Notes on Cardiology: Heart Failure, Tamponade, and Pulmonary Hypertension

CARDIOLOGY 2024/2025

Nicholas Raccagni

Nicholas Raccagni

1SMS

2024/2025

Emergency Diseases

Heart Failure (HF) Definition

Heart failure (HF) is a clinical syndrome due to structural and/or functional abnormality of the heart resulting in elevated intracardiac pressures and/or inadequate CO, at rest and/or during exercise. It is a chronic progressive condition in which the heart muscle is unable to pump blood efficiently enough to meet the body needs for oxygen and nutrients causing elevation of the filling pressures. The [LVJEF is determined by ([LVJEDV-[LVJESV)/[LVJEDV therefore a normal [LVJEF can't be 100%, a value is normal if <70% since some blood always remains in the left ventricle at every systole.

1. Left-sided heart failure: occurs when the left ventricle fails to pump blood effectively.

• HF with reduced ejection fraction (HFrEF): when LVEF <40%. The heart muscle is weakened, and the left ventricle can't contract forcefully enough to push adequate blood into circulation.
• HF with mildly reduced ejection fraction (HFmrEF): when LVEF 40%-49%, elevated natriuretic peptides and one additional criteria (as left ventricular hypertrophy or left atrial enlargement).
• HF with preserved ejection fraction (HFpEF): when LVEF >50%, elevated natriuretic peptides and one additional criteria (LA enlargement or LV hypertrophy). The heart contracts normally, but the ventricle is stiff and doesn't relax properly, preventing it from filling in enough blood.

1. Right-sided heart failure: occurs when the right ventricle cannot pump blood into the lungs, causing fluid buildup in abdomen, legs and feet. It often results from left-sided heart failure.
2. Congestive heart failure (CHF): occurs when the fluid buildup (congestion) in tissues such as the lungs and/or the lower extremities due to impaired pumping ability of the heart muscle.

. Left atrial enlargement (LAE) is an additional criteria for HFpEF and HFmrEF since being the LA, a compliant chamber, an high [LVJEDV cause an increased LV pressure then reflected on the LA. . Left ventricular hypertrophy (LVH) is an additional criteria for HFpEF and HFmrEF, as a thicker the LV chamber can be filled by a lower blood amount than a chamber with regular thickness.

Epidemiology of Heart Failure

Heart failure is the first cause of hospitalisation in patients older than 65 years old. Furthermore, the prevalence is increasing as people are getting older and we are now able to treat diseases like myocardial infarction. In Italy, nowadays there are more than 1,000,000 people that are suffering from heart failure and 50% of them are affected by HFpEF. In these patients, nevertheless the use of foundational therapies (ACEi, ARBs, Beta-blockers), we still have a residual risk of progression.

Pathophysiology of Heart Failure

The Frank-Starling Curve represents the mechanism by which the normal subject can increase the cardiac output (CO=SVxHR where SV=EDV-ESV) after an increase in end-diastolic volume (EDV): for instance, following an increase in EDV in patients with HFrEF we assist at a lower increase in SV than in patients with an hypertrophic cardiomyopathy where we have an higher increase in SV. The best value to correctly define the left ventricular function is the ejection fraction (EF=SV/EDV) that allows us to define the heart functionality and it's strongly correlated with the stroke volume. Stroke volume (and therefore also cardiac output) depends on preload, contractility and afterload:

• Cardiomyopathy: heart muscle weakening, potentially caused by genetic, viral, or toxic causes, cause heart malfunctioning which can lead to a reduced stroke volume and so cardiac output.
• Heart valve disease: mitral or aortic regurgitation but also aortic stenosis cause some blood to turn back to the left ventricle or atrium during systole instead of being expelled from the heart.
• Arrhytmias: if a LV desynchrony develops the pumping systems become inefficient. It can be intraventricular or interventricular: an example of desynchrony is the left bundle branch block.
• Coronary artery disease: narrowed (coronary artery disease) or occluded arteries (myocardial infarction) reduce heart perfusion affecting its pumping ability and reducing its stroke volume.

These conditions decrease the stroke volume reducing the left ventricular ejection fraction (LVEF). Nicholas Raccagni

2SMS

2024/2025

Left Ventricle Performance and Remodelling

Looking now at the global performance of the left ventricle, we can see two main determinants: preload (diastole), which is related to relaxation and compliance, and afterload (systole), which is related to contractility. These two processes, systole and diastole, lead to the generation of stroke volume (SV) and end-diastolic pressure (EDV), from which we can understand the clinical picture:

• Reduced stroke volume (SV) leads to uncorrect peripheral organs perfusions leading to fatigue and multiple organ damage. Moreover, the stroke volume also influences the venous return, and in case it is reduced, venous congestion can develop as the blood remain trapped in the veins.
• Increased end-diastolic pressure (EDV) leads to increased left atrial pressure (LAP); which is reflected to the pulmonary circulation, causing pulmonary hypertension and lung congestion.

In heart failure (HF) we assist to a vicious cycle since all the aspects involved, in the end, lead to left ventricle (LV) remodelling where the heart switches from an elliptical shape (resembling rugby ball) to a circular shape (resembling football ball) to compensate for the reduced ejection fraction (EF). This occurs since the heart undergoes through LV dilation to increase EDV and in this way also the SV and the CO; until a point the compensation mechanism ceases since the CO cannot increase anymore and therefore the EF decreases. Moreover, as the heart becomes more dilated, getting spherical, the contracting forces push blood in all the directions, and not only towards the direction of the aortic valve, further diminishing the EF. Apart from LV dilation, in heart failure we also assists at a LV hypertrophy. This is phenomenon is explained by the Laplace's Law, which express the cardiac wall stress [o=(2Pxr/)t] as the result of the left endoventricular pressure [P] multiplied by the radius [r] and then divided by the wall thickness [t]. On the basis of this law, the enlarged chamber radius of the chronically failing heart exposes myocytes to increased systolic wall stress causing chamber hypertrophy, which acts to renormalize wall stress. This increased afterload impairs the weakened myocytes ability to shorten deteriorating cardiac performance.

Neurohormonal Activation in Heart Failure

Apart from remodelling, the LV tries to compensate for damage by neurohormonal activation:

• Sympathetic Nervous System (SNS): maintain high blood pressure and concentrate blood flow to the main organs by secreting adrenaline/noradrenaline, that cause vasoconstriction. Thus, it increases the heart walls (not affected by damage) contractility and the HR to maintain the CO.
• Renin Angiotensin Aldosterone System (RAAS): is another system leading to vasoconstriction.
• Natriuretic Peptides: increase diuresis and natriuresis, cause vasodilation, inhibit SNS+RAAS.

SNS and RAAS are good in the short term but in the long run, they become deleterious, because vasoconstriction increases the peripheral vascular resistance (afterload). Natriuretic peptides work trying to compensate the previous mechanisms decreasing the arterial pressure and sympathetic tone by increasing diuresis and natriuresis. However, their action is not enough to compensate for the other mechanisms, causing a chronic hemodynamic stress to which the heart responds with cardiac remodelling. Many heart failure patients stay asymptomatic thanks to these physiological compensating mechanisms; however this neurohormonal imbalance causes the HF progression.

Mitral Regurgitation in Heart Failure

Patients with heart failure (HF) may also present mitral regurgitation (MR) which can be caused by:

• LV dilation: causes dilation of the mitral annulus and tending of the chordae tendineae, leading to an ineffective leaflets coaptation (point of contact between the leaflets is lower than 1 cm).
• LA dilation: causes dilation of the mitral annulus; especially in case of in atrial fibrillation (AF), which can occur as a consequence of the dilation (leading to secondary mitral regurgitation).
• LV-EDP increase: causes a reduced closing force as the force produced by the poor contractile ventricle is not enough to push up the leaflets efficiently, hence the valve doesn't close properly.

Manifestation of Heart Failure

Heart failure is not a single pathological diagnosis, but it's a clinical syndrome characterised by:

• Fatigue and weakness: caused by a reduced oxygen delivery and a decreased cardiac output.
• Palpitations: caused by compensatory mechanisms triggered by the increased heart workload.
• Cyanosis: bluish skin or lips, due to inadequate oxygenation, particularly in severe heart failure.

Left-Sided Heart Failure Symptoms

Left-Sided HF: left ventricle's inability to pump blood, causing pulmonary congestion.

• Dyspnea: the earliest symptom, especially on exertion, and in advanced stages, even at rest. This can present with orthopnea (difficulty in breathing when lying flat), paroxysmal nocturnal dyspnea (night episodes of dyspnea), pulmonary edema (accumulation of fluids in the lungs).
• Decreased Urination: often occurs during the day since the kidneys perfusion is reduced.
• Confusion or syncope: in severe cases, left-heart failure can lead to reduced brain perfusion.

Nicholas Raccagni

3SMS

2024/2025

Right-Sided Heart Failure Symptoms

Right-Sided HF: right ventricle's inability to pump blood, causing systemic congestion.

• Peripheral edema: swelling in the lower legs, ankles, and feet caused by buildup of fluid.
• Ascites and hepatomegaly: fluid accumulation in the abdomen due to venous congestion.
• Jugular vein distention (JVD): is caused by the increased pressure in the venous system.

When we must carefully start from the legs, from which we can look at the hemodynamic state of the patient. We must check for edema, temperature, and afterwards we can feel the pulse which give us information about peripheral perfusion; if the heart doesn't pump enough, the legs will be less perfused, since it is more important to provide good brain perfusion. Then we have to check the abdomen, the liver and the spleen to look for ascites and hepatosplenomegaly that may hint systemic congestion. We must look at the radial pulses that should be stronger than the leg ones. In the end we perform auscultation which may give us signs of S3 and S4 due to heart stiffness.

NYHA Classification of Heart Failure Severity

The severity of impairment is classified using the NYHA (New York Heart Association) system:

1. NYHA I: no limitation of physical activity; ordinary activities cause no symptoms.
2. NYHA II: low limitation of physical activity; normal activity cause fatigue, palpitation, dyspnea.
3. NYHA III: marked limitation of physical activity; less-than-ordinary activity causes symptoms.
4. NYHA IV: severe limitation of physical activity; symptoms of heart failure present even at rest.

Diagnosis of Heart Failure

The following tests are the standard diagnostic tests which are used to assess heart failure (HF).

Blood Tests for Heart Failure

A. Blood tests: check for blood count, markers, organ function tests, electrolytes and glucose.

• Complete blood count: assesses anemia or infection, that may exacerbate HF symptoms.
• Natriuretic peptides: B-type NP (BPN<100 pg/mL) + N-terminal-proBNP (NT-proBNP<450 pg/mL) are hormonal markers released by a stressed heart, which are often elevated in HF.
• Organ functional tests: renal and hepatic functions can be affected by heart failure due to reduced blood flow or congestion, especially in advanced stages. Instead, thyroid function tests are important since hypo- or hyperthyroidism can mimic or exacerbate HF symptoms.
• Electrolytes and glucose: checks for imbalances that complicate treatment or reveal issues.

Electrocardiogram (ECG) for Heart Failure

B. Electrocardiogram (ECG): looks for heart rhythm irregularities (atrial fibrillation or arrhythmias), for evidence of prior heart attack (myocardial infarction) and/or for left ventricular hypertrophy.

Echocardiography for Heart Failure

C. Echocardiography: crucial to visualise heart's structure, together with heart wall motion and valves function but also to measure ejection fraction which is useful to classify heart failure.

Chest X-ray (CXR) for Heart Failure

D. Chest X-ray (CXR): allows to detect the fluid buildup in the lungs (pulmonary edema) and to assess the heart size (cardiomegaly), and other lung issues which exacerbate HF symptoms.

Stress Test for Heart Failure

E. Stress test: evaluates heart's response to exertion, revealing potential cardiac abnormalities.

Advanced Diagnostic Tests for Heart Failure

Advanced diagnostic tests for heart failure include cardiac MRI to evaluate cardiac hypertrophy, invasive coronary angiography in case of CADs is suspected as the underlying cause and right heart catheterisation to measure the pressure in the right side of the heart (Swan Ganz catheter).

Diagnosing HFpEF

HFpEF is one of the most difficult diagnoses in cardiovascular diseases since these patients are mostly asymptomatic at rest but they can have exercise intolerance. There are neither signs nor symptoms specific for HFpEF but there are many mimics: for example, COPD, obesity, anaemia.

• Patients with HFpEF may present only with unexplained dyspnoea on exertion. So, we perform a stress test to assess the pulmonary arterial pressure (PAP): high PAP suggests HFpEF as the LV is stiff and doesn't properly relax, preventing its diastolic filling. Several cardiac conditions may mimic HFpEF, like hypertrophic cardiomyopathy, restrictive cardiomyopathy, constrictive pericarditis, but we can distinguish the disease evaluating increased natriuretic peptides levels.

Classification of Heart Failure Stages

These are the HF stages according to the American College of Cardiology and the American Heart Association, however the most followed are the European guidelines that have some differences:

A. Stage A: asymptomatic patients only with risk factors and no structural abnormality. B. Stage B: asymptomatic patients with risk factors and mild structural abnormalities. C. Stage C: mildly symptomatic patients with risk factors and moderate structural abnormalities. D. Stage D: severe symptomatic patients with risk factors and advanced structural abnormalities.

Nicholas Raccagni

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