexia, as well as a feeling of fullness or a dull pain in the right upper quadrant (hepatic congestion). Advanced HF may manifest as nausea and a lack of appetite.

clinical assessment 

Rales and occasionally wheezing, peripheral edema, S3 gallop, hepatomegaly, jugular venous distention, hepatojugular reflux, and ascites are symptoms of increased filling pressures.
Poor cardiac output is characterized by hypotension, pulsus alternans, tachycardia, narrow pulse pressure, chilly extremities, and cyanosis. Remodeling is characterized by an enlarged or displaced point of maximal impulse.

Multiple Diagnoses 
Constrictive pericarditis, nephrotic syndrome, cirrhosis, simple dependent edema, pulmonary embolism, exertional asthma, cardiac ischemia, asthma/chronic obstructive pulmonary dysfunction

Laboratory Results 

Laboratory results should be used as an addition to the clinical diagnosis and as a sign of potential problems.
Initial examinations (lab, imaging)
BNP and N-terminal pro-BNP (NT-proBNP) are useful in an emergency situation to determine the source of dyspnea (a value of 100 effectively rules out heart failure). In those with structural heart disease or risk factors for developing HF but no symptoms, a BNP level can aid in predicting the onset of symptomatic HF (1).[A].
BNP may be increased by renal failure, acute coronary syndromes, and pulmonary embolism. BNP levels can be increased by sacubitril/valsartan, however NT-proBNP levels are less affected.
BNP levels could be lowered by obesity. Although a predischarge BNP can predict the probability of readmission and survival, the use of BNP-guided therapy in chronic HF and abruptly decompensated HF is not well established.

Lab results: proteinuria, increased creatinine (cardiorenal syndrome), dilutional hyponatremia (poor prognosis), pulmonary alkalosis, azotemia, reduced erythrocyte sedimentation rate, and hyperbilirubinemia
Chest x-ray findings include an enlarged heart, vascular redistribution (cephalization) with a "butterfly" pattern of pulmonary edema, interstitial and alveolar edema, Kerley B lines, and pleural effusions (changes lag clinical symptoms).
In long-standing HF, pulmonary edema findings may not be present.

Diagnostic Nuclear imaging to estimate ventricular size, assess for ischemia or infarction, amyloidosis, and systolic function. Echocardiogram: most useful test to determine LVEF, which is crucial for proper diagnosis and management of HF. RV function, diastolic dysfunction, ventricular size, wall thickness, and valvular abnormalities are other tests to consider. When there is a possibility of cardiac sarcoidosis, arrhythmogenic RV CM, acute myocarditis, amyloidosis, or hemochromatosis, a cardiac MRI may be recommended. In the presence of risk factors, cardiac catheterization is crucial for ruling out CAD as the cause; endomyocardial biopsy should only be performed in exceptional cases (such as suspected giant cell myocarditis).

Management 
The goal of treatment is to increase hemodynamics, reduce symptoms, and prevent the neurohormonal response to increase survival.
MEDICATION
Nitrates and diuretics are used to treat acute HF.
Aldosterone antagonists and ACE-I can be introduced at any moment, especially for HFrEF. Once acute HF has cleared, the blocker should be started. NSAIDs should be avoided because they make HF worse. Diltiazem and verapamil should not be used in patients with systolic dysfunction due to increased mortality and harmful inotropic effects.
Initial Line
In all NYHA classes, ACE-I is utilized to reduce afterload, boost survival, alleviate symptoms, and raise exercise capacity; patients with systolic dysfunction and post-MI benefit most from this treatment. Number required to treat (NNT) for mortality is 25 per year. All ACE-Is are thought to be equally efficient. Start with modest doses and increase to the desired doses as tolerated.
Angiotensin receptor blockers (ARBs) are recommended if an ACE-I intolerance exists. The starting doses for these medications are as follows: captopril: 6.25 mg PO TID; enalapril: 2.5 mg PO BID; lisinopril: 2.5 to 5.0 mg daily; and ramipril: 1.25 mg daily. Do not combine ACE-I and ARB.
- The recommended starting doses for losartan, valsartan, and candesartan are 4 to 8 mg orally once day, respectively.
Blockers are applied in diastolic or systolic HF. Start with a modest dose in individuals who are hemodynamically stable or compensated, then gradually increase the dose. NNT for mortality is 25 per year. Death rates dropped in systolic HF, suggesting that heart rate (HR) should be adjusted rather than dose.
– Carvedilol: 3.125 mg PO BID; metoprolol succinate ER: 12.5 mg/day PO; bisoprolol: 1.25 to 10.00 mg once daily; bisoprolol: 1.25 to 10.00 mg once daily; sacubitril/valsartan (Entresto): an ARNI that has been shown to lower the risk of CV death and HF hospitalizations in patients with HFrEF.
24/26 mg or 49/51 mg PO BID, with an aim of 97/103 mg PO BID, is the recommended dose. To minimize morbidity and mortality in patients with HFrEF and NYHA classes II and III who tolerate an ACE-I or ARB with CrCl >30, substitution with an ARNI is advised (NNT to prevent one CV death over 3.5 years: 31). At least 36 hours should pass before beginning ARNIs after stopping ACE-Is. The most frequent side effects include hypotension, edema, and renal failure.

 Based on randomized clinical trials, DAPA-HF and EMPEROR-Reduced, serum glucose cotransporter-2 (SGLT-2) inhibitors dapagliflozin and empagliflozin, used to treat type 2 diabetes mellitus, improved in worsening HF or CV death in patients with EF 40% and NYHA class II/IV, regardless of diabetes, and may decrease overall death (NNT 50 to 60/year). The suggested daily dose for both is 10 mg PO. The FDA authorized the use of SGLT-2 inhibitors for the treatment of HFrEF on the basis of evidence. Urogenital infections, ketoacidosis, decreased blood pressure, and increased diuresis are side effects.

Vericiguat, a guanylate cyclase simulator, was approved by the FDA for use in patients with an EF 45%, recent hospitalization for HF, or need for IV diuretics based on the VICTORIA trial. Diuretics are useful to manage volume overload/reduce preload.
- Torsemide (Demadex): 10 to 200 mg/day PO split dosage; furosemide (Lasix): 40 to 120 mg/day PO divided dose; bumetanide (Bumex): 0.5 to 10.0 mg/day IV/PO divided dose
- Chlorothiazide (Diuril): 250 to 2,000 mg/day IV/PO divided dosage; metolazone (Zaroxolyn): 2.5 to 20.0 mg/day PO split dose; hydrochlorothiazide: 12.5 to 100.0 mg/day PO divided dose
- Spironolactone, eplerenone: spironolactone 12.5 to 25.0 mg/day PO; maximum 50 mg/day PO; eplerenone 25 to 50 mg/day; warning with reference to hyperkalemia and chronic kidney disease (CKD)
Digoxin: lessens symptoms, but has little beneficial impact on mortality. The suggested dosage for people with maintained renal function (CrCl >50 mL/min) is 0.125 mg/day.
If a patient is unable to take an ACE-I/ARB, the combination of isosorbide dinitrate and hydralazine (20 mg/37.5 mg PO TID) can be utilized to improve survival and lower hospitalization rates among African Americans.
Ivabradine (Corlanor) may be used to prevent hospitalization in NYHA classes II and III HF patients with EF 35% and maximally tolerated -blockers with HR >70.

ADHF, hypotension (90/50 mm Hg), severe liver disease, pacemaker dependency, bradyarrhythmias, or powerful CYP3A4 inhibitors are contraindications. Patients with AF should not receive medication, and treatment should be stopped if AF develops.
No therapy has increased survival in HFpEF. Spironolactone and ARBs have the potential to cut down on hospitalizations.


Further Therapies 

It has been demonstrated that device therapy, such as cardiac resynchronization therapy (CRT) and implantable cardioverter-defibrillators (ICDs), improves outcomes.
Left bundle branch block (LBBB)-related sinus rhythm with a QRS width 150 ms, LVEF 35%, persistent mild to moderate HF despite goal-directed medical therapy (GDMT), decreasing LVEF with continuous RV pacing or with bradyarrhythmias, and an expected need for a pacemaker are all indications for CRT.
CRT is taken into account when the following criteria are met: LVEF 35%, sinus rhythm, QRS width >150 ms, non-LBBB pattern, and NYHA class II or ambulatory NYHA class IV symptoms. Consider CRT in ambulatory NYHA class IV patients if the QRS width is more than 150 ms as a result of the LBBB pattern. Despite GDMT, consider CRT in NYHA classes II to IV if the QRS width is between 120 and 150 ms with an LBBB pattern.
The ICDs recommend primary prevention in individuals with nonischemic and ischemic CM, at least 40 days after a MI; LVEF 35%; NYHA class II or III HF; or LVEF 30%; and on optimal medical therapy and >1 year expected survival; generally not advised in endstage HF.

Surgery Mitral valve repair if mitral regurgitation (MR) is the main problem and is not functional Advanced therapies like cardiac transplantation and LV assist device (LVAD) implantation can be considered in patients with HF that is resistant to treatment. Cardiac transplantation is a possibility for individuals under the age of 70 who have estimated 1-year survival rates that are lower than those offered by transplantation.
The indications for implanting an LVAD are comparable but changing.


Admission 
Acute renal damage, mental status change, hemodynamic/respiratory impairment, considerable volume overload, and electrolyte abnormalities (such as hyponatremia) were present upon admission. Upon discharge, there had been a subjective improvement, euvolemia on assessment, improved vitals, and outpatient education had been completed.

Take Action 
After hospitalization, stop outpatient follow-up to reduce the likelihood of readmission.
DIET
Reduce sodium load; unknowable optimum level

After diagnosis, the prognosis is: 75% of patients survive for one year, 50% for five years, and 25% for ten years.
COMPLICATIONS
sudden demise and gradual pump failure