Copia - Copia - Heart failure

Gonzalez MD

START

HY Heart Failure

clinical syndrome with symptoms caused by impairment of one or both ventricles to provide adequate cardiac output at a normal filling pressure due to a structural or functional cardiac disorder

Cardiac dysfunction leads to elevated cardiac filling pressures at rest AND during stress.

HF is a chronic condition punctuated by periods of instability.

Despite advances in therapy and management, HF remains a deadly clinical syndrome (fluid retention).

HF is the final common stage of many diseases of the heart (abnormal LV-RV filling and elevated filling pressures). **Hemodynamic: heart can not pump blood or can do so only at the cost of high filling pressures.Many of its features are not organ-specific, and there may be few signs or symptoms early in the disease process (such as elevated jugular venous pressure, pulmonary rales, or a third heart sound, hepatomegaly)

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Concept: Heart Failure

Heart failure is a typical result of extended periods of extreme mechanical activity.

Acute heart failure is a syndrome defined as the new onset (de novo heart failure (HF)) or worsening (acutely decompensated heart failure (ADHF)) of symptoms and signs of HF, mostly related to systemic congestion. In the presence of an underlying structural or functional cardiac dysfunction, one or more precipitating factors can induce AHF, although sometimes de novo HF can result directly from the onset of a new cardiac dysfunction, most frequently an acute coronary syndrome. Fluid retention and redistribution result in systemic congestion, eventually causing organ dysfunction due to hypoperfusion. Current treatment of AHF is centred on decongestive drugs.AHF is associated with high mortality and hospital readmission rates. There is an unmet need for increased individualization of management.

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Acute Heart Failure

High blood pressure: An increase in blood pressure exposes cardiac myocytes to elevated mechanical stress and neurohormones, which increase myocardial mass and result in left ventricular hypertrophy.

Ischemic heart disease is thought to be the most important risk factor for HF.In the 7 to 8 years after an MI, more than one-third of patients will develop HF

The more severe the elevation in blood pressure, the worse the risk of developing HF.The lifetime risk for individuals with blood pressure ≥160/90 mmHg is double that of those with blood pressure <140/90 mmHg.*** The combined presence of hypertension and HF is associated with worse outcomes

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Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Review article. Signal Transduction and targeted therapy 2022.

Heart Failure: Etiopathogenesis

HF is often referred to as left-sided failure when caused primarily by left heart pathologies (eg, LV, mitral valve, or aortic valve dysfunction). HF is called right-sided when caused by right heart conditions (eg, pulmonary hypertension or RV, pulmonic valve, or tricuspid valve dysfunction). Left HF and right HF may each occur separately or concurrently. Left HF is a common cause of right HF, and most patients with right HF have some element of left HF.

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***** Over time, pulmonary venous capacitance and lymphatic drainage accommodates to the chronic state of volume overload, leading to less or no fluid accumulation in the alveoli, despite the increase in total lung water and high filling pressures.

Chronic heart failure: patients with diagnosed heart failure for a period of time (minimum of 3 months). Patients tend to gradaully withdraw from physical activity.Acute heart failure: acute onset(days to weeks) or significant worsening of symptoms (decompensation), it always requires prompt diagnosis and management. Subgroups of acute heart failure (Medical emergencies)Acute (cardiogenic) pulmonary oedema —acute left heart failure with redistribution of fluid into the pulmonary interstitium. Cardiogenic shock—Acute reduced cardiac output (cardiac index <2.2 L/min/m2 ) and hypotension (systolic blood pressure <90 mm Hg) in the setting of heart failure (PCWP > 18 mm Hg) to the point where endorgan perfusion is compromised. Acute decompensated —The most common form is an acute deterioration in a previously stable patient.

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Heart Failure: Onset

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Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Review article. Signal Transduction and targeted therapy 2022.

Congestion in Heart Failure: Stages

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Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Review article. Signal Transduction and targeted therapy 2022.

Congestion in Heart Failure: AHA classification

Vital signs and appearance —

1. An irregular pulse is suggestive of AF, which frequently accompanies HF.
2. Evidence of decreased tissue perfusion caused by a major decline in cardiac output.
3. Four key findings suggest greater severity of cardiac dysfunction even at steady state: resting sinus tachycardia, narrow pulse pressure, diaphoresis, and peripheral vasoconstriction (cool, pale, and cyanotic extremities due to the combination of decreased perfusion and increased oxygen extraction).
4. The pulse pressure is reduced below 25 mmHg (neurohumoral adaptation to compensate for a fall in cardiac output by increasing sympathetic outflow with resultant shunting of the cardiac output to vital organs).
5. Pulsus alternans, pathognomonic of severe LV systolic dysfunction.

Some of the physical examination findings of HF, while not very specific on their own, can be very specific in the setting of typical symptoms of HF, but sensitivity is low, so the absence of physical findings does not exclude HF. E.g. patients with HF and preserved ejection fraction (HFpEF) typically have a nondilated heart, so displacement of the apical impulse is not a helpful finding for diagnosis of HFpEF.

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Congestion in Heart Failure: Physical examination

Volume assessment

• There are three major manifestations of volume overload: pulmonary congestion, peripheral edema, and elevated jugular venous pressure.
• Pulmonary congestion that may manifest as rales is more prominent in acute or subacute disease: rales (crackles).
• Pulmonary edema
• Pleural effusion (chronic elevation in pulmonary venous pressure)
• Peripheral edema, ascites, scrotal edema, hepatomegaly, and splenomegaly
• Hepatojugular reflux/abdominojugular test/Liver congestion (manual compression of the right upper quadrant to increase venous return may elevate jugular venous pressure above the transient 1 to 3 cm elevations seen in normal individuals
• Elevated jugular venous pressure (patient sitting at 45 degrees, jugular venous pressure can be estimated from the height above the right atrium of venous pulsations in the internal jugular vein).
• Gallops: sign of elevated left heart filling pressure

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Congestion in Heart Failure: Physical examination

Cardiac examination

• Ventricular chamber size can be estimated by precordial palpation (an apical impulse that is laterally displaced past the midclavicular line is usually indicative of LV enlargement).
• The S3 may be palpable in severe ventricular failure (left atrial pressures exceeding 20 mmHg and increased LV end-diastolic pressures >15 mmHg) *** low sensitivity
• Physical signs of pulmonary hypertension: a murmur of pulmonary or tricuspid insufficiency

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Congestion in Heart Failure: Physical examination

Screening with 12-lead electrocardiography, echocardiography, and plasma B-type natriuretic peptide or N-terminal proBNP has been considered in ambulatory patients at high risk of developing heart failure to identify abnormalities in cardiac structure and function

Chest radiography. Chest radiography can be used to assess the degree of congestion. Radiographic congestion scores correlate well with directly measured mass of lungs . Pulmonary ultrasonography. Ultrasonography of the lungs is becoming a generally accepted tool for the evaluation of pulmonary oedema. The quantity of water in the lungs corresponds to the degree of echogenicity found on ultrasonography. Thoracic ultrasonography can also be used to identify existing pleural effusion. Thoracic CT scans. Increased density on high-resolution pulmonary CT scans correlates well with lung weight and has been suggested as a gold standard for the assessment of pulmonary interstitial oedema. T

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Heart Failure: Work up

*** add each drug sequentially, to allow for identification of the source of any adverse effect or intolerance(ie, ARNI, beta blocker, MRA, and, finally, SGLT2 inhibitor). However, patient characteristics (potassium, blood pressure, HF severity) can allow for a different sequence of therapy,

the goals of therapy are to reduce symptom severity, decrease the risk of mortality and morbidity, and attenuate or possibly reverse the process of adverse remodeling of the LV. REGIMEN FOR PATIENTS WITH MILD TO MODERATE SYMPTOMS (NYHA class II to III)A combination therapy with one agent from each of the following classes of medications:

1. Renin-angiotensin-aldosterone system antagonist, with a preference for an angiotensin receptor-neprilysin inhibitor (ARNI; ie, sacubitril-valsartan)
2. Beta blocker.
3. Mineralocorticoid receptor antagonist
4. Sodium-glucose co-transporter 2 inhibitor.

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Heart Failure treatment: Primary components of therapy

Selected Potential Causes of Elevated Natriuretic Peptide Levels

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Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Review article. Signal Transduction and targeted therapy 2022.

Heart Failure treatment