Integrated control of CO & HF stuff Flashcards
What can CO be defined as?
The volume of blood ejected by one ventricle in one minute
What is a normal value for CO?
5 litres per minute at rest
this can rise to >25litres/min during strenuous exercise
Go over Guyton model
OneNote - BP section
Describes Starlings law
Starling’s law of the heart states that the force generated upon contraction is dependent upon muscle stretch. In stretched muscle there is less filament overlap so more cross-bridges can form, increasing contractile force. In addition, stretch increases Ca2+ sensitivity, so in stretched muscle, more Ca2+ binds to troponin C and more cross-bridges form.
Describe what preload and afterload are?
filling pressure of the right ventricle is the preload (this is set by the central venous pressure)
resistantce to outflow from the left ventricle (i.e. the arterial resistance) is the afterload
How may intracellular Na+ levels affect force of contraction?
Elevated intracellular concentrations of Na+ reduces Ca2+ extrusion via the Na-Ca exchanger (because the Na+ gradient is reduced), and so induces a rise in the baseline intracellular Ca2+ concentration. This Ca2+ rise stimulates SERCA pumps, which enhance Ca2+ loading into the SR, and thus enhance subsequent Ca2+ release from the SR during an action potential. This increases the amplitude of the cytoplasmic Ca2+ transient seen during the cardiac action potential, which means more Ca2+ is available to bind to troponin C which increases the force of contraction.
What does SV increase in response to?
Increase EDV (PRELOAD) which depends on:
- filling pressure (CVP)
- filling time (longer filling time means more EDV)
- ventricular compliance
Draw Frank-Starling graph
OneNote
Define mean circulatory filling pressure
The average integrated pressure throughout the circulatory system - can be measured by stopping blood flow and allowing the pressure throughout the circulatory system to reach equilibrium
Define systemic vascular resistence
Refers to the resistance to blood flow offered by all of the systemic vasculature, excluding some of the pulmonary vasculature
Sometimes referred to as the TPR
What is central venous pressure?
The blood pressure in the vena cava, near the right atrium of the heart
It reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system
Often used as a surrogate for preload
What is EDV?
- end diastolic volume
- ‘pre-pumping volumr’
What can SV be broken down into?
Preload
Contractility
Afterload
What is HF?
When CO is insufficient to meet the body’s needs
What is the most common cause of HF?
Ischaemia - may or may not be associated with MI → causes destruction of a part of the myocardium → reduced contraction
How is ischaemic HF a vicious cycle?
a reduction in CO
- Lowered BP activates the SNS and RAAS (due to reduced renal perfusion) in attempt to
boost BP back to normal retention of Na+ and water to increase blood volume, diluting
plasma proteins, thus leading to oedema where excess fluid enters tissues
- As shown in the figure, this increased work eventually results in a reduced CO as a result of
ventricular remodelling
- Vicious cycle gradual deterioration of the condition
How does HF result in oedema? Discuss oedema
one of the most characteristic symptoms; pulmonary oedema in left-sided
failure and peripheral oedema in right-sided failure.
This is due to the reduction in CO, which leads to blood backing up into veins and
increasing the hydrostatic pressure at the venous end of capillaries
extravasation of fluid, which is exacerbated by fluid retention that often also
occurs
Pulmonary oedema impaired gas exchange – can cause respiratory failure. Signs
of pulmonary oedema include breathlessness + cyanosis.
Aside from oedema, what is another characteristic of HF?
Acidaemia from reduced CO leading to poor tissue perfusion and increased anaerobic respiration
What do a combination of oedema and acidaemia lead to?
Marked exercise intolerane
What do drugs used to treat HF aim for?
1 - reduce symptoms
2 - prevent further ischaemic damage to the heart
List main drug classes used in the treatment of HF
Diuretics:
Including thiazide, loop and potassium-sparing diuretics.
Vasodilators: Angiotensin converting enzyme (ACE) inhibitors. Angiotensin receptor blockers (ARBs). Nitric oxide donors. Natriuretic peptides. Phosphodiesterase inhibitors.
Cardio-stimulatory (inotropic) drugs:
Digitalis.
Sympathomimetic drugs (beta-agonists.
Phosphodiesterase inhibitors.
Cardio-inhibitory drugs:
Beta-blockers.
Ca2+-channel blockers
What is first line for HF treatment. Discuss
Diuretic
Descibe using ACE inhibitor for HF? Why are they good? Downsides?
Antagonist the RAAS by inhibiting ACE (AI🡪AII)
This increases Na+ elimination from the body as AII and aldosterone synthesis = inhibited, causing a diuresis to treat the oedema
Also has a vasodilatory effect as AII is a vasoconstrictor 🡪 reduces peripheral resistance and hence reduces the contractile force needed to pump a sufficient CO
But this treatment has downsides e.g. can promote postural hypotension + reduce venous return, potentially causing the heart to work harder
These treatments are successful at alleviating the problems in 25% of patients
Describe using a beta blocker for HF? Why are they good?
This also relieves oedema by inhibiting sympathetically-mediated renin release, and protects the myocardium from further ischaemia by reducing sympathetic tone and so O2
