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The umbilical arteries
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A. originate from the fetal internal iliac arteries
B. convey venous blood from the fetus
C. contain blood at a PO2 of 5.3 KPa (40mmHg)
D. insert into the fetal inferior vena cava
E. are unaffected by autoregulation
A. TRUE B. TRUE C. FALSE D. FALSE E. FALSE
In the fetus, the umbilical vein carries the oxygenated blood from the placenta (with a pKa of 4.7 kPa and 80-90% saturation) while a pair of umbilical veins carry the deoxygenated blood back to the placenta/ maternal circulation (with a pKa of 2.7 kPa and 25-40% saturation).
Umbilical arteries stem from the anterior division of the internal iliac artery of the fetus.
Although, there are no detectable adrenergic or cholinergic nerve fibres in the human placenta or the human umbilical cord vessels (indicating that these vessels are not under direct neural control). Nonetheless, several systemic and placental-derived vasoconstrictors contribute to umbilical–placental blood flow regulation, including angiotensin II, bradykinin, catecholamines, thromboxane, prostaglandins, endothelin-1, histamine, peptides, and serotonin. These factors appear to play an important role in the maintenance of low vascular resistance in this vascular bed
Which of the following ECG Changes favour a diagnosis of acute anterolateral STEMI
A. ST elevation of 1 mm in V2/V3.
B. Hyperacute T elevation V2-V6, I, aVL.
C. Q waves in anteroseptal leads.
D. LBBB, the patient’s earlier records also show an LBBB pattern.
E. 1.5 mm ST elevation in II, III, aVF.
A. FALSE B. TRUE C. FALSE D. FALSE E. FALSE
ECG CHANGES IN ACUTE MI:
• Hyperacute T wave elevation.
• New ST-segment elevation > 1mm at the J point in at least two contiguous leads, except for V2/V3.
o For leads V2 or V3, the elevation must be 2mm in men and 1.5 mm in women (AHA guidelines).
ST-elevation is convex upwards and frequently overwhelms T wave, which is called tombstoning.
• Reciprocal ST depression confirms the diagnosis.
• New-onset LBBB accompanied by ischemic symptoms should be treated as STEMI.
• Pathological Q waves (Q wave > 0.04 second and > 25% of the size of the following R waves in that lead, except for leads III and aVR). Because pathological Q waves may take hours to develop and can last for a long time, new pathological Q waves indicate acute myocardial infarction, but the mere presence of Q waves does not necessarily mean that myocardial infarction is taking place.
ECG changes in old MI
• Q waves
• Loss of R wave/ Poor R wave progression
• T inversion/flattening/ normal T waves
Changes in leads V2-V6, I, aVL indicate anterolateral MI.
ECG IN ACUTE ANTEROLATERAL MI
ECG changes in II, III, aVF are indicative of inferior MI.
The digoxin effect includes
A. flattening of T waves
B. frequent ventricular ectopics
C. upsloping ST depression
D. absent P wave
E. the reverse tick sign
A. TRUE B. FALSE C. FALSE D. FALSE E. TRUE
Digitalis belongs to the group of cardiac glycosides that inhibit cellular Na+/K+-ATPase.
Therapeutic blood levels are accompanied by multiple ECG changes, the digoxin effect. The effects on cardiac conduction are a combination of its direct cardiac effects and indirect effects due to modification (↑) of vagal tone.
• Decreased T wave amplitude (most common and earliest sign, biphasic T waves may be seen occasionally).
• Scooped or sagging ST-segment depression (downsloping, resembles the shape of a tick made by a left-handed person, the ‘Reverse tick sign.’
• Increase in U wave amplitude.
• Shortening of the Q-T interval.
THE DIGOXIN EFFECT
Any arrhythmia observed while on digoxin is regarded as a sign of digoxin toxicity and not included in the digoxin effect.
FOR COMPLETE DISCUSSION ON ECG IN PATIENTS ON DIGOXIN, DOWNLOAD THE ECG FOR THE ANAESTHETIST MODULE BY TARGETEDAIC.
Successful countershock for ventricular fibrillation requires
A. energy levels of 200 to 360 joules
B. ECG monitoring
C. simultaneous depolarization of all myocardial fibres
D. synchronized DC countershock
E. prior administration of adrenaline
A. TRUE B. TRUE C. TRUE D. FALSE E. FALSE
VF is an irregular ventricular rhythm incompatible with life. Unless advanced life support is rapidly instituted, this rhythm is invariably fatal.
Ventricles generate multifocal electrical signals at a very fast and erratic rate producing rivulets of independently contracting units. The cardiac pump fails to generate an effective CO, being reduced to a mere quivering mess.
Defibrillation aims to restore a rhythm compatible with cardiac output and tissue perfusion with minimal insult to the myocardium while ensuring patient and staff safety. The defibrillation current depolarizes all the myocardial cells at once, making it transiently refractory. This gives the fastest pacemaker (hopefully SA node) a chance to take over and restore myocardial synchrony.
In VF, there are no discernable R waves, and synchronisation is impossible. Unsynchronized cardioversion (defibrillation) is a HIGH ENERGY shock delivered as soon as the shock button is pushed on a defibrillator.
The likelihood of restoring a perfusing rhythm is optimized with immediate CPR and defibrillation. Defibrillation should be done as soon as possible. The success is not dependent upon prior adrenaline administration, although the incidence of ROSC is much higher when adrenaline is used in CPR. As per ACLS guidelines, adrenaline is given after the third shock.
For defibrillation, the appropriate energy dose is determined by the design of the defibrillator—monophasic or biphasic. For a monophasic defibrillator, give a single 360 J shock, and use the same energy dose on subsequent shocks. Biphasic defibrillators use various waveforms and are more effective for terminating a fatal arrhythmia. When using biphasic defibrillators, providers should use the manufacturer’s recommended energy dose. The usual initial shock dose is 120-200J (as per ACLS).
ECG monitoring is beneficial in management; it allows differentiation of wide complex tachycardias from narrow complex rhythms and VT from VF.
FOR A COMPREHENSIVE DISCUSSION ON ECG IN CARDIAC ARRHYTHMIAS AND THE ANAESTHETIC IMPLICATIONS, DOWNLOAD THE ECG FOR THE ANAESTHETIST MODULE AND BE THE ECG EXPERT YOU ALWAYS WANTED TO BE.
Traction on the medial rectus muscle of the eye produces
A. hypertension
B. bradycardia
C. mydriasis
D. Homer’s syndrome
E. cardiac dysrhythmias
A. FALSE B. TRUE C. FALSE D. FALSE E. TRUE
Traction or torsion on the extraocular muscles (most commonly when the medial rectus muscle is manipulated) results in oculocardiac reflex.
Oculomedullary reflex is a trigemino-vagal reflex: the afferent arc is via long and short ciliary nerves to the ciliary ganglion and the ophthalmic division of the trigeminal nerve. At the same time, the vagus conveys the efferent impulses.
The reflex is powerful in children and is often witnessed during squint surgery (up to 60%).
Sensitizing factors: Hypercarbia, Hypoxia, acidosis, and light anaesthesia.
Attenuation of the afferent limb can be achieved by local infiltration of LA or giving peribulbar block during the surgery while anti-muscarinic drugs block the efferent limb.
Presentation: bradycardia, cardiac dysrhythmias (ectopic beats, nodal rhythm, atrial or ventricular arrhythmias, even sinus arrest and asystole). When severe or prolonged, it is associated with a fall in BP (hypotension).
Horner syndrome and mydriasis are not a part of the oculocardiac reflex.
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