Week 4 - Heart Failure Flashcards
What is the pathophysiological definition of heart failure?
Heart failure is abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a sufficient rate to meet the metabolic demands of the body tissues.
What is the clinical definition (signs and symptoms) of heart failure?
Heart failure is defined clinically as a syndrome in which patients have typical symptoms (e.g. breathlessness, peripheral oedema and fatigue) and signs (elevated JVP, pulmonary crackles and displaced apex beat) resulting from abnormality of cardiac structure or function.
Describe the pressure changes in the heart during the normal cardiac cycle
Diastole:
After the ventricles have contracted and start relaxing they reach the isovolumic relaxation stage- where the aortic valve is shut due to large pressure drop in the ventricles as they relax but the AV valve is not yet open. The pressure in the ventricles continues to drop hitting a minimum, pressure in the atria rises with filling, forcing the AV valve open- ventricles enter rapid filling phase, where there is passive flow of blood from A-V which reaches a plateau- diastasis. Contraction of atria forces final blood volume into the ventricles and there is a blip of increased pressure. The ventricles have reached EDV.
Systole:
Ventricles start to contract and pressure shoots up. AV valve closes and blood is ejected into the aorta, pressure rising enough to force open the aortic valve. Pressure continues to rise as the ventricles finish their contraction. Pressure then sharply falls, the aortic pressure overcomes ventricular and the aortic valve closes. Pressure continues to fall sharply away during isovolumic relaxation, reaching minumum at the start of rapid filling.
What is the frank starling mechanism? How does this relate to heart failure?
The frank starling mechanism describe the relationship between the end diastolic volume (filling pressure of ventricles) and the stroke volume (volume of blood ejected by the heart with each contraction) in systole.
At higher EDV’s, myocytes are stretched more which increases the sarcomere length and the number of actin-myosin cross bridges formed. The amount of active tension created is greater and myocytes contract with greater velocity and force. This forces more blood out the heart thereby increasing Stroke Volume.
This relates to diastolic heart failure- where the compliance of the ventricle is reduced (hypertrophy/ scarring) and the ventricles cannot relax enough to fill adequately. The EDV decreases which decreases the stroke volume by F/S mechanism above. F/S mechanism will also play a part in the compensation of a failing heart (to a point). Systolic heart failure can be buffered by the F/S mechanism, where decreased CO will lead to increased EDV and therefore increase stroke volume.
List the factors that affect stroke volume of the heart.
What does each of these factors affect ultimately (thinking volumes in heart during a cardiac cycle).
What is the equation for stroke volume?
three main factors 1) preload 2) contractility 3) afterload
1) Preload is affected by both venous return and filling time of the heart and refers to the end diastolic volume.
2) contractility is affected by both the ANS (increased symp stimulation leads to increased contractility) and hormones (noradrenaline). Contractility will affect the end systolic volume.
3) afterload refers to the systemic vascular resistance (vasocontriction or vasodilation of systemic vascualture). Afterload of the heart will also affect the end systolic volume.
Stroke volume = EDV- ESV
Describe the balance between hydrostatic and osmotic forces in the capillaries
