Graphic Anaesthesia. Tim Hooper

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Graphic Anaesthesia - Tim Hooper

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With high PEEP, error may be more difficult to predict.

      Central venous pressure waveform – abnormalities

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      Examination of the CVP waveform may aid diagnosis of various pathophysiological conditions.

      Cardiac arrhythmias

      A – Atrial fibrillation is characterized by an absent ‘a wave’. The ‘c wave’ is more prominent due to a greater than normal right atrial volume at the end of diastole.

      B – In isorhythmic AV dissociation, the atria and ventricles beat independently of each other but at the same rate. As such, the atria contract against a closed tricuspid valve producing an enlarged ‘a wave’ termed a ‘cannon a wave’.

      Other arrhythmias also affect the CVP waveform. Sinus tachycardia is characterized by a shortening of diastole and therefore alters the diastolic waveform components (shortening of ‘y descent’ with merger of the ‘v’ and ‘a’ waves). In contrast, sinus bradycardia leads to increased distinction between the three waves.

      Valvular disease

      C – Tricuspid stenosis is a diastolic abnormality impeding right atrial emptying. As the right atrium contracts against a narrowed tricuspid valve, a prominent ‘a wave’ is produced. Right atrial pressure remains elevated for longer than normal, attenuating the ‘y descent’.

      D – In tricuspid regurgitation, systolic flow of blood back into the right atrium through an incompetent valve leads to a persistent elevation of right atrial pressure. As such, the ‘c’ and ‘v’ waves gradually merge over time with subsequent loss of the ‘x descent’.

      Elevation of CVP may be observed with raised intrathoracic pressure (positive-pressure ventilation), cardiac dysfunction (cardiac tamponade, cardiac failure) and circulatory overload.

      Reduction in CVP may occur in association with reduced venous return (hypovolaemia, vasodilatation) and a reduction in intrathoracic pressure (spontaneous inspiration).

      Einthoven triangle

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      Bipolar leads (I, II, III) electrically form an equilateral triangle named after Willem Einthoven, the scientist who developed the ECG. These leads, combined with unipolar augmented leads (aVL, aVR, aVF) examine the heart in the frontal plane. Rearranging these six limb leads, allowing an intersection representing the heart, forms the hexaxial reference system. The arrows represent the normal path of electrical current for each lead. This graphical representation of cardiac electrical activity aids interpretation of ventricular axis in the frontal plane.

      Frontal ventricular axis determination

      Normal cardiac electrical activity progresses systematically from the SA node, via internodal fibres to the AV node. Conduction continues via the bundle of His, through right and left bundle branches to Purkinje fibres, resulting in ventricular contraction. Depolarization towards a positive electrode produces a positive deflection on the ECG. When viewing the heart in the frontal plane, mean ventricular depolarization (as denoted by the QRS complex) lies between −30° and +90°. Ventricular axis may be determined using the limb leads. The simplest approach is the quadrant method, examining leads I and aVF. These perpendicular limb leads outline the majority of the normal axis.

       Normal axis – positive QRS complex in both leads.

       Extreme right axis deviation – negative QRS complex in both leads.

       Right axis deviation – negative complex in lead I, positive complex in aVF.

       Left axis deviation – positive complex in lead I, negative complex in aVF. However, as the normal axis ranges from −30° to +90°, this average vector may represent a normal axis. Examination of lead II is also required; if QRS complex is positive the axis is normal (ranging from 0° to −30°).

      An alternative equiphasic approach exists, founded on the principle that depolarization travelling perpendicular to a lead produces an equiphasic QRS complex.

      Ejection fraction equation

      EF = SVEDV ×100

      SV = EDV – ESV

      EF = ejection fraction

      EDV = end-diastolic volume

      ESV = end-systolic volume

      SV = stroke volume

      The ejection fraction simply describes the amount of blood that is ejected from the ventricle during systolic contraction (stroke volume) as a proportion of the amount of blood that is present in the ventricle at the end of diastole (end-diastolic volume). A 70 kg individual would normally have a stroke volume of about 70 ml and an end-diastolic volume of about 120 ml.

      The ejection fraction equation is used to calculate the stroke volume as a percentage of the end-diastolic volume. It gives an indication of the percentage of the ventricular volume that is ejected during each systolic contraction. It can be applied to the left or the right ventricles, with normal values being 50–65%. Right and left ventricular volumes are roughly equal and therefore ejection fractions are broadly similar.

      In clinical practice, it can be calculated using echocardiography, pulmonary artery catheterization, nuclear cardiology or by contrast angiography.

      In aortic stenosis, the ventricle will compensate for the increased obstruction to outflow by hypertrophy. This will initially maintain the ejection fraction and the pressure gradient across the valve. As the disease progresses and the valve area narrows, the hypertrophied ventricle becomes stiff and less compliant and will no longer be able to compensate. A reduction in the stroke volume (and ejection fraction) is seen, resulting in a fixed reduced cardiac output. The myocardium will eventually fail as compliance continues to worsen.

      Electrocardiogram

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      An electrocardiogram (ECG) is a non-invasive, transthoracic interpretation of cardiac electrical activity over time. Thorough assessment requires a systematic approach including rate, rhythm, axis (normal axis is −30° to +90°), and wave morphology/interval.

      Morphology and intervals

       P wave – represents atrial depolarization. A positive deflection should be present in all leads except aVR.

       PR interval – from the start of the P wave to the end of the PR segment. Normal value 0.12–0.2 s (3–5 small squares). This interval is rate dependent; as heart rate increases, the PR interval decreases.

       QRS wave – represents ventricular depolarization. The normal duration is ≤0.12 s. A Q wave in leads V1–V3 is abnormal.

       ST segment – from the junction of the QRS complex and the ST segment to the beginning of the T wave. A normal ST segment is isoelectric.

       T

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