Heart Failure Concepts Quiz

Dentistry Degree - Unit III: Heart Failure

• Unit 3 covers the physiopathology and semiology of the cardiovascular system.
• Lesson 17 specifically focuses on heart failure.

Unit III. Lesson 17 Index

• Circulatory insufficiency
• Heart failure
• Decompensated Heart Failure
• Shock

Circulatory Insufficiency (1.1 General concepts)

• The circulatory system's inability to provide tissues with the necessary blood volume for their needs.
• Consequences include decreased tissue oxygenation, reduced substrate contribution for metabolism, and impaired removal of residual products.

Circulatory Insufficiency (1.2 Classification)

• Global, affecting the entire body.
• Organ-specific, impacting only certain organs.
• Heart failure is a type of global circulatory insufficiency
• Shock is another possible outcome.

Heart Failure (2.1 Concept)

• Heart failure is a complex condition combining the heart's inability to pump sufficient blood volume to meet tissue needs with a neurohormonal compensatory response.

Heart Failure (2.2 Classification)

• Low-output HF (Lo-HF): Failure of the heart's pumping mechanism. Subcategories include systolic dysfunction and diastolic dysfunction.
• High-output HF: The heart pumps adequately but with high volume demands.

Heart Failure (2.3 Mechanisms and Causes)

• Low-output HF due to systolic dysfunction involves arrhythmias, myocardial injury (ischemia, myocarditis, toxic/metabolic myocardiopathies), and mechanical/pressure/volume overload (valve stenosis, insufficiency, anomalous communication).
• Low-output HF due to diastolic dysfunction involves arrhythmias, atrioventricular flow obstruction (valve stenosis), reduced ventricular distensibility (pericardial effusion, ischemia, hypertrophy).
• High-output HF can arise from conditions such as anemia, beriberi, hyperthyroidism, and Paget's disease.

Heart Failure (2.4 Compensatory Mechanisms)

• The body initially responds to heart failure through compensatory mechanisms.
• Two main mechanisms are systemic neuro-endocrine responses and ventricular remodeling.
• Systemic neuro-endocrine response: The body activates the sympathetic nervous system, releases catecholamines, activates the renin-angiotensin-aldosterone system (RAAS) and increases ADH secretion to elevate blood volume, pressure and heart rate.
• Ventricular remodeling occurs in response to pressure or volume overload. It can manifest as concentric (pressure overload) or eccentric (volume overload) hypertrophy. This involves changes in myocardial structure, impacting its efficiency and leading to further damage.

Heart Failure (2.5 Pathogeny)

• Increased myocardial oxygen consumption
• Reduced myocardial contractility/distensibility
• Less efficient sarcomere function, as the presence of fetal sarcomere isoforms.
• Reduced contractile myocardial mass from factors like catecholamine cytotoxicity, increased apoptosis, or necrosis.

Decompensated Heart Failure (3.1 Concept)

• Decompensated heart failure occurs when compensatory mechanisms fail, leading to adverse effects such as sudden or gradual onset of heart failure symptoms that require unplanned medical attention (e.g., office visits, ER).

Decompensated Heart Failure (3.2 Clinical Manifestations)

• Manifestations include tissue hypoperfusion or ischemia, lung congestion, and systemic venous congestion.

Decompensated Heart Failure (3.3 Classification)

• Left-sided heart failure
• Right-sided heart failure
• High-output heart failure
• 3.3.1 Left-sided heart failure: Symptoms and Physical Exam findings are described
• 3.3.2 Right-sided heart failure: Symptoms and Physical exam findings are described.
• 3.3.3 High-output heart failure: Defined and explained
• 3.3.3.1 High-output heart failure: Symptoms including hyperdynamic state, hot skin, elevated heart rate, and potential functional murmurs.

Decompensated Heart Failure (3.3.1 Left-sided Heart Failure, 3.3.2 Right-sided Heart Failure, 3.3.3 High-output Heart Failure) (Complementary Exploration)

• ECG for hypertrophy
• X-Rays showing pulmonary congestion
• Echocardiogram to assess hypertrophy, dilation, cardiac function, and pulmonary artery pressure. Explaining those tests.

Shock (4.1 Concept)

• Global circulatory failure causing generalized ischemia (inadequate blood flow to tissues) due to inadequate perfusion.
• Characterized as cellular and tissue hypoxia due to reduced oxygen delivery, increased oxygen consumption, or inadequate oxygen utilization.

Shock (4.2 Classification)

• Cardiogenic shock
• Hypovolemic shock
• Distributive shock
• Obstructive shock
• 4.2.1 Cardiogenic shock: Lower cardiac output and hypoxia with adequate blood volume.
• 4.2.2 Hypovolemic shock: Inadequate blood volume due to various, severe blood/fluid losses.
• 4.2.3 Distributive shock: Abnormal dilation of blood vessels impacting blood flow to organs.
• 4.2.4 Obstructive Obstructive shock: Physical obstructions impede blood flow into/out of the heart

Shock (4.3 Compensatory Mechanisms)

• The body attempts a neuro-endocrine response (sympathetic system, catecholamines, RAAS, increased ADH secretion).
• These responses aim to restore normal circulatory function but are often less intense given the speed of shock progression.

Shock (4.4 Manifestations and Consequences)

• Anamnesis: Confusion, progressive clouding of consciousness, oliguria (low urine output), and dyspnea (difficulty breathing)
• Physical Examination: Pale, cold skin, peripheral cyanosis, sweating, and changes in heart rate and breathing
• Laboratory findings include metabolic acidosis. Explaining the types of acidosis and the significance of measuring them.