Oxygen delivery Medical Assignment Help

Oxygen delivery (oxygen flux) is defined as the total amount of oxygen delivered to the tissues per unit time. It is dependent on the volume of blood flowing through the microcirculation per minute (i.e. the total cardiac output – Q,) and the amount of oxygen contained in that blood (i.e. the arterial oxygen content- C.02). Oxygen is transported in combination with haemoglobin or dissolved in plasma. The amount combined with haemoglobin is determined by the oxygen capacity of the haemoglobin (usually taken as 1.34 ml O2 per gram of haemoglobin) and its percentage saturation with oxygen (So2)’ while the volume dissolved in plasma depends on the partial pressure of oxygen (P02). Except when hyperbaric oxygen is administered, the amount of dissolved oxygen in plasma is sufficiently small to be ignored for most practical purposes.
Clinically, however, the concept of oxygen flux provides little information about the relative flow to individual organs. Furthermore, some organs have high oxygen requirements relative to their blood flow and maybecome hypoxic even if the overall oxygen flux is apparently adequate.

CARDIAC OUTPUT

Cardiac output is the product of heart rate and stroke volume, and is affected by changes in either.

Heart rate

Increased heart rate

When heart rate increases, the duration of systole remains essentially unchanged, whereas diastole, and thus the time available for ventricular filling, becomes progressively shorter, and the stroke volume eventually falls. In the normal heart this occurs at rates greater than about 160 beats per minute, but in those with cardiac pathology, especially when this restricts ventricular filling (e.g. mitral stenosis), stroke volume may fall at much lower heart rates. Furthermore, tachycardias cause a marked increase in myocardial oxygen consumption and this may precipitate ischaemia in areas of the myocardium that have reduced coronary perfusion.
Decreased heart rate When the heart rate falls, a point is reached at which the increase in stroke volume is insufficient to compensate for the bradycardia and again cardiac output falls. Alterations in heart rate are often caused by disturbances of rhythm (e.g. artrial fibrillation, complete heart block or junctional arrhythmias), in which ventricular filling is not augmented by atrial contraction and stroke volume therefore falls.

Stroke volume

Three factors determine the stroke volume: pre-load, myocardial contractility and after-load.

Pre-load

This is defined as the tension of the myocardial fibres at the end of diastole, just before the onset of ventricular contraction, and is therefore related to the degree of stretch of the fibres. As the end-diastolic volume of the ventricle increases, tension in the myocardial
fibres is increased and stroke volume .rises.
Myocardial oxygen consumption (Vm02) increases only slightly with an increase in pre-load and this is therefore the most efficient way of improving cardiac output.

Myocardial contractility

This refers to the ability of the heart to perform work, independent of changes in pre-load and after-load. The state of myocardial contractility determines the response of the ventricles to changes in pre-load and after-load. Contractility is often reduced in intensive care patients, either as a result of pre-existing myocardial damage, e.g. ischaemic heart disease, or the acute disease process itself. Changes in myocardial contractility alter the slope and position of the Starling curve; the resulting worsening ventricular performance is manifested as a depressed, flattened curve.

The determinants of cardiac output.

The determinants of cardiac output.

The relationship between myocardial

The relationship between myocardial

Ventricular function (Starling curve).

Ventricular function (Starling curve).

The effect of changes in after-load

The effect of changes in after-load

After-load

This is defined as the myocardial wall tension developed during systolic ejection. In the case of the left ventricle the resistance imposed by the aortic valve, the peripheral vascular resistance and the elasticity of the major blood vessels are important determinants of after -load. Decreasing the after-load can increase the stroke volume achieved at a given pre-load, whilst also reducing the ventricular wall tension and the myocardial oxygen consumption. The reduction in wall tension may lead to an increase in coronary blood flow, thereby improving the myocardial oxygen supply-demand ratio. Excessive reductions in after-load will cause hypotension. An increase in after-load, on the other hand, can cause afall in stroke volume and is a potent cause of increased Vm02. Right ventricular after-load is normally negligible because the resistance of the pulmonary circulation is very low.

OXYGENATION OF THE BLOOD

Oxygen content (Ca02) is dependent on the amount of haemoglobin present per unit volume of blood, its oxygen capacity and its percentage saturation with oxygen. For this reason, maintenance of an ‘adequate’ haemoglobin concentration is essential in critically ill patients. Tissue oxygenation is, however, also dependent on blood flow. This is in turn determined not only by the cardiac output and its distribution, but also by the viscosity of the blood. The latter depends largely on the packed cell volume (PCv) and it is generally considered that the optimal balance between oxygen-carrying capacity and tissue flow is achieved at a PCV of approximately 30-35%.

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