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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
Table8.7 ECG features ofbradyarrhythmias and types ofheartblock
Sinus bradycardia P waves precede each QRS, rate <60bpm
st- degree AV block P– R interval >5 small squares (>0.2s)
Möbitz I
(Wenckebach)
Möbitz II Intermittent P waves fail to conduct to ventricles, but
3rd- degree AV
block
Digoxin
eect/ toxicity
Rate- controlled AF No P waves; irregularly irregular rhythm
Sinus
bradycardia
1st-degree
AV block
Möbitz type I
P– R interval lengthens from beat to beat, until failure of
AV conduction, then pattern restarts. Ausually benign
and asymptomatic disease of the AVN that improves
with exercise and rarely requires pacemaker insertion
P– R interval does not lengthen, unlike Möbitz type I;
typically 2: (P waves:QRS complexes):Ratios of 3:
and above are considered
benign and more symptomatic infranodal disease that
is worsened by exercise and more commonly requires
pacemaker implantation
Complete dissociation between P waves and QRS
complexes, which may be narrow or broad. Amalign
and usually symptomatic disease that invariably requires
urgent permanent pacemaker implantation
Down- sloping ST segment (reversed tick), inverted T
waves; often present even when drug is at non- toxic
levels
ECG, lead II (rhythm strip) view; arrows indicate P wave
high- grade AV block. Aless
273BRADYARRHYTHMIAS
Möbitz II with
3:1 AV block
3rd-degree
(complete)
AV block
Digoxin
eect/
toxicity
Fig.8.7 Typical appearances of various bradyarrhythmias and types of
heartblock.
274 CHAPTER8 Cardiovascular
Sinus bradycardia(E OHAM4p. 88.)
2
Worrying signs Features of heart failure, hypotension,dGCS.
Symptoms Asymptomatic, dizziness (±on standing), falls, palpitations,
shortness of breath, oedema, symptoms of iICP, hypothermia, ordT
SignsOrthostatic dBP, hypothermia, evidence of iICP (Ep. 372).
Investigations ECGQRS complex will be preceded by a P wave, rate <60,
QRS will be narrow unless BBB; exclude ischaemia/ infarction;
2+
U+E, Ca
pacing);
Acute treatmentIf symptomatic (dizzy or GCS <5) or systolic <90mmHg,
, Mg2+, TFT, troponin, coagulation (if considering transvenous
CXRUnlikely to be helpful in resuscitationphase.
monitor heart rate on debrillator, lay at with legs elevated (as long as
iICP not suspected). O
signs present, 3call for senior help/ ARREST TEAM. Titrate 500micro-
, secure IV access and take bloods. If worrying
2
grams atropine IV every 2– 3min (to a maximum of 3mg) followed by a
large ush, until HR improves. Identify and correct precipitant. Consider
sedation and external pacing/ pacing- wire via central line/ permanent
pacemaker (E pp. 562–3); a rhythmical precordial thump (percussion
pacing) can be used in extremis when an external pacing machine is not
immediately available.
Chronic treatmentConsider 24h tape; frequent symptomatic episodes of
bradycardia or pauses are sign of sick sinus syndrome (E p. 275) and
may need a permanent pacemaker system (E OHCM11p. 28).
ComplicationsSevere bradycardia and high vagal tone can deteriorate into
asystole so prompt treatment is required. Remember to talk continually
to the patient and/ or check for a pulse since pulseless electrical activity
(PEA) is common and the ECG trace may not change.
Box 8.4 Vasovagal attacks
K Sudden reex bradycardia from unopposed parasympathetic inhibition upon heart rate is common. Often brief loss of consciousness preceded by eg light- headedness, visual disturbance, nausea, or sweating.
Recovery of consciousness is prompt— consider other diagnoses if not.
Typical precipitants are listed.
• Fear and pain (including needles)
• Post- micturition (especially in oldermen)
• Nausea and vomiting
• Dilatation of anal sphincter and cervix (during surgery)
• Pulling of extra- ocular muscles/ pressure on eye (during ophthalmic surgery)
• iIntra- abdominal pressure (during laparoscopic surgery, straining on
the toilet).
bldsFBC,
.
4
Box 8.5 Drugs which can precipitate bradycardia
β
- blockers Reports of bradycardia even from β- blocking eyedrops
Digoxin Rhythm likely to be AF, but may be sinus if reverted
Ca2+ antagonists Verapamil and diltiazem slow heartrate
Amiodarone Can cause conduction defects and bradycardia
- agonists Phenylephrine is mainly used by anaesthetists and can cause
α
reex bradycardia by increasing peripheral vascular resistance
Ivabradine Used for prognosis in heart failure to slow the sinusnode.
Complete (3rd- degree) heart block(E OHAM4p. 90.)
2
Worrying signs Features of heart failure, hypotension,dGCS.
Symptoms Asymptomatic, dizziness (±on standing), palpitations, short-
ness of breath, ±chestpain.
Causes Frequently underlying ischaemic damage (typically after inferior
MI); also post- cardiac surgery, drug- induced (β- blockers, Ca
2+
channel
blockers), amyloid, sarcoid, myeloma, infective (Chagas,Lyme).
Signs dBP (and potentially dGCS), often iBP, cannon waves in iJVP (due
to asynchronous 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 implies proximal rhythm (may respond to atropine),
broad QRS implies distal rhythm (less likely to respond to atropine); look
for evidence of myocardial infarction;
blds FBC, U+E, Ca
troponin, coagulation (if considering transvenous pacing);
2+
, Mg2+, TFT,
CXR Unlikely
to be helpful in immediate resuscitationphase.
Acute treatmentIf symptomatic (dizzy or GCS <5) or systolic <90mmHg,
monitor heart rate on debrillator, lay at with legs elevated. O
tation, secure IV access and take bloods. 3Call for senior help/ ARREST
supplemen-
2
TEAM. Titrate 500micrograms atropine IV every 2– 3min (to a maximum
of 3mg), followed by a large ush, until HR improves. Identify and correct precipitant. Consider external pacing/ pacing- wire via central line (E
pp. 562–3); a rhythmical precordial thump (percussion pacing) can be used
in extremis when an external pacing machine is not immediately available.
Chronic treatment Likely to need permanent pacemaker (E OHCM11
p. 28) and/ or correction of precipitant. Discuss with cardiology.
ComplicationsSevere bradycardia and high vagal tone can deteriorate into
asystole so prompt treatment is required. Remember to talk continually
to the patient and/ or check for a pulse since PEA is common and the
ECG trace may not change.
Sick sinus syndrome
Dysfunction of the sinoatrial node often precipitated by ischaemia/
brosis. Results in bradycardia (±arrest), sinoatrial block, or SVT with
alternating bradycardia/ asystole (tachy- brady syndrome). Needs
pacing if symptomatic.
275BRADYARRHYTHMIAS
Other types ofheart block(E OHAM4p. 90.)
st- degree AV block and Möbitz I These do not require treatment unless
the patient is symptomatic or there is a reversible cause (usually drugs).
Möbitz II and high- grade AV block These may deteriorate into complete
heart block and may require temporary/ permanent pacing, especially
when associated with an ACS or general anaesthesia— seek cardiology
advice.
276 CHAPTER8 Cardiovascular
2Hypertension emergency
2 Airway
2 Breathing
2 Circulation
2 Disability
3Call for senior help early if patient deteriorating.
If systolic BP >200 or diastolicBP >20:
•
Sit patientup
• 5L/ min O2 if SOB or sats<94%
•
Monitor pulse oximeter, BP, debrillator ECG leads ifunwell
• Request full set of
• Take brief
•
Examine patient:condensed RS, CVS, abdo, and eye examination
• Rule out serious causes and establish
•
review history and previous observations:is hypertensionnew?
•
Do not give STAT dose of antihypertensive without seniorreview
•
Initiate further treatment Ep. 280
•
Venous access, take bloods:
•
FBC, U+E, troponin, TFT, glucose, cortisol
• Consider requesting urgent CXR, portable if toounwell
• Urinalysis and β- hCG (in women of child- bearingage)
• Call for
• Re- assess, starting with A, B, C…
2Life- threatening causes
• Pre- eclampsia/ eclampsia
• Malignant hypertension >200/ 20
• Hypertensive encephalopathy
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort— CALL ARREST TEAM
If no palpable pulse— CALL ARREST TEAM
If GCS <8— CALL ANAESTHETIST
observations andECG
history if possible/ check notes/ ask wardsta
likelycauses:
senior help foradvice
• Phaeochromocytoma
• Thyrotoxicstorm
• Cushing’s reex (raised ICP).
277HYPERTENSION EMERGENCY
278 CHAPTER8 Cardiovascular
Hypertension
2Worrying features Altered mentation, seizures, retinal haemor-
rhages, AKI, chest pain, pregnancy, arterial aneurysms, acute changes in BP.
2
Is this a hypertensive crisis? If any of above, or acute iBP >200
systolic or >20 diastolic (Ep. 276).
Think about Life- threatening Hypertensive crisis (acute iBP, typically
>200 systolic or >20 diastolic; E p. 280), pre- eclampsia;
pain, primary (essential) or secondary hypertension (including thyroid
storm and phaeochromocytoma).
Ask aboutThe majority of patients will be asymptomatic, but consider
possibility of end- organ damage (visual symptoms, headache, chest/
back pains, haematuria, confusion) or
secondary causes (Table 8.8);
PMH Previous hypertension, Cushing’s syndrome, acromegaly, Conn’s
syndrome, phaeochromocytoma, coarctation, thyroid disease, DM, renal
artery stenosis;
DHCardiac and antihypertensive medications, steroids,
contraceptive pill, levothyroxine/ carbimazole, MAOI, antipsychotics,
recreational drugs (cocaine, amphetamines);
crine disease, polycystic kidney disease;
FH Hypertension, endo-
SH Exercise tolerance, smoking.
ObsHR, BP (use correct cu size & highest value from two arms), sitting
& standing BP, sats, temp, GCS, repeat BP after period of prone relaxation.
Look for Signs ofprecipitating disease Radiofemoral delay, striae, cen-
tral obesity, large hands/ feet/ face, tremor, exophthalmos, proximal myopathy, gravid uterus, renal bruits/ polycystic kidneys;
Fundoscopy (papilloedema, hypertensive retinopathy), displaced
damage
apex beat or S
(suggest left ventricular hypertrophy), haematuria.
4
Table8.8 Key secondary causes ofhypertension
Features Investigations Cross-ref
Renal disease or
renal artery stenosis
Phaeochromocytoma
Thyroid dysfunction Cold/ heat
Acromegaly Headache, visual eld
Cushing’s
syndrome
Other causes include pregnancy (gestational, pre- eclampsia/ eclampsia), Conn’s syndrome
(E p. 347), hyperparathyroidism (E p. 411), scleroderma, coarctation of the aorta, drugs
(steroids, MAOI, OCP), and obstructive sleep apnoea.
Renal failure,
abnormal urine
dipstick, FH may be
relevant, renal bruit
Sweating, labile
hypertension,
palpitations
intolerance, sweating,
lack of energ y
disturbance, change in
facial features
Centripetal obesity,
skin thinning,
weakness
Urine microscopy,
renal Doppler USS,
autoantibodies ±renal
biopsy
Plasma metanephrines;
24h urinary
catecholamines +VMA
TFTs
IGF- and pituitary
hormone levels
Urinary free cortisol;
dexamethasone
suppression test
Other Anxiety,
Signs of end- organ
E p. 395
E p. 347
E pp. 348–9
E p. 345
E p. 346
Investigations BP Ensure correct cu and repeat manually; a new diag-
nosis of HTN should be conrmed with BP monitoring (BPM) which can
be ambulatory (a 24h monitor measuring every 30min) or at home (selfmonitoring BD forwk);
cholesterol, HDL, TFT;
8
ECGLVH (Ep. 601); bldsFBC, U+E, glucose,
UrineBlood, protein,ACR, β- hCG; CXRUnhelpful
in immediate setting, but will show heart size and aortic contours.
TreatmentLifestyle advice (smoking cessation, regular exercise, reduce
alcohol and caeine, weight loss, balanced low- salt diet). Identify and treat
modiable risk factors (DM and dyslipidaemia). Pharmacological therapy
if appropriate, based upon BP, risk factors, and comorbidities (Box 8.6).
Box 8.6 Hypertension:who and how totreat
The following is adapted from NICE guidelines CG26, NG85, NG36,
NG203, and NG7:
• If clinic BP is <40/90 or BPM is <35/85, perform 5-yearly BP checks
& oer lifestyle advice. Any patient with a clinic BP >60/ 00 and BPM
>50/ 95 should be oered lifestyle advice and an antihypertensive. This
also applies to those <80yr with a clinic BP >40/90, a BPM >35/85,
and either CVSD, CKD, DM, end-organ damage (LVH on ECG, eGFR
<60mL/ min, hypertensive retinopathy, microalbuminuria, or haematuria)
or a QRISK >0%. Also, consider medication if <60yr and a QRISK
<0%, or if >80yr with clinic BP >50/90
• Same-day specialist review is recommended if clinic BP is >80/20
and there is evidence of retinal haemorrhage, papilloedema, new-onset
confusion, chest pain, LVF, AKI, or suspected phaeo++chromocytoma.
Routine specialist review is recommended if <40yr and BPM >50/95, or
taking >3 antihypertensives
• Monitor BP using clinic BPs, including a BPM for those with white-coat HTN,
or patients wishing to self-monitor. Routinely measure standing & sitting BPs
in patients with symptoms of postural hypotension or those who are >80yr
• BP targets depend on age, comorbidity, and frailty. If <80yr, aim for a clinic BP
of <40/90, or 35/85 if on BPM. If >80yr, aim for a clinic BP of <50/90, or
45/85 if on BPM. In DM or CKD, clinic BP targets are <40/90 if urine ACR
<70mg/mmol, or <30/80 if urine ACR >70mg/mmol
• Antihypertensive choice depends on age, ethnicity, comorbidity, & tolerance.
For patients with CVSD, treat BP as per ACS or angina guidelines, using the
below HTN guidance if their BP remains uncontrolled thereafter.
• For patients with (i) DM, (ii) CKD and ACR >30mg/mmol, or (iii) who are
<55yr and not of Black African or African-Caribbean origin, step is an ACEi
or ARB; step 2 is to add a calcium-channel blocker or thiazide-like diuretic.
For remaining patients, step is a calcium-channel blocker, and step 2 is an
ACEi/ARB or thiazide-like diuretic. Step 3 for all patients is an ACEi/ARB,
calcium-channel blocker, and thiazide-like diuretic in combination
• If BP is still uncontrolled, step 4 is to re-conrm the diagnosis with BPM, check
for postural hypotension, discuss adherence, consider referral, and add either
spironolactone (if K <4.5mmol/L) or α/β-blocker (if K >4.5mmol/L)
• At each stage, in the presence of frailty/multimorbidity, use clinical
judgement.
8
Follow- upIf treatment is initiated or altered in hospital, ensure the GP
knows what investigations 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 medications.
Complications End- organ damage, malignant HTN, CV disease.
8
NICE guidelines available at Mguidance.nice.org.uk/ NG36
279HYPERTENSION
280 CHAPTER8 Cardiovascular
Hypertensive crises
K Elevation of BP >200/ 20 is a 2hypertensive emergency when ac-
companied by evidence of end- organ damage (Table8.9) or 2hyperten-
sive urgency in the absence of end- organ damage (E OHAM4p. 138).
Symptoms and signs iBP, often acute, in presence of end- organ damage
(Table8.9).
Table8.9 End- organ damage inhypertension
Organ Symptoms/ signs Investigations
CNS
dGCS, headache,
confusion, vomiting,
new motor weakness,
seizures, coma
Eyes Headache, visual
disturbance
Heart Chest pain,
orthopnoea
Aorta Sudden tearing chest
pain radiating to back;
collapse
Kidneys Haematuria, lethargy,
anorexia
CT head may show subarachnoid or
intracranial haemorrhage; hypertensive
encephalopathy occurs with cerebral oedema
following loss of vascular autoregulation
Fundoscopy shows retinal haemorrhages
±papilloedema; often coexists with damage
elsewhere
ECG changes, elevated cardiac markers.
pulmonary oedema on CXR
Echo or CT may reveal aortic dissection
(E p. 261)
Rapidly worsening renal function; proteinuria,
red cell casts on urine microscopy
Investigations See Table8.9. Always conrm BP yourself, using correct
sized cu. Consider secondary causes (Table8.8). Request formal ophthalmic assessment if suspect retinal disease.
DiagnosisThis relies on a compatible history, often with previously com-
paratively normal BP, and presence or absence of end- organ damage.
Acute treatment In the absence of end- organ damage, oral therapy with
a calcium-channel blocker or ACEi should be instigated. If end- organ
damage is present, admit patient to a monitored area (HDU/ ICU),
with close monitoring of BP (Box 8.7), ECG, neurological state, and
uid balance (consider arterial line, central line, catheterization). Rapid
reduction in BP can be dangerous, resulting in cerebral hypoperfusion,
and is only necessary in an acute MI or aortic dissection. Otherwise,
aim to reduce diastolic BP to 00mmHg or by 25% (whichever value
is higher) over 24h (see Tables8.0 and 8. for treatment options).
Patients with early features of end- organ damage may be started 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
furosemide (20– 50mg IV) ±hydralazine. Consider ACEi to counteract
high circulating levels of renin. Nitroprusside and hydralazine are still
used as adjuncts in severe crises under expert guidance.
Chronic treatmentBP needs checking regularly once discharged from hos-
pital. Ensure GP knows what investigations have been undertaken, their
results, and what the therapeutic plan/ targetBPis.
K Box 8.7 BP control inacuteCVA
In acute ischaemic stroke, cerebral autoregulation is impaired and aggressive lowering of BP results in hypoperfusion and poor outcomes.
3Seek expert help. Generally, only treat if BP >220/ 20 or clear
evidence of end- organ damage. Suitable agents include IV labetalol.
Table8.0 Oral antihypertensives foracute management ofhypertensive crises (E OHAM4p. 143)
Drug Dose Comment
Atenolol 50– 00mg/
Amlodipine 5– 0mg/ 24 PO Ca2+ channel blocker; st line in elderly and
Hydralazine 25– 50mg/
Nifedipine 0– 20mg/ 8h PO Avoid sublingual as rapidly drops BP. OK
24h PO
8h PO
Many β- blockers available. Contraindicated
in asthma, peripheral vascular disease, DM
when β- blocker contraindicated
Vasodilator. Safe in pregnancy
to use in conjunction with β- blocker (avoid
verapamil or diltiazem with β- blockers)
Table8. IV antihypertensives foracute management ofhypertensive
crises (E OHAM4 p. 142)
K Patient must be inHDU/ ICU, ideally withinvasive BP monitoring. Intravenous
therapy can result inrapid falls inBP so drugs must be titrated cautiously.
Drug Dose Comment
Isoket® 0.05%*
(0.5mg/ mL)
GTN – 0mg/ h IVI Venodilates. Useful in LVF and angina
Hydralazine 5– 0mg/ 20min IVI Vasodilates, can cause compensatory
Labetalol 20– 80mg/ 0min IVI Used in eg aortic dissection. Avoid in
Nitroprusside 0.25– 8micrograms/
*Isosorbide dinitrate:available as 25mL 0.% solution (25mg in25mL).
2– 0mL/ h IVI
(– 5mg/ h)
kg/ min IVI
Venodilates. Useful in LVF/ angina. Easy
for nurses to set up infusion. Drug of
choice
rise in heart rate; use with a β- blocker
LVF
Rapid onset. Useful in LVF or hypertensive
encephalopathy. Rarely used now:toxic
cyanide metabolites may accumulate
causing sweating, iHR, iRR, and dpH
281HYPERTENSION
282 CHAPTER8 Cardiovascular
Heart failure
K HF has high morbidity/ mortality and is increasingly common. Reduced
EF is <40%, mildly reduced EF 4–49%, and preserved EF >50%.
SymptomsBreathlessness, orthopnoea, PND, wheeze, oedema, fatigue.
CausesOften multifactorial. Assess history, exam, BNP, and echo. Mostly
ischaemic. Non- ischaemic can be due to eg HTN, DM, valve disease, and
toxins eg chemo, stimulants, alcohol. Can also be primary (inherited eg
HCM, ARVC, DCM, or acquired, eg peripartum or Takotsubo). Nonischaemic secondary causes are inltrative (amyloid, iron overload, Fabry),
inammatory (sarcoid, giant cell), infectious (myocarditis, HIV), neuromuscular (muscular dystrophy, Friedrich’s), and tachyarrhythmia.
SignsCachexia, iRR, iHR, iJVP, murmur (if valvular disease), 3rd heart
sound, bibasal creps, pitting oedema (typically ankles but check sacrum).
Investigations ECG No specic features, look for arrhythmias, is-
chaemia, conduction disease or broad QRS (?device therapy);
(?anaemia), U+E (?renal injury), TFTs, fasting lipids, glucose, iron (?supplement), NPs (secreted by the failing ventricle— normal levels unlikely
in untreated HF);
sions, upper lobe diversion, Kerley Blines;
motion abnormalities, LVEF. HF with preserved LVEF (Box 8.8) may
show ventricular hypertrophy, left atrial dilatation, diastolic dysfunction,
and/or raised lling pressures.
Acute treatment
(Ep. 296).
Chronic treatment Conservative measures are HF team involvement,
treating the cause, smoking cessation, exercise, and cardiac rehab.st-line therapies to reduce mortality in reduced EF are a β- blocker, ACEi/ARNI (ARB if
not tolerated), MRA, and SGLT2i, and to reduce hospitalization are furosemide/
bumetanide (thiazides if resistant). Patients must be stable and euvolaemic on
oral therapies prior to discharge. 2nd line if EF <40% and symptomatic include
cardiac resynchronization therapy (if SR and QRS >30ms), ivabradine (if SR
and HR >70bpm), or hydralazine/ISDN (if Black ethnicity). At any time, consider ICD (if EF <35% and prognosis >yr) and ferric carboxymaltose (if
Fe <00ng/mL or 00–299ng/mL and TSAT <20%). Advanced HF therapies
(transplant/ mechanical circulatory support) or palliation may follow.
CXR Cardiomegaly, pulmonary oedema, pleural eu-
EchoValvular pathology, wall
Treat pulmonary oedema in acute decompensation
9
bldsFBC
K Box 8.8 Heart failure withpreserved ejection fraction
Much understanding in HF comes from patients with echo evidence of
poor LV contraction. However, the signs and symptoms of HF often manifest in those with ‘preserved LVEF’. Such patients have raised LV lling
pressures with LV stiening and reducing lling eciency in diastole. These
patients are more likely to be older, female, overweight, and hypertensive (a demographic increasing in size) but underrepresented in clinical
trials. Despite good theoretical backing, no evidence of mortality benet
exists for ACEi, ARBs, β- blockers, or CCBs. Diuretics should be used
carefully (since acute reductions in lling pressures may worsen failure).
Management involves close attention to correction of dysrhythmias and
comorbidities, BP control, and careful uid balance.
9
European Society of Cardiology Guidelines available at Mhttps://www.escardio.org/Guidelines/
Clinical-Practice-Guidelines/Acute-and-Chronic-Heart-Failure