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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
Chapter8
Cardiovascular
2Chest pain emergency 254
Chest pain 255
2Tachyarrhythmia emergency 262
Tachyarrhythmias 264
2Bradyarrhythmia emergency 270
Bradyarrhythmias 272
2Hypertension emergency 276
Hypertension 278
Heart failure 282
253
254 CHAPTER8 Cardiovascular
2Chest pain emergency
2 Airway
2 Breathing
2 Circulation
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort— CALL ARREST TEAM
If no palpable pulse— CALL ARREST TEAM
3Call for senior help early if patient unwell or deteriorating.
•
Sit patientup
• 5L/ min O2 if SOB or sats<94%
•
Monitor pulse oximeter, BP, debrillator ECG leads ifunwell
• Obtain a full set of
• Take brief
•
Examine patient:condensed CVS, RS, abdoexam
• Establish
•
•
likely causes and rule out serious causes:
•
consider percutaneous coronary intervention (PCI) (Epp. 564–5)
•
consider giving aspirin 300mg POSTAT
•
consider needle decompression (Ep. 293)
Initiate further treatment, including analgesia, see following sections
Venous access, take bloods:
•
FBC, U+E, LFT, CRP, glucose, troponin, D- dimer, lactate
observations including BP in both arms andECG
history if possible/ check notes/ ask wardsta
• Request urgent CXR, portable if toounwell
• Call for
senior help if no improvement or worsening
• Call cardiology if suspected acute cardiac event
• Repeat ECG after 20min if no improvement
•
Reassess, starting with A, B, C. . .
2Life- threatening causes
• (Tension) pneumothorax
• Acute coronary syndrome
• Pericardial eusion/ cardiac tamponade
• Aortic dissection
• Pulmonary embolism
• Sickle- cell crisis.
Chestpain
2Worrying features idHR, idBP, iRR, dGCS, collapse, sudden-
onset/ ongoing pain, arm, jaw, or back pain, sweating, nausea, vomiting,
radio- radial/ femoral delay, neurology, pregnancy, ECG changes.
Think about Common Acute coronary syndromes, pulmonary embolism,
musculoskeletal, pneumonia, pneumothorax (tension or simple), myocarditis, pericarditis, reux, peptic ulcer disease;
cardiac tamponade, sickle- cell crisis, Takotsubo cardiomyopathy (Table8.).
Ask aboutSite of onset, radiation, quality (heavy, aching, sharp, tearing),
intensity (scale of – 0), time of onset, duration, associated symptoms
(sweating, nausea, palpitations, breathless, cough, fever), exacerbating/
relieving factors (breathing, position, exertion, eating), recent trauma/
exertion/ stress, similarity to previous pain;
issues, DM, GORD, icholesterol;
antacids;
FHIHD, early cardiacdeath; SHSmoking, exercise tolerance.
Risk factors
IHD iBP, ichol, FH, smoker, iBMI, DM, prevIHD, Asian/African ethnicity.
PE/ DVT Previous PE/ DVT, immobility, ioestrogens, recent surgery, FH,
pregnancy, hypercoagulable states, smoking, long- distance travel.
GIKnown GORD (E p. 308), known peptic ulcer, alcoholbinge.
ObsHR, BP (both arms), RR, sats, temp, GCS, pain, cardiac monitor.
Look for Sweating, pallor, dyspnoea, cyanosis, pulse rate/ rhythm/
volume, cool peripheries, clammy, iJVP, mediastinal shift, tracheal tug, chest
wall tenderness, asymmetric chest expansion/ percussion/ breath sounds,
crepitations, pericardial rub, heart murmurs, calf pain/ swelling/ erythema.
Investigations ECG(E p. 556, pp. 600–9 for procedure/ interpret-
ation.);
BloodsVBG, FBC, U+E, LFT, D- dimer, troponin, lactate; ABGTaken
on O
if patient acutely unwell (E pp. 550–1, pp. 612–13 for procedure/
2
interpretation);
CXRIf you suspect a tension pneumothorax clinically per-
form immediate needle decompression (E p. 293), otherwise request a
portable CXR if the patient is severely ill (poorer image quality) or standard
CXR (E pp. 610–11 for interpretation);
PE, acute MI, or aortic dissection;
CTTo rule out PE or aortic dissection.
TreatmentMonitoring, escalation, and re-review. 5L/ min O
or sats <94%. Consider IV opioids (and an antiemetic) if pain is severe.
Diagnoses toexcludeIf you are unable to conrm a diagnosis im-
mediately, consider life- threatening causes and investigate until excluded:
Cardiac ischaemia Abnormal ECG, typical history, itroponin(s), echo.
PE dsats, abnormal ECG, clinical risk (E p. 292), iD- dimer,CTPA.
PneumothoraxMediastinal shift, dbreath sounds, reviewCXR.
Aortic dissectionTypical history, evidence of shock, left and right systolic
BP dier by >5mmHg, CXR mediastinal widening, abnormal CT/ echo.
Contact medical/cardiology registrar on- call for advice if unsure.
Uncommon Aortic dissection,
DH Cardiac/ respiratory medications,
PMH Cardiac/ respiratory
Bedside echoFor suspected large
if SOB
2
255CHESTPAIN
256 CHAPTER8 Cardiovascular
Table8. Common causes of chest pain
History Examination Investigations
Sudden- onset pain/
ACS
3
(STEMI)
3
(NSTEMI)
3
(unstable
angina)
Angina
(stable)
Myocarditis/
pericarditis
3
dissection
Pulmonary
embolism
Pneumothorax
Pneumonia Productive cough,
Musculoskeletal chest
pain
Reux or
spasm
ACS
ACS
Aortic
tightness, radiating
to left arm/ jaw,
>5min, SOB,
sweating, nausea
Sudden- onset
pain or tightness,
radiating to left
arm/ jaw, >5min,
breathlessness,
sweating, nausea
Anginal pain at rest
or with ifrequency/
severity/ duration,
>5min
Exertional pain
or tightness,
radiating to left
arm/ jaw, <5min,
breathlessness, dby
rest/ GTN
Recent viral illness,
pleurisy, ion lying,
dsitting forward
Severe tearing
interscapular pain,
breathlessness,
neurological ndings
Breathlessness, PE
risk factors (E
p. 292), pleurisy,
collapse
Sudden- onset
pleurisy ±trauma;
tall and slim patient;
COPD, smoker
pleurisy, feels unwell
Mechanical, may be
pleuritic, worse on
palpation/ movement
Previous indigestion,
reux, known hiatus
hernia, dby antacids
Unwell, dyspnoea,
±arrhythmia,
pale, clammy,
sweaty
Unwell, dyspnoea,
±arrhythmia,
pale, clammy,
sweaty,
non- tender chest
wall
Unwell, dyspnoea,
±arrhythmia, pale,
clammy, nontender chest wall
Dyspnoea,
tachycardia,
non- tender, may
be normal after
pain resolves
Pericardial rub,
otherwise normal
CVS and RS exam
iHR, dBP,
dierence in
brachial pulses
and pressures,
iRR, neurology
Often normal,
swollen/ red
leg, tachycardia,
dyspnoea, dBP
Mediastinal
shift, unequal air
entry/ expansion,
hyper- resonance
Febrile, coarse
creps, dullness to
percussion
Tender, normal RS
exam
UGI tenderness,
normal CVS and
RS examinations
ST elevation/ new
LBBB, itroponin(s).
Troponin(s) are not
needed to make the
diagnosis of STEMI
ST depression, T- wave
inversion, Q waves,
ECG can be normal,
itrop, echo may show
regional wall motion
abnormalities
ST depression, T- wave
inversion, ECG can be
normal, troponin not
elevated
Transient ECG changes,
troponin not elevated,
+ve cardiac stress
test, +ve CT/ invasive
coronary angiogram,
responds to anti anginals
Saddle- shaped STE
on most ECG leads,
iCRP/ ESR, itroponin if
myocardial involvement,
echo, cardiac MRI
Widened mediastinum
on CXR, iD-dimer,
dissection ap/ aortic
dilation on echo/ CTA
ABG:PaO
clear CXR, iD- dimer,
sinus tachy, S
new RBBB, thrombus/
dilated/dysfunctional RV
on echo, CTPA
Pleura separated from
ribs on CXR, other
investigations often
normal, CT if unclear
iWCC/ iNØ/ iCRP,
consolidation on CXR
(E pp. 610–11)
ECG to exclude cardiac
cause, normal bloods,
normal CXR
ECG to exclude cardiac
cause, normal bloods/
CXR, trial PPI/antacids
n/ d, CO2d,
2
,
Q3T3
3Acute coronary syndromes(ACS)
K ACS is a general term referring to presentations of varying severities
of unstable myocardial ischaemia (Tables8.2 and 8.3). The aim is to allow
a prospective rather than a retrospective diagnosis to be made to improve acute management and patient outcomes (E OHCM11p. 4).
Table8.2 ACS classication inpatients withtypical cardiac- sounding
chest pain lasting>5min
ECG ndings Troponin (3– 2h post pain) Diagnosis
ST elevation Not needed to make a diagnosis,
T- wave inversion/
attening, ST depression,
absence of ST elevation.
ECG may still be normal
but will be i
Troponin T above 99th percentile
of the upper reference limit
Troponin T below 99th percentile
of the upper reference limit
STEMI
(E p. 258)
NSTEMI
(E p. 259)
Unstable angina
(E p. 260)
Table8.3 Interpreting troponin measurements insuspected ACS
Raised troponin can be detected – 2h aftermyocardial necrosis using highsensitivity assays. Consider thefollowing wheninterpreting troponins:
Time
Troponins should not be interpreted in isolation. Use the ‘pre- test
probability’ of acute MI (history, ECG, and echo ndings) both at
course
presentation and over time to help interpret troponin levels
History In patients with cardiac- sounding chest pain, a raised troponin is usually
diagnostic of ACS. Remember that diabetics, the elderly, and females can
present dierently (weakness, confusion, nausea, pain outside the chest)
Levels While cardiac- sounding chest pain and a markedly raised troponin
should be treated as MI until proven otherwise, myocarditis and
Takotsubo cardiomyopathy can also cause both. There are many
causes of moderately raised troponins (see PMH below)
Trend Acute MI causes a sharp rise in troponin over – 2d, falling again over 3– 5d.
The value over time can therefore help determine the cause
PMH Trop is excreted renally and released in times of CV stress (when cardiac
O
demand outstrips supply). It can also ‘leak’ from the myocardium,
2
without cardiac necrosis. Causes of raised trop are critical illness, renal
(AKI, CKD), cardiac (acute MI, heart failure, arrhythmias, myocarditis),
respiratory (hypoxia, PE), anaemia, neurological (ischaemic stroke,
haemorrhage), and trauma (cardiac contusion, DC cardioversion). The
PMH is therefore vital to interpret a troponin level
ECGs In patients who may present dierently (females, elderly, diabetics)
or who cannot provide a history (agitated, comatose, low GCS,
dementia), the ECG and troponin levels become more important.
Inspect serial ECGs for evidence of MI (pathological Q waves),
ischaemia (T- wave inversion/ attening, ST depression), and coronary
instability (T- wave normalization/ ipping, changing ST segments)
Echo An echo can show features in keeping with acute MI (loss of viable
myocardium, new regional wall motion abnormalities) and other
diagnoses (eg dissection, PE, cardiomyopathy, Takotsubo)
Bleeding Bleeding risk should be balanced against thrombosis risk in suspected
ACS, especially where there is diagnostic uncertainty. Exclude aortic
dissection and talk to seniors before starting ACS treatment
257CHESTPAIN
258 CHAPTER8 Cardiovascular
Normal Hours Days Weeks Months
3STEMI (ST elevation MI) (E OHCM11 p. 16.)
2Worrying signs Features of LV failure, AV block, cardiac dysrhythmia.
SymptomsCentral, crushing, heavy chest pain/ tightness, ±radiating to left
arm/ jaw, shortness of breath, nausea, sweating, palpitations, anxiety.
Risk factorsSmoking, obesity, DM, iBP, icholesterol, FH, previousIHD.
SignsTachycardia, cool and sweaty (‘clammy’), ±LV failure or hypotension.
Investigations ECG ST elevation (>mm in 2 or more contiguous limb leads
or >2mm in chest leads); later Q waves ±T- wave inversion (Fig. 8.);
CXRCardiomegaly, signs of LV failure; Tro pWill be raised, but treatment is
not withheld as ECG+history are alone sucient and early treatment isvital.
Acute treatment Aim for immediate reperfusion by PCI (angiography with
angioplasty and stenting) within 2h of onset and 2h of rst presentation—
seek senior help. Give O
(60mg; clopidogrel 600mg if already anticoagulated), diamorphine (2.5–
(5L/ min), aspirin (300mg), prasugrel
2
5mg IV), antiemetic (E p. 84), GTN (two pus SL/ 5min until pain
free; infusion if ongoing pain after 3 doses 5min apart and not hypotensive E p. 200). Consider thrombolysis if 2h since onset and PCI
cannot occur within 2h of presentation (E pp. 564–5). β- blockade (eg
bisoprolol 5– 0mg/ PO STAT) reduces infarct size and mortality but
avoid in asthma, hypotension, AV block, acute heart failure, and haemodynamic instability. See Box8..
Secondary prophylaxis drisk factors (smoking, obesity, DM, iBP, ichol), β-
blocker (at least yr, indenite if low EF), statin (indenite), anti platelets
(aspirin indenite, P2Y
MRA (if low EF), anti anginals if required, and consider revascularization.
inhibitor usually for yr), ACEi/ARB (indenite),
2
Complications Dysrhythmias (AV block, bradycardia, VF/ VT), LVF, valve
prolapse, ventricular septal/ free wall rupture, ventricular aneurysm, pericarditis, Dressler’s syndrome (E OHAM4 p. 60), and recurrentpain.
Fig.8. Typical sequential ECG changes following an acuteSTEMI.
Box 8. Care aftermyocardial infarction
• Echo, continuous ECG, and symptom monitoring while in-patient
• Daily 2- lead ECG and thorough clinical examination ofCVS/ RS
• CBG: insulin infusion, HbA
• Thromboembolism prophylaxis (Epp. 428–30)
, and fasting CBG after 4d if >mmol/L
c
• β- blockade and ACEi/ARB unless contraindicated, with uptitration
• High-dose statin (eg atorvastatin 80mg PO OD)
• Discuss modiable risk factors, cardiac rehab, and lifestyle advice
• PCI patients have lower risk of complications and shorter stays; lysis
patients need risk stratication and likely in-patient angiography
• Review in OP clinic to review symptoms, lipids+BP, titrate medications,
and optimize cardiovascular risk (E OHCM11p. 6).
• Ask GP to monitor HbA
NICE guidelines available at Mguidance.nice.org.uk/NG85
(if high CBG), bleeding risk, BP, U&E.
c
3NSTEMI (non- ST elevationMI)
K Diagnosis and intervention often less ‘dramatic’ than STEMI, but yr
survival poorer. High GRACE score, markedly raised troponins, ongoing
cardiac symptoms, dynamic ECG changes, and a large area of aected
myocardium suggest higher risk (Box 8.2); ask cardiology early to identify
patients needing emergency PCI (E OHAM4p. 20).
2
2Worrying signs LV failure, AV block, cardiac dysrhythmia, ongoingpain.
Symptoms, risk factors, and signsOverlap with STEMI; patients are older,
more comorbid, and present more atypically.
Investigations ECG Can be normal or show ST depression, T- wave inver-
sion/attening/ normalization, or complete resolution of changes;
Cardiomegaly, signs of LV failure;
Troponin K Dierentiate from UA by raised
CXR
troponin (Tables8.2 and 8.3); taken according to local protocols, typically on
presentation and 3– 2h after maximum symptomonset.
Echo To assess for
loss of viable myocardium, regional wall motion abnormalities, structural complications of MI, and dierential diagnoses (eg PE, aortic dissection).
Acute treatment O
(clopidogrel 300mg if already anticoagulated), diamorphine (2.5– 5mg IV),
, aspirin (300mg), prasugrel 60mg or ticagrelor 80mg
2
antiemetic (E p. 84), GTN (two pus SL/ 5min until pain free; infusion if
ongoing pain after 3 doses unless low BP E p. 200), anticoagulation (2.5mg
fondaparinux SC unless Cr >265 or for immediate PCI, in which case consider
unfractionated heparin E p. 428). β- blockade (eg bisoprolol 5– 0mg), beware those with asthma, low BP, AV block, or acute LVF. Consider glycoprotein IIb/ IIIa inhibitors and immediate PCI if high risk/ chest pain despite GTN.
Secondary prophylaxis and complications These are broadly the same as in
STEMI, though complications are less common. See Box 8..
K Box 8.2 Risk straticationinACS
Estimation of mortality in ACS allows assessment of the risks and
benets of interventions and targeting of resources to patients who
will benet the most. Many scores have been developed from major
trial data. The Global Registry of Acute Coronary Events (GRACE) algorithms were developed from a large registry (94 hospitals, 4 countries, 22,645 patients) involving patients with all subtypes of ACS
(STEMI, NSTEMI, and UA). Risk scores can be calculated on admission
(to predict in hospital and 6mth mortality) and on discharge (to predict
6mth mortality).
2
Unstable patients Require a cardiology review, CCU bed, immediate
PCI, and consideration of glycoprotein IIb/ IIIa inhibitor infusion.
Intermediate/high GRACE score Require observation to ensure pain free
and clinically stable, cardiology review, and angiography within 72h.
Low GRACE score As for intermediate/high score except in-patient angiog-
raphy can be delayed or performed as an out-patient. The threshold for
in-patient angiography is lower in younger patients.
259CHESTPAIN
2
NICE guidelines available at Mguidance.nice.org.uk/ NG85
260 CHAPTER8 Cardiovascular
3Unstableangina
K Diagnosis based on typical history without raised troponin (E OHAM4 p. 10).
2
Worrying signs Features of LV failure, cardiac dysrhythmia, ongoing chest pain.
Symptoms, risk factors, and signs These overlap with other forms of ACS;
typically episodes of angina occurring on minimal provocation or at rest,
with poor response to GTN; more frequent and more severe than patient’s
‘usual’ angina; few symptoms or signs between episodes ofpain.
Investigations ECG ST depression, T- wave attening/ inversion/ ipping, dynamic
ST/ T- wave changes over time, signs of previousMI;
Troponins Negative.
Acute treatment As for NSTEMI (E p. 259); analgesia (morphine, GTN),
antiplatelet agents (prasugrel or ticagrelor), limit ischaemia (β- blockade),
and disrupt thrombus (fondaparinux). Risk stratify, further management
and secondary prophylaxis as for NSTEMI (Ep. 259).
Stable angina(E OHCM11 p. 2.)
3
K Frequently encountered in primary care, retrosternal chest discomfort
occurring predictably upon exertion and relieved by rest and nitrates.
SymptomsCentral, heavy chest pain (lasting <5min) radiating to left arm
and jaw, precipitated by exertion and relieved by rest or rapidly by GTN
(<5min), shortness of breath, nausea, sweating, palpitations.
Risk factorsCommon for IHD; see ACS (E p. 257); severe aortic stenosis.
SignsTachycardia, cool and sweaty (‘clammy’), pallor. Normal after epi-
sode. See Box8.3.
Investigations ECG Transient ST depression during pain; at or inverted T
waves; signs of previousMI;
NSTEMI);
CT coronary angiogram If rst presentation of typical chest pain or
Troponin Not elevated (if elevated, diagnosis is
atypical symptoms with ECG ndings (ST changes or Q waves);
If positive CTCA or previous CAD (eg myocardial perfusion scan,
testing
SPECT imaging, stress echo, or cardiacMRI);
inconclusive functionaltest.
4
Invasive coronary angiogramIf
Acute treatment Pain relief with rest and GTN is characteristic. If pain lasts
>5min, investigate and treat as for NSTEMI/ UA (NSTE-ACS).
Prophylaxis Assessment/ reduction of modiable risk factors (smoking,
obesity, DM, BP, cholesterol), statin, aspirin, ACEi, anti anginals (β- blockade,
calcium-channel blockers, nitrates, nicorandil, ranolazine, revascularization).
Functional
K Box 8.3 Angina withnormal coronaries?
Throughout your career, you will encounter numerous patients with
atypical chest pain who require basic investigations to exclude serious pathology and subsequent reassurance. However, some patients
experience convincing ischaemic heart pain despite angiographically
normal coronary arteries. In this situation, considerations include coronary artery spasm (Prinzmetal’s angina), cocaine- induced vasospasm,
microvascular angina (post- menopausal women with perfusion defects
on functional imaging), hypertrophic cardiomyopathy, hypertension,
and aortic stenosis.
3
NICE guidelines available at Mguidance.nice.org.uk/ CG26
4
See NICE guidelines at Mguidance.nice.org.uk/ CG95
3Aortic dissection
K If you suspect aortic dissection, get help and arrange an urgent CT aorta
(E OHCM11 p. 647, or E OHAM4p. 150).
Symptoms Sudden- onset severe chest pain, anterior or interscapular,
tearing in nature, dizziness, breathlessness, sweating, neurological decits.
Risk factorsSmoking, obesity, DM, iBP, icholesterol, FH, previousIHD.
SignsUnequal radial pulses, tachycardia, hypotension/ hypertension, dif-
ference in brachial pressures of ≥5mmHg, aortic regurgitation, pleural
eusion (L>R), neurological decits from carotid artery dissection.
Investigations ECG Normal or may show LV strain/ ischaemia (E
pp. 600–2);
CXR Widened mediastinum >8cm (rarely seen), irregularity
of aortic knuckle and small left pleural eusion can develop from blood
trackingdown;
or pericardial eusion.
treatment
EchoMay show aortic root leak, aortic valve regurgitation,
Urgent CT/ MR angiography/ transoesophageal echo. Acute
Seek seniorhelp. HypotensiveTreat as shock (E pp. 480–5). O
(5L/ min), two large- bore cannulae, X- match 6units, analgesia (IV opioids);
Hypertensive Aim to keep systolic BP <00mmHg (Epp. 280–1).
Further treatment Surgery (for type A: involves the ascending aorta) or
conservative management (for type B:involves descending aortaonly).
Musculoskeletal chestpain
Symptoms Localized chest wall pain, worse on movement and/ or
breathing, recent trauma or exertion (eg lifting).
SignsFocal tenderness, erythema, absence of other signs in CVSorRS.
Investigations ECG Normal (no ischaemia/ MI); CXR Normal (no pneumo-
thorax);
D- dimer Normal and low probability of PE (Ep. 292).
Acute treatment Reassurance and simple analgesia (Epp. 92–4).
Chronic treatment Should settle in 2wk, avoid further injury (eg heavy
lifting), regular analgesia to permit ADLs, deep breathing and coughing
(to prevent chest infection). Stop smoking.
Pericarditis(E OHAM4p. 56.)
Symptoms Pleuritic chest pain, worse on lying at and deep inspiration,
relieved by sitting forwards, fever, recent viral illnesses.
SignsMay be no abnormalities, ±pericardial rub. Exclude tamponade.
Investigations ECG Saddle- shaped ST in most leads (Fig. 8.2); blds iWCC
and inammatory markers, ±iviral titres, troponin;
Echo Bright pericar-
dium ± pericardial eusion; exclude tamponade and purulent pericarditis.
Acute treatment Reassurance and analgesia; paracetamol, NSAIDs. High
troponin suggests myopericarditis, but treat as ACS until proven otherwise.
Chronic treatmentUsually settles in 2– 4wk. If recurrent, discuss with car-
diology and consider cardiac MRI/ colchicine/ steroids/rheum review.
261CHESTPAIN
2
Fig.8.2 Typical saddle- shaped ST segment seen in pericarditis.
262 CHAPTER8 Cardiovascular
2Tachyarrhythmia emergency
2 Airway
2 Breathing
2 Circulation
22Call for senior help early if patient ‘unstable’ (Fig.8.3):
2Signs of an unstable patient
• Reduced consciouslevel
• Systolic BP <90mmHg
•
Sit patient up unless hypotensive, then lay at with legs elevated
•
5L/ min O
•
Monitor pulse oximeter, BP, debrillator pads ifunwell
• Request full set of
• Take brief
•
Examine patient:condensed CVS, RS, ±abdoexam
• Establish
• Initiate further treatment Ep. 263
•
Venous access, take bloods:
•
VBG, FBC, U+E, D- dimer, troponin, TFT, lactate, magnesium, calcium
• Consider requesting urgent CXR, portable if toounwell
• Call for
• Reassess, starting with A, B, C....
2Life- threateningcauses
• Ventricular tachycardia (VT) or ventricular brillation(VF)
• Torsades de pointes
• Supraventricular tachycardia with haemodynamic compromise
• Fast atrial brillation/ utter with haemodynamic compromise
• Sinus tachycardia:
•
secondary to shock, includingPE
•
iatrogenic (drugs).
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort— CALL ARREST TEAM
If no palpable pulse— CALL ARREST TEAM
• Chestpain
• Heart failure.
if SOB or sats<94%
2
observations andECG
history if possible/ check notes/ ask wardsta
likely causes and rule out seriouscauses
seniorhelp