densed CVS, RS, abdo exam \200 Establish likely causes and rule out serious causes \200 Consider IV atropine, 500micrograms, repeat at 2 \200\2233min intervals (max 3mg) Initiate further treatment, including transcutaneous pacing, see following pages Venous access, take bloods: FBC, U+E, LFT, cardiac markers, TFT Consider requesting urgent CXR, portable if too unwell \200 Call for senior help. \200 Reassess, starting with A, B, C \200 Life-threatening causes Complete (3rd degree) heart block ( following MI) \200 M bitz type II \200 Pauses >3s on ECG \200 Hypoxia in children OHFP.indb 256 OHFP.indb 256 30/05/2014 16:18 30/05/2014 16:18 257 BRADYARRHYTHMIA EMERGENCY Assess using the ABCDE approach \200 Give oxygen if appropriate and obtain IV access \200 Monitor ECG, BP, SpO2, record 12-lead ECG \200 Identify and treat reversible causes (eg electrolyte abnormalities) Adverse features? Shock \200 Syncope \200 Myocardial ischaemia \200 Heart failure YES NO Atropine 500 mcg IV YES Satisfactory response? NO Interim measures: \200 Atropine 500 mcg IV repeat to maximum of 3 mg \200 Isoprenaline 5 mcg min \210\2221 IV \200 Adrenaline 2 \200\22310 mcg min \210\2221 IV \200 Alternati ve drugs* OR \200 Transcutaneous pacing Risk of asystole? Recent asystole \200 M bitz II AV block \200 Complete heart block with broad QRS \200 Ventricular pause >3s YES NO Seek expert help Arrange transvenous pacing Observe Alternatives include: \200 Aminophylline \200 Dopamine \200 Glucagon (if beta-blocker or calcium-channel blocker overdose) \200 Glycopyrrolate can be used instead of atropine Fig. 7.7 Adult bradycardia algorithm; 2010 guidelines. Reproduced with the kind permission of the Resuscitation Council (UK). _OHFP.indb 257 _OHFP.indb 257 30/05/2014 16:18 30/05/2014 16:18 258 CHAPTER 7 Cardiovascular Bradyarrhythmias Worrying features systolic BP <90mmHg, HR <40bpm, heart failure, ventricular arrhythmia. Think about sinus bradycardia MI (typically inferior MI) drugs (including digoxin toxicity) , vasovagal, dT4, hypothermia, Cushing \200\231s refl ex (bradycardia and hypertension 2 to iICP), sleep, anorexia nervosa, physical fi tness; complete or 3rd-degree atrioventricul ar (AV) heart block. Ask about dizziness, postural dizziness, fi ts/faints, weight change, visual disturbance, n ausea, vomiting; PMH cardiac disease (IHD/AF), thyroid disease/surgery, DM, head injury or intracranial pathology, glaucoma, eating disorder; DH cardiac medications (B-blockers, Ca2+ antagonists, amiodarone, digoxin), eye drops (B-blockers); SH exercise tolerance. \200 I HD risk factors iBP, icholesterol, FH, smoking, obesity, DM, previous angina/MI. Obs HR, BP, postural BP, RR, sats, temp, GCS. Look for pulse rate/rhythm/volume, pallor, shortness of breath, dGCS, drowsy, iJVP (cannon waves in 3rd-degree AV block), signs of cardiac failure (iJVP, pulmonary oedema, swollen an kles), features of iICP (papilloedema, focal neurology \200\223 b p360). Investigations ECG sinus bradycardia or complete heart block (see Table 7.7 and Fig. 7.8), evidence of ischaemia or infarction (b p572) or of digoxin toxicity (see opposite); blds FB C, U+E, glucose, Ca2+, Mg2+, TFT, cardiac markers, digoxin level, coagulation (if consideri ng pacing-wire); CXR unlikely to be helpful in the immediate setting, but may reveal heart size and evidence of pulmonary oedema; head CT useful if you suspect raised intracranial pr essure, though patient will be in extremis (about to cone, b p338) if iICP causing bradycar dia (speak to on-call neurosur- geon). Treatment \200 Airway, Breathing (with O2) and monitor Circulation \200 If either dGCS or dBP (<90mmHg systolic), 3call senior help/ ARREST TEAM IV cannula and take bloods \200 Consider giving IV atropine if systolic BP <90mmHg (500mi crograms at 2 \200\2233min intervals to a maximum of 3mg) Check ECG to exclude myocardial infarction and to identify heart block or extreme sinus bra dycardia or very slow atrial fi brillation. OHFP.indb 258 OHFP.indb 258 30/05/2014 16:18 30/05/2014 16:18 259 BRADYARRHYTHMIAS Table 7.7 ECG features of bradyarrhythmias and types of heart block Sinus bradycardia 1st-degree AV block M bitz I (Wenkebach) M bitz II P waves precede each QRS, rate <60 P \200\223R interval >5 small squares (>0.2s) P \200\223R interval lengthens from beat to beat, until failure of AV conduction, then patt ern restarts Intermittent P waves fail to conduct to ventricles, but P \200\223R interval d oes not lengthen, unlike M bitz type I; typically 2:1 (P waves:QRS complexes): Ratios of 3 :1 and above are considered high-grade AV block Complete dissociation between P waves and Q RS complexes, which will be broad as a result Down-sloping ST segment (reversed tick), inve rted T waves; often present even when drug is at non-toxic levels No P waves; irregularly i rregular rhythm 3rd-degree AV block Digoxin eff ect/ toxicity Rate controlled AF ECG, lead II (rhythm strip) view; arrows indicate P wave Sinus bradycardia 1st-degree AV block M bitz type I M bitz II with 3:1 AV block 3rd-degree (complete) AV block Digoxin effect/ toxicity Fig. 7.8 Typical appearances of various bradyarrhythmias and types of heart block. _OHFP.indb 259 _OHFP.indb 259 30/05/2014 16:18 30/05/2014 16:18 260 CHAPTER 7 Cardiovascular Sinus bradycardia (OHAM3 b p82) Worrying signs features of heart failure, hypotension, dGCS . Symptoms asymptomatic, dizziness ( on standing), recurrent falls, palpitations, shortnes s of breath, symptoms of iICP, hypothermia or dT4. Signs orthostatic dBP, hypothermia, evid ence of iICP (b p360). Investigations ECG QRS complex will be preceded by a P wave, rate <6 0, QRS will be narrow unless BBB; exclude ischaemia/infarction; blds FBC, U+E, Ca2+, Mg2+, TFT, cardiac markers, coagulation (if considering pacing- wire); CXR unlikely to be helpful in immediate resuscitation phase. Acute treatment if symptomatic (dizzy or GCS <15) or sys tolic <90mmHg, monitor heart rate on defi brillator, lay fl at with legs elevated (as long as iICP not suspected). O2, secure IV access and take bloods. If worrying signs present, 3C all senior help/ARREST TEAM. Titrate 500micro- grams atropine IV every 2 \200\2233min (to a maximum of 3mg) followed by a large fl ush, until HR improves. Identify and correct precip itant. Consider external pacing/pacing-wire via central line (b p534); a rhythmical precord ial thump (percussion pacing) can be used in extremis when an external pacing machine is no t immediately available. Chronic treatment consider 24h tape; frequent symptomatic episodes of bradycardia or pauses are sign of sick sinus syndrome (b p261) and may need a permanent pacemaker (OHCM9 b p126). Complications severe bradycardia and high vagal tone can deterio rate into asystole so prompt treatment is required. Remember to talk con- tinually to the p atient and/or check for a pulse since pulseless electrical activity (PEA) is common and the ECG trace may not change. Vasovagal attacks Sudden refl ex bradycardia from unopposed parasympathetic inhibition upon heart rate is com mon. Often brief loss of consciousness, preceded by eg light- headedness, visual disturbanc e, nausea or sweating. Recovery of consciousness is prompt \200\223 consider other diagnos es if not. Typical precipitants are listed. Fear and pain (including needles) Post-micturition (especially in older men) Nausea and vom iting Dilatation of anal sphincter and cervix (during surgery) Pulling of extra-ocular musc les/pressure on eye (during ophthalmic surgery) iIntra-abdominal pressure (during laparosco pic surgery, straining on the toilet) Drugs which can precipitate bradycardia B-blockers Digoxin Ca2+ antagonists Verapamil and diltiazem slow heart rate Amiodarone A-ag onists Reports of bradycardia even from B-blocking eye drops Rhythm likely to be AF, but may be si nus if reverted Can cause conduction defects and bradycardia Phenylephrine is mainly used by anesthetists a nd can cause refl ex bradycardia by increasing peripheral vascular resistance OHFP.indb 260 OHFP.indb 260 30/05/2014 16:18 30/05/2014 16:18 261 BRADYARRHYTHMIAS Complete (3rd-degree) heart block (OHAM3 b p86) Worrying signs features of heart failure, h ypotension, dGCS. Symptoms asymptomatic, dizziness ( on standing), palpitations, short- ne ss of breath, chest pain. Causes frequently underlying ischaemic damage (typically after inferior MI); also post-card iac surgery, drug-induced (B-blockers, Ca2+channel blockers), amyloid, sarcoid, myeloma, in fective (Chagas, Lyme). Signs dBP (and potentially dGCS), cannon waves in iJVP (due to asyn - chronous contraction of the right atria against a closed tricuspid valve), signs of heart failure, features of underlying disease. Investigations ECG complete dissociation of P waves from QRS com- plexes; narrow QRS implie s proximal lesion (may respond to atropine), broad QRS implies distal lesion (less likely t o respond to atropine); look for evidence of myocardial infarction; blds FBC, U+E, Ca2+, Mg 2+, TFT, cardiac markers, coagulation (if considering pacing-wire); CXR unlikely to be help ful in immediate resuscitation phase. Acute treatment if symptomatic (dizzy or GCS <15) or systolic <90mmHg, monitor heart rate o n defi brillator, lay fl at with legs elevated. O2 supplementation, secure IV access and ta ke bloods. 3Call senior help/ARREST TEAM. Titrate 500micrograms atropine IV every 2 \200 \2233min (to a maximum of 3mg), followed by a large fl ush, until HR improves. Identify and correct precipitant. Consider external pacing/pacing-wire via central line (b p534); a rhy thmical precordial thump (percussion pacing) can be used in extremis when an external pacin g machine is not immediately available. Chronic treatment likely to need permanent pacemaker (OHCM9 b p126) and/or correction of pr ecipitant. Complications severe bradycardia and high vagal tone can deteriorate into asystole so promp t treatment is required. Remember to talk con- tinually to the patient and/or check for a p ulse since pulseless electrical activity (PEA) is common and the ECG trace may not change. Sick sinus syndrome Dysfunction of the sinoatrial node often precipitated by ischaemia/ fi brosis. Results in bradycardia ( arrest), sinoatrial block or SVT with alternating bradyca rdia/asystole (tachy-brady syndrome). Needs pacing if symptomatic. Other types of heart block (OHAM3 b p86) 1st-degree AV block and M bitz I do not require t reatment unless the patient is symptomatic or there is a reversible cause (usually drugs). M bitz II and high-grade AV block may deteriorate into complete heart block and may requir e temporary/permanent pacing, especially when associated with an ACS or general anesthesia \200\223 seek cardiology advice. _OHFP.indb 261 _OHFP.indb 261 30/05/2014 16:18 30/05/2014 16:18 262 CHAPTER 7 Cardiovascular Hypertension emergency Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM If no palpable pulse \200\223 CALL ARREST TEAM If GCS <8 \200\223 CALL anes thetist Airway Breathing Circulation Disability 3Call for senior help early if patient deteriorating. If systolic >200 or diastolic >120: \200 Sit patient up \200 15l/min O2 if SOB or sats <94% \200 Monitor pulse oximeter, B P, defi brillator ECG leads if unwell \200 Request full set of observations and ECG \200 Take brief history if possible/check notes/ask ward staff \200 Examine patient: condens ed RS, CVS, abdo and eye examination \200 Rule out serious causes and establish likely ca uses Review history and previous observations: is hypertension new? \200 Do not give STAT dose of antihypertensive without senior review \200 Initiate further treatment, see b p264 \200 Venous access, take bloods: FBC, U+E, cardiac markers, TFT, glucose, cortisol \200 Consider requesting urgent CXR, po rtable if too unwell \200 Urinalysis and B-hCG (in women of child-bearing age) \200 Cal l for senior help for advice \200 Re-assess, starting with A, B, C \200 Life-threatening causes Pre-eclampsia/eclampsia \200 Malignant hypertension >200/120 \200 Hypertensive encephal opathy Phaeochromocytoma \200 Thyrotoxic storm \200 Cushing \200\231s refl ex (raised ICP). OHFP.indb 262 OHFP.indb 262 30/05/2014 16:18 30/05/2014 16:18 263 HYPERTENSION Hypertension (systolic >140 or diastolic >90) Worrying features altered mental status, seizures, retinal hemorrhages, acute renal failure , chest pain. Is this a hypertensive crisis? If any of above, or acute iBP >200 systolic or >120 diastolic (b p262). Think about life-threatening hypertensive crisis (acute iBP, typically >200 systolic or >12 0 diastolic; b p265), pre-eclampsia; other anxiety, pain, primary (essential) or secondary hypertension (including thyroid storm and phaeochromocytoma). Ask about The majority of pat ients will be asymptomatic, but consider possibility of end organ damage (visual symptoms, headache, chest/back pains, haematuria) or secondary causes (see Table 7.8) PMH pre- vious hypertension, Cushing \200\231s syndrome, acromegaly, Conn \200\231s syndrome, phaeochromoc ytoma, coarctation, thyroid disease, DM, renal artery ste- nosis; DH cardiac and antihypert ensive medications, steroids, contracep- tive pill, levothyroxine/carbimazole, MAOI, antips ychotics, recreational drugs (cocaine, amphetamines); FH hypertension, endocrine disease, p olycystic kidney disease; SH exercise tolerance, smoking. Obs HR, BP (both arms with correc t sized cuff ), sats, temp, GCS, repeat BP after a period of prone relaxation. Look for sig ns of precipitating disease radiofemoral delay, striae, central obesity, large hands/feet/f ace, tremor, exophthalmos, proximal myopathy, gravid uterus, renal bruits/polycystic kidney s; signs of end-organ damage fundoscopy (papilloedema, hypertensive retinopathy), displaced apex beat of S4 (suggest left ventricular hypertrophy), haematuria. Table 7.8 Key secondary causes of hypertension Features Investigations Ref b p373 Urine microscopy, renal Doppler USS, autoantibodies renal biopsy Plasma metanephrines; 24 h urinary catecholamines +VMA TFTs Renal failure, abnormal urine dipstick, FH may be relevant, renal bruit Renal disease or renal artery stenosis b p333 Phaeochromocytoma Sweating, labile hypertension, palpitations Thyroid dysfunction Cold/heat b p334 intolerance, sweating, lack of energy Headache, visual fi eld disturbance, change in facial features Centripetal obesity, skin thinning, weakness b p331 IGF-1 and pituitary hormone levels Acromegaly b p332 Urinary free cortisol; dexamethasone suppression test Cushing \200\231s syndrome Other causes include pregnancy (gestational, pre-eclampsia/eclampsia), Conn \200\231s syndr ome (b p333), hyperparathyroidism (b p389), scleroderma, coarctation of the aorta, drugs (s teroids, MAOI, OCP) and obstructive sleep apnoea. _OHFP.indb 263 _OHFP.indb 263 30/05/2014 16:18 30/05/2014 16:18 264 CHAPTER 7 Cardiovascular Investigations BP ensure correct sized cuff and repeat manually; a new diagnosis of hyperte nsion should be confi rmed with ambulatory or home BP monitoring;1 ECG features of LVH (b p 573); blds FBC, U+E, glucose, cholesterol, TFT; urine blood, protein, B-hCG; CXR unhelpful in immediate setting, but will show heart size and aortic contours. Consider investigations for secondary causes, especially if BP >180/110 (see Table 7.8). Treatment Off er lifestyle advice (smoking cessation, regular exercise, reduce alcohol and caff eine intake, balanced low-salt diet). Identify and treat modifi able risk factors (DM and dyslipidaemia). Recommend pharmacolog- ical therapy if appropriate, based upon BP and r isk factors (see box). Hypertension: Who and How to treat1 Pharmacological therapy for hypertension should be init iated in: \200 All patients with BP >160/100, aiming for BP <140/90 in those aged <80 and BP <150/90 in those aged >80 Patients with type 2 DM, aiming for BP <140/80, or <130/80 if evidence of end-organ damage (microalbuminuria or eGFR<60ml/ min, retinopathy, or history o f TIA/CVA) Patients with type 1 DM, aiming for BP <135/80, or <130/80 if microalbuminuria or retinopathy Patients aged <80 with BP >140/90 and existing evidence of cardiovascular disease or end-organ damage, or a predicted 10yr risk of cardiovascular dise ase >20%, aiming for BP <140/90. Choice of antihypertensive for non-diabetic patients should be guided by Fig. 7.9 and patie nt tolerability. Calcium-channel blockers (or thiazide-type diuretics D, if C not suit- abl e) represent the best fi rst choice drug for most patients. Limited data from younger patie nt groups suggest that ACE-inhibitors or angiotensin receptor blockers (A) have better bloo d pressure lowering eff ects. Fig. 7.9 Treating hypertension. \200 B-blockers are less ef f ective than other classes at reducing cardiovascular events, especially stroke. Their use is as an additive treatment, or to avoid polypharmacy in patients with other indications f or a B-blocker (eg angina) \200 For patients with DM, ACEi are the preferred fi rst-line anti- Age <55 Age >55 or black (C) A C (or D) A & C (or A & D) A & C & D hypertensive agents. Exceptions include patients with type 1 DM without nephropathy (D pref erred) or female patients who may become pregnant (C preferred). Follow-up If treatment initiated or altered in hospital, ensure GP knows what investigation s have been undertaken, their results, and what the therapeutic plan is. Once BP control is acceptable, patients should have annual GP follow-up to review BP, lifestyle and medicatio n. Complications end-organ damage, malignant hypertension. 1 NICE guidelines available at ( cid:27)guidance.nice.org.uk/CG127 Thresholds and targets given in the box are based upon clinic measurements, but note that improved home monitoring equip- m ent availability has led to increased emphasis on diagnosis and monitoring of hypertension in the patient s usual surroundings with slightly lower target values as per guidance. OHFP.indb 264 OHFP.indb 264 30/05/2014 16:18 30/05/2014 16:18 265 HYPERTENSION Hypertensive crises (OHAM3 b p132) Elevation of BP >200/120 is a hypertensive emergency whe n accompanied by evidence of end-organ damage (see Table 7.9) or hypertensive urgency in th e absence of end-organ damage. Symptoms and signs iBP, often acute, in presence of end-orga n damage (see Table 7.9). Table 7.9 End-organ damage in hypertension Investigations Organ Symptoms/signs CT head may show subarachnoid or intracranial hemorrhage; hypertensive encephalopathy occurs with cereb ral oedema following loss of vascular autoregulation Fundoscopy shows retinal hemorrhages papilloedema; often coexists with damage elsewhere dGCS, headache, confusion, vomiting, new motor weakness, seizures, coma Headache, visual di sturbance CNS Eyes Heart Chest pain, orthopnoea ECG changes, elevated cardiac markers. pulmonary oedema on CXR Echo or CT may reveal aortic dissection (b p247) Rapidly worsening renal function; proteinuria, red cell casts on urine microscopy Sudden tearing chest pain radiating to back; collapse Aorta Kidneys Haematuria, lethargy, anorexia Investigations see Table 7.9. Always confi rm blood pressure yourself, using correct sized cuff . Consider secondary causes (see Table 7.8). Request formal ophthalmic assessment if s uspect retinal disease. Diagnosis relies on a compatible history, often with previously com parat ively normal BP, and presence or absence of end-organ damage Acute treatment in the a bsence of end-organ damage, oral therapy with a calcium-channel blocker or ACE-inhibitor sh ould be instigated. If end-organ damage is present, admit patient to a monitored area (HDU/ ICU), with close monitoring of BP, ECG, neurological state, and fl uid balance (consider ar terial line, central line, catheterisation). Rapid reduction in BP can be dan- gerous, resu lting in cerebral hypoperfusion and is only necessary in an acute MI or aortic dissection. Otherwise, aim to reduce diastolic BP to 100mmHg or by 25% (whichever value is higher) over 24h (see Tables 7.10 and 7.11 for treatment options). Patients with early features of end- organ damage may be commenced on oral therapy, though more severe organ damage may require treatment with IV agents. If no evidence of LVF use labetalol; if LVF present commence furo semide (20 \200\22350mg IV) hydralazine. Consider ACEi to counteract high circulating lev els of renin. Nitroprusside and hydralazine are still used as adjuncts in severe crises und er expert guidance. Chronic treatment BP needs checking regularly once discharged from hosp ital. Ensure GP knows what investigations have been undertaken, their results and what the therapeutic plan/target BP is. their results and what the therapeutic plan/target BP is. BP control in acute CVA In acute ischaemic stroke, cerebral autoregulation is impaired and aggressive lowering of BP results in hypoperfusion and poor outcomes. 3Seek expert help. Ge nerally, only treat if BP>220/120 or clear evidence of end-organ damage. Suitable agents in clude IV labetalol. _OHFP.indb 265 _OHFP.indb 265 30/05/2014 16:18 30/05/2014 16:18 266 CHAPTER 7 Cardiovascular Table 7.10 Oral antihypertensives for acute management of hypertensive crises (OHAM3 b p137 ) Drug Dose 50 \200\223100mg/24h PO Many B-blockers available. Contraindicated in asthma, peripher al vascular disease, DM 5 \200\22310mg/24 PO Ca2+ channel blocker; 1st line in elderly and Comment Atenolol Amlodipine when B-blocker contraindicated Hydralazine Nifedipine 25 \200\22350mg/8h PO Vasodilator. Safe in pregnancy 10 \200\22320mg/8h PO Avoid sublingual as rapidly drops BP. OK to use in conjunction with B-blocker (avoid verapamil or diltiazem with B-blockers) Table 7.11 IV antihypertensives for acute management of hypertensive crises (OHAM3 b p136) Patient must be in HDU/ICU, ideally with invasive BP monitoring. Intravenous therapy can re sult in rapid falls in BP so drugs must be titrated cautiously Drug Isoket 0.05%1 (0.5mg/ml) GTN Hydralazine Dose Comment 2 \200\22310ml/h IVI (1 \200\2235mg/h) Venodilates. Useful in LVF/angina. Easy for nurses to set up infusion. Drug of choice Venod ilates. Useful in LVF and angina 1 \200\22310mg/h IVI 5 \200\22310mg/20min IVI Vasodilates, can cause compensatory rise in heart rate; use with a B-blocker Used in eg aortic dissection. Avoid in LVF Labetalol 20 \200\22380mg/ 10min IVI Nitroprusside 0.25 \200\2238micrograms/ Rapid onset. Useful in LVF or hypertensive encephalopathy. Rarely used now: toxic cyanide m etabolites may accumulate causing sweating, iHR, iRR, and dpH kg/min IVI 1 Isosorbide dinitrate: available as 25ml 0.1% solution (25mg in 25ml). OHFP.indb 266 OHFP.indb 266 30/05/2014 16:18 30/05/2014 16:18 267 HEART FAILURE Heart failure 1 Failure of the heart as a pump leads to well-recognized signs and symp- tom s with signifi cant morbidity and mortality; rapidly growing prevalence. Symptoms shortness of breath, orthopnoea, PND, dexercise tolerance, wheeze, ankle swelling, anorexia, nocturi a. Causes multiple factors may combine to reduce cardiac contractility and fi lling effi ci ency: ischaemia (post-MI), cardiomyopathy, dysrhythmia (eg AF), hypertension, valvular dysf unction, infections (eg HIV), infi ltra- tive disease (eg amyloid, sarcoid), chemotherapy; also consider excess demands (eg hyperthyroidism, Paget s disease). Signs cachexia, iRR, iH R, iJVP, displaced apex beat, ventricular heave, cardiac murmur (if valvular disease), 3rd heart sound, bibasilar crepitations, dependent oedema (typically ankles but check sacrum if bed-bound). Investigations ECG no specifi c features but check for dysrhythmias or con- du ction blocks; blds FBC (exclude anemia), U+E (?renal hypoperfusion), TFTs, fasting lipids a nd glucose, BNP (secreted by the failing ventricle \200\223 normal levels unlikely in untr eated heart failure); CXR cardiomegaly, pulmo- nary oedema, pleural eff usions, upper lobe diversion, Kerley B lines; echo will show valvular pathology, wall motion abnormalities and estimate left ventricular ejection fraction (LVEF). Heart failure with preserved LVEF (see box) may show evidence of ventricular hypertrophy and altered fi lling by Doppler fl ow ac ross mitral valve. Acute treatment of pulmonary oedema in acute decompensation (b p282). Ch ronic treatment Support smoking cessation and a graded exercise pro- gramme. In failure wit h reduced LVEF, ACEi and B-blockers2 both reduce mortality and morbidity and should be fi r st-line therapy; if intolerant of ACEi, try ARB. 2nd-line options include cautious addition of an aldos- terone antagonist, or combination hydralazine/nitrate (especially in those of African or Caribbean origin). Loop diuretics are useful for symptomatic management (with c autious addition of a thiazide if resistant). Consider aspirin statin if ischaemic heart disease. Those refractory to medical therapy with LVEF \211 35% and QRS prolongation may b enefi t from cardiac resychronisation therapy with a biventricular pacemaker. resychronisat ion therapy with a biventricular pacemaker. Heart failure with preserved ejection fraction Much understanding in heart failure comes fr om the study of patients with clear echocardiographic evidence of inadequate left ventricul ar contraction. However, the signs and symptoms of heart failure frequently manifest in tho se with preserved LVEF . Many of these patients will have raised left ven- tricular fi lli ng pressures with ventricular stiff ening, reducing fi lling effi ciency in diastole. This population is more likely to be older, female and hypertensive (a demographic rapidly incre asing in size) but poorly represented in clinical trials. Despite good theoretical backing, little or no evidence of mortality benefi t exists for ACEi, ARBs, B-blockers, or calcium channel blockers, whilst diuretics should be used with caution (since acute reductions in f i lling pressures may worsen failure). Management should involve close attention to cor- re ction of dysrhythmias and comorbid conditions, as well as control of blood pressure, and ca reful fl uid balance. 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG108 2 Avoid B-blockers in COP D. Few B-blockers are licensed for heart failure (eg bisoprolol, carve- dilol, and nebivolo l): Patients already on a B-blocker for another indication may need to switch. _OHFP.indb 267 _OHFP.indb 267 30/05/2014 16:18 30/05/2014 16:18 This page intentionally left blank Chapter 8 Respiratory 269 Breathlessness and low sats emergency 270 Breathlessness and low sats 271 Stridor in a cons cious adult patient 284 Cough 285 _OHFP.indb 269 _OHFP.indb 269 30/05/2014 16:18 30/05/2014 16:18 270 CHAPTER 8 Respiratory y Breathlessness and low sats emergency g Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM Airway Breathing Circulation If no palpable pulse \200\223 CALL ARREST TEAM 3Call for senior help early if patient deteriorating. \200 Sit patient up \200 15l/min O2 in all patients if acutely unwell \200 Monitor pulse oximeter, BP, defi brillator \200 \231s ECG leads if unwell \200 Obtain a full set of observations including temp \200 Ta ke brief history if possible/check notes/ask ward staff \200 Examine patient: condensed R S, CVS, abdo exam \200 Establish likely causes and rule out serious causes \200 Init iate further treatment, see b p271 \200 Venous access, take bloods: FBC, U+E, LFT, CRP, bld cultures, D-dimer, cardiac markers Arterial blood gas, but don \200\231t leave the patient alone \200 ECG to exclude arrhyth mias and acute MI \200 Request urgent CXR, portable if too unwell \200 Call for senior help \200 Reassess, starting with A, B, C \200 \200 In COPD/known CO2 retention, rapi dly titrate down O2 to lowest fl ow to maintain normal sats for this patient (usually 88 \200\22392%). Beware of CO2 retention and have a low threshold for repeat ABG. Life-threatening causes Asthma/COPD \200 Pulmonary oedema (LVF) \200 (Tension) pneumothorax \200 MI/arrhythmi a Pneumonia \200 Pulmonary embolism (PE) \200 Pleural eff usion \200 Anaphylaxis/airway obstruction OHFP.indb 270 OHFP.indb 270 30/05/2014 16:18 30/05/2014 16:18 271 BREATHLESSNESS AND LOW SATS Breathlessness and low sats Worrying features RR >30, sats <92%, systolic <100mmHg, chest p ain, confusion, inability to complete sentences, exhaustion, tachy/bradycardia. Think about life-threatening see Table 8.1 b p272; most likely COPD/ asthma, pneumonia, pul monary oedema (LVF), PE, MI; other pneumo- thorax, pleural eff usion, arrhythmia, acute res piratory distress syndrome (ARDS), sepsis, metabolic acidosis, anemia, pain, panic, foreign body/aspi- ration; chronic COPD, lung cancer, bronchiectasis, fi brosing alveolitis, TB. A sk about speed of onset, cough, sputum (quantity, color), haemoptysis, chest pain (related to movement, pleuritic), chest trauma, palpitations, dizzi- ness, diffi culty lying fl at, recent travel, weight loss; PMH cardiac or respira- tory problems, malignancy, TB; DH inhal ers, home nebulisers, home O2, cardiac medication, allergies; SH smoking, pets, exercise to lerance, previous and current occupation. \200 PE risk factors recent surgery/immobility/ fracture/travel, estrogen (pregnancy, HRT, the pill), malignancy, previous PE/DVT, thrombophilia, varicose v eins, obesity, central lines. Obs temp, RR (11 \200\22320 is normal), BP, HR, sats (should be >94%1), O2 requirements (im proving or worsening?). Look for ability to speak full sentences, confusion, cyanosis, CO2 tremor, clubbing, rashes, itching, swollen lips/eyes, raised JVP, tracheal shift and tug, u se of accessory muscles, abnormal percussion, unequal air entry, crackles, stridor, wheeze, bronchial breathing, swollen/red/hot/ tender legs, swelling of ankles, cold peripheries. I nvestigations PEFR if asthma suspected (may be too ill); blds FBC, U+E, LFT, CRP, D-dimer ( if PE suspected), cardiac markers, blood cultures; sputum (may need physio or saline nebs t o help) inspect and send for M,C+S; AFBs if TB risk; ABG (b p584), keep on O2 if acutely SO B; ECG (b p572); CXR (b p582); portable if unwell, though image quality may be poor; spirom etry should be done once the patient has been stabilized to help confi rm the diagnosis (b p586). Treatment Sit all patients up and give 15l/min O2 \200\223 this saves lives. This c an be reduced later since CO2 retention in COPD takes a while to develop. Check sats and EC G in all patients: \200 Stridor \200\223 call an anesthetist (b p284) \200 Wheeze \200\223 give nebuliser (b p273) eg salbutamol 5mg ipratropium 500micrograms STAT (drive by oxygen or air as appropriate) Unilateral resonance, reduced air entry tracheal deviation and shock \200\223 consider t ension pneumothorax and treat urgently (b p279) Asymmetrical crackles, dair entry \200\223 consider pneumonia (b p276) \200 Symmetrical crackles, dair entry, iJVP \200\223 consider LVF (b p282) \200 Normal examination \200 \223 consider PE, cardiac and systemic causes. 1 Patients with chronic lung disease may normally have sats <92%. 88 \200\22392% is a bette r target. See BTS guidelines on emergency use of oxygen in adults at (cid:27)www.brit-thora cic.org.uk _OHFP.indb 271 _OHFP.indb 271 30/05/2014 16:18 30/05/2014 16:18 272 CHAPTER 8 Respiratory Table 8.1 Common causes of breathlessness History Examination Investigations COPD Known respiratory problems, usually smoker, productive cough worse than usual Known asthma, recent exposure to cold air, allergens or drugs (NSAIDS, B-blockers) wheeze/crackles, cyanosed/pursed- lip breathing, look for infection and pneumothorax Wh eeze crackles, look for signs of infection or pneumothorax CXR hyperexpanded, fl at diaphragms; exclude pneumonia and pneumothorax dPEFR; CXR; exclude pneumonia and pneumothorax Asthma iWCC/N \230/CRP, consolidation or blunted angles on CXR (b p582) dPaCO2 hypoxia on ABGs, iD-dimer, CXR often normal Cardiomegaly + fl uid overload on CXR (b p582), ECG may show isc haemia or previous MI Needle decompression of tension pneumothorax; CXR shows pleura separa ted from ribs Eff usion on CXR Pneumonia Productive cough, Febrile, asymmetrical air entry, crackles, bronchial breath sounds dpercussion iJVP, iHR (may be only sign); may have evidence of DVT; can be severely shocked iJVP, symmetrical fi ne crackles, pink frothy sputum, dependent oedema, cold peripheries green sputum, feels unwell pleuritic pain PE risk factors, leg pain, pleuritic chest pain and haemoptysis Known cardiac problems, orthopnoea, swollen legs Pulmonary embolism Pulmonary oedema Pneumo- thorax Sudden onset pleuritic chest pain trauma. Underlying lung disease and previous episodes o r tall, thin, male Gradual onset breathlessness, pleuritic chest pain Concurrent severe i llness Chest pain, palpitations, dizziness, tiredness Sudden onset, itching, swelling, urti carial rash, new drugs/food Unequal air entry and expansion, hyperresonant displaced trachea (late) Pleural eff usion Reduced expansion, stony dull base ARDS Hypoxic New bilateral infi ltrates on CXR Abnormal ECG (b p572), dHb, icardiac markers IM adrenalin e, IV steroids (b p470); acute and convalescent serum tryptase Anemia/ MI/ arrhythmias 3 Anaphylaxis Irregular or fast pulse, shocked, pale Stridor, wheeze, shock, swollen lips and eyes, blanching rash OHFP.indb 272 OHFP.indb 272 30/05/2014 16:18 30/05/2014 16:18 273 BREATHLESSNESS AND LOW SATS Asthma1 (OHAM3 b p178) Common, chronic infl ammatory airway disorder characterized by airwa y hypersensitivity resulting in episodic obstruction, wheeze and dyspnoea. Symptoms episodi c breathlessness, dyspnoea and wheeze, night or morning cough, excess sputum; triggers may include exercise, NSAIDs, B-blockers, allergens, cold; family or personal Hx of atopy (hayf ever, eczema, asthma). Signs wheeze, prolonged expiration, tachypnoea, hyperinfl ated chest . Investigations PEFR reduced in acute setting compared with best or pre- dicted based upon age/height,1 or diurnal variation on self-monitoring as out-patient; ABG normal or dPaO2 w ith a dPaCO2 due to hyperventilation 3beware normal/rising CO2 ?Pt tiring; CXR hyperexpande d, exclude pneumonia and pneumothorax; spirometry dFEV1, dFEV1:FVC ratio. Acute exacerbatio n sit up and give 15l/min O2. Salbutamol 5mg NEB ipratropium 500micrograms NEB and predni solone 40mg PO (or hydrocortisone 200mg IV). Drive the nebuliser mask from O2 supply, not a ir. Repeat salbutamol 2.5mg nebs every 10 \200\22315min and reassess PEFR and sats frequent ly. Antibiotics if evidence of infection. 3Severe 3Life- threatening Incomplete sentences, PEFR <50% of best, HR >110, RR >25 PEFR <33% of best, silent chest, s ats <92%, PaO2 <8kPa, normal PaCO2, poor respiratory eff ort, exhaustion, cyanosis, altered GCS, arrhythmia CO2 retention \200\223 call ICU 3Near-fatal Beware those with previous ICU admissions \200 No improvement Call for senior help. Consi der: ICU input/assessment \200 Aminophylline 5mg/kg IV bolus over 20min unless the patient is on oral aminophylline or theophylline \200 Mg2+ sulfate 2g (8mmol) IV over 20min Improving admit those in whom PEFR<75% predicted after 1h therapy; gradually reduce supplemental O2 and step from nebs back to inhalers over several days; always check inhaler technique and ensure follow-up plan in place before discharge. Chronic treatment (OHCM9 b p174) Stepwise management (see Table 8.2) aiming for minimum tre atment resulting in symptom control; monitor PEFR; always check inhaler technique before es calation; consider allergen testing; smoking cessation; oral steroids for exacerbations. Table 8.2 Simpli \201 ed stepwise management of asthma1 Oral steroids (cid:57) High-dose steroid inhaler Long-acting B-agonist Low-dose steroid inhaler (cid:57) (cid:57) (cid:57) (cid:57) (cid:57) (cid:57) (cid:57) (cid:57) Salbutamol/terbutaline (cid:57) (cid:57) Step 1 Step 2 Step 3* Step 4 Step 5 (cid:57) (cid:57) (cid:57) (cid:57) Either low-dose steroid inhaler and long-acting B-agonist or high-dose steroid inhaler. 1 B TS Asthma guidelines available at (cid:27)www.brit-thoracic.org.uk/guidelines/asthma-guidel ines. aspx These include tables to predict PEFR where not known. _OHFP.indb 273 _OHFP.indb 273 30/05/2014 16:18 30/05/2014 16:18 274 CHAPTER 8 Respiratory COPD1 (OHAM3 b p186) Relatively fi xed airfl ow obstruction due to loss of elastic recoil i n alveoli (emphysema) and narrowing of airways with excess secretions (bronchitis) Worrying signs dGCS, rising CO2. Symptoms breathlessness, cough, isputum, tight chest, confusion, d exercise tolerance. NB dindex of suspicion in (ex-)smoker. Signs wheeze, cyanosis, barrel-c hested, poor expansion, tachypnoea. Investigations ABG often deranged in COPD, compare with previous samples and pay close attention to FiO2; repeat after 30min in seriously ill pati ents; CXR hyperexpanded, fl at diaphragm (look for evidence of infection, pneumothorax or b ullae); spirometry (see b p586) dFEV1, dFEV1:FVC ratio (<70%). Acute exacerbation sit the p atient up and give the minimum amount of O2 to maintain sats \211 88% (aim for PaO2 78kPa) . Give salbutamol 5mg ipra- tropium 500micrograms nebs (drive by air, leaving nasal O2 ca nnulae on under mask if necessary) and prednisolone 30mg PO (or hydrocortisone 200mg IV). S putum for M,C+S. Get an ABG and CXR (portable if unwell). Use ABG results and clinical obse rvations to guide further management: \200 Normal ABG (for them) continue current O2 and give regular nebs \200 Worsening hypoxaemia iFiO2, repeat ABG <30min, watch for confusion which should prompt a repeat ABG sooner; consider NIV (see box) iCO2 retention or dGCS request senior help urgently; consider: ICU input/assessment \200 aminophylline 5mg/kg IV bolus over 20min unless the patient is on oral aminophylline or theophylline NIV (see box). Antibiotics consider prescribing antibiotics (eg doxycycline 200mg PO loading then 100mg/24 h PO or amoxicillin 500mg/8h PO) if the patient has increased SOB, fevers, worsening cough, purulent sputum, or focal changes on CXR. Chronic treatment (OHCM9 b p176) Smoking cessati on and graded exer- cise are vital. Stepwise therapy with inhalers (see Table 8.3) is based upon inhaled short-acting B-agonist or anti-cholinergic, then inhaled long-acting agents, then adding inhaled steroid before oral theophylline. If still breathless despite maximal i nhaler therapy give home nebulisers. If PaO2 consistently \211 7.3kPa (or \211 8kPa with additional risk factors) long-term O2 therapy aiming for a minimum of 15h/d confers surviva l advantage. Complications exacerbations, infection, cor pulmonale, pneumothorax, respirato ry failure, lung cancer (beware haemoptysis and weight loss). respiratory failure, lung can cer (beware haemoptysis and weight loss). Non-invasive ventilation (NIV) These are machines that assist ventilation through a tightly fi tting mask rather than tracheal intubation. Bi-level positive airway pressure (BiPAP) u sed in COPD patients with a pH \211 7.35 and CO2 \211 6.0kPa who have failed to respond t o initial medical therapy reduces mortality and length of admission. Patients who need NIV are usually allocated specialist beds on the respiratory ward or on HDU/ICU. Continuous pos itive airway pressure (CPAP) is not a type of NIV since it does not help with the mechanics of ventilation (b p282).