Rapid Cardiac Care Emma Menzies‐Gow Ebook Free Download

Rapid Cardiac Care Emma Menzies‐Gow Ebook Free Download

Rapid Cardiac Care Emma Menzies‐Gow Ebook Free Download

Rapid Cardiac Care Emma Menzies‐Gow Ebook Free Download Cardiac output is the volume of blood ejected from the left ventricle  (LV) in one minute, i.e. heart rate×stroke volume. It is approximately  4–7L/min. The cardiac conduction system controls heart rate variability  and co‐ordinated systolic (contraction) and diastolic (relaxation and  filling) activity of the cardiac chambers to maximise cardiac output.

The superior and inferior vena cava empty into the right atrium,
enabling the return of deoxygenated blood to the heart. The coronary .sinus, a large cardiac vein, also drains deoxygenated blood from the  myocardium into the right atrium. The tricuspid valve opens to permit  blood to enter the right ventricle (RV); atrial contraction provides extra  force to expel blood from the chamber, known as the ‘atrial kick’,  to optimise the end diastolic volume (EDV) of the ventricles.

During systole, the three papillary muscles in the RV contract,
tightening the chordae tendineae, attached to the cusps of the
tricuspid valve to ensure the valve leaflets remain closed, preventing
regurgitation of blood into the right atrium. Pressure within the RV  will rise until it exceeds the pressure within the pulmonary circulation  beyond, forcing the pulmonary valve to open and blood to flow into  the pulmonary arterial trunk. During ventricular diastole, the
pulmonary arteries will rapidly recoil to enable blood to fall back
towards the RV, closing the pulmonary valve.

Having completed gaseous exchange within the alveoli and
pulmonary capillaries, oxygenated blood returns to the left atrium  via four pulmonary veins. The increase in pressure within the atrial  chamber forces the mitral valve to open and ventricular filling to begin.

During diastole, the ventricular myocytes will stretch to accommodate  the volume of blood, which directly correlates with the force of  contraction that occurs during systolic contraction (Frank Starling’s  Law). The two papillary muscles contract first, once systole begins,  tightening the chordae tendineae attached to the two cusps of the
mitral valve to prevent regurgitation. The LV and septum then contract   to increase the pressure (preload) within the LV. Once the preload  pressure exceeds the pressure in the aorta beyond the aortic valve
(afterload), blood will leave the LV, referred to as the stroke volume,
crossing the aortic valve into the aorta to supply the arterial circulation.

The term ‘ejection fraction’ refers to the stroke volume as a percentage  of the left ventricular EDV (LVEDV), usually approximately 60–70% at  rest. As systole ends, diastole begins again and a small volume of  blood in the aorta will return towards the LV, closing the aortic valve  cusps and simultaneously perfusing the coronary arteries originating  at the aortic root.





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