Learn — Cardiovascular

19 notes · 65 questions on the topic

Deep vein thrombosis (DVT)

Deep vein thrombosis is the formation of thrombus inside the deep veins, usually of the calf and thigh, where it obstructs venous return and can break off and embolise to the pulmonary arteries. It matters after every operation because immobility, tissue injury and the postoperative hypercoagulable state complete Virchow's triad, and a pulmonary embolus from an unrecognised leg thrombus is one of the leading preventable causes of hospital death.

Virchow's triad is venous stasis, endothelial injury and hypercoagulability; the surgical risk factors that stack on it are age over 40, major pelvic, hip or knee surgery, malignancy, obesity, immobility beyond about 3 days, previous venous thromboembolism, oestrogen therapy and pregnancy.
Timing on the ward: postoperative deep vein thrombosis most often becomes apparent between day 5 and day 10, although calf thrombus can start on the operating table — which is why calf inspection, hydration and early mobilisation are daily tasks and not admission-day tasks.
The clinical signs are unreliable on their own: unilateral leg swelling, calf pain, warmth, redness and dilated superficial veins, with a calf circumference difference of more than 3 cm measured 10 cm below the tibial tuberosity. Homans' sign is neither sensitive nor specific and forced dorsiflexion should not be used as a test.
The Wells score stratifies probability; with a low score a negative D-dimer excludes the diagnosis, while a raised D-dimer proves nothing after surgery, infection or in pregnancy. Compression ultrasonography with Doppler is the confirmatory test.
Prophylaxis is the examinable answer and combines all three: early ambulation and hydration for everyone, graduated compression stockings or intermittent pneumatic compression, and low-molecular-weight heparin — enoxaparin 40 mg subcutaneously once daily (reduced in renal impairment) started about 12 hours after surgery, or unfractionated heparin 5000 units subcutaneously every 8 to 12 hours; mechanical methods alone when the bleeding risk is high.
Treatment doses are different from prophylactic doses: enoxaparin 1 mg/kg subcutaneously twice daily (or 1.5 mg/kg once daily), overlapping with warfarin to an INR of 2 to 3, or a direct oral anticoagulant such as rivaroxaban or apixaban; anticoagulation continues for at least 3 months, and longer with cancer or recurrent events.
An inferior vena cava filter is only for the patient in whom anticoagulation is contraindicated or has failed — it is not an addition to anticoagulation and it does not treat the clot.
Nursing an established thrombosis: bed rest is no longer routine, so mobilise once anticoagulation is running, elevate the leg at rest, apply graduated compression, never massage the calf, measure the limb daily at a marked level, and watch for bleeding (gums, haematuria, melaena, falling haemoglobin) and for a platelet count falling after day 5 on heparin.
Post-thrombotic syndrome — chronic pain, oedema, pigmentation and venous ulceration — follows in up to a third of patients, so discharge teaching covers compression stockings, leg care, anticoagulant adherence and INR checks, avoiding long immobile journeys, and reporting sudden breathlessness or chest pain at once.

Fluid and electrolyte imbalance with ECG changes

Electrolyte imbalance is a deviation of the serum concentration of potassium, sodium, calcium or magnesium outside its reference range, and the heart is the organ that announces it first because these ions generate the cardiac action potential. Potassium and calcium have signature ECG patterns that appear before the patient looks unwell, so the monitor is the earliest warning the nurse gets and the ECG, not the laboratory value, sets the speed of treatment.

Serum potassium is normally 3.5 to 5.0 mmol/L; hyperkalaemia progresses on the ECG as tall peaked narrow-based T waves first (about 5.5 to 6.5 mmol/L), then a flattened or absent P wave with PR prolongation (6.5 to 7.5), then a widening QRS (7.0 to 8.0), then the sine wave that precedes ventricular fibrillation and asystole.
Emergency treatment of hyperkalaemia runs in three steps: calcium gluconate 10 percent, 10 mL intravenously over 2 to 3 minutes to stabilise the myocardium (it works within 1 to 3 minutes, lasts 30 to 60 minutes and lowers no potassium at all); then 10 units of regular insulin with 25 g of dextrose intravenously plus 10 to 20 mg of nebulised salbutamol to shift potassium into the cells; then removal by a potassium binder or dialysis.
Hypokalaemia below 3.5 mmol/L gives ST depression, a flat or inverted T wave, a prominent U wave and a long QU interval, with ventricular ectopy and torsades de pointes as it deepens; it also potentiates digoxin toxicity at a therapeutic digoxin level.
Potassium is replaced no faster than 10 mmol per hour through a peripheral line and 20 mmol per hour through a central line with continuous ECG monitoring, and it is never given as an intravenous push.
Hypokalaemia that will not correct is hypomagnesaemia until proved otherwise; the magnesium has to be replaced first or the potassium will not stay up.
Hypocalcaemia prolongs the QT interval and shows Trousseau sign (carpopedal spasm after the blood pressure cuff is held above systolic pressure for 3 minutes) and Chvostek sign (a facial twitch when the facial nerve is tapped in front of the ear); hypercalcaemia shortens the QT interval.
Sodium disorders have no ECG signature, and that is the discriminator the exam tests: hyponatraemia causes cerebral oedema and seizures, hypernatraemia causes thirst, irritability and confusion, and either is corrected by no more than about 8 to 10 mmol/L in 24 hours to avoid osmotic demyelination or cerebral oedema.
Magnesium below the normal range prolongs the QT and causes torsades de pointes, which is treated with intravenous magnesium sulfate whatever the serum magnesium level.

Vagal manoeuvre

A vagal manoeuvre is a bedside action that raises parasympathetic tone and so slows conduction and lengthens the refractory period of the atrioventricular node. It is the first treatment for a stable, regular narrow-complex tachycardia because the AV node is part of the re-entry circuit in most supraventricular tachycardias, and breaking it there terminates the arrhythmia without a drug; when it does not terminate the rhythm, the transient AV block it produces still unmasks the underlying atrial flutter or fibrillation on the strip.

The modified Valsalva manoeuvre is the most effective version: the patient blows into a 10 mL syringe hard enough to just move the plunger (about 40 mmHg) for 15 seconds while semi-recumbent, then is laid flat with both legs passively raised to about 45 degrees for 15 seconds; it converts roughly two to three times as many patients as the standard strain.
Carotid sinus massage is applied to one side only, at the level of the upper border of the thyroid cartilage below the angle of the jaw, for 5 to 10 seconds with continuous ECG running; both sides are never massaged together or in quick succession.
Carotid sinus massage is contraindicated when there is a carotid bruit, known carotid disease, a stroke or transient ischaemic attack within the last 3 months, or a recent myocardial infarction, and it is avoided in the elderly.
Cold stimulation of the face triggers the diving reflex and is the preferred manoeuvre in infants and small children: a bag of iced water or an ice pack applied to the forehead, eyes and bridge of the nose for up to 15 to 30 seconds, without occluding the airway.
Ocular (eyeball) pressure is obsolete and must not be used because it causes retinal detachment, and it is a common wrong option in the paper.
The manoeuvre is both a treatment and a test: a rhythm strip must run throughout, because gradual slowing that then speeds up again means atrial flutter or sinus tachycardia, while abrupt termination means an AV nodal re-entrant tachycardia.
When the manoeuvre fails, the next step is adenosine 6 mg by rapid intravenous push into a large proximal vein followed immediately by a 20 mL saline flush with the arm elevated, then 12 mg if needed; the half-life is under 10 seconds, so a slow push simply wastes the dose.
Vagal manoeuvres and adenosine belong only to the stable patient. Hypotension, altered mental status, ischaemic chest pain, acute heart failure or shock with the tachycardia means immediate synchronised cardioversion instead.

Basic ECG interpretation

The 12-lead ECG is a surface recording of the heart's electrical activity from twelve viewpoints, printed at a standard paper speed of 25 mm per second and a standard gain of 10 mm per millivolt. Reading it is a fixed sequence rather than pattern spotting: calibration, rate, rhythm, axis, intervals, chamber enlargement, then ischaemia and infarction, and the value of the sequence is that it makes a nurse able to name the one abnormality that must be shown to a doctor within minutes.

At 25 mm per second one small square is 1 mm and 0.04 second, one large square is 5 mm and 0.20 second; vertically 10 mm equals 1 millivolt, and the calibration mark at the start of the strip must be checked before any measurement is trusted.
Rate for a regular rhythm is 300 divided by the number of large squares between two R waves, or 1500 divided by the number of small squares; for an irregular rhythm count the QRS complexes in a 6-second strip (30 large squares) and multiply by 10.
Normal intervals: PR 0.12 to 0.20 second, QRS under 0.12 second, and a corrected QT up to about 440 ms in men and 460 ms in women, with a QTc above 500 ms carrying a real risk of torsades de pointes.
Axis is read from leads I and aVF: both positive is a normal axis, lead I positive with aVF negative is left axis deviation, lead I negative with aVF positive is right axis deviation, and both negative is an extreme axis.
Right bundle branch block gives a QRS of 0.12 second or more with an RSR pattern (the letter M) in V1 and a wide slurred S wave in leads I and V6; left bundle branch block gives the opposite, a W pattern in V1 and an M in V6, and a new left bundle branch block with ischaemic chest pain is treated as a STEMI equivalent.
STEMI is new ST elevation at the J point in two contiguous leads: 1 mm or more in the limb leads and in V4 to V6, and 2 mm or more in V2 and V3 in men (2.5 mm in men under 40) or 1.5 mm or more in V2 and V3 in women.
Territories: leads II, III and aVF are inferior (usually the right coronary artery), V1 to V4 anterior (left anterior descending), leads I, aVL, V5 and V6 lateral (left circumflex), tall R waves with ST depression in V1 and V2 suggest a posterior infarct, and V4R is added whenever the inferior leads are involved to look for right ventricular infarction.
Lead II is the best single rhythm lead because the P wave is largest there; V1 is the best lead for deciding whether a wide beat is ventricular or a bundle branch block.
A pattern read on the strip must always be matched to the patient: an ECG is never reported without the pulse, blood pressure and symptoms recorded at the same time.

Heart sounds — rhonchi, wheezes, pleural rub, crackles

Auscultation is the systematic listening to the sounds the heart valves and the airways make, using the diaphragm for high-pitched sounds and the bell for low-pitched ones. Naming a sound correctly is what turns a vague complaint of breathlessness into a working diagnosis at the bedside, because crackles, wheeze, rhonchi, a pleural rub and stridor each point to a different level of the airway and a different immediate action.

The first heart sound is the closure of the mitral and tricuspid valves at the start of systole and is loudest at the apex; the second is closure of the aortic and pulmonary valves at the end of systole and is loudest at the base, and it splits normally on inspiration.
Auscultation areas: aortic in the second right intercostal space, pulmonary in the second left intercostal space, tricuspid at the left lower sternal border in the fourth or fifth space, and mitral at the apex in the fifth intercostal space in the mid-clavicular line.
A third heart sound is a low-pitched early diastolic gallop from rapid ventricular filling: normal in children, young adults and pregnancy, but in an adult over 40 it means volume overload and heart failure. A fourth heart sound is late diastolic, comes from atrial contraction against a stiff ventricle in hypertension or aortic stenosis, and can never occur in atrial fibrillation because there is no organised atrial contraction.
Crackles are discontinuous, non-musical sounds: fine late-inspiratory crackles at the bases mean pulmonary oedema or interstitial fibrosis, coarse crackles mean secretions, pneumonia or bronchiectasis, and crackles that clear completely after a cough are of no significance.
Wheeze is continuous, musical and high-pitched, mainly expiratory; polyphonic wheeze across both lungs means asthma or COPD, while a fixed monophonic wheeze in one place means a localised obstruction such as a tumour or an inhaled foreign body.
Rhonchi are continuous low-pitched snoring sounds from secretions in the large airways and typically change or clear with coughing or suction, which is exactly what separates them from wheeze.
A pleural rub is a leathery creaking heard in both inspiration and expiration over one localised area, does not clear with coughing and stops when the breath is held; it accompanies pleurisy, pneumonia and pulmonary embolism.
Stridor is a harsh, mainly inspiratory sound from the upper airway (croup, epiglottitis, an inhaled foreign body, anaphylaxis or post-extubation oedema) and is an airway emergency, not a chest sign.
Absent or reduced breath sounds on one side with a hyper-resonant percussion note suggest pneumothorax, and with a stony dull note suggest pleural effusion; bronchial breathing heard over a peripheral lung field means consolidation.

Pulse pressure

Pulse pressure is the difference between the systolic and diastolic blood pressure, normally 30 to 40 mmHg in an adult, and it reflects the stroke volume the ventricle ejects against the stiffness of the arterial tree. It is the vital sign that changes earliest in shock, because a compensating patient maintains the systolic pressure while the diastolic pressure climbs with vasoconstriction, so the pulse pressure narrows long before the systolic reading falls.

Pulse pressure equals systolic minus diastolic pressure; a reading of 120/80 mmHg gives a normal pulse pressure of 40 mmHg, and the mean arterial pressure derived from it is the diastolic pressure plus one third of the pulse pressure, normally 70 to 100 mmHg with 65 mmHg the usual floor for organ perfusion.
A narrow pulse pressure, under 25 mmHg or under about a quarter of the systolic value, points to a low stroke volume: hypovolaemia and early shock, cardiac tamponade, constrictive pericarditis, severe aortic stenosis and cardiogenic shock.
A wide pulse pressure, over about 60 mmHg, points to a large stroke volume or a stiff aorta: aortic regurgitation, thyrotoxicosis, severe anaemia, beriberi from thiamine deficiency, arteriovenous fistula, patent ductus arteriosus, fever, pregnancy and the isolated systolic hypertension of older age.
In children a narrowing pulse pressure with cool peripheries and a prolonged capillary refill is a decompensating sign, because a child holds the systolic pressure until very late and then falls abruptly.
Aortic regurgitation gives the wide pulse pressure its collapsing or water-hammer character, together with Corrigan sign in the neck, Quincke sign in the nail bed, de Musset head nodding and Traube pistol-shot femoral sounds.
Pulse pressure is not pulsus paradoxus: pulsus paradoxus is an inspiratory fall in systolic pressure of more than 10 mmHg and is the sign of tamponade, severe asthma and constrictive pericarditis, while pulse pressure is a single-beat difference.
A widening pulse pressure with bradycardia in a head-injured patient is part of the Cushing response and means rising intracranial pressure, not a healthy circulation.

Myocardial infarction and enzyme markers

Myocardial infarction is myocardial cell death caused by prolonged ischaemia, and the Fourth Universal Definition requires a rise and or fall of cardiac troponin with at least one value above the 99th percentile upper reference limit, together with evidence of ischaemia such as symptoms, new ischaemic ECG changes, new pathological Q waves, imaging evidence of new loss of viable myocardium, or intracoronary thrombus. Type 1 infarction follows plaque rupture with thrombus, while type 2 follows a supply-demand mismatch from anaemia, tachyarrhythmia, sepsis or hypotension, and the two are treated very differently, which is why the marker is always read alongside the story and the ECG.

Cardiac troponin I and T are the most sensitive and specific markers: they begin to rise within 3 to 4 hours of injury, peak at about 18 to 24 hours, and stay elevated for 7 to 14 days, which is why troponin cannot diagnose reinfarction in the same week.
Creatine kinase MB rises at 3 to 6 hours, peaks at about 24 hours and returns to normal by 48 to 72 hours, and that fast clearance is exactly why it remains the marker used to detect reinfarction.
Myoglobin is the earliest marker to rise at 1 to 2 hours but is not specific because it also comes from skeletal muscle; lactate dehydrogenase and aspartate transaminase peak late and are of historical interest only.
High-sensitivity troponin assays allow rule-in and rule-out algorithms using a baseline sample and a repeat at 1 to 3 hours, and it is the pattern of rise and fall, not a single number, that separates infarction from a chronically raised troponin.
Troponin is raised without an acute coronary syndrome in chronic kidney disease, sepsis, myocarditis, pulmonary embolism, decompensated heart failure and prolonged tachyarrhythmia, and that list is a favourite examination question.
STEMI reperfusion targets: primary percutaneous coronary intervention within 90 minutes of first medical contact at a PCI centre, or within 120 minutes if transfer is needed; where that is impossible, fibrinolysis within 30 minutes of arrival, followed by transfer for angiography.
Immediate drug treatment is aspirin 300 mg chewed, a loading dose of a second antiplatelet such as clopidogrel or ticagrelor, high-intensity statin and anticoagulation as prescribed; oxygen is given only when the saturation is below 90 percent, because routine oxygen in a normoxic patient increases infarct size.
Nitrates are withheld in inferior infarction with right ventricular involvement (ST elevation in V4R), in hypotension, and within 24 hours of sildenafil or 48 hours of tadalafil, because the infarcted right ventricle is preload dependent and collapses without it; those patients need intravenous fluid instead.
Silent or atypical infarction is common in people with diabetes, the elderly and women, presenting as breathlessness, epigastric discomfort, sweating, fatigue or collapse without classical chest pain.

Varicose vein

Varicose veins are dilated, tortuous, elongated superficial veins of the leg, 3 mm or more in diameter when the patient is standing, produced by incompetent valves that let blood reflux down the great or small saphenous system. They matter far beyond appearance because sustained venous hypertension produces skin damage, and the end point of untreated disease is the chronic venous ulcer above the medial malleolus that occupies months of nursing care.

The great saphenous vein and the saphenofemoral junction are the commonest site; primary disease comes from valve incompetence, while secondary disease follows a previous deep vein thrombosis that has obstructed or damaged the deep system.
Risk factors are occupations involving prolonged standing, pregnancy, obesity, increasing age, female sex and a family history; the symptoms are aching heaviness worse at the end of the day and relieved by elevation, night cramps, itching and ankle swelling.
Duplex ultrasonography is the investigation of choice and defines reflux (usually taken as reverse flow lasting more than 0.5 second in a superficial vein); the bedside Brodie-Trendelenburg test localises saphenofemoral incompetence and the Perthes test checks that the deep veins are patent.
The CEAP clinical grades run from C0 with no visible signs, C1 telangiectasia or reticular veins, C2 varicose veins, C3 oedema, C4 skin changes such as pigmentation, eczema, lipodermatosclerosis and atrophie blanche, C5 a healed ulcer and C6 an active ulcer.
A venous ulcer sits in the gaiter area just above the medial malleolus, is shallow with sloping edges and a granulating base, is relatively painless and is surrounded by haemosiderin staining; an arterial ulcer is punched out, on the toes or pressure points, painful and has absent pulses, which is the discriminator that decides treatment.
Graduated compression stockings of class II (about 20 to 30 mmHg at the ankle) are the mainstay of conservative treatment, put on first thing in the morning before the leg swells and removed at night, alongside leg elevation above heart level, calf exercises and weight reduction.
The ankle-brachial pressure index is measured before any compression is applied, because compression on a limb with arterial disease causes necrosis; an index below 0.8 means compression is not applied without vascular advice.
Definitive treatment is endovenous thermal ablation by laser or radiofrequency, ultrasound-guided foam sclerotherapy, or open surgery with high ligation and stripping, and after any of them compression and early walking are prescribed while prolonged standing and sitting are avoided.

Coronary artery bypass grafting (CABG)

Coronary artery bypass grafting is open surgical revascularisation in which an arterial or venous conduit is used to carry blood from the aorta or the subclavian system to a coronary artery beyond a significant obstruction. It is chosen over percutaneous intervention in left main disease, in multivessel disease especially with diabetes or impaired left ventricular function, and in complex anatomy, and the nursing importance lies in the first 48 postoperative hours, when arrhythmia, bleeding, tamponade and pulmonary complications are all common and all detectable at the bedside.

The left internal mammary (internal thoracic) artery grafted to the left anterior descending artery is the graft with the best long-term patency, over 90 percent at 10 years, whereas a reversed saphenous vein graft is patent in only about half to two-thirds of cases at 10 years; the radial artery is the other common arterial conduit.
The saphenous vein is reversed before it is grafted because its valves would otherwise obstruct flow, and the leg from which it was harvested is elevated and observed for haematoma, infection and neuropathy.
Surgery may be on-pump with cardiopulmonary bypass and cardioplegic arrest, or off-pump on the beating heart; cardiopulmonary bypass accounts for the coagulopathy, the systemic inflammatory response, fluid shifts and the transient cognitive changes seen afterwards.
Sternal precautions run for 6 to 8 weeks while the sternum heals: no lifting, pushing or pulling more than about 5 kg, no driving, no pulling on the bed rails, and splinting the chest with a pillow for every cough and change of position.
Pulmonary care is the nurse's daily work: incentive spirometry hourly while awake, deep breathing and supported coughing, early mobilisation from the first postoperative day, and adequate analgesia given before physiotherapy so the patient can breathe deeply.
Chest drains are monitored hourly; drainage exceeding about 100 mL per hour for two consecutive hours, or a drain that abruptly stops draining while the venous pressure rises and the blood pressure falls, both need immediate medical review because the second means tamponade.
Postoperative atrial fibrillation occurs in up to a third of patients and peaks on the second to third day; other complications are bleeding, tamponade, sternal wound infection and mediastinitis, stroke, acute kidney injury and graft occlusion.
Sternal wound infection is much more likely in patients with diabetes, obesity and smokers, so the blood glucose is kept under about 180 mg/dL perioperatively, the sternum is supported, and the wound is inspected daily for sternal clicking, discharge or instability.
Secondary prevention is lifelong: aspirin restarted within 24 hours, a high-intensity statin, a beta-blocker, blood pressure and glycaemic control, smoking cessation, and enrolment in cardiac rehabilitation.

Angina — types (variant/Prinzmetal)

Angina is chest discomfort caused by reversible myocardial ischaemia, classically retrosternal, described as heaviness, tightness or burning, and radiating to the left arm, jaw, neck or epigastrium. It divides into stable angina brought on by a predictable amount of exertion and relieved by rest or nitrate, unstable angina which is an acute coronary syndrome, and variant or Prinzmetal angina caused by focal coronary spasm rather than a fixed obstruction, and the distinction changes both the drug given and the urgency.

Stable angina is provoked by a reproducible level of exertion, cold or emotion, lasts about 2 to 10 minutes, and settles with rest or sublingual nitroglycerin within about 5 minutes; the resting ECG is often normal and stress testing shows ST depression.
Unstable angina is new-onset, occurs at rest, follows a crescendo pattern or lasts more than 20 minutes; it is an acute coronary syndrome with a normal troponin, and once the troponin rises the same picture is a non-ST-elevation myocardial infarction.
Prinzmetal or variant angina comes from focal coronary artery spasm, typically at rest between midnight and the early morning, in younger patients and smokers, with preserved exercise tolerance and transient ST elevation on the ECG that resolves completely when the spasm relieves.
Prinzmetal angina is treated with a calcium channel blocker such as diltiazem or amlodipine together with a long-acting nitrate, and smoking cessation is essential; cocaine use must be asked about because it causes the same picture.
Beta-blockers, especially non-selective ones, can worsen coronary spasm by leaving alpha-mediated vasoconstriction unopposed, so they are avoided in variant angina even though they are first-line for stable angina, and this contrast is the single most examined point in the topic.
Sublingual nitroglycerin 0.5 mg is taken while sitting (never standing, because of syncope), repeated every 5 minutes for up to three doses, and emergency help is called if the pain persists beyond the first dose or after the third; a burning sensation under the tongue suggests the tablet is still potent, and tablets are stored in the original dark glass bottle and replaced within about 6 months of opening.
Nitrates are absolutely contraindicated within 24 hours of sildenafil or vardenafil and 48 hours of tadalafil, and in right ventricular infarction and severe aortic stenosis, because the fall in preload causes profound hypotension.
Microvascular angina, once called cardiac syndrome X, gives typical angina with objective ischaemia but normal epicardial coronary arteries and is commoner in women; the Canadian Cardiovascular Society class I to IV grades how much exertion provokes the pain.

Bacterial endocarditis

Infective endocarditis is microbial infection of the endocardial surface, usually of a heart valve, in which platelets, fibrin and organisms build a vegetation that destroys the valve and showers emboli around the body. It presents as prolonged fever with a new or changing murmur, and in India rheumatic valve disease is still the commonest underlying lesion, so any patient with known valve disease and unexplained fever is assumed to have it until blood cultures say otherwise.

The modified Duke criteria make a definite diagnosis on two major criteria, one major plus three minor, or five minor criteria.
The major criteria are typical organisms grown from two separate blood cultures or persistently positive cultures, and evidence of endocardial involvement on echocardiography such as a vegetation, an abscess, new dehiscence of a prosthetic valve or new valvular regurgitation.
The minor criteria are a predisposing heart lesion or injecting drug use, fever of 38 degrees Celsius or more, vascular phenomena (arterial emboli, septic pulmonary infarcts, mycotic aneurysm, conjunctival haemorrhage, Janeway lesions), immunological phenomena (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor) and microbiological evidence that falls short of a major criterion.
Organisms follow the setting: viridans streptococci in subacute native-valve disease after dental work, Staphylococcus aureus in acute disease, injecting drug use and healthcare-associated infection, coagulase-negative staphylococci in early prosthetic valve infection, enterococci after genitourinary procedures, and Streptococcus gallolyticus (bovis) which should prompt a search for colonic carcinoma.
Three sets of blood cultures are taken from three separate venepuncture sites over at least an hour and always before antibiotics start; taking cultures after the first dose is the commonest reason endocarditis is never proved.
Transthoracic echocardiography is the first test but transoesophageal echocardiography is far more sensitive and is done when the transthoracic study is negative with continuing suspicion, when a prosthetic valve is involved, or when an abscess is suspected.
Treatment is 4 to 6 weeks of intravenous bactericidal antibiotics chosen by culture and sensitivity, and surgery is indicated for heart failure from valve destruction, uncontrolled infection or abscess, persistently positive cultures, fungal infection, and a large mobile vegetation that has already embolised.
Janeway lesions are painless haemorrhagic macules on the palms and soles and are embolic, while Osler nodes are painful tender nodules on the finger pulps and are immune-mediated; the memory hook is that Osler equals ouch.
Antibiotic prophylaxis is now restricted to the highest-risk patients (a prosthetic valve or prosthetic repair material, previous endocarditis, specified congenital heart disease, and cardiac transplant valvulopathy) undergoing dental procedures that manipulate gingival tissue or perforate the oral mucosa, using amoxicillin 2 g orally (50 mg per kilogram in children) 30 to 60 minutes before the procedure; it is not given routinely for gastrointestinal or genitourinary procedures.

Constrictive pericarditis

Constrictive pericarditis is a thickened, fibrosed and often calcified pericardium that encases the heart and prevents the ventricles from filling in mid and late diastole, so filling is rapid and early and then stops abruptly. It produces the picture of right heart failure with a raised venous pressure, ascites and hepatomegaly in a patient whose lungs are clear and whose ventricular contraction is normal, and in India the commonest cause by far is healed tuberculous pericarditis.

Causes in India are led by tuberculosis; elsewhere the leading causes are previous cardiac surgery, mediastinal radiotherapy, and idiopathic or viral pericarditis, with uraemia and connective tissue disease adding to the list.
The jugular venous pressure is high with prominent x and y descents, and Kussmaul sign is present, meaning the venous pressure rises rather than falls with inspiration because the rigid pericardium cannot accommodate the extra venous return.
A pericardial knock is an early diastolic high-pitched sound produced when ventricular filling halts against the rigid shell, and it is heard where a third heart sound would otherwise be.
Ascites and hepatomegaly are out of proportion to the peripheral oedema, the pulse pressure is narrow, and the lungs stay clear, which is what distinguishes it from left ventricular failure.
Investigations: the chest radiograph may show pericardial calcification, which is classic after tuberculosis; CT or cardiac magnetic resonance shows a pericardium thicker than about 4 mm; echocardiography shows a septal bounce and exaggerated respiratory variation in transvalvular flow; catheterisation shows equalisation of end-diastolic pressures in all four chambers and the dip-and-plateau or square root sign.
Restrictive cardiomyopathy is the differential that matters: constriction shows marked respiratory variation in mitral inflow, a septal bounce and a preserved or increased medial mitral annular velocity, while restriction shows a markedly raised natriuretic peptide and reduced annular velocities.
Tamponade is the other differential: tamponade has pulsus paradoxus with a blunted y descent and no Kussmaul sign, whereas constriction has a prominent y descent and Kussmaul sign, and this pair of discriminators is what examinations ask.
Pericardiectomy is the only definitive treatment; diuretics with salt restriction relieve congestion in the meantime, and tuberculous disease is treated with the full anti-tuberculosis regimen under the National Tuberculosis Elimination Programme, sometimes with corticosteroids added.

Intra-aortic balloon pump (IABP)

The intra-aortic balloon pump is a catheter-mounted balloon sitting in the descending thoracic aorta, with its tip just distal to the origin of the left subclavian artery and above the renal arteries, that inflates and deflates in time with the cardiac cycle. This counterpulsation raises diastolic pressure to improve coronary and cerebral perfusion and drops aortic end-diastolic pressure to reduce the afterload the failing ventricle has to overcome, so it improves oxygen supply and lowers oxygen demand at the same time.

Timing is taken either from the R wave of the ECG or from the dicrotic notch of the arterial waveform: the balloon inflates at the dicrotic notch, which marks aortic valve closure and the start of diastole, and deflates just before the next systole.
Inflation in diastole augments coronary artery perfusion, which happens only in diastole; deflation before systole creates a vacuum effect that lowers aortic end-diastolic pressure, reduces left ventricular wall stress and myocardial oxygen demand, and increases stroke volume.
Assist ratios of 1:1, 1:2 and 1:3 describe how many cardiac cycles the balloon assists, and weaning is done by stepping the ratio down while the haemodynamics are watched.
Indications are cardiogenic shock, the mechanical complications of infarction such as acute mitral regurgitation and ventricular septal rupture, refractory unstable angina, and support as a bridge to revascularisation, surgery or transplantation.
Contraindications are aortic regurgitation (the augmented diastolic pressure worsens the regurgitation), aortic dissection or aneurysm, severe peripheral arterial disease, uncontrolled sepsis and uncontrolled bleeding.
The four timing errors are early inflation (before the aortic valve shuts, increasing afterload), late inflation (loss of augmentation), early deflation (loss of afterload reduction and possible coronary steal) and late deflation, which impedes ejection and is the most harmful of the four.
Nursing surveillance is limb and organ perfusion: check the pedal pulses, colour, temperature, capillary refill and sensation of the cannulated limb hourly, keep that leg straight with the head of the bed no higher than 30 to 45 degrees, and watch the left radial pulse and the urine output because a catheter that migrates occludes the subclavian or renal arteries.
Daily bloods include platelet count and haemoglobin, since thrombocytopenia and haemolysis are expected; anticoagulation is given per unit protocol and puncture sites are watched for bleeding.
The balloon must never sit still: if the pump stops for more than a few minutes a thrombus forms on the balloon, so a stopped console is an emergency that is reported at once and the balloon is manually cycled per protocol.

Cardiac tamponade

Cardiac tamponade is the accumulation of fluid, blood, pus or gas in the pericardial sac at a pressure high enough to compress the heart and stop the chambers filling in diastole, producing obstructive shock. What decides whether tamponade occurs is the speed of accumulation, not the volume, because 150 to 200 mL collecting quickly will tamponade a heart while one to two litres collecting over months may not, and that is why a small traumatic effusion can kill within minutes.

Beck triad is hypotension, muffled or distant heart sounds and distended neck veins, and it is accompanied by tachycardia, tachypnoea, a narrow pulse pressure, restlessness and cold peripheries.
Pulsus paradoxus greater than 10 mmHg is the classic sign: with the cuff deflated slowly, the Korotkoff sounds are first heard only in expiration and only later in all phases, and the difference between those two pressures is the measurement.
Kussmaul sign is characteristically absent in tamponade and present in constrictive pericarditis, and the y descent of the venous waveform is blunted in tamponade and prominent in constriction; these two pairs are the standard examination discriminators.
The ECG shows low-voltage complexes and may show electrical alternans, a beat-to-beat change in QRS amplitude produced by the heart swinging in the fluid; the chest radiograph shows a globular water-bottle heart only when the effusion is large and slow.
Echocardiography is the confirming test and shows diastolic collapse of the right atrium and right ventricle, a dilated inferior vena cava that fails to collapse by more than 50 percent on inspiration, and exaggerated respiratory variation across the valves.
Causes are malignancy, uraemia, tuberculosis, trauma and cardiac surgery, free wall rupture after myocardial infarction, aortic dissection leaking into the pericardium, and procedures such as pacemaker lead placement, central line insertion and coronary intervention.
Definitive treatment is drainage: emergency pericardiocentesis by the subxiphoid route under echocardiographic guidance, or surgical drainage and a pericardial window when the blood is clotted, traumatic or recurrent.
While drainage is arranged, intravenous fluid is given to maintain filling pressure, and diuretics, vasodilators and nitrates are withheld because they drop the preload the patient is surviving on.
Positive-pressure ventilation reduces venous return further and can precipitate cardiac arrest on induction, so intubation is deferred until the pericardium is drained wherever that is possible.

Pacemaker — types and settings

A cardiac pacemaker is a pulse generator with one or more leads that delivers an electrical stimulus to the myocardium when the heart's own rate or conduction fails, so it treats bradyarrhythmia and conduction block rather than tachyarrhythmia. Pacing may be temporary (transcutaneous or transvenous) while a reversible cause is corrected, or permanent, and the nurse's work is to recognise on the monitor when the device is not doing what it was programmed to do.

The NBG code names the device in five positions: chamber paced, chamber sensed, response to a sensed beat (I for inhibited, T for triggered, D for dual, O for none), rate modulation (R), and multisite pacing.
VVI paces and senses the ventricle and is inhibited by the patient's own beat, so it suits permanent atrial fibrillation with a slow ventricular response; DDD paces and senses both chambers and preserves atrioventricular synchrony, so it suits complete heart block with sinus rhythm; AAI paces the atrium where atrioventricular conduction is intact, as in sinus node disease.
Indications for permanent pacing are symptomatic sinus node dysfunction, second-degree Mobitz type II block, third-degree (complete) atrioventricular block, symptomatic bradycardia with no reversible cause, and alternating bundle branch block.
In transcutaneous pacing the rate is usually set around 60 to 80 per minute and the current in milliamperes is increased until electrical capture appears as a wide QRS with a broad T wave after every spike, and capture is only confirmed when a pulse is felt to match, which is mechanical capture; the procedure is painful and needs sedation and analgesia.
Failure to capture is a pacing spike with no complex following it, caused by lead dislodgement, too low an output, electrolyte disturbance, fibrosis or infarction at the lead tip. Failure to sense (undersensing) is a spike that falls where it should have been inhibited and risks a shock on the T wave, while oversensing is a missing spike when one was due.
Early complications are pneumothorax, cardiac perforation with tamponade, pocket haematoma, infection and lead dislodgement, which is commonest in the first month; later problems are pacemaker syndrome from loss of atrioventricular synchrony in VVI pacing, twiddler syndrome and diaphragmatic stimulation causing persistent hiccups.
Post-implant nursing: keep the arm on the implant side below shoulder level and avoid heavy lifting for 4 to 6 weeks, inspect the pocket for swelling, redness or discharge, take the pulse daily and report a rate persistently below the programmed lower rate, and confirm the device card is issued before discharge.
Patient education: household appliances including microwave ovens are safe, but the mobile phone is held to the opposite ear and kept at least 15 cm from the generator, arc welding and strong magnetic fields are avoided, airport screening wands are not held over the device, and magnetic resonance imaging is done only if the whole system is labelled MRI-conditional.
Every implanted patient carries the identification card at all times and attends the device clinic for battery and threshold checks, because the battery is replaced electively before it depletes.

Pulmonary embolism

Pulmonary embolism is obstruction of the pulmonary arterial tree by thrombus that has almost always broken off from a deep vein of the leg or pelvis, so it is the dangerous end of the same disease as deep vein thrombosis. It kills by acute right ventricular failure rather than by hypoxaemia alone, and because the classic triad of pleuritic pain, breathlessness and haemoptysis is present in only a minority, it is the diagnosis that must be actively considered in any patient with sudden unexplained breathlessness or collapse.

Risk follows Virchow's triad: stasis (immobility, long travel, plaster cast, paralysis), endothelial injury (surgery, especially hip and knee replacement, trauma, central lines) and hypercoagulability (malignancy, pregnancy and the puerperium, oestrogen-containing contraceptives, nephrotic syndrome, inherited thrombophilia).
Symptoms are sudden breathlessness, pleuritic chest pain, cough, haemoptysis, presyncope or syncope; signs are tachypnoea, tachycardia, hypoxaemia, a low-grade fever, and in large emboli hypotension with a raised jugular venous pressure and a loud pulmonary second sound.
The Wells score for pulmonary embolism scores clinical signs of DVT and an alternative diagnosis being less likely at 3 points each, heart rate above 100, immobilisation or surgery within 4 weeks and previous DVT or PE at 1.5 each, and haemoptysis and active malignancy at 1 each; 4 points or less means PE is unlikely and a D-dimer is used to exclude it, above 4 means imaging.
D-dimer is sensitive but not specific — it is raised in sepsis, malignancy, pregnancy, trauma and the post-operative state — so it rules out only in low or intermediate probability; above 50 years the age-adjusted cut-off is the age multiplied by 10 micrograms per litre.
CT pulmonary angiography is the confirmatory test; a ventilation-perfusion scan is used when contrast is contraindicated, in renal failure and in pregnancy, and a bedside echocardiogram showing a dilated, poorly moving right ventricle supports the diagnosis when the patient is too unstable to move.
Supporting tests: the ECG most often shows only sinus tachycardia, with the classic S1Q3T3 pattern, right bundle branch block or anterior T-wave inversion in larger emboli; arterial blood gas shows hypoxaemia with a low carbon dioxide and a widened alveolar-arterial gradient; the chest X-ray is usually normal or near-normal, which is itself a clue.
Anticoagulation is started as soon as the diagnosis is suspected and imaging is not immediate: low molecular weight heparin such as enoxaparin 1 mg/kg subcutaneously twice daily, fondaparinux, or a direct oral anticoagulant (rivaroxaban 15 mg twice daily for 21 days then 20 mg daily, or apixaban 10 mg twice daily for 7 days then 5 mg twice daily); if warfarin is used it overlaps with heparin for at least 5 days and until the INR is 2 to 3 on two consecutive days.
High-risk (massive) pulmonary embolism means sustained hypotension, and it is treated with systemic thrombolysis such as alteplase, or with catheter-directed therapy or surgical embolectomy when thrombolysis is contraindicated; an inferior vena cava filter is reserved for patients in whom anticoagulation truly cannot be given.
Duration of anticoagulation is at least 3 months for a provoked event, and extended or indefinite treatment when the event was unprovoked, recurrent, or associated with active cancer; prevention on the ward is early mobilisation, graduated compression stockings or intermittent pneumatic compression, adequate hydration and prophylactic low molecular weight heparin in immobile and post-operative patients.

Heart failure — classification and nursing

Heart failure is a clinical syndrome in which the heart cannot fill or eject enough blood to meet the body's metabolic demand at normal filling pressures, so the patient has symptoms such as breathlessness, orthopnoea and fatigue together with signs of congestion, supported by an objective abnormality of cardiac structure or function. It is classified two ways at once — by ejection fraction (HFrEF 40% or less, HFmrEF 41 to 49%, HFpEF 50% or more) and by functional limitation (NYHA class I to IV) — and the two are not interchangeable, because a patient with an ejection fraction of 20% can be NYHA class I on good treatment.

Ejection fraction sorts the treatment: HFrEF is 40% or less and follows ischaemic heart disease and dilated cardiomyopathy, HFmrEF is 41 to 49%, and HFpEF is 50% or more with evidence of raised filling pressure, which is the picture in the elderly hypertensive, diabetic or obese patient.
NYHA class describes symptoms and can change week to week — I no limitation, II slight limitation on ordinary activity, III marked limitation on less than ordinary activity, IV symptoms at rest — while the ACC/AHA stages only move forward: A at risk, B structural change without symptoms, C symptomatic heart failure, D advanced or refractory disease.
Left-sided failure is a lung picture of exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, bibasal crackles, an S3 gallop and pink frothy sputum; right-sided failure is a systemic picture of raised jugular venous pressure, tender hepatomegaly with hepatojugular reflux, ascites and dependent pitting oedema, and the commonest cause of right heart failure is left heart failure.
Natriuretic peptides rule the diagnosis out more reliably than in: in the acute setting a BNP under 100 pg/mL or an NT-proBNP under 300 pg/mL makes untreated heart failure very unlikely, while levels rise with age, atrial fibrillation and renal impairment and are lower than expected in obesity.
Four drug classes together are the pillars of HFrEF treatment, each started low and uptitrated: an ARNI (sacubitril/valsartan) or an ACE inhibitor or ARB, a beta-blocker proven in heart failure (carvedilol, bisoprolol or metoprolol succinate), a mineralocorticoid receptor antagonist (spironolactone or eplerenone) and an SGLT2 inhibitor (dapagliflozin or empagliflozin); diuretics relieve congestion but do not prolong life.
The sequencing rules are examined often: a beta-blocker is started only when the patient is euvolaemic and never during acute decompensation, a switch from an ACE inhibitor to sacubitril/valsartan needs a 36-hour washout because of angio-oedema risk, and potassium and creatinine are checked 1 to 2 weeks after starting or increasing an ACE inhibitor or an MRA, with a creatinine rise of up to about 30% accepted.
Devices: an implantable cardioverter-defibrillator for an ejection fraction of 35% or less in NYHA class II to III after at least 3 months of optimal drug therapy and at least 40 days after a myocardial infarction, and cardiac resynchronisation therapy when the ejection fraction is 35% or less in sinus rhythm with left bundle branch block and a QRS of 150 ms or more.
Self-monitoring taught before discharge: weigh at the same time each morning after voiding, before breakfast and in the same clothing, and report a gain of 2 kg or more in 3 days or about 2.5 kg in a week, because that is retained fluid and it appears days before the breathlessness.
Sodium is restricted to about 2 g a day, which is roughly 5 g of salt, fluid to 1.5 to 2 litres a day in advanced disease or hyponatraemia, alcohol and tobacco are stopped, and influenza and pneumococcal immunisation are given; NSAIDs, pioglitazone and most non-dihydropyridine calcium channel blockers are avoided because they worsen failure.
Digoxin reduces hospitalisation without prolonging life, the serum level aimed at in heart failure is low at about 0.5 to 0.9 ng/mL, and hypokalaemia, hypomagnesaemia and renal impairment precipitate toxicity, which shows as nausea, confusion, yellow-green visual haloes and bradyarrhythmia.

Acute coronary syndrome — MONA

Acute coronary syndrome covers the three presentations of a suddenly unstable coronary plaque — unstable angina, non-ST-elevation myocardial infarction and ST-elevation myocardial infarction — separated from one another by the electrocardiogram and the troponin. MONA (morphine, oxygen, nitrates, aspirin) is the ward mnemonic for the first drugs, but only the aspirin has a proven mortality benefit and the other three are now conditional, so the mnemonic is a checklist to think through rather than a set of orders to carry out.

Aspirin 162 to 325 mg, chewed rather than swallowed whole and never enteric-coated, is the one component of MONA that saves lives, and it is given at first contact unless there is a true allergy or active bleeding.
Oxygen is given only when the saturation is below 90% or the patient is in respiratory distress, because routine oxygen in a normoxic patient increases infarct size.
Nitroglycerin relieves pain and preload but is withheld in inferior infarction with right ventricular involvement, in hypotension with a systolic below 90 mmHg, in severe aortic stenosis, in marked bradycardia or tachycardia, and within 24 hours of sildenafil or 48 hours of tadalafil.
Morphine is reserved for pain that persists after nitrates, since it slows gastric emptying and delays absorption of oral P2Y12 inhibitors, and it is avoided in right ventricular infarction where preload must be preserved.
The 12-lead ECG must be recorded and shown to a doctor within 10 minutes of arrival, which is the single most time-critical nursing action in chest pain; ST elevation of 1 mm or more in two contiguous limb leads, 2 mm in V2 to V3 in men or 1.5 mm in women, or a new left bundle branch block with typical pain, defines a STEMI.
Territories: II, III and aVF is inferior and usually the right coronary artery, so right-sided leads including V4R are recorded because a large minority have right ventricular involvement; V1 to V4 is anterior (left anterior descending); I, aVL, V5 and V6 is lateral (circumflex); and tall R waves with ST depression in V1 to V2 is a posterior infarct needing leads V7 to V9.
Reperfusion timing decides the outcome in STEMI: primary PCI with a first-medical-contact-to-device time of 90 minutes or less at a PCI-capable hospital and 120 minutes or less when transfer is required, and where that is impossible, fibrinolysis within 30 minutes of arrival and within 12 hours of symptom onset, followed by transfer for angiography.
Beyond MONA the initial package is dual antiplatelet therapy (aspirin plus a loading dose of ticagrelor 180 mg or clopidogrel 300 to 600 mg), an anticoagulant such as unfractionated heparin or enoxaparin, a high-intensity statin such as atorvastatin 80 mg, and a beta-blocker within 24 hours provided there is no heart failure, low-output state, heart block or bronchospasm.
High-sensitivity cardiac troponin rises within 3 to 4 hours, peaks at about 24 hours and stays elevated for 7 to 14 days, so a rise-and-fall pattern on serial samples defines infarction, while CK-MB, which returns to normal within 48 to 72 hours, is the marker used to detect reinfarction.
Absolute contraindications to fibrinolysis that the nurse checks before the drug is drawn up: any previous intracranial haemorrhage, ischaemic stroke within 3 months, a known cerebral vascular malformation or intracranial tumour, suspected aortic dissection, active bleeding, and significant closed head or facial trauma within 3 months.
Ventricular fibrillation is commonest in the first hour after infarction, so continuous ECG monitoring with a defibrillator at the bedside is standard, and two wide-bore cannulae are secured before any thrombolytic is started.

Peripheral arterial disease

Peripheral arterial disease is atherosclerotic narrowing or occlusion of the arteries supplying the limbs, almost always the legs, so that blood flow meets resting demand but fails as soon as the muscle works. It presents as intermittent claudication — a cramping muscle pain that appears after a reproducible walking distance and settles within minutes of standing still — and progresses through ischaemic rest pain to ulceration and gangrene. It matters twice over: the limb is at risk, but the patient is far more likely to die of myocardial infarction or stroke, because peripheral arterial disease is a marker of atherosclerosis everywhere else.

The ankle-brachial index is the bedside test: the higher ankle systolic pressure (dorsalis pedis or posterior tibial) divided by the higher of the two brachial systolic pressures. Normal is 1.00 to 1.40, borderline is 0.91 to 0.99, 0.90 or less is diagnostic of peripheral arterial disease and 0.40 or less is severe disease.
An index above 1.40 is not reassurance but a warning of incompressible calcified vessels, typical of long-standing diabetes and chronic kidney disease, and the assessment is then repeated as a toe-brachial index, which is abnormal below 0.70, or with Doppler waveform analysis.
The site of the pain localises the block: buttock and hip claudication with absent femoral pulses and erectile dysfunction is aortoiliac disease (Leriche syndrome), thigh pain is common femoral, calf pain is superficial femoral or popliteal and is the commonest of all, and foot pain is tibial or peroneal disease.
Fontaine staging runs I asymptomatic, IIa claudication after more than 200 m, IIb claudication within 200 m, III ischaemic rest pain and IV ulceration or gangrene; rest pain that wakes the patient at night and is relieved by hanging the leg out of bed is stage III and means the limb is threatened.
Chronic limb-threatening ischaemia — rest pain for more than 2 weeks, an ischaemic ulcer or gangrene — is the term that replaced critical limb ischaemia, and it is a same-week vascular referral rather than an outpatient review.
Acute limb ischaemia is the emergency, recognised by the 6 Ps of pain, pallor, pulselessness, perishing cold, paraesthesia and paralysis; paraesthesia and paralysis are the two that mark a threatened limb, and irreversible muscle and nerve injury begins after about 6 hours.
The arterial ulcer is punched-out with a dry pale base, sits on the toes, heel, lateral malleolus or pressure points, is painful with absent pulses and hurts more when the leg is elevated; the venous ulcer sits in the gaiter area near the medial malleolus, is shallow and exudative with granulation, haemosiderin staining and oedema, and is relieved by elevation.
Compression bandaging treats the venous ulcer and can destroy the arterial one, so compression is never applied without an ankle-brachial index, and an index below 0.8 contraindicates full compression; the diabetic neuropathic ulcer is a third pattern again, painless and plantar over a metatarsal head with surrounding callus.
Medical treatment that changes outcome: absolute smoking cessation, a high-intensity statin, an antiplatelet (aspirin 75 to 150 mg or clopidogrel 75 mg daily), tight blood pressure and glycaemic control, and supervised exercise therapy — walking into near-maximal claudication pain for 30 to 45 minutes at least 3 times a week for at least 12 weeks, which lengthens the walking distance more than any drug does.
Cilostazol 100 mg twice daily improves claudication distance but is contraindicated in heart failure of any severity because it is a phosphodiesterase-3 inhibitor; revascularisation by angioplasty or bypass is reserved for lifestyle-limiting claudication that has failed exercise and drug therapy, and for all limb-threatening ischaemia.
Foot care is nursing work that prevents amputation: inspect the feet and between the toes daily with a mirror, never walk barefoot, wash in lukewarm water tested with the elbow or a thermometer, dry between the toes, moisturise the skin but not between the toes, cut nails straight across, never cut corns or use corn caps, check shoes for stones before wearing them, and never use a hot water bottle or heating pad on an insensate foot.
In a young male smoker with distal ischaemia, migratory superficial thrombophlebitis and corkscrew collaterals on angiography the diagnosis is thromboangiitis obliterans (Buerger disease), and complete tobacco cessation is the only treatment that saves the limb.

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