Heart Failure and Diastolic Dysfunction Quiz

A condition where the heart cannot pump blood effectively to meet the body's needs.

A condition where the heart's ability to pump blood is so compromised that it causes symptoms and complications.

Conditions that directly damage the heart muscle, leading to impaired pumping ability.

Conditions that put excessive strain on the heart, forcing it to work harder than usual, eventually leading to failure.

Conditions that restrict the ability of the heart to fill with blood effectively, leading to reduced output.

Factors that trigger or worsen existing heart failure.

The heart compensates for reduced pumping ability by increasing its workload, but this can eventually lead to further damage.

The underlying mechanisms and processes that contribute to the development and progression of heart failure.

A type of heart failure characterized by rapid onset and a significant decrease in cardiac output within a short period.

A type of heart failure characterized by a gradual onset and often accompanied by compensatory mechanisms like increased blood volume and heart muscle remodeling.

Heart failure affecting the left side of the heart, causing congestion in the lungs.

Heart failure affecting the right side of the heart, causing congestion in the body.

Heart failure affecting both the left and right sides of the heart.

A type of heart failure where the heart's ability to pump blood is significantly reduced.

A type of heart failure where the heart pumps enough blood but the body has an increased demand.

Heart failure caused by a weakened heart muscle, resulting in a decrease in the heart's ability to contract.

The body's natural response to heart failure, aiming to maintain adequate blood flow and organ function despite the weakened heart.

The heart beats faster to pump more blood per minute.

Hormones like adrenaline increase the strength of heart contractions.

The chambers of the heart enlarge to hold more blood, potentially improving output.

The heart muscle thickens, allowing it to pump more forcefully.

The amount of blood pumped by the heart per minute.

The law describing the relationship between the initial length of heart muscle fibers and the force of contraction.

The overlap of thin and thick filaments in heart muscle fibers, which determines the strength of contraction.

Destruction of heart muscle cells, primarily caused by factors like oxygen deprivation (ischemia), infection, toxins, and calcium overload.

A key mechanism in heart failure, where the heart muscle cells die due to lack of oxygen or other harmful conditions.

A programmed cell death process that also contributes to heart failure. It can be initiated by factors like oxidative stress and calcium overload.

A vital aspect of heart failure pathogenesis that involves the heart's response to damage. It can lead to hypertrophy (enlargement) or dilation (expansion) of the heart chambers.

A condition where the heart muscle's ability to relax and fill with blood is impaired, leading to reduced cardiac output.

The ability of the ventricle to expand and accommodate increasing volumes of blood during diastole.

A decrease in ventricular compliance, making it harder for the ventricle to fill with blood during diastole.

The inability of the myosin-actin complex to detach quickly enough, leading to delayed relaxation and reduced filling.

Calcium ions are not taken up by the sarcoplasmic reticulum fast enough, prolonging the contraction and hindering relaxation.

Reduced production of ATP (energy) within the heart muscle due to problems with glycolysis, pyruvate metabolism, or mitochondrial function.

Insufficient storage of energy in the heart muscle due to low levels of creatine phosphate (CP), which is the main energy storage molecule.

Inability of the heart muscle to use energy effectively due to increased workload, leading to inefficient muscle contraction.

A complex process where electrical signals trigger muscle contraction. It is impaired when there are problems with calcium (Ca2+) influx, storage, or binding to troponin.

Problems with the voltage-operated calcium channel (VOC) and receptor-operated calcium channel (ROC) can reduce calcium influx into heart cells.

Acidosis (excess acidity) and increased hydrogen ions (H+) can interfere with calcium influx, impair the function of calcium channels, and make the heart more susceptible to potassium (K+) competition.

The sarcoplasmic reticulum (SR) is the heart cell's calcium storage unit. Reduced SR uptake, reserves, or release of calcium can lead to impaired muscle contraction.

Hydrogen ions (H+) compete with calcium for binding to troponin, preventing the triggering of muscle contraction.