The pressure measured in the right atrium or superior vena cava is known as central venous pressure (CVP). In a spontaneously breathing subject, the usual CVP value is 0-8 cmH2O (0-6 mmHg).At the conclusion of expiration, the CVP should be measured with the patient resting flat. The catheter’s tip should be at the intersection of the superior vena cava and the right atrium. An electronic transducer is installed and zeroed at the level of the right atrium to measure it (usually in the 4th intercostal space in the mid-axillary line).CVP is a good predictor of preload in the right ventricle. Hypovolaemia is indicated by a volume challenge of 250-500 mL crystalloid eliciting an increase in CVP that is not sustained for more than 10 minutes.CVP is influenced by a number of factors, including:Mechanical ventilation (and PEEP)Pulmonary hypertensionPulmonary embolismHeart failurePleural effusionDecreased cardiac outputCardiac tamponadeCVP is reduced by the following factors:Distributive shockNegative pressure ventilationHypovolaemiaDeep inhalation

Arm oedema is one of the sequelae after breast cancer surgery and radiation therapy. Arm oedema in the breast cancer patient is caused by interruption of the axillary lymphatic system by surgery or radiation therapy, which results in the accumulation of fluid in subcutaneous tissue in the arm, with decreased distensibility of tissue around the joints and increased weight of the extremity. Chronic inflammatory changes result in both subcutaneous and lymph vessel fibrosis.

Beta-blockers are contraindicated in Raynaud’s syndrome. Beta-blockers may be indicated in:HypertensionPheochromocytoma (only with an alpha-blocker)AnginaSecondary prevention after ACSArrhythmias including atrial fibrillationHeart failureThyrotoxicosisAnxietyProphylaxis of migraineEssential tremorGlaucoma

Gluteus minimus is innervated by the superior gluteal nerve.Gluteus medius is innervated by the superior gluteal nerve.Gluteus maximus is innervated by the inferior gluteal nerve.

The commonest implicated organisms in hospital-acquired bacteraemia following cannulation are Staphylococcus aureus and Staphylococcus epidermidis. The risk is directly proportional to the length of time in-situ. Peripheral cannula should be replaced after 48 hours.

A suprascapular nerve injury causes numbness in the shoulder, as well as weakness in abduction and external rotation. Damage to the axillary nerve can result in shoulder or arm muscle weakness, as well as difficulty lifting the arm. This is because the deltoid and supraspinatus muscles, which are innervated by the axillary and suprascapular nerves, are responsible for abduction of the arm at the shoulder joint.

In non-shockable (PEA/asystole) cardiac arrests, adrenaline should be given as soon as circulatory access is gained. The dose is 1 mg via IV or IO (10 mL of 1:10,000 or 1 mL of 1:1000).Once chest compressions have been resumed after the third shock in a shockable (Vf/pVT) cardiac arrest, adrenaline should be administered. The dosage is one milligram (10 mL of 1:10,000 or 1 mL of 1:1000)It should be given every 3-5 minutes after that (i.e. alternate loops) and without interrupting chest compressions.Systemic vasoconstriction is caused by the alpha-adrenergic effects of adrenaline, which raises coronary and cerebral perfusion pressures.Adrenaline’s beta-adrenergic effects are inotropic (increased myocardial contractility) and chronotropic (increased heart rate), and they can increase coronary and cerebral blood flow. However, concomitant increases in myocardial oxygen consumption and ectopic ventricular arrhythmias (especially in the absence of acidaemia), transient hypoxemia due to pulmonary arteriovenous shunting, impaired microcirculation, and increased post-cardiac arrest myocardial dysfunction may offset these benefits.Although there is no evidence of long-term benefit from its use in cardiac arrest, the improved short-term survival reported in some studies justifies its use.

Atrial natriuretic peptide (ANP) is released from cardiac atrial muscle cells in response to atrial stretch caused by an increase in intravascular fluid volume and is also produced in collecting duct cells.Atrial natriuretic peptide acts to inhibit sodium reabsorption in the distal nephron.

In most cases of atrial flutter, ventricular rate control is used as a stopgap measure until sinus rhythm is restored. A beta-blocker (e.g. bisoprolol), diltiazem, or verapamil can be used to reduce the rate of contractions in the heart.Electrical cardioversion, pharmacological cardioversion, and catheter ablation can all be used to return the heart to a normal rhythm. Cardioversion should not be attempted until the patient has been fully anticoagulated for at least three weeks if the duration of atrial flutter is unknown or it has lasted longer than 48 hours. Emergency electrical cardioversion is the treatment of choice when there is a sudden onset of symptoms and haemodynamic compromise. For recurrent atrial flutter, catheter ablation is preferred.Verapamil is a calcium-channel blocker that is non-dihydropyridine phenylalkylamine and can be used to treat supraventricular arrhythmias. It’s a calcium channel blocker with a high negative inotropic effect that lowers cardiac output, slows the heart rate, and may impair atrioventricular conduction. At high doses, it can cause heart failure, exacerbate conduction disorders, and cause hypotension.Adults should take 240-480 mg of verapamil in 2-3 divided doses. 5-10 mg IV over 30 seconds is the corresponding intravenous (IV) dose. After an IV injection, the peak effect lasts 3-5 minutes, and the action lasts 10-20 minutes.Verapamil should not be taken with beta-blockers like atenolol or quinidine because the combination of their negatively inotropic and negatively chronotropic effects can result in severe hypotension, bradycardia, impaired atrioventricular conduction, heart failure (due to impaired cardiac contractility), and sinus arrest.The use of verapamil is contraindicated in the following situations:Acute porphyrias are a type of porphyria that occurs suddenly.Accessory conducting pathways are linked to atrial flutter or fibrillation (e.g. Wolff-Parkinson-White-syndrome)BradycardiaShock caused by the heartInsufficiency of the heart (with reduced ejection fraction)Left ventricular function has been significantly harmed in the past (even if controlled by therapy)Hypotension (blood pressure less than 90 mmHg)AV block in the second and third degreesSinusitis is a condition in which the sinuses becomeSino-atrial occlusion

Prevention of spread of measles is extremely important and infected patients should be isolated. The infectious stage is from 3 days before the rash emerges and patients are advised to stay away from school/nursery/work for 4 days from onset of the rash.

Current and previous smoking reduces the effectiveness of inhaled corticosteroids and higher doses may be necessary.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline. Glucagon then causes:GlycogenolysisGluconeogenesisLipolysis in adipose tissueThe secretion of glucagon is also stimulated by:AdrenalineCholecystokininArginineAlanineAcetylcholineThe secretion of glucagon is inhibited by:InsulinSomatostatinIncreased free fatty acidsIncreased urea productionGlycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

CREST syndrome is usually associated with anti-centromere antibodies.Primary biliary cirrhosis is associated with anti-mitochondrial antibodies.Sjogren’s syndrome is associated with anti-Ro and anti-La antibodies.Polymyositis is associated with anti-Jo1 antibodies.Anti-double stranded DNA antibodies are highly characteristic of systemic lupus erythematosus (SLE). They are a group of anti-nuclear antibodies (ANA) that target double stranded DNA and are implicated in the pathogenesis of lupus nephritis.

Chemical cardioversion, or pharmacologic cardioversion, is the treatment of abnormal heart rhythms using drugs. Flecainide and propafenone are examples of drugs used as chemical cardioverters. However, given the situation of the patient, these drugs are contraindicated for his ischaemic heart disease. Amiodarone is also an antiarrhythmic drug and is the best choice for this situation.

Absolute risk reduction (ARR) of treatment = risk of death in control group – risk of death in treatment groupARR = (10/1000) – (5/1000) = 5/1000 = 0.005Number needed to treat (NNT) = 1/ARR = 1/0.005 = 200Therefore 200 people would need to be treated to prevent one extra death.

Gentamicin is the aminoglycoside of choice in the UK and is used widely for the treatment of serious infections. It has a broad spectrum but is inactive against anaerobes and has poor activity against haemolytic streptococci and pneumococci. When used for the blind therapy of undiagnosed serious infections it is usually given in conjunction with a penicillin or metronidazole (or both). The main toxic effects are nephrotoxicity and ototoxicity due to damage to the vestibulocochlear nerve (CN VIII).Gentamicin is contraindicated in myasthenia gravis and should be used with caution in renal disease which may result in accumulation and a greater risk of toxic side effects.

Haemoglobin is a 64.4 kd tetramer consisting of two pairs of globin polypeptide chains: one pair of alpha-like chains, and one pair of non-alpha chains. The chains are designated by Greek letters, which are used to describe the particular haemoglobin (e.g., Hb A is alpha2/beta2).Two copies of the alpha-globin gene (HBA2, HBA1) are located on chromosome 16 along with the embryonic zeta genes (HBZ). There is no substitute for alpha globin in the formation of any of the normal haemoglobins (Hb) following birth (e.g., Hb A, Hb A2, and Hb F). Thus, absence any alpha globin, as seen when all 4 alpha-globin genes are inactive or deleted is incompatible with extrauterine life, except when extraordinary measures are taken. A homotetramer of only alpha-globin chains is not thought to occur, but in the absence of alpha chains, beta and gamma homotetramers (HbH and Bart’s haemoglobin, respectively) can be found, although they lack cooperativity and function poorly in oxygen transport. The single beta-globin gene (HBB) resides on chromosome 11, within a gene cluster consisting of an embryonic beta-like gene, the epsilon gene (HBE1), the duplicated and nearly identical fetal, or gamma globin genes (HBG2, HBG1), and the poorly expressed delta-globin gene (HBD). A heme group, consisting of a single molecule of protoporphyrin IX co-ordinately bound to a single ferrous (Fe2+) ion, is linked covalently at a specific site to each globin chain. If the iron is oxidized to the ferric state (Fe3+), the protein is called methaemoglobin.Alpha globin chains contain 141 amino acids (residues) while the beta-like chains contain 146 amino acids. Approximately 75 percent of haemoglobin is in the form of an alpha helix. The non helical stretches permit folding of the polypeptide upon itself. Individual residues can be assigned to one of eight helices (A-H) or to adjacent non helical stretches.Heme iron is linked covalently to a histidine at the eighth residue of the F helix (His F8), at residue 87 of the alpha chain and residue 92 of the beta chain. Residues that have charged side groups, such as lysine, arginine, and glutamic acid, lie on the surface of the molecule in contact with the surrounding water solvent. Exposure of the hydrophilic (charged) amino acids to the aqueous milieu is an important determinant of the solubility of haemoglobin within the red blood cell and of the prevention of precipitation.The haemoglobin tetramer is a globular molecule (5.0 x 5.4 x 6.4 nm) with a single axis of symmetry. The polypeptide chains are folded such that the four heme groups lie in clefts on the surface of the molecule equidistant from one another.

About 80% of bicarbonate is reabsorbed in the proximal tubule. HCO3-is not transported directly, tubular HCO3-associates with H+secreted by epithelial Na+/H+antiporters to form carbonic acid (H2CO3) which readily dissociates to form carbon dioxide and water in the presence of carbonic anhydrase. CO2and water diffuse into the tubular cells, where they recombine to form carbonic acid which dissociates to H+and HCO3-. This HCO3-is transported into the interstitium largely by Na+/HCO3-symporters on the basolateral membrane (and H+is secreted back into the lumen). For each H+secreted into the lumen, one Na+and one HCO3-are reabsorbed into the plasma. H+is recycled so there is little net secretion of H+at this stage.

A pareto diagram, or pareto chart, consists of a vertical bar graph in which values are plotted in decreasing order of relative frequency from left to right. The independent variables on the chart are shown on the horizontal axis and the dependent variables are portrayed as the heights of bars.A point-to-point graph, which shows the cumulative relative frequency, may be superimposed on the bar.Because the values of the statistical variables are placed in order of relative frequency, the graph clearly reveals which factors have the greatest impact and where attention is likely to yield the greatest benefit. It is extremely useful for analysing what problems need attention first, because the taller bars on the chart clearly illustrate which variable have the greatest cumulative effect on a given system.

Clostridium tetaniis a Gram positive, rod shaped, obligate anaerobic bacterium.The incubation period is quoted as anywhere between 4-21 days and can occur after several months but symptoms usually occur within the first 7 days after exposure.Approximately 80% of patients develop generalised tetanus. The commonest presenting feature of generalised tetanus is trismus (lockjaw), occurring in approximately 75% of affected individuals. Other clinical features include:Facial spasms (risus sardonicus)Opisthotonus (characteristic body shape during spasms)Neck stiffnessDysphagiaCalf and pectoral muscle rigidityFeverHypertensionTachycardiaSpasms can occur frequently and last for several minutes, they can continue to occur for up to 4 weeks. Current mortality rates are between 10 and 15%.Tetanic spasms are caused by the exotoxin tetanospasmin. The effects of tetanolysin are not fully understood but it is not believed to have clinical significance.Localised tetanus is a rare form of the disease, occurring in around 1% of affected individuals. Patients have persistent contraction of muscles in the same anatomic area as the injury. It may precede generalised tetanus.