Smoking is a major risk factor associated with perioperative respiratory and cardiovascular complications. Evidence also suggests that cigarette smoking causes imbalance in the prostaglandins and promotes vasoconstriction and excessive platelet aggregation. Two of the constituents of cigarette smoke, nicotine and carbon monoxide, have adverse cardiovascular effects. Carbon monoxide increases the incidence of arrhythmias and has a negative ionotropic effect both in animals and humans.

Smoking causes an increase in carboxyhaemoglobin levels, resulting in a leftward shift in which appears to represent a risk factor for some of these cardiovascular complications.

There are two mechanisms responsible for the leftward shift of oxyhaemoglobin dissociation curve when carbon monoxide is present in the blood. Carbon monoxide has a direct effect on oxyhaemoglobin, causing a leftward shift of the oxygen dissociation curve, and carbon monoxide also reduces the formation of 2,3-DPG by inhibiting glycolysis in the erythrocyte. Nicotine, on the other hand, has a stimulatory effect on the autonomic nervous system. The effects of nicotine on the cardiovascular system last less than 30 min.

With regards to the autonomic nervous system (ANS)

1. It is not under voluntary control
2. It uses reflex pathways and different to the somatic nervous system.
3. The hypothalamus is the central point of integration of the ANS. However, the gut can coordinate some secretions and information from the baroreceptors which are processed in the medulla.

With regards to the central nervous system (CNS)
1. There are myelinated preganglionic fibres which lead to the
ganglion where the nerve cell bodies of the non-myelinated post ganglionic nerves are organised.
2. From the ganglion, the post ganglionic nerves then lead on to the innervated organ.

Most organs are under control of both systems although one system normally predominates.

The nerves of the sympathetic nervous system (SNS) originate from the lateral horns of the spinal cord, pass into the anterior primary rami and then pass via the white rami communicates into the ganglia from T1-L2.

There are short pre-ganglionic and long post ganglionic fibres.
Pre-ganglionic synapses use acetylcholine (ACh) as a neurotransmitter on nicotinic receptors.
Post ganglionic synapses uses adrenoceptors with norepinephrine / epinephrine as the neurotransmitter.
However, in sweat glands, piloerector muscles and few blood vessels, ACh is still used as a neurotransmitter with nicotinic receptors.

The ganglia form the sympathetic trunk – this is a collection of nerves that begin at the base of the skull and travel 2-3 cm lateral to the vertebrae, extending to the coccyx.

There are cervical, thoracic, lumbar and sacral ganglia and visceral sympathetic innervation is by cardiac, coeliac and hypogastric plexi.

Juxta glomerular apparatus, piloerector muscles and adipose tissue are all organs under sole sympathetic control.

The PNS has a craniosacral outflow. It causes reduced arousal and cardiovascular stimulation and increases visceral activity.

The cranial outflow consists of
1. The oculomotor nerve (CN III) to the eye via the ciliary ganglion,
2. Facial nerve (CN VII) to the submandibular, sublingual and lacrimal glands via the pterygopalatine and submandibular ganglions
3. Glossopharyngeal (CN IX) to lungs, larynx and tracheobronchial tree via otic ganglion
4. The vagus nerve (CN X), the largest contributor and carries ¾ of fibres covering innervation of the heart, lungs, larynx, tracheobronchial tree parotid gland and proximal gut to the splenic flexure, liver and pancreas

The sacral outflow (S2 to S4) innervates the bladder, distal gut and genitalia.

The PNS has long preganglionic and short post ganglionic fibres.
Preganglionic synapses, like in the SNS, use ACh as the neuro transmitter with nicotinic receptors.
Post ganglionic synapses also use ACh as the neurotransmitter but have muscarinic receptors.

Different types of these muscarinic receptors are present in different organs:
There are:
M1 = pupillary constriction, gastric acid secretion stimulation
M2 = inhibition of cardiac stimulation
M3 = visceral vasodilation, coronary artery constriction, increased secretions in salivary, lacrimal glands and pancreas
M4 = brain and adrenal medulla
M5 = brain

The lacrimal glands are solely under parasympathetic control.

Skeletal muscle blood flow is in the range of 1-4 ml/min per 100 g when at rest. Blood flow can reach 50-100 ml/min per 100 g during exercise. With maximal vasodilation, blood flow can increase 20 to 50 times.

The adrenal medulla releases catecholamines and increases neural sympathetic activity during exercise. Normally, alpha-1 and alpha-2 would cause vasoconstriction in the muscle groups being used, but vasodilatory metabolites override these effects, resulting in a so-called functional sympathectomy. Local hypoxia and hypercarbia, nitric oxide, K+ ions, adenosine, and lactate are some of the stimuli that cause vasodilation.

However, the splanchnic and cutaneous circulations, which supply inactive muscles, vasoconstrict.

Sympathetic cholinergic innervation of skeletal muscle arteries is found in some species (such as cats and dogs, but not humans). Vasodilation is induced by stimulating smooth muscle beta-2 adrenoreceptors, but at rest, the alpha-adrenoreceptor effects of adrenaline and noradrenaline predominate. During exercise, the skeletal muscle pump promotes venous emptying, but it does not necessarily increase blood flow.

Primary FRCA is concerned with two issues. The first is a working knowledge of the Henderson-Hasselbalch equation, and the second is a working knowledge of logarithms and antilogarithms.

The pH at which the drug exists in 50 percent ionised and 50 percent unionised forms is known as the pKa.

To calculate the proportion of ionised to unionised form of a drug, use the Henderson-Hasselbalch equation.

pH = pKa + log ([A-]/[HA])

or

pH = pKa + log [(salt)/(acid)]
pH = pKa + log ([ionised]/[unionised])

Hence, if the pKa ˆ’ pH = 0, then 50% of drug is ionised and 50% is unionised.

In this example:
7.4 = 8.4 + log ([ionised]/[unionised])
7.4 ˆ’ 8.4 = log ([ionised]/[unionised])
log ˆ’1 = log ([ionised]/[unionised])

Simply put, the antilog is the inverse log calculation. In other words, if you know the logarithm of a number, you can use the antilog to find the value of the number. The antilogarithm’s definition is as follows:

y = antilog x = 10x

Antilog to the base 10 of 0 = 1, ˆ’1 = 0.1, ˆ’2 = 0.01, ˆ’3 = 0.001 and, ˆ’4 = 0.0001.

[A-]/[HA] = 0.1

Assuming that we can apply the approximation [A-] << [HA} then this means the acid is 0.1 x 100% = 10% ionised so the percentage of (non-ionized) acid will be 100% – 10% = 90%

Since an arterial pressure transducer, and every other measuring apparatus, is prone to errors due to offset and gradient drifts, regular calibration is required to maintain accuracy of the instrument. The two-point calibration pressure values of 0 mmHg and 200 mmHg are within the physiologic range and can best compensate for the gradient drift.

The ureter starts from the hilum of the kidney and has different relations with structures along its journey to the bladder.
It runs anterior to the psoas major muscle.
The testicular vessels (males) or the ovarian vessels (females) cross in front of the ureter.
The ureter passes in front of the common iliac artery where it bifurcates into the internal and external iliac arteries.
The ureter passes medial to the branches of the internal iliac vessel downwards and forwards to towards the bladder.
In males, the ductus deferens crosses the pelvic ureter medially.
In females. the ureter passes through the base of the broad ligament
In females, the pelvic part initially has the same relations as in males but, anterior to the internal iliac artery, it is immediately behind the ovary, forming the posterior boundary of the ovarian fossa. It is in extraperitoneal connective tissue in the inferomedial part of the broad ligament of the uterus. In the broad ligament, the uterine artery is anterosuperior to the ureter for approximately 2.5 cm and then crosses to its medial side to ascend alongside the uterus. The ureter turns forwards slightly above the lateral vaginal fornix and is, generally, 2 cm lateral to the supravaginal part of the uterine cervix in this location. It then inclines medially to reach the bladder.

The answer is anterior to the spermatic cord.

The inguinal canal in men contains the ilioinguinal nerve, the genitofemoral nerve and the spermatic cord.

The ilioinguinal nerve arises of the L1 nerve root with the Iliohypogastric nerve, before entering the inguinal canal from the side, through the muscles of the abdomen, travelling superficial to the spermatic cord.

Cardiac conduction

Phase 0 – Rapid depolarization. Opening of fast sodium channels with large influx of sodium

Phase 1 – Rapid partial depolarization. Opening of potassium channels and efflux of potassium ions. Sodium channels close and influx of sodium ions stop

Phase 2 – Plateau phase with large influx of calcium ions. Offsets action of potassium channels. The absolute refractory period

Phase 3 – Repolarization due to potassium efflux after calcium channels close. Relative refractory period

Phase 4 – Repolarization continues as sodium/potassium pump restores the ionic gradient by pumping out 3 sodium ions in exchange for 2 potassium ions coming into the cell. Relative refractory period

Refractometers measure the degree to which the light changes direction, called the angle of refraction. A refractometer takes the refraction angles and correlates them to refractive index (nD) values that have been established. Using these values, you can determine the concentrations of solutions.

Thermodilution is the most common dilution method used to measure cardiac output (CO) in a hospital setting.

During the procedure, a Swan-Ganz catheter, which is a specialized catheter with a thermistor-tip, is inserted into the pulmonary artery via the peripheral vein. 5-10mL of a cold saline solution with a known temperature and volume is injected into the right atrium via a proximal catheter port. The solution is cooled as it mixes with the blood during its travel to the pulmonary artery. The temperature of the blood is the measured by the catheter and is profiled using a computer.

The computer also uses the profile to measure cardiac output from the right ventricle, over several measurements until an average is selected.

Cardiac output changes at each point of respiration, therefore to get an accurate measurement, the same point during respiration must be used at each procedure, this is usually the end of expiration, that is the end-expiratory pause.

The bispectral index (BIS) is one of several systems used in anaesthesiology as of 2003 to measure the effects of specific anaesthetic drugs on the brain and to track changes in the patient’s level of sedation or hypnosis. It is a complex mathematical algorithm that allows a computer inside an anaesthesia monitor to analyse data from a patient’s electroencephalogram (EEG) during surgery. It is a dimensionless number (0-100) that is a summative measurement of time domain, frequency domain and high order spectral parameters derived from electroencephalogram (EEG) signals.

Sleep and anaesthesia have similar behavioural characteristics but are physiologically different but BIS monitors can be used to measure sleep depth. With increasing sleep depth during slow-wave sleep, BIS levels decrease. This correlates with changes in regional cerebral blood flow when measured using positron emission tomography (PET).

BIS shows a dose-response relationship with the intravenous and volatile anaesthetic agents. Opioids produce a clinical change in the depth of sedation or analgesia but fail to produce significant changes in the BIS. Ketamine increases CMRO2 and EEG activity.

BIS is unable to predict movement in response to a surgical stimulus. Some of these are spinal reflexes and not perceived by the cerebral cortex.

BIS is used during cardiopulmonary bypass to measure depth of anaesthesia and an index of cerebral perfusion. However, it cannot predict subtle or significant cerebral damage.

Bilirubin is formed by metabolizing heme, mostly from haemoglobin in red blood cells.

Bilirubin is conjugated to glucuronic acid in the hepatocytes by the glucuronyl transferase enzyme in order to enable it to become soluble and allow for its secretion across the canalicular membrane and into bile.

The conjugation process is increased by rifampicin and decreased by valproate.

Gilbert’s syndrome is caused by a decrease in glucuronyl transferase in the hepatic system, decreasing the transport of bilirubin into the hepatocyte, causing unconjugated bilirubinaemia.

Crigler-Najjer syndrome is caused by mutations in the genes responsible for hepatic glucuronyl transferase, decreasing the activity of the enzyme, meaning bilirubin cannot be conjugated, causing unconjugated bilirubinaemia.

Dubin-Johnson syndrome does not cause an impairment in the conjugation of bilirubin, but it blocks the transport of bilirubin out of the hepatocyte resulting in conjugated bilirubinaemia.

A prospective randomised double blind controlled trial against cyclizine in multiple centres is the most likely to change your practice.

Case controlled studies are efficient in identifying an association between a drug treatment and outcome and are usually conducted retrospectively. They are generally less valued than prospective randomised trials. They cannot generate incidence data, are subject to bias, have difficult selection of controls and can be made more difficult if note keeping is not reliable.

The gold standard in intervention-based studies is randomised controlled double blind trials. Its features are:

Treating all intervention groups identically
Reduction of bias by random allocation to intervention groups
Patients and researchers unaware of which treatment was given until at completion of study
Patients analysed within the group to which they were allocated, and
Analysis focused on estimating the size of the difference in predefined outcomes between intervention groups.

New healthcare interventions should be evaluated through properly designed randomised controlled trials (though there are some potential ethical disadvantages)

Conducting trials in multiple centres is an accepted way of evaluating a new drug as it may be the only way of recruiting sufficient number of patients within a reasonable time frame to satisfy the objectives of the trial. Type II statistical errors will occur if a small numbers of patients is used in study group.

The level of statistical significance required influences the sample size used. This is because sample size is used in the calculation of SD/SE.

Sample size does not affect

The level of acceptance
The alternative hypothesis with a general level set at p<0.05
The test to be used.

Experience of the investigator and the type of patient recruited should have no bearing on the required sample size.

Atrial natriuretic peptide (ANP) is secreted mainly from myocytes of right atrium and ventricle in response to increased blood volume.
It is secreted by both the right and left atria (right >> left).

It is a 28 amino acid peptide hormone, which acts via cGMP
degraded by endopeptidases.

It serves to promote the excretion of sodium, lowers blood pressure, and antagonise the actions of angiotensin II and aldosterone.

Cardiac conduction

Phase 0 – Rapid depolarization. Opening of fast sodium channels with large influx of sodium

Phase 1 – Rapid partial depolarization. Opening of potassium channels and efflux of potassium ions. Sodium channels close and influx of sodium ions stop

Phase 2 – Plateau phase with large influx of calcium ions. Offsets action of potassium channels. The absolute refractory period

Phase 3 – Repolarization due to potassium efflux after calcium channels close. Relative refractory period

Phase 4 – Repolarization continues as sodium/potassium pump restores the ionic gradient by pumping out 3 sodium ions in exchange for 2 potassium ions coming into the cell. Relative refractory period

To begin, one must determine the child’s approximate weight. There are a variety of formulas to choose from. It is acceptable to use the advanced paediatric life support formula:

(age + 4) 2 = weight

A 5-year-old child will weigh around 18 kilogrammes.

The following are the appropriate doses of the drugs listed above:

Gentamicin (once daily) – 5-7 mg/kg = 90-126 mg and subsequent dose modified according to plasma levels
Ondansetron – 0.1 mg/kg, but a maximum of 4 mg as a single dose = 1.8 mg
Codeine should be administered orally at a dose of 1 mg/kg rather than intravenously, as the latter can cause ‘dangerous’ hypotension due to histamine release.
15 mg/kg paracetamol = 270 mg orally or intravenously (a loading dose of 20 mg/kg, or 360 mg, is sometimes recommended, which is not far short of the doses listed above).
Cefuroxime – the initial intravenous dose is 20 mg/kg (360 mg) depending on the indication (again, similar to the dose given in the answer options above).

Parotidectomy is basically an anatomical dissection. Identification of the facial nerve trunk is essential during parotid gland surgery because facial nerve injury is the most daunting potential complication of parotid gland surgery owing to the close relation between the gland and the extratemporal course of the facial nerve. After exiting the stylomastoid foramen, the facial nerve enters the substance of the parotid gland and then gives off five terminal branches:
From superior to inferior, these are the:
– Temporal branch supplying the extrinsic ear muscles, occipitofrontalis and orbicularis oculi
– Zygomatic branch supplying orbicularis oculi
– Buccal branch supplying buccinator and the lip muscles
– Mandibular branch supplying the muscles of the lower lip and chin
– Cervical branch supplying platysma.

There are two approaches to identify the facial nerve trunk during parotidectomy€”conventional antegrade dissection of the facial nerve, and retrograde dissection. Numerous soft tissue and bony landmarks have been proposed to assist the surgeon in the early identification of this nerve. Most commonly used anatomical landmarks to identify facial nerve trunk are stylomastoid foramen, tympanomastoid suture (TMS), posterior belly of digastric (PBD), tragal pointer (TP), mastoid process and peripheral branches of the facial nerve.

Campylobacter is the commonest bacterial cause of infectious intestinal disease in the UK. The majority of cases are caused by the Gram-negative bacillus Campylobacter jejuni which is spread by the faecal-oral route. The incubation period is 1-6 days.

Features include a prodrome phase with headaches and malaise, then diarrhoea occurs which is often bloody.
There is often abdominal pain which may mimic appendicitis.

It is usually self-limiting but treatment is warranted if the infection is severe or the infection occurs in an immunocompromised patient.
Severe infection comprises of high fever, bloody diarrhoea, or more than eight stools per day or symptoms last for more than one week.
This management would include antibiotics and the first-line antibiotic is clarithromycin.
Ciprofloxacin is an alternative but there are strains with decreased sensitivity to ciprofloxacin which can be frequently isolated.

Complications include:
1.Guillain-Barre syndrome may follow Campylobacter
2. Jejuniinfections
3. Reactive arthritis
4. Septicaemia, endocarditis, arthritis

The posterior cerebral arteries are the terminal branches of the basilar artery and are connected to the circle of Willis via the posterior communicating artery. The posterior cerebral artery supplies the visual areas of the cerebral cortex and other structures in the visual pathway.

The posterior cerebral artery is separated from the superior cerebellar artery near its origin by the oculomotor nerve (3rd cranial nerve) and, lateral to the midbrain, by the trochlear nerve.

PCA strokes will primarily cause a visual field loss or homonymous hemianopia to the opposite side. This large occipital or PCA stroke causes people to be €œblind€� on one side of the visual field. This is the most common symptom of a large occipital lesion or PCA stroke.

ICP is significant because it influences cerebral perfusion pressure and cerebral blood flow. The normal ICP ranges from 5 to 13 mmHg.

The components within the skull include the brain (80%/1400 ml), blood (10%/150 ml), and cerebrospinal fluid (CSF) (10%/150 ml).

Because the skull is a rigid box, if one of the three components increases in volume, one or more of the remaining components must decrease in volume to compensate, or the ICP will rise (Monroe-Kellie hypothesis).

Primary brain injury occurs as a result of a head injury and is unavoidable unless precautions are taken to reduce the risk of head injury. A reduction in oxygen delivery due to hypoxemia (low arterial PaO2) or anaemia, a reduction in cerebral blood flow due to hypotension or reduced cardiac output, and factors that cause a raised ICP and reduced CPP are all causes of secondary brain injury. Secondary brain injury can be avoided with proper management.

The most important initial management task is to make certain that:

There is protection of the airway and the cervical spine
There is proper ventilation and oxygenation
Blood pressure and cerebral perfusion pressure are both adequate (CPP).

Following the implementation of these management principles, additional strategies to reduce ICP and preserve cerebral perfusion are required. The volume of one or more of the contents of the skull can be reduced using techniques that can be used to reduce ICP.

Reduce the volume of brain tissue
Blood volume should be reduced.
CSF volume should be reduced.

The following are some methods for reducing the volume of brain tissue:
Abscess removal or tumour resection
Steroids (especially dexamethasone) are used to treat oedema in the brain.
To reduce intracellular volume, use mannitol/furosemide or hypertonic saline.
To increase intracranial volume, a decompressive craniectomy is performed.

The following are some methods for reducing blood volume:

Haematomas must be evacuated.
Barbiturate coma reduces cerebral metabolic rate and oxygen consumption, lowering cerebral blood volume as a result.
Hypoxemia, hypercarbia, hyperthermia, vasodilator drugs, and hypotension should all be avoided in the arterial system.
PEEP/airway obstruction/CVP lines in neck: patient positioning with 30° head up, avoid neck compression with ties/excessive rotation, avoid PEEP/airway obstruction/CVP lines in neck

The following are some methods for reducing CSF volume:

To reduce CSF volume, an external ventricular drain or a ventriculoperitoneal shunt is inserted (although more a long term measure).

Staphylococcus aureus infection is the most likely cause.

Surgical site infections (SSI) occur when there is a breach in tissue surfaces and allow normal commensals and other pathogens to initiate infection. They are a major cause of morbidity and mortality.

SSI comprise up to 20% of healthcare associated infections and approximately 5% of patients undergoing surgery will develop an SSI as a result.
The organisms are usually derived from the patient’s own body.

Measures that may increase the risk of SSI include:
-Shaving the wound using a single use electrical razor with a disposable head
-Using a non iodine impregnated surgical drape if one is needed
-Tissue hypoxia
-Delayed prophylactic antibiotics administration in tourniquet surgery, patients with a prosthesis or valve, in clean-contaminated surgery of in contaminated surgery.

Measures that may decrease the risk of SSI include:
1. Intraoperatively
– Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
-Cover surgical site with dressing

In contrast to previous individual RCT’s, a recent meta analysis has confirmed that administration of supplementary oxygen does not reduce the risk of wound infection and wound edge protectors do not appear to confer benefit.

2. Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention

Use of diathermy for skin incisions
In the NICE guidelines the use of diathermy for skin incisions is not advocated. Several randomised controlled trials have been undertaken and demonstrated no increase in risk of SSI when diathermy is used.

Barbituric acid is the barbiturates’ pharmacologically inactive precursor. A pyrimidine heterocyclic nucleus is formed by the condensation of urea and malonic acid. Its pharmacological activity can be influenced by minor structural changes (structure function relationship).

The duration of action and potency as a sedative are influenced by the length of the side chains at C5. Barbiturates with three carbon atoms in their chain last longer than those with two. Anticonvulsant properties are enhanced by branched chains.

The addition of a methyl group at N1 causes a faster onset/offset of action, but it also causes excitatory phenomena (twitching/lower convulsive threshold).

The addition of oxygen and sulphur to C2 increases the molecule’s lipid solubility and thus its potency. Thiopentone (thiobarbiturate) has sulphur groups at C2, making it 20-200 times more lipid soluble than oxybarbiturates.

30 mmol Na+ and 30 mmol Cl- are found in 1 litre of 0.18 percent N. saline with 4% dextrose. Percent (percent) refers to the number of grammes of a compound per 100 mL, so a litre of 4 percent dextrose solution contains 40 grammes.

As a result, a 500 mL bag of 1/5th N. saline and 4% dextrose contains approximately 15 mequivalents of sodium and 20 g of glucose. It is hypotonic due to its osmolarity of 284.

Because of the risk of hyponatraemia, it is no longer considered the crystalloid of choice for fluid maintenance in children.

Detsky’s Modified cardiac risk classification system in patients undergoing non-cardiac surgery:

Age more than 70: 05 points

History of myocardial infarction:

Less than 6 months: 10 points
More than 6 months: 5 points

Angina Pectoris:

Angina with minimal exertion: 10 points

Angina at any level of exertion: 20 points

Pulmonary Oedema:

Within 7 days: 10 points
At any time: 5 points

Suspected aortic valve stenosis with valve area <0.6cm2: 20 points Arrhythmia: Any rhythm other than sinus or sinus with premature atrial complexes (PACs): 5 points More than 5 premature ventricular contractions: 5 points
Emergency Surgery: 10 points
Deficient general medical condition: 5 points

Risk classification:

Grade I: 0-15 points = low risk
Grade II: 15-30 points = moderate risk
Grade III: >30 points = high risk.

Normally, at rest vagal influence is dominant producing the heart rate of 60-80 beats per minute even if the intrinsic automaticity of Sinoatrial Node is 100-110 beats per minute.

The transplanted heart has no autonomic nervous supply. So, it will respond to endogenous and exogenous catecholamine. This loss of parasympathetic innervation is responsible for the tachycardia in this patient.

Hypokalaemia can cause myocardial excitability and potential for ventricular ectopic and supraventricular arrhythmias. Hypothyroidism is also unlikely to cause tachycardia in this patient.

Awareness during general anaesthesia is a frightening experience, which may result in serious emotional injury and post-traumatic stress disorder.

The incidence of awareness during general anaesthesia with current anaesthetic agents and techniques has been reported as 0.2-0.4% in nonobstetric and noncardiac surgery, as 0.4% during caesarean section, and as 1.5% in cardiac surgery.

The incidence during major trauma surgery is higher. Incidence of recall has been reported to be as high as 11-43% in major trauma cases.

The liver receives blood supply from two sources.
1. Hepatic artery proper
It arises from the celiac trunk via the common hepatic artery and brings oxygenated blood to the liver.
It contributes to approximately 30% of the blood supply of the liver.
2. Hepatic portal vein – supplies the liver with partially deoxygenated blood, carrying nutrients absorbed from the small intestine. It gets tributaries from the inferior mesenteric vein, splenic vein, and superior mesenteric vein

The inferior mesenteric artery supplies the hindgut.
The superior mesenteric artery supplies the pancreas and intestine up to the proximal two-thirds of the transverse colon.
The inferior phrenic artery supplies the inferior surface of the diaphragm and oesophagus.

Moderately high doses of dopamine produce a positive inotropic (direct β1 and D1 action + that due to Noradrenaline release), but the little chronotropic effect on the heart.

Vasoconstriction (α1 action) occurs only when large doses are infused.

At doses normally employed, it raises cardiac output and systolic BP with little effect on diastolic BP. It has practically no effect on nonvascular α and β receptors; does not penetrate the blood-brain barrier€”no CNS effects.

Blood vessels (except capillaries and venules) have three distinctive layers (innermost to outermost):
1. Tunica intima
2. Tunica media
3. Tunica adventitia

The tunica media contains smooth muscle cells and is separated from the intima layer by the internal elastic lamina and the adventitia by the external elastic lamina.