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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
263TACHYARRHYTHMIA EMERGENCY
Fig.8.3 Adult tachycardia (with a pulse) algorithm; 202 guidelines.
Reproduced with the kind permission of the Resuscitation Council(UK).
264 CHAPTER8 Cardiovascular
Tachyarrhythmias
2Worrying features dGCS, dBP (systolic <90mmHg), chest pain,
heart failure, broad QRS complexes.
Think about Common Sinus tachycardia, AF or utter with fast ven-
tricular response, AV nodal re- entrant tachycardia;
tachycardia (VT), AV re- entrant tachycardia (eg accessory pathway/
Wol– Parkinson– White), atrial tachycardia;
appropriate tachycardia in eg sepsis, shock, pain, anxiety, PE.
Ask about Onset, associated Sx (chest pain, shortness of breath, dizzi-
ness, palpitations, collapse), previous episodes;
(IHD, valvular lesions, hypertension), thyroid disease, DM;
drugs, levothyroxine, salbutamol, anticholinergics, caffeine, nicotine, allergies; SHSmoking, alcohol, recreational druguse.
AF risk factors iBP, coronary artery and valvular heart disease, pulmonary
embolism, pneumonia, thyrotoxicosis, alcohol, sepsis.
Sinus tachycardia risk factors Shock (hypovolaemic, cardiogenic, septic, ana-
phylactic, spinal), pain/ anxiety, fever, drugs (levothyroxine, salbutamol, anticholinergics, caeine, nicotine, cocaine).
Obs Pulse (check apical pulse as radial can underestimate), BP, cap rell,
RR, O
sats, GCS, temp, cardiac monitor.
2
Look for Any ‘worrying features’ classify arrhythmia as ‘unstable’ (Fig.8.3).
Investigations ECG P waves before each QRS imply sinus rhythm,
irregular QRS without clear P waves implies AF, saw- tooth baseline implies atrial utter, rate of ≥40 (narrow complexes) suggests SVT (including
utter with 2: block), broad regular complexes suggests VT (always
check for a pulse) (Fig.8.4, Tables8.4 and 8.5);
D- dimer (if PE suspected), troponin, Mg
picion (eg X- match if haemorrhage);
2+
, Ca2+, others as indicated by sus-
ABG and CXROnly once treatment has
been initiated or if results are likely to alter management;
large PE, acute valve lesion, poor LV, or pericardial eusion.
Treatment
In all patients
• Airway, Breathing (with O2), Circulation (HR, BP, and capillary rell)
• IV access (two large- bore cannulae in both antecubitalfossae)
• Obtain ECG or view trace on debrillator to decide onrhythm
• If hypotensive or dizzy lay at with legs up— call for seniorhelp
• If semi- conscious lay in recovery position— call senior/ 2ARRESTTEAM.
Specic arrhythmias
Sinus tachycardia
AFOld or new AF? Consider urgent rate/ rhythm control (Ep. 266).
SVT Usually time to call for help and get drugs ready (Ep. 267).
VT no pulse 3Call ARREST TEAM and start BLS/ ALS (Ep. 226).
VT with pulse If haemodynamically stable, attempt chemical cardioversion
Establish and treat cause, eg shock, sepsis (Epp. 480–5).
(eg amiodarone or β- blocker E p. 83); if fails or if unstable, will need DC
cardioversion (E p. 560), with sedation or GA unless lowGCS.
UncommonVentricular
Non- cardiac causes Beware
PMH
Cardiac problems
bldsFBC, U+E, TFT, CRP,
EchoIf suspected
DH
Cardiac
Table8.4 ECG features oftachyarrhythmias
Rate Regular P waves Broad/ narrow
Sinus tachycardia >00
Fast AF >00
SVT ≥40
VT (with pulse) ≥50
VT (pulseless) As for ‘VT with pulse’; always perform a pulse- check
VF Chaotic irregular electrical activity; never has a pulse
*80% of wide complex tachycardias (WCTs) are ventricular (VT) and 20% are supraventricular
(90% VT if previous CAD). Supraventricular rh ythms can produce a WCT if there is bundle
branch block (BBB; ‘aberrancy’) or an accessory pathway (‘pre- excitation’), as part of the heart
is depolarized from outside the conduction system, and therefore more slowly. Because ()it is
dicult to distinguish VT from SVT with aberrancy/ pre- excitation on the ECG, (2)treatments
are similar, and (3)VT is a more unstable rhythm, if there is any doubt at all a WCT should be
treated as VT until proven otherwise.
(carotid)
✓ ✓
✘ ✘
✓ ✓or ✘
✓ ✘
ECG, lead II view (rhythm strip)
Sinus tachycardia
Fast AF
SVT
Narrow (unless BBB)*
Narrow (unless BBB)*
Narrow (unless BBB)*
Wide, not typical BBB QRS*
265TACHYARRHYTHMIAS
VT with or without a
pulse
VF
Torsades de pointes
Fig.8.4 Typical appearance of various tachyarrhythmias.
266 CHAPTER8 Cardiovascular
Atrial brillation (AF)(E OHAM4p. 76.)
5
2Worrying signs Heart failure, hypotension, dGCS, or chestpain.
Symptoms Palpitations, SOB, heart failure, chest pains, dizziness, malaise.
Risk factors/ cause Prev AF, age, acute illness, valve disease, heart failure, car-
diomyopathy, IHD, cardiac surgery, HTN, PE, COPD, hyperthyroidism.
SignsIrreg irreg pulse, hypotension if compromised, signs of a cause/ risk factors.
Investigations ECG Absent P waves, irreg irreg QRS complexes; blds FBC
(iWCC), U+E, TFT, alcohol, Mg
possible ischaemic cause);
dilatation/ impairment, LA volume, valvular lesion;
2+
, Ca2+, ±D- dimer (PE), troponin (if
CXRHeart size, oedema, pneumonia; Echo LV
CTC ATo excludeCAD.
Treatment
2Haemodynamic compromise Seek immediate help. Treat with shock (see
E p. 560); O
IV ±further cardioversion. Chronic AF very unlikely to cause compromise:
, IV access, DC cardioversion; if unsuccessful, amiodarone
2
do not shock, but consider other causes of compromise, eg sepsis, bleeding.
Haemodynamically stableTreatment options include:
•
Conservative: if AF is new and the precipitant is obvious then treating
the cause and close monitoring may suce. Discuss with cardiology.
•
Rate control: if not, rate (target <0bpm) over rhythm control
(cardioverting to SR) is st line because symptoms are usually raterelated, rate- controlling meds are safer more successful drugs, and
anticoagulation usually continues regardless. β- blockers (E p. 87) or
non- dihydropyridine calcium-channel blockers (E p. 89) are st line,
adding digoxin if needed (E p. 95). Consider pacemaker ± ablation if
ipping from sinus bradycardia to fastpAF (tachy-brady syndrome).
•
Rhythm control: reverting to and staying in SR is less likely in old age,
established AF, LA dilatation, and mitral valve disease, but younger patients
with new AF and normal hearts may achieve and maintain SR, so could be
spared the risks of AF cardiomyopathy and long- term anticoagulation. Also,
if there are disabling symptoms or AF- induced heart failure, rhythm control
can be tried with DC/ chemical cardioversion rst (ecainide/ sotalol if no
structural heart disease, or amiodarone), and AF ablation second.
AnticoagulationMost patients need lifelong anticoag, inc the 4wk before DC
cardioversion and 4wk after. Exceptions are patients with excessive bleeding
risk (eg ORBIT score, aim to reduce bleeding risk),
low stroke risk (CHA
times those in sustained SR (discuss with cardio rst). Non- vitamin K oral
VASc score of 0 in men, in women)7, and some-
2DS2
6
contraindications, very
anticoagulants are st line (DOACs; apixaban, dabigatran, edoxaban, and
rivaroxaban) (E pp. 428–30). Warfarin if contraindicated. Aspirin is no
longer monotherapy for stroke prevention.
ComplicationsThromboembolic disease (eg ischaemic stroke). Drug side
eects from amiodarone, warfarin, DOACs, β- blockers, digoxin,etc.
5
NICE guidelines available at Mguidance.nice.org.uk/ NG96
6
ORBIT score: 2 points for Hb<130g/L in men or 120g/L in women, point for age >74yr, 2
points for bleeding history (GIB, intracranial bleed, haemorrhagic stroke), point if eGFR<60,
and point if taking antiplatelets. A score of 4–7 = high risk, 3 = medium, 0–2 = low.
7
CHA2DS2VASc score: point for each of CCF, HTN, DM, vascular disease, age 65– 74yr, and
female sex category. 2 points for each of age >75yr and stroke/ TIA. After assessing and reducing
the bleeding risk, the stroke risk outweighs the anticoagulation risks for patients with AF and a
CHA
VASc score of 2 or more (‘consider’ anticoagulation in men with point).
2DS2
Atrial utter
K ‘Saw-tooth’ utter waves reecting atrial activity, with ventricular response
around 50bpm. Management similar to AF, except drugs less successful, and
electrical and ablative cardioversion more so (E OHAM4p. 82).
Supraventricular tachycardia(SVT)
2Worrying signs Heart failure, hypotension, dGCS, or chest pain
(E OHAM4p. 72).
Symptoms Palpitations, shortness of breath, dizziness, ±chestpains.
Risk factors Previous SVT, structural cardiac anomaly, alcohol,iT
SignsTachycardia, anxiety, hypotension if haemodynamic compromise.
.
4
Investigations ECG Narrow complex tachycardia (unless concurrent BBB)
with P waves (which may merge into QRST so be dicult to see), regular
QRS complexes, rate usually ≥40;
Further investigations Only required if
diagnosis is in question, otherwise initiate treatment as follows.
Acute treatment O
rhythm on debrillator:
, large- bore IV access (antecubital fossa). Monitor
2
• Vagal manoeuvres (Ep. 559)
• Chemical (Ep. 559).
Chronic treatmentIf recurrent, seek cardiology advice as may require elec-
trophysiological testing of cardiac conduction pathways/ablation.
ComplicationsHypotension, ischaemia, heart failure in individuals with ex-
isting cardiac disease, deterioration into more sinister arrhythmia.
Wol– Parkinson– White syndrome (WPW)
(E OHAM4p. 84.)
AetiologyThis is a re- entrant tachycardia
which results from an accessory conduction pathway between the atria
and the ventricles (bundle of Kent). It
classically appears as a short PR interval
and a δ/ delta wave (arrow in Fig.8.5).
Treatment Avoid digoxin and verapamil.
Refer to a cardiologist for consideration of electrophysiology studies and
ablation of accessory pathway.
Fig.8.5 δ wave inWPW.
267TACHYARRHYTHMIAS
Table8.5 Anti- dysrhythmics commonly used intachyarrhythmias
3These drugs should only be used after discussion with a senior.
Amiodarone (should
be given via a central
vein, butcan be given
peripherally in an
emergency)
Verapamil (avoid if patient
on β- blockers)
Flecainide (not if patient
has IHD)
Patient must be in a monitored bed during IV administration of these agents.
Loading dose 300mg/ over 60min IVI via central line
followed by 900mg/ over 24h IVI via central line OR
200mg/ 8h PO for wk then 200mg/ 2h PO for
wk then
Maintenance dose 200mg/ 24h PO
5mg/ over 2min IV; further 0.5– mg doses every
5min until target rate achieved (total maximum
20mg) OR 40– 20mg/ 8h PO
2mg/ kg/ over 0min IV (maximum 50mg) OR
00– 200mg/ 2h PO
268 CHAPTER8 Cardiovascular
Ventricular tachycardia (VT)(E OHAM4p. 64.)
2
Worrying signs Sustained (>30s), symptomatic, heart failure, hypoten-
sion, dGCS, chest pain, or absent pulse (pulselessVT).
Symptoms Palpitations, dizziness, shortness of breath, ±chest pain, arrest.
Risk factors IHD, trauma, hypoxia, acidosis, long QT, electrolyte disturbances.
SignsTachycardia, anxiety, pallor, hypotension, dGCS,shock.
Investigations ECGBroad complex tachycardia, P waves not before every
QRS, rate usually >50;
2+
and Mg
; Other investigations Should be directed by clinical situation
blds Check urgent TSH, U+E (especially K
though cardioversion is main priority at thisstage.
Acute treatment 2 Call for seniorhelp immediately.
3
Pulseless VT Call ARREST TEAM. Commence BLS/ ALS (Epp. 228–9).
VT witha pulseO
of sinus rhythm with either drugs (eg sotalol, amiodarone loading) or
, large- bore IV cannula in antecubital fossa; restoration
2
DC cardioversion (under sedation unless lowGCS).
Either SVT withaberrancy/ pre- excitation or VT.Treataspresumed VT.
Chronic treatmentThis may need drug therapy to maintain sinus rhythm,
electrophysiological studies/ ablation, or implantable cardioverter/ debrillator (E OHAM4 p. 64). Try to keep Mg >0.9 and K>4.0.
ComplicationsVF (or other dysrhythmia), tachycardia cardiomyopathy.
Torsades de pointes
This looks like VF but has a rotating axis (E p. 265). Develops on background of iQT interval (Table8.6). Give Mg
2+
sulfate 2g/ IV (8mmol)
over 5min (dilute in small volume, eg 50mL of 0.9% saline) ±overdrive
pacing (E OHAM4p. 68).
+
),
Table8.6 Causes ofprolonged QT interval
QTc =QT/ √(RR interval)— this allows correction of the QT interval for heart rate
and is usually calculated automatically on an ECGtrace.
Normal QTc Values are sex specic:values <430ms (♂) and <450ms (♀) are
considered normal; values >450ms (♂) and >470ms (♀) are abnormal; values in
between these are borderline. There is a dose– response relationship between risk
of cardiac death and prolongation of QTc.*
Congenital Romano– Ward syndrome (autosomal dominant),
Drugs Anti- dysrhythmics (amiodarone, sotalol,
Electrolyte disturbance
Severe bradycardia Complete heart block, sinus bradycardia
IHD Ischaemia, myocarditis
i
intracranial bleed
*Straus, M.etal. J Am Coll Cardiol. 2006;47:362 available free online.
Jervel and Lange– Nielsen syndrome (autosomal
recessive associated with deafness)
quinidine), psychoactives (thioridazine, haloperidol,
uoxetine), antihistamines (terfenadine, loratadine),
antimicrobials (erythromycin, clarithromycin,
uconazole)
dK+, dMg2+, dCa
2+
Subarachnoid haemorrhage
269TACHYARRHYTHMIAS
270 CHAPTER8 Cardiovascular
2Bradyarrhythmia 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 has ‘adverse features’ (Fig.8.6):
2Adverse features/features
• Systolic BP <90mmHg
• Syncope
•
Sit patient up unless hypotensive/ dizzy, then lay at with legs elevated
•
5L/ min O
•
Monitor pulse oximeter, BP, debrillator ECG leads if veryunwell
• Request full set of
if SOB or sats<94%
2
observations and ECG with long rhythmstrip
• Ischaemic chestpain
• Heart failure.
• Take brief history if possible/ check notes/ ask wardsta
•
Examine patient:condensed CVS, RS, abdoexam
• Establish
likely causes and rule out seriouscauses
• Consider IV atropine, 500micrograms, repeat at 2– 3min intervals
(max3mg)
•
Initiate further treatment, including transcutaneous pacing, see following
sections
•
Venous access, take bloods:
•
VBG, FBC, U+E, LFT, troponin, TFT, lactate, calcium, magnesium
• Consider requesting urgent CXR, portable if toounwell
• Call for
•
seniorhelp.
Reassess, starting with A, B, C…
2Life- threatening causes
• Complete (3rd- degree) heart block (±followingMI)
• Möbitz typeII 2nd-degree heart block
• Pauses >3sonECG
• Hypoxia in children.
271BRADYARRHYTHMIA EMERGENCY
Fig.8.6 Adult bradycardia algorithm; 202 guidelines.
Reproduced with the kind permission of the Resuscitation Council(UK).
272 CHAPTER8 Cardiovascular
Bradyarrhythmias
2Worrying features Systolic BP <90mmHg, symptomatic hypo-
tension, HR <40bpm, broad QRS, heart failure,runs of VT/ VF.
Think aboutSinus bradycardiaMI (typically inferior MI), drugs (including
digoxin toxicity), vasovagal (Box 8.4), dT
(bradycardia and hypertension 2° to iICP), sleep, anorexia nervosa,
physical tness;
Complete or 3rd-degree AV heartblock.
Ask about Dizziness, postural dizziness, ts/ faints, weight change, visual
disturbance, nausea, vomiting;
PMH Cardiac disease (IHD/ AF), thyroid
disease/ surgery, DM, head injury or intracranial pathology, glaucoma, eating
disorder;
DHCardiac medications (β- blockers, Ca
digoxin), eye drops (β- blockers), anticoagulants, and antiplatelets (they may
need pacemaker urgently) (Box8.5);
independence.
IHD risk factors iBP, icholesterol, FH, smoking, obesity, DM, previous
angina/ MI.
ObsHR, BP, postural BP, RR, sats, temp, GCS, cardiac monitor.
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 ankles), features of
iICP (papilloedema, focal neurology Ep. 355).
Investigations ECG Sinus bradycardia or complete heart block
(Table8.7, Fig.8.7), evidence of ischaemia or infarction (E pp. 600–2)
or of digoxin toxicity (Table8.7, Fig.8.7);
2+
Mg
, TFT, cardiac markers, digoxin level, troponin, coagulation (if con-
sidering transvenous pacing);
CXRUnlikely to be helpful in the immediate
setting, but may reveal heart size and evidence of pulmonary oedema;
Head CT Useful if you suspect raised ICP, though patient will be in ex-
tremis (i.e. about to cone E p. 353) if iICP causing bradycardia (speak
to on- call neurosurgeon);
Echo for structural defects and cardiac func-
tion, to assess the need for ICD/ CRT device on top of a pacemaker.
Treatment
• Airway, Breathing (with O2), and monitor Circulation
• If either dGCS or dBP (<90mmHg systolic), 3call for senior help/
ARRESTTEAM. Discuss urgently with cardiology
• IV cannula and takebloods
• Bed rest and cardiac monitoring
• Consider giving IV atropine if systolic BP <90mmHg (500micrograms at
2– 3min intervals to a maximum of3mg)
• Check ECG to exclude myocardial infarction and to identify heart
block, extreme sinus bradycardia, or very slow atrial brillation.
, hypothermia, Cushing’s reex
4
2+
antagonists, amiodarone,
SH Exercise tolerance, ADLs, level of
bldsFBC, U+E, glucose, Ca
2+
,