Cardiovascular System _ PLAB_Passmed _Theory

7/26/2019 Cardiovascular System _ PLAB_Passmed _Theory

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CardiovascularSystem



Chest pain

Assessment of patients with suspected cardiacchest pain

NICE issued guidelines in 2010 on the 'Assessment and diagnosis of recentonset chest pain or discomfort of suspected cardiac origin'.

Patients presenting with acute chest pain

immediate management of suspected acute coronary syndrome ACS!

• "lyceryl trinitrate

•Aspirin #00mg. Nice do not recommend giving other antiplatelet agents (i.e.Clopidogrel) outside of hospital

• $o not routinely give o%ygen& only give if sats ()*+

• ,erform an ecg as soon as possi-le -ut do not delay transfer tohospital. A normal ecg does not e%clude ACS

eferral

• Current chest pain or chest pain in the last 12 hours /ith an a-normalEC" emergency admission

• Chest pain 122 hours ago refer to hospital the sameday forassessment

• Chest pain 3 2 hours ago perform full assessment /ith EC" and

troponin measurement -efore deciding upon further action

+NICE suggest the follo/ing in terms of oxygen therapy

• $o not routinely administer o%ygen& -ut monitor o%ygen saturationusing pulse o%imetry as soon as possi-le& ideally -efore hospitaladmission. 4nly o5er supplemental o%ygen to

Dr.Afsana BhuiyanSource ,assmed



,eople /ith o%ygen saturation spo2! of less than ()* /ho are

not at ris6 of hypercapnic respiratory failure& aiming for spo2 of94-98%

,eople /ith chronic o-structive pulmonary disease /ho are at

ris6 of hypercapnic respiratory failure& to achieve a target spo2of 88-92% until -lood gas analysis is availa-le.

Patients presenting with stabe chest pain

7ith all due respect to NICE the guidelines for assessment of patients /ithsta-le chest pain are rather complicated. 8hey suggest an approach /herethe ris6 of a patient having coronary artery disease CA$! is calculated -asedon their symptoms /hether they have typical angina& atypical angina or

nonangina chest pain!& age& gender and ris6 factors.

NICE de9ne angina pain as the follo/ing

!. "onstricting discomfort in the front of the chest# nec$#shouders# aw or arms

&. Precipitated by physica exertion

'. (eie)ed by rest or *+, in about minutes

,atients /ith all # features have typical angina

,atients /ith 2 of the a-ove features have atypical angina

,atients /ith 1 or none of the a-ove features have nonangina chest

pain

If patients have typical anginal symptoms and a risk of CAD is greater than90* then no further diagnostic testing is re:uired. It should -e noted that allmen over the age of 70 years /ho have typical anginal symptoms fall into

this category.

;or patients /ith an estimated ris6 of 10(0* the follo/ing investigations arerecommended. Note the a-sence of the e%ercise tolerance test




stimated

i$eihood of "AD

Diagnostic testing

/!-90% Coronary angiography'0-/0% ;unctional imaging& for e%ample

• <yocardial perfusion scan /ith S,EC8

• Stress echocardiography

• ;irstpass contrastenhanced magnetic

resonance <! perfusion

• < imaging for stressinduced /all motion

a-normalities.

!0-&9% C8 calcium scoring

,ulses

Pusus parodoxus

•"reater than the normal 10 mm=g! fall in systolic -lood pressureduring inspiration > faint or a-sent pulse in inspiration

• evere asthma! cardiac tamponade

1ow-rising2pateau

• Aortic stenosis

"oapsing

• Aortic regurgitation

• "atent ductus arteriosus

• #yperkinetic (anemia! thyroto$icosis! fever! e$ercise%pregnancy)




Pusus aternans

• egular alternation of the force of the arterial pulse

1e)ere 35

Bisferiens puse

• '$ou-le pulse' t/o systolic pea6s

• &i$ed aortic valve disease

67er$y6 puse

• =ypertrophic o-structive cardiomyopathy+

+=4C< may occasionally -e associated /ith a -isferiens pulse

=eart sounds

8he 9rst heart sound S1! is caused -y closure of the mitral and tricuspidvalves /hilst the second heart sound S2! is due to aortic and pulmonaryvalve closure

1!

• Closure of mitral and tricuspid valves

• Soft if long , or mitral regurgitation

• ?oud in mitral stenosis

1&

• Closure of aortic and pulmonary valves

• Soft in aortic stenosis

• Splitting during inspiration is normal




1' third heart sound

• Caused -y diastolic 9lling of the ventricle

• Considered normal if #0 years old may persist in /omen up to @0years old!

• =eard in left ventricular failure e.g. $ilated cardiomyopathy!&constrictive pericarditis called a pericardial 6noc6!

14 fourth heart sound

• <ay -e heard in aortic stenosis& =4C<& hypertension

• Caused -y atrial contraction against a sti5 ventricle

• In =4C< a dou-le apical impulse may -e felt as a result of a palpa-leS)

=eart sounds S2

S2 is caused -y the closure of the aortic valve A2! closely follo/ed -y that of

the pulmonary valve ,2!




"auses of a oud 1&

• =ypertension systemicloud A2! or pulmonaryloud ,2!

• =yperdynamic states

• Atrial septal defect /ithoutpulmonary hypertension

"auses of a soft 1&

• Aortic stenosis

"auses of :xed spit 1&

• Atrial septal defect

"auses of a widey spit 1&

• $eep inspiration

•

• ,ulmonary stenosis

• Severe mitral regurgitation


"auses of a re)ersed

paradoxica spit 1&

P& occurs before A&

• ?

• Severe aortic stenosis

• ight ventricular pacing



<urmurs

EBection systolic

• Aortic stenosis

• ,ulmonary stenosis& =4C<

• AS$& ;allot's

=olosystolic pansystolic!

• <itraltricuspid

regurgitation highpitchedand '-lo/ing' in character!

• DS$ 'harsh' in character!

?ate systolic

• <itral valve prolapse

•

Coarctation of aorta

Early diastolic

• Aortic regurgitation highpitched and '-lo/ing' in character!

• "rahamSteel murmur pulmonary regurgitation& again highpitchedand '-lo/ing' in character!

<idlate diastolic

• <itral stenosis 'rum-ling' in character!

• Austin;lint murmur severe aortic regurgitation& again is 'rum-ling' incharacter!




Continuous machineli6e mumur

• ,atent ductus arteriosus

Adult advanced life support

8he Boint European esuscitation Council and esuscitation Council F!2010 guidelines do not alter signi9cantly from the 200@ guidelines. ,leasesee the lin6 for more details& -elo/ is only a very -rief summary of 6eypoints changes.

<aBor points include

• atio of chest compressions to ventilation is #02

• Chest compressions are no/ continued /hile a de9-rillator is charged

• $uring a D;D8 cardiac arrest& adrenaline 1 mg is given once chestcompressions have restarted after the third shoc6 and then every #@minutes during alternate cycles of C,!. In the 200@ guidelines&adrenaline /as given Bust -efore the third shoc6. Amiodarone #00 mgis also given after the third shoc6

• Atropine is no longer recommended for routine use in asystole orpulseless

Electrical activity ,EA!.

• A single shoc6 for D;pulseless D8 follo/ed -y 2 minutes of C,& ratherthan a series of # shoc6s follo/ed -y 1 minute of C,

• Asystolepulselesselectrical activity should -e treated /ith 2 minutes

of C,& rather than #& prior to reassessment of the rhythm

• $elivery of drugs via a tracheal tu-e is no longer recommended




• ;ollo/ing successful resuscitation o%ygen should -e titrated to achievesaturations of ()(G*. 8his is to address the potential harm caused -yhypero%aemia

+++8he a-sence of a carotid pulse in the presence of sinus tachycardiaindicates that this is a nonshoc6a-le rhythm& and the appropriate algorithmshould -e follo/ed as e%plained -elo/. 8he only shoc6a-le rhythms areventricular 9-rillation and ventricular tachycardia.

Syncope

Syncope may -e de9ned as a transient loss of consciousness due to glo-alcere-ral hypoperfusion /ith rapid onset& short duration and spontaneouscomplete recovery. Note ho/ this de9nition e%cludes other causes of collapsesuch as epilepsy.

8he European Society of Cardiology pu-lished guidelines in 200( on the

investigation and management of syncope. 8hey suggested the follo/ingclassi9cation

(e;ex syncope neuray mediated

• Dasovagal triggered -y emotion& pain or stress. 4ften referred to as'fainting'

• Situational cough& micturition& gastrointestinal

• Carotid sinus syncope

<rthostatic syncope

• ,rimary autonomic failure ,ar6inson's disease& ?e/y -ody dementia




• Secondary autonomic failure e.g. $ia-etic neuropathy& amyloidosis&uraemia

• $ruginduced diuretics& alcohol& vasodilators

• Dolume depletion haemorrhage& diarrhoea

"ardiac syncope

• Arrhythmias -radycardias sinus node dysfunction& AD conductiondisorders! or tachycardias supraventricular& ventricular!

• Structural valvular& myocardial infarction& hypertrophic o-structivecardiomyopathy

• 4thers pulmonary em-olism

eHe% syncope is the most common cause in all age groups althoughorthostatic and cardiac causes -ecome progressively more common in olderpatients.

Evaluation

• Cardiovascular e%amination

Postura bood pressure readings= a symptomatic fa insystoic BP > &0 mm?g or diastoic BP > !0 mmhg or decreasein systoic BP @ 90 mm?g is considered diagnostic

• EC"

• Carotid sinus massage

• 8ilt ta-le test

• 2) hour EC"

,eriarrest rhythms tachycardia

8he 2010 esuscitation Council F! guidelines have simpli9ed the advicegiven for the management of periarrest tachycardias. Separate algorithms




for the management of -roadcomple% tachycardia& narro/ comple%tachycardia and atrial 9-rillation have -een replaced -y one uni9edtreatment algorithm;ollo/ing -asic AC assessment& patients are classi9ed as -eing sta-le orunsta-le according to the presence of any adverse signs

• Shoc6 hypotension systolic -lood pressure (0 mmhg!& pallor&s/eating&

Cold& clammy e%tremities& confusion or impaired consciousness

• Syncope

• <yocardial ischaemia

• =eart failure

If any of the a-ove adverse signs are present then synchronised $C shoc6sshould -e given 8reatment follo/ing this is given according to /hether the S comple% isnarro/ or -road and /hether the rhythm is regular or irregular. 8he fulltreatment algorithm can -e found at the esuscitation Council /e-site&-elo/ is a very limited summary

Broad-compex tachycardia

'egular Assume ventricular tachycardia unless previously con9rmed SD8 /ith

-undle -ranch -loc6! ?oading dose of amiodarone follo/ed -y 2) hour infusion

rregular A; /ith -undle -ranch -loc6 treat as for narro/ comple% tachycardia

,olymorphic D8 e.g. 8orsade de pointes! ID magnesium

,arrow-compex tachycardia

'egular

Dagal manoeuvres follo/ed -y ID adenosine If a-ove unsuccessful consider diagnosis of atrial Hutter and control

rate e.g. eta-loc6ers!rregular

,ro-a-le atrial 9-rillation

If onset )G hr consider electrical or chemical cardioversion




ate control e.g. eta-loc6er or digo%in! and anticoagulation

,eriarrest rhythms -radycardia

8he 2010 esuscitation Council F! guidelines emphasise that the

management of -radycardia depends on

!. dentifying the presence of signs indicating haemodynamiccompromise - 6ad)erse signs6

&. dentifying the potentia ris$ of asystoe

Ad)erse signs

8he follo/ing factors indicate haemodynamic compromise and hence the

need for treatment

• Shoc6 hypotension systolic -lood pressure (0 mmhg!& pallor&s/eating&

Cold& clammy e%tremities& confusion or impaired consciousness

• Syncope


• =eart failure

Atropine is the 9rst line treatment in this situation. If this fails to /or6& orthere is the potential ris6 of asystole then transvenous pacing is indicated

Potentia ris$ of asystoe 8he follo/ing indicate a potential ris6 of asystole and hence the need fortreatment /ith transvenous pacing

• Complete heart -loc6 /ith -road comple% S

• ecent asystole

• <o-itJ type II AD -loc6

• Dentricular pause 3 # seconds




If there is a delay in the provision of transvenous pacing the follo/inginterventions may -e used

• Atropine& up to ma%imum of #mg

• 8ranscutaneous pacing

• Adrenaline infusion titrated to response

Dentricular tachycardia

Dentricular tachycardia D8! is -roadcomple% tachycardia originating from aventricular ectopic focus. It has the potential to precipitate ventricular9-rillation and hence re:uires urgent treatment.

8here are t/o main types of D8 onomorphic + most commonly caused -y myocardial infarction

Poymorphic + A su-type of polymorphic D8 is torsades de pointes

/hich is precipitated -y prolongation of the 8 interval. 8he causes ofa long 8 interval are listed -elo/

"auses of a proonged C+ inter)a

"ongenita Drugs <ther

7er)e-3ange-

,iesen syndrome

incudes deafness

and is due to an

abnorma

potassium channe

(omano-ard

syndrome nodeafness

amiodarone&

sotalol& class 1a

antiarrhythmic

drugs tricyclic

antidepressants&

Huo%etine chloro:uine

terfenadine

erythromycin

electrolyte

hypocalcaemia&

hypo6alaemia&

hypomagnesaemia acute myocardial

infarction myocarditis

hypothermia

su-arachnoid

haemorrhage

anagement

If the patient has adverse signs systolic , (0 mmhg& chest pain& heart




failure or rate 3 1@0 -eatsmin! then immediate cardioversion is indicated. Inthe a-sence of such signs antiarrhythmics may -e used. If these fail& thenelectrical cardioversion may -e needed /ith synchronised $C shoc6s

$rug therapy

• Amiodarone ideally administered through a central line

• ?idocaine use /ith caution in severe left ventricular impairment

• ,rocainamide

erapami shoud ,<+ be used in +

If drug therapy fails

• Electrophysiological study E,S!

• Implant a-le cardioverterde9-rillator IC$! this is particularlyindicated in patients /ith signi9cantly impaired ?D function

+++=ypo6alemia is the most important cause of ventricular tachycardia D8!

clinically& follo/ed -y hypomagnesaemia. Severe hyper6alaemia may causeD8 in certain circumstances& for e%ample in patients /ith structural heartdisease& -ut it is not as common a cause as hypo6alemia.

8orsades de pointes

8orsades de pointes 't/isting of the points'! is a rare arrhythmia associated/ith a long 8 interval. It may deteriorate into ventricular 9-rillation and

hence lead to sudden death

Causes of long 8 interval

• Congenital Kervell?angeNielsen syndrome& omano7ard syndrome




• Antiarrhythmics amiodarone& sotalol& class 1a antiarrhythmic drugs

• 8ricyclic antidepressants

• Antipsychotics

• Chloro:uine

• 8erfenadine

• Erythromycin

• Electrolyte hypocalcaemia& hypo6alaemia& hypomagnesaemia

• <yocarditis

• =ypothermia

• Su-arachnoid haemorrhage

<anagement

• ID magnesium sulphate

Supraventricular tachycardia




7hilst strictly spea6ing the term supraventricular tachycardia SD8! refers toany tachycardia that is not ventricular in origin the term is generally used inthe conte%t of paro%ysmal SD8. Episodes are characterised -y the suddenonset of a narro/ comple% tachycardia& typically an atrioventricular nodal re

entry tachycardia ADN8!. 4ther causes include atrioventricular reentrytachycardias AD8! and Bunctional tachycardias.

Acute management

• Dagal manoeuvres e.g. Dalsalva manoeuvre

• Intravenous adenosine Lmg > 12mg > 12mg contraindicated inasthmatics verapamil is a prefera-le option

• Electrical cardioversion

,revention of episodes

• eta-loc6ers

• adiofre:uency a-lation

Atrial 9-rillationrate control and maintenance

of sinus rhythm

8he oyal College of ,hysicians and NICE pu-lished guidelines on the

management of atrial 9-rillation A;! in 200L. 8he follo/ing is also -ased onthe Boint American =eart Association A=A!& American College of CardiologyACC! and European Society of Cardiology ESC! 2012 guidelines

Agents used to control rate in patients /ith atrial 9-rillation

Beta-boc$ers




"acium channe boc$ers

Digoxin not considered :rst-ine anymore as they are esseEecti)e at controing the heart rate during exercise.?owe)er# they are the preferred choice if the patient has

coexistent heart faiure

Agents used to maintain sinus rhythm in patients /ith a history of atrial9-rillation

1otao

Amiodarone

5ecainide

<thers ess commony used in FG= disopyramide# dofetiide#procainamide# propafenone# Huinidine

8he ta-le -elo/ indicates some of the factors /hich may -e considered /henconsidering either a rate control or rhythm control strategy

5actors fa)ouring rate

contro

5actors fa)ouring rhythm contro

4lder than L@ years

=istory of ischaemic heartdisease

7ith contraindications to

antiarrhythmic drugs.

nsta-le for cardioversion.

Mounger than L@ years

Symptomatic;irst presentation

?one A; or A; secondary to a corrected

precipitant e.g. Alcohol!

Congestive heart failure

8he 9rst thing is to determine the type of A;& so here are some importantsimpli9ed! de9nitions.

• Acute onset /ithin the previous )G hours.




• ,aro%ysmal spontaneous termination /ithin seven days and mostoften /ithin )G hours.

• ecurrent t/o or more episodes.

• ,ersistent not selfterminating lasting longer than seven days& orprior cardioversion.

• ,ermanent longstanding A; de9ned as over a year! that is notsuccessfully terminated -y

Atrial 9-rillation anticoagulation

NICE updated their guidelines on the management of atrial 9-rillation A;! in201). 8hey suggest using the "?A&D1&-)asc score to determine the most

appropriate anticoagulation strategy. 8his scoring system superceded theC=A$S2 score.

(is$ factor Poin

ts

" Congestive heart failure 1

? =ypertension or treated hypertension! 1

A

&

Age 3O @ years 2

Age L@) years 1

D $ia-etes 11

&

,rior Stro6e or 8IA 2

Dascular disease including ischaemic heart disease and

peripheral arterial disease!

1

1 Se% female! 1

8he ta-le -elo/ sho/s a suggested anticoagulation strategy -ased on thescore

1core Anticoaguation

0 No treatment

! <ales Consider anticoagulation

;emales No treatment this is -ecause their score of 1 is only

reached due to their gender!

& or 45er anticoagulation




more

NICE recommend that /e o5er patients a choice of anticoagulation& including/arfarin and the novel oral anticoagulants noacs!. 8here are complicatedrules surrounding /hich N4AC is licensed for /hich ris6 factor these can -e

found in the NICE guidelines. Aspirin is no longer recommended for reducingstro6e ris6 in patients /ith A;

$octors have al/ays thought carefully a-out the ris6-ene9t pro9le ofstarting someone on /arfarin. A history of falls& old age& alcohol e%cess and ahistory of previous -leeding are common things that ma6e us consider/hether /arfarinisation is in the -est interests of the patient. NICE no/recommend /e formalise this ris6 assessment using the =AS?E$ scoringsystem.

8here are no formal rules on ho/ /e act on the =AS?E$ score although a

score of 3O # indicates a 'high ris6' of -leeding& de9ned as intracranial

haemorrhage& hospitalisation& haemoglo-in decrease 32 g?& andor

transfusion.

Atrial 9-rillation pharmacological cardioversion


Atrial fibrillation - cardioversion: amiodarone +

(is$ factor Points

? =ypertension& uncontrolled& systolic , 3 1L0

mmhg

1

A A-normal renal function dialysis or creatinine 3

200!

4r

A-normal liver function cirrhosis& -iliru-in 3 2

times normal& A?8AS8A?, 3 # times normal

1 for any renal

a-normalities

1 for any liver

a-normalities

1 Stro6e& history of 1

B leeding& history of -leeding or tendency to -leed 1

3 ?a-ile inrs unsta-lehigh inrs& time in therapeuticrange L0*!

1

Elderly 3 L@ years! 1

D $rugs ,redisposing to leeding Antiplatelet agents&

nsaids!

4r

Alcohol se 3G drin6s/ee6!

1 for drugs

1 for alcohol



8he oyal College of ,hysicians and NICE pu-lished guidelines on themanagement of atrial 9-rillation A;! in 200L. 8he follo/ing is also -ased onthe Boint American =eart Association A=A!& American College of CardiologyACC! and European Society of Cardiology ESC! 2012 guidelinesAgents /ith proven ePcacy in the pharmacological cardioversion of atrial

9-rillation

Amiodarone

5ecainide if no structura heart disease

<thers ess commony used in FG= Huinidine# dofetiide#ibutiide# propafenone

?ess e5ective agents

• eta-loc6ers including sotalol!

• Calcium channel -loc6ers

• $igo%in

• $isopyramide

• ,rocainamide

Atrial 9-rillation cardioversion

8here are t/o scenarios /here cardioversion may -e used in atrial9-rillation

• Electrical cardioversion as an emergency if the patient is

haemodynamically unsta-le

• Electrical or pharmacological cardioversion as an elective procedure/here a rhythm control strategy is preferred.

8he notes -elo/ refer to cardioversion -eing used in the elective scenario forrhythm control. 8he /ording of the 201) NICE guidelines is as follo/s




*er rate or rhythm control if the onset of the arrhythmia is less than +,hours! and start rate control if it is more than +, hours or is uncertain

<nset @ 48 hours

If the atrial 9-rillation A;! is de9nitely of less than )G hours onset patientsshould -e heparinised. ,atients /ho have ris6 factors for ischaemic stro6eshould -e put on lifelong oral anticoagulation. 4ther/ise& patients may -ecardioverted using either

• Electrical '$C cardioversion'

• ,harmacology amiodarone if structural heart disease& Hecainide or

amiodarone in those /ithout structural heart disease

;ollo/ing electrical cardioversion if A; is con9rmed as -eing less than )Ghours duration then further anticoagulation is unnecessary

<nset > 48 hours

If the patient has -een in A; for more than )G hours then anticoagulationshould -e given for at least # /ee6s prior to cardioversion. An alternativestrategy is to perform a transoesophageal echo 84E! to e%clude a left atrialappendage ?AA! throm-us. If e%cluded patients may -e heparinised and

cardioverted immediately.

NICE recommend electrical cardioversion in this scenario& rather thanpharmacological.

If there is a high ris6 of cardioversion failure e.g. ,revious failure or A;recurrence! then it is recommend to have at least ) /ee6s amiodarone orsotalol prior to electrical cardioversion

5oowing eectrica cardio)ersion patients shoud be

anticoaguated for at east 4 wee$s. After this timedecisions about anticoaguation shoud be ta$en on anindi)idua basis depending on the ris$ of recurrence




Atrial 9-rillation poststro6e

NICE issued guidelines on atrial 9-rillation A;! in 200L. 8hey included adviceon the management of patients /ith A; /ho develop a stro6e or transientischaemic attac6 8IA!.

ecommendations include

• ;ollo/ing a stro6e or 8IA /arfarin should -e given as the anticoagulantof choice. Aspirindipyridamole should only -e given if needed for thetreatment of other comor-idities

In acute stro6e patients& in the a-sence of haemorrhage& anticoagulation

therapy should -e commenced after 2 /ee6s. If imaging sho/s a very large

cere-ral infarction then the initiation of anticoagulation should -e delayed

Fey ,oints

ate control algorithm step 1 administer throm-oprophyla%is

Side e5ects of amiodarone has some important side e5ects such ashypohyperthyroidism due to loo6ing similar to thyro%ine and causes

throm-ophle-itis.A calcium channel -loc6er CC! i.e. Derapamil! for rate control& /ithdigo%in only -eing indicated in sedentary patients. 8hese are correct-ut N48 9rst line. ;or further reading




If the presentation is atrial 9-rillation as seen -y palpitations anda-sent , /aves on EC"!& the options for management include rate orrhythm control& /ith the possi-ility of throm-oprophyla%is.

=o/ever& as he has an unmeasura-le , and signs of

haemodynamic insta-ility& patient is acutely un/ell and so his

arrhythmia must -e treated as soon as possi-le /ith $Ccardioversion /ithout delaying for throm-oprophyla%is.Anticoagulation should -e continued for ) /ee6s aftercardioversion ho/ever.

If patient is clinically sta-le and had atrial 9-rillation of over )G

hours duration& the ris6 of stro6e /ould mean parenteralanticoagulation /ould ta6e precedence over cardioversion.source NICE& https///.nice.org.u6guidancecg1G0!

• Asthma is a contraindication to the prescription of a -eta-loc6er.NICE therefore recommend a ratelimiting calcium channel-loc6er.Consideration should also -e given to antithrom-otic therapy.

• 'If pharmacological cardioversion has -een agreed on clinical andresource grounds for ne/onset atrial 9-rillation& o5er

• ;lecainide or amiodarone if there is no evidence ofstructural or ischaemic heart disease or

• Amiodarone if there is evidence of structural heart

disease.'

=ypertension


https://www.nice.org.uk/guidance/cg180

https://www.nice.org.uk/guidance/cg180



DA*,<11 A,D A,A*,+

NICE pu-lished updated guidelines for the management of hypertension in2011. Some of the 6ey changes include

"assifying hypertension into stages

(ecommending the use of ambuatory bood pressuremonitoring ABP and home bood pressure monitoring?BP

"acium channe boc$ers are now considered superior tothiaIides

Bendro;umethiaIide is no onger the thiaIide of choice

Diagnosing hypertension

;irstly& NICE recommend measuring -lood pressure in -oth arms /henconsidering a diagnosis of hypertension.

If the di5erence in readings -et/een arms is more than 20 mmhg then themeasurements should -e repeated. If the di5erence remains 3 20 mmhgthen su-se:uent -lood pressures should -e recorded from the arm /ith thehigher reading.

It should of course -e remem-er that there are pathological causes ofune:ual -lood pressure readings from the arms& such as supravalvular aorticstenosis. It is therefore prudent to listen to the heart sounds if a di5erencee%ists and further investigation if a very large di5erence is noted.

NICE also recommend ta6ing a second reading during the consultation& if the9rst reading is 3 1)0(0 mmhg. 8he lo/er reading of the t/o shoulddetermine further management.

NICE suggest o5ering A,< or =,< to any patient /ith a -lood pressure 3O

1)0(0 mmhg.

If ho/ever the -lood pressure is 3O 1G0110 mmhg

• Immediate treatment should -e considered




• If there are signs of papilloedema or retinal haemorrhages NICErecommend same day assessment -y a specialist

• NICE also recommend referral if a phaeochromocytoma is suspectedla-ile or postural hypotension& headache& palpitations& pallor and

diaphoresis!

Ambuatory bood pressure monitoring ABP

• At least 2 measurements per hour during the person's usual /a6inghours for e%ample& -et/een 0G00 and 2200!

• se the average value of at least 1) measurements

If A,< is not tolerated or declined =,< should -e o5ered.

?ome bood pressure monitoring ?BP

• ;or each , recording& t/o consecutive measurements need to -eta6en& at least 1 minute apart and /ith the person seated

• , should -e recorded t/ice daily& ideally in the morning and evening

• , should -e recorded for at least ) days& ideally for days

•$iscard the measurements ta6en on the 9rst day and use the averagevalue of all the remaining measurements

Bood pressure cassi:cation

1tage "riteria

1tage !

hypertensio

n

Clinic , 3O 1)0(0 mmhg and su-se:uent A,< daytime

average or =,< average , 3O 1#@G@ mmhg

1tage &

hypertension

Clinic , 3O 1L0100 mmhg and su-se:uent A,<

daytime average or =,< average , 3O 1@0(@ mmhg

1e)ere

hypertensio

n

Clinic systolic , 3O 1G0 mmhg& or clinic diastolic , 3O

110 mmhg




anaging hypertension

• A lo/ salt diet is recommended& aiming for less than Lgday& ideally#gday. 8he average adult in the F consumes around G12gday ofsalt. A recent <K paper+ sho/ed that lo/ering salt inta6e can have asigni9cant e5ect on -lood pressure. ;or e%ample& reducing salt inta6e-y Lgday can lo/er systolic -lood pressure -y 10mmhg

• Ca5eine inta6e should -e reduced

• 8he other general -its of advice remain stop smo6ing& drin6 lessalcohol& eat a -alanced diet rich in fruit and vegeta-les& e%ercise more&

lose /eight

ABP2?BP >J !'28 mm?g i.e. 1tage ! hypertension

• 8reat if G0 years of age AN$ any of the follo/ing apply target organdamage& esta-lished cardiovascular disease& renal disease& dia-etes ora 10year cardiovascular ris6 e:uivalent to 20* or greater

ABP2?BP >J !029 mmhg i.e. 1tage & hypertension

• 45er drug treatment regardless of age

;or patients )0 years consider specialist referral to e%clude secondarycauses.

1tep ! treatment

•

,atients @@yearsold ACE inhi-itor A!

• ,atients 3 @@yearsold or of AfroCari--ean origin calcium channel

-loc6er




1tep & treatment

• ACE inhi-itor Q calcium channel -loc6er A Q C!

1tep ' treatment

• Add a thiaJide diuretic $& i.e. A Q C Q $!

• NICE no/ advocate using either chlorthalidone 12.@[email protected] mg oncedaily! or indapamide 1.@ mg modi9edrelease once daily or 2.@ mgonce daily! in preference to a conventional thiaJide diuretic such as-endroHumethiaJide

NICE de9ne a clinic , 3O 1)0(0 mmhg after step # treatment /ith optimalor -est tolerated doses as resistant hypertension. 8hey suggest step )treatment or see6ing e%pert advice

1tep 4 treatment

• Consider further diuretic treatment

• If potassium ).@ mmoll add spironolactone 2@mg od

•

If potassium 3 ).@ mmoll add higherdose thiaJideli6e diuretictreatment

• If further diuretic therapy is not tolerated& or is contraindicated or

ine5ective& consider an alpha or -eta-loc6er

,atients /ho fail to respond to step ) measures should -e referred to aspecialist. NICE recommend

f -lood pressure remains uncontrolled ith the optimal or ma$imumtolerated doses of four drugs! seek e$pert advice if it has not yet -een

o-tained.

Bood pressure targets

"inic BP ABP 2 ?BP

Age @ 80 years 1)0(0 mmhg 1#@G@ mmhg




Age > 80 years 1@0(0 mmhg 1)@G@ mmhg

,ew drugsDirect renin inhibitors

• E.g. Alis6iren -randed as asileJ!

• y inhi-iting renin -loc6s the conversion of angiotensinogen toangiotensin I

• No trials have loo6ed at mortality data yet. 8rials have onlyinvestigated fall in -lood pressure. Initial trials suggest alis6irenreduces -lood pressure to a similar e%tent as angiotensin convertingenJyme ACE! inhi-itors or angiotensinII receptor antagonists

•

Adverse e5ects /ere uncommon in trials although diarrhoea /asoccasionally seen

• 4nly current role /ould seem to -e in patients /ho are intolerant ofmore esta-lished antihypertensive drugs

Isolated systolic hypertension

Isolated systolic hypertension IS=! is common in the elderly& a5ecting

around @0* of people older than 0 years old

. 8he Systolic =ypertension in the Elderly ,rogram S=E,! -ac6 in 1((1esta-lished that treating IS= reduced -oth stro6es and ischaemic heartdisease.

$rugs such as thiaJides /ere recommended as 9rst line agents. 8his

approach is contradicated -y the 2011 NICE guidelines /hichrecommends treating IS= in the same step/ise fashion as standardhypertension.

$ia-etes mellitus hypertension management

NICE recommend the follo/ing -lood pressure targets for type 2 dia-etics

f end-organ damage e.g. (ena disease# retinopathy @!'0280 mmhg

<therwise @ !40280 mmhg




Gey Points=

8he 2011 NICE guidelines recognise that in the past there /as

overtreatment of '/hite coat' hypertension. 8he use of am-ulatory

-lood pressure monitoring A,<! aims to reduce this. 8here is also

good evidence that A,< is a -etter predictor of cardiovascular ris6

than clinic -lood pressure readings. See the follo/ing study for more

details NICE no/ only recommend diagnosing people over the age of G0 years

as hypertensive if they have stage 2 hypertension A,< daytimeaverage or =,< average , 3O 1@0(@ mmhg!.

A 2012 <K article <K 2012#)@e)#! on resistant hypertension

highlighted the importance of correcting lifestyle factors in patients/ith resistant hypertension. 4nly around 10* of patients /ith resistanthypertension have a secondary case& e.g. Conn's syndrome.

Isolated hypertension perspectiveQ 3 @@ yearsQ eBection fraction is

))* O An ACE inhi-itor rather than a CC. A -eta-loc6er should also-e added due to the evidence of heart failure.

8he use -loc6er in the treatment of =8N has declined recently as

?ess li6ely to prevent stro6e Q potential impairment of glucosetolerance

If a calcium channel -loc6er is not suita-le& for e%ample -ecause of oedema

or intolerance& or if there is evidence of heart failure or a high ris6 of heartfailure& o5er a thiaJideli6e diuretic

8ight -lood pressure remains a 6ey management aim in patients /ith

dia-etic nephropathy. ACE inhi-itors are clearly the most evidence-ased management in this arena.

,ersistently high ,Q$ia-etic retinopathyO thiaJide -ased diuretice.g. Indapamide!

If the egfr is less than #0 mlmin1.#mR then thiaJides should -e

avoided as the N; states/hiaides and related diuretics are ine*ective if egfris less than 10 ml%minute%.71 m2 and should -e avoided3 metolaone remainse*ective -ut ith a risk of e$cessive dieresis

Spironolactone and angiotensin II receptor -loc6ers may ris6

precipitating hyper6alaemia. A 201# Cochrane revie/ casted dou-t on the /isdom of lo/er -lood

pressure targets for patients /ith dia-etes. It compared patients /hohad tight -lood pressure control targets 1#0G@ mmhg! /ith more

rela%ed control 1)01L0(0100 mmhg!. ,atients /ho /ere moretightly controlled had a slightly reduced rate of stro6e -ut other/iseoutcomes /ere not signi9cantly di5erent.

ecause ACEinhi-itors have a renoprotective e5ect in dia-etes theyare the 9rstline antihypertensives recommended for NICE. ,atients of




African or Cari--ean family origin should -e o5ered an ACEinhi-itorplus either a thiaJide diuretic or calcium channel -loc6er. ;urthermanagement then reverts to that of nondia-etic patients.Autonomic neuropathy may result in more postural symptoms inpatients ta6ing antihypertensive therapy.

,rimary hyperaldosteronism

,rimary hyperaldosteronism /as previously thought to -e most commonly

caused -y an adrenal adenoma& termed Conn's syndrome. =o/ever& recent

studies have sho/n that -ilateral idiopathic adrenal hyperplasia is the cause

in up to 0* of cases. $i5erentiating -et/een the t/o is important as this

determines treatment. Adrenal carcinoma is an e%tremely rare cause of

primary hyperaldosteronism

5eatures

• =ypertension

• =ypo6alaemia e.g. <uscle /ea6ness!

• Al6alosis

n)estigations

• =igh serum aldosterone

• ?o/ serum renin

• =ighresolution C8 a-domen

• Adrenal vein sampling

anagement

Adrenal adenoma surgery

ilateral adrenocortical hyperplasia aldosterone antagonist e.g.

1pironoactone




C8 a-domen sho/ing a rightsided adrenaladenoma in a patient /ho presented /ith

hypertension and hypo6alaemia. 8headenoma can -e seen 'ne%t to' or '-elo/'the liver.

,haeochromocytoma

,haeochromocytoma is a rare catecholamine secreting tumour. A-out 10*are familial and may -e associated /ith <EN type II& neuro9-romatosis andvon =ippel?indau syndrome

asics

• ilateral in 10*

• <alignant in 10*

• E%traadrenal in 10* most common site O organ of uc6er6andl&

adBacent to the -ifurcation of the aorta!

5eatures are typicay episodic

?ypertension around 90% of cases# may be sustained

?eadaches

Papitations

1weating

Anxiety




+ests

• 2) hr urinary collection of metanephrines sensitivity (*+!

8his has replaced a &4 hr urinary coection of catechoaminessensiti)ity 8/%

Surgery is the de9nitive management. 8he patient must 9rst ho/ever -esta-iliJed /ith medical management

• Alpha-loc6er e.g. ,heno%y-enJamine!& given -efore a

• eta-loc6er e.g. ,ropranolol!

+<K 2012 #)) doi httpd%.doi.org10.11#L-mB.e10)2 ,u-lished 20;e-ruary 2012!

Acute Coronary SyndromeAngina ,ectoris

Angina pectoris= drug management

8he management of sta-le angina comprises lifestyle changes& medication&percutaneous coronary intervention and surgery. NICE produced guidelines in2011 covering the management of sta-le angina

<edication

• All patients should receive aspirin and a statin in the a-sence ofany contraindication

• 1ubingua gycery trinitrate to a-ort angina attac6s




• NICE recommend using either a beta-boc$er or a caicumchanne boc$er 9rstline -ased on 'comor-idities&contraindications and the person's preference'

• If a calcium channel -loc6er is used as monotherapy a ratelimiting one

such as )erapami or ditiaIem should -e used. If used incom-ination /ith a -eta-loc6er then use a longactingdihydropyridine calciumchannel -loc6er e.g. <odi9edreleasenifedipine!. Beta-boc$ers shoud not be prescribed concurrentywith )erapami ris$ of compete heart boc$

• If there is a poor response to initial treatment then medication should

-e increased to the ma%imum tolerated dose e.g. ;or atenolol 100mgod!

• If a patient is still symptomatic after monotherapy /ith a -eta-loc6eradd a calcium channel -loc6er and vice versa

• If a patient is on monotherapy and cannot tolerate the addition of acalcium channel -loc6er or a -eta-loc6er then consider one of thefollo/ing drugs a longacting nitrate& iva-radine& nicorandil orranolaJine

• If a patient is ta6ing -oth a -eta-loc6er and a calciumchannel -loc6erthen only add a third drug /hilst a patient is a/aiting assessment for,CI or CA"

Nitrate tolerance

• <any patients /ho ta6e nitrates develop tolerance and e%periencereduced ePcacy

• 8he N; advises that patients /ho develop tolerance should ta6e thesecond dose of isosor-ide mononitrate after G hours& rather than after12 hours. 8his allo/s -loodnitrate levels to fall for ) hours andmaintains e5ectiveness

• 8his e5ect is not seen in patients /ho ta6e modi9ed release isosor-idemononitrate

)abradine




• A ne/ class of antianginal drug /hich /or6s -y reducing the heartrate

• Acts on the If 'funny'! ion current /hich is highly e%pressed in thesinoatrial node& reducing cardiac pacema6er activity

• Adverse e5ects visual e5ects& particular luminous phenomena& arecommon. radycardia& due to the mechanism of action& may also -eseen

• 8here is no evidence currently of superiority over e%isting treatmentsof sta-le angina

Nitrates

Nitrates are a group of drugs /hich have vasodilating e5ects. 8he mainindications for their use is in the management of angina and the acutetreatment of heart failure. Su-lingual glyceryl trinitrate is the most commondrug used in patients /ith ischaemic heart disease to relieve angina attac6s.

<echanism of action

• Cause release of nitric o%ide in smooth muscle& increasing cgmp /hich

leads to a fall in intracellular calcium levels

• In angina they -oth dilate the coronary arteries and also reducevenous return /hich in turn reduces left ventricular /or6& reducingmyocardial o%ygen demand

Sidee5ects

?ypotension

+achycardia

?eadaches

5ushing




xercise toerance tests

E%ercise tolerance tests E88& also e%ercise EC"! are used for a variety ofindications

• Assessing patients /ith suspected angina ho/ever the 2010 NICEChest pain of recent onset guidelines do not support the use of etts forall patients

• is6 stratifying patients follo/ing a myocardial infarction

• Assessing e%ercise tolerance

• is6 stratifying patients /ith hypertrophic cardiomyopathy

E88 has a sensitivity of around G0* and a speci9city of 0* for ischaemicheart disease.

=eart rate

• <a%imum predicted heart rate O 220 patient's age

•

8he target heart rate is at least G@* of ma%imum predicted to allo/reasona-le interpretation of

A test as lo/ris6 or negative

Contraindications

• <yocardial infarction less than days ago

• nsta-le angina

• ncontrolled hypertension systolic , 3 1G0 mmhg! or hypotensionsystolic , (0 mmhg!

• Aortic stenosis




• ?eft -undle -ranch -loc6 this /ould ma6e the EC" very diPcult tointerpret

Stop if

• E%haustion patient re:uest

• 'Severe'& 'limiting' chest pain

• 3 #mm S8 depression

• 3 2mm S8 elevation.Stop if rapid S8 elevation and pain

• Systolic -lood pressure 3 2#0 mmhg

• Systolic -lood pressure falling 3 20 mmhg

• Attainment of ma%imum predicted heart rate

• =eart rate falling 3 20* of starting rate

• Arrhythmia develops

Acute Coronary Syndrome <yocardial

infarction<I!

A,A*,+ <5 1+A num-er of studies over the past 10 years have provided an evidence for themanagement of S8elevation myocardial infarction S8E<I!




In the a-sence of contraindications& all patients should -e given

Aspirin

"opidogre= the two maor studies "3A(+K and "<+ bothcon:rmed bene:t but used diEerent oading doses '00mg andLmg respecti)ey

3ow moecuar weight heparin

NICE suggest the follo/ing in terms of o%ygen therapy

• $o not routinely administer o%ygen& -ut monitor o%ygen saturationusing pulse o%imetry as soon as possi-le& ideally -efore hospitaladmission. 4nly o5er supplemental o%ygen to

• ,eople /ith o%ygen saturation spo2! of less than ()* /ho are not atris6 of hypercapnic respiratory failure& aiming for spo2 of ()(G*

• ,eople /ith chronic o-structive pulmonary disease /ho are at ris6 ofhypercapnic respiratory failure& to achieve a target spo2 of GG(2*until -lood gas analysis is availa-le.

,rimary percutaneous coronary intervention ,CI! has emerged as the goldstandard treatment for S8E<I -ut is not availa-le in all centres. 8hrom-olysisshould -e performed in patients /ithout access to primary ,CI

7ith regards to throm-olysis




• 8issue plasminogen activator tpa! has -een sho/n to o5er clearmortality -ene9ts over strepto6inase

• 8enecteplase is easier to administer and has -een sho/n to have noninferior ePcacy to alteplase /ith a similar adverse e5ect pro9le

An EC" should -e performed (0 minutes follo/ing throm-olysis to assess/hether there has -een a greater than @0* resolution in the S8 elevation

• If there has not -een ade:uate resolution then rescue ,CI is superior torepeat throm-olysis

• ;or patients successfully treated /ith throm-olysis ,CI has -een sho/nto -e -ene9cial. 8he optimal timing of this is still under investigation

"lycaemic control in patients /ith dia-etes mellitus

• In 2011 NICE issued guidance on the management of hyperglycaemiain acute coronary syndromes

• It recommends using a doseadBusted insulin infusion /ith regular

monitoring of -lood glucose levels to glucose -elo/ 11.0 mmoll

• Intensive insulin therapy an intravenous infusion of insulin and

glucose /ith or /ithout potassium& sometimes referred to as '$I"A<I'!regimes are not recommended routinely

MMM $eep S8 depression in D1D# /ith tall 8 /aves is a sign of a severe

posterior myocardial infarction. 8hese patients should -e treated as a S8E<I.

If posterior leads are placed on the -ac6 of the patient and EC" redone S8

elevation /ill -e seen. 8herefore the patient should -e treated /ith primary

percutaneous coronary intervention.

NICE guidelines on S8E<I care 201#

4*er coronary angiography! ith follo5on primary "C if indicated! as the preferred coronary reperfusion strategy for people ith acute /6& if




• "resentation is ithin 2 hours of onset of symptoms and

• "rimary "C can -e delivered ithin 20 minutes of the time hen

8-rinolysis could have -een given4

MMM S8 elevation of 1mm in leads II& III and avf reHects signi9cant cardiac

ischaemia due to the right coronary artery occlusion. 8he medical registrar should

-e contacted to urgently assess the patient. Note right coronary artery occlusions

puts the patient at ris6 of cardiac arrhythmias due to -lood supply to the sino atrial

node!.

8hrom-olysis or percutaneous intervention in myocardial

infarction

8hrom-olytic drugs activate plasminogen to form plasmin. 8his in turn degrades

9-rin and help -rea6s up throm-i. 8hey in primarily used in patients /ho present

/ith a S8 elevation myocardial infarction. 4ther indications include acute ischaemic

stro6e and pulmonary em-olism& although strict inclusion criteria apply.

E%amples

Atepase

+enectepase

1trepto$inase

Contraindications to throm-olysis

• Active internal -leeding

• ecent haemorrhage& trauma or surgery including dental e%traction!

•

Coagulation and -leeding disorders

• Intracranial neoplasm

• Stro6e # months

• Aortic dissection




• ecent head inBury

• ,regnancy

• Severe hypertension

Sidee5ects

• =aemorrhage

• =ypotension more common /ith strepto6inase

• Allergic reactions may occur /ith strepto6inase

Acute coronary syndrome management ofNS8E<I

NICE produced guidelines in 201# on the econdary prevention in primaryand secondary care for patients folloing a myocardial infarction

management of unsta-le angina and non5/ elevation myocardial infarction(/6&). 8hese superceded the 2010 guidelines /hich advocated a ris6-ased approach to management /hich determined /hether drugs such asclopidogrel /ere given.

All patients should receive

Aspirin '00mg

,itrates or morphine to reie)e chest pain if reHuired

7hilst it is common that nonhypo%ic patients receive o%ygen therapy thereis little evidence to support this approach. 8he 200G ritish 8horacic Societyo%ygen therapy guidelines advise not giving o%ygen unless the patient ishypo%ic.




Antithrombin treatment. ;ondaparinu% should -e o5ered to patients /hoare not at a high ris6 of -leeding and /ho are not having angiography /ithinthe ne%t 2) hours. If angiography is li6ely /ithin 2) hours or a patientscreatinine is 3 2L@ Tmoll unfractionated heparin should -e given.

"opidogre #00mg should -e given to all patients and continued for 12months.

Intravenous gycoprotein iib2iiia receptor antagonists epti9-atide ortiro9-an! should -e given to patients /ho have an intermediate or higherris6 of adverse cardiovascular events predicted Lmonth mortality a-ove#.0*!& and /ho are scheduled to undergo angiography /ithin (L hours ofhospital admission.

"oronary angiography should -e considered /ithin (L hours of 9rstadmission

to hospital to patients /ho have a predicted Lmonth mortality a-ove #.0*.It should also -e performed as soon as possi-le in patients /ho are clinicallyunsta-le.

8he ta-le -elo/ summaries the mechanism of action of drugs commonlyused in the management of acute coronary syndrome

edicatio

n

echanism of action

Aspirin Antiplatelet inhi-its the production of throm-o%ane A2

"opidogr

e

Antiplatelet inhi-its A$, -inding to its platelet receptor

noxapar

in

Activates antithrom-in III& /hich in turn potentiates the

inhi-ition of coagulation factors Ua

5ondaparinux

Activates antithrom-in III& /hich in turn potentiates theinhi-ition of coagulation factors Ua

Bi)airudi

n

eversi-le direct throm-in inhi-itor




Gey Points

• A modest rise in troponin is seen in around onethird of patients /ithacute pericarditis. 8he /idespread nature of the EC" changes acrosscoronary territories! points a/ay from an ischaemic cause. It /ouldalso -e very unusual for a #0yearold /oman to su5er an acute

coronary syndrome.• 8he 201# NICE myocardial infarction guidelines replaced the 2010

advice ris6 scores are no longer needed to determine /hetherclopidogrel is given.

• NICE NS8E<Iunsta-le angina guidelines are -ased on L monthmortality ris6

• If 3 1.@* clopidogrel for 12 months

• If 3 #* angiography /ithin (L hours

<yocardial infarction complications

,atients are at ris6 of a num-er of immediate& early and late complicationsfollo/ing a myocardial infarction <I!.

"ardiac arrest

8his most commonly occurs due to patients developing ventricular 9-rillation




and is the most common cause of death follo/ing a <I. ,atients are

managed as per the A?S protocol /ith de9-rillation.

"ardiogenic shoc$

If a large part of the ventricular myocardium is damaged in the infarction the

eBection fraction of the heart may decrease to the point that the patient

develops cardiogenic shoc6. 8his is diPcult to treat. 4ther causes of

cardiogenic shoc6 include the 'mechanical' complications such as left

ventricular free /all rupture as listed -elo/. ,atients may re:uire inotropic

support andor an intraaortic -alloon pump.

"hronic heart faiure

As descri-ed a-ove& if the patient survives the acute phase their ventricularmyocardium may -e dysfunctional resulting in chronic heart failure. ?oop

diuretics such as furosemide /ill decrease Huid overload. oth ACEinhi-itors

and -eta-loc6ers have -een sho/n to improve the longterm prognosis of

patients /ith chronic heart failure.

+achyarrhythmias

Dentricular 9-rillation& as mentioned a-ove& is the most common cause of

death follo/ing a <I. 4ther common arrhythmias including ventricular

tachycardia.

Bradyarrhythmias

Atrioventricular -loc6 is more common follo/ing inferior myocardial

infarctions.

Pericarditis

,ericarditis in the 9rst )G hours follo/ing a transmural <I is common c. 10*

of patients!. 8he pain is typical for pericarditis /orse on lying Hat etc!& a

pericardial ru- may -e heard and a pericardial e5usion may -e

demonstrated /ith an echocardiogram.




$ressler's syndrome tends to occur around 2L /ee6s follo/ing a <I. 8he

underlying pathophysiology is thought to -e an autoimmune reaction against

antigenic proteins formed as the myocardium recovers. It is characterised -y

a com-ination of fever& pleuritic pain& pericardial e5usion and a raised ES. It

is treated /ith nsaids.

3eft )entricuar aneurysm

8he ischaemic damage sustained may /ea6en the myocardium resulting in

aneurysm formation. 8his is typically associated /ith persistent S8 elevation

and left ventricular failure. 8hrom-us may form /ithin the aneurysm

increasing the ris6 of stro6e. ,atients are therefore anticoagulated.

3eft )entricuar free wa rupture

8his is seen in around #* of mis and occurs around 12 /ee6s after/ards.

,atients present /ith acute heart failure secondary to cardiac tamponade

raised KD,& pulsus parado%us& diminished heart sounds!. rgent

pericardiocentesis and thoracotomy are re:uired.

entricuar septa defect

upture of the interventricular septum usually occurs in the 9rst /ee6 and is

seen in around 12* of patients. ;eatures acute heart failure associated /ith

a pansystolic murmur. An echocardiogram is diagnostic and /ill e%clude

acute mitral regurgitation /hich presents in a similar fashion. rgent surgical

correction is needed.

Acute mitra regurgitation

<ore common /ith inferoposterior infarction and may -e due to ischaemia

or rupture of the papillary muscle. An earlytomid systolic murmur is

typically heard. ,atients are treated /ith vasodilator therapy -ut oftenre:uire emergency surgical repair.

<yocardial infarction secondary prevention




NICE produced guidelines on the management of patients follo/ing amyocardial infarction <I! in 201#. Some 6ey points are listed -elo/

All patients should -e o5ered the follo/ing drugs

Dua antipateet therapy aspirin pus a second antipateetagent

A" inhibitor

Beta-boc$er

1tatin

1ome seected ifestye points=

• $iet advise a <editerranean style diet& s/itch -utter and cheese forplant oil -ased products. $o not recommend omega# supplements oreating oily 9sh

• E%ercise advise 20#0 mins a day until patients are 'slightly -reathless'

• Se%ual activity may resume ) /ee6s after an uncomplicated <I.eassure patients that se% does not increase their li6elihood of a

further <I. ,$E@ inhi-itors e.g& sildena9l! may -e used L months aftera <I. 8hey should ho/ever -e avoided in patient prescri-ed eithernitrates or nicorandil

"opidogre

• Since clopidogrel came o5 patent it is no/ much more /idely usedpost<I

• S8E<I the European Society of Cardiology recommend dual

antiplatelets for 12 months. In the F this means aspirin Q clopidogrel

• NonS8 segment elevation myocardial infarction NS8E<I! follo/ingthe NICE 201 econdary prevention in primary and secondary carefor patients folloing a myocardial infarction guidelines clopidogrelshould -e given for the 9rst 12 months




Adosterone antagonists

• ,atients /ho have had an acute <I and /ho have symptoms andorsigns of heart failure and left ventricular systolic dysfunction&treatment /ith an aldosterone antagonist licensed for post<I

treatment e.g. Eplerenone! should -e initiated /ithin #1) days of the<I& prefera-ly after ACE inhi-itor therapy

Acute pericarditis

,ericarditis is one of the di5erentials of any patient presenting /ith chestpain.

;eatures

• Chest pain may -e pleuritic. Is often relieved -y sitting for/ards

• 4ther symptoms include nonproductive cough& dyspnoea and Huli6esymptoms

• ,ericardial ru-

• 8achypnoea

• 8achycardia

Causes

• Diral infections Co%sac6ie!

• 8u-erculosis

• raemia causes '9-rinous' pericarditis!

• 8rauma

• ,ostmyocardial infarction& $ressler's syndrome

• Connective tissue disease




• =ypothyroidism

EC" changes

• 7idespread 'saddleshaped' S8 elevation

• , depression most speci9c EC" mar6er for pericarditis

EC" sho/ing pericarditis. Note the /idespread nature of the S8 elevationand the , depression

<yocarditis

<yocarditis is an acute inHammatory condition of the heart /hich often

occurs in patients /ith no underlying cardiac disease. Clinical features

include chest pain usually due to coe%istant pericarditis!& acute heart failure

and arrhythmias. 7hile the most common aetiology in Europe is viral& the

most common cause /orld/ide is /rypanosoma crui Chaga's disease!.

Causes

• Diral co%sac6ie& =ID

• acteria diphtheria& clostridia

• Spirochaetes ?yme disease




• ,rotoJoa Chagas' disease& to%oplasmosis

• Autoimmune

• $rugs do%oru-icin

,resentation

• sually young patient /ith acute history

• Chest pain& S4

Aortic dissection management

Stanford classi9cation

• 8ype A ascending aorta& 2# of cases

• 8ype descending aorta& distal to left su-clavian origin& 1# of cases

$e-a6ey classi9cation

• 8ype I originates in ascending aorta& propagates to at least the aorticarch and possi-ly -eyond it distally




• 8ype II originates in and is con9ned to the ascending aorta

• 8ype III originates in descending aorta& rarely e%tends pro%imally -ut

/ill e%tend distally

8ype A

• Surgical management& -ut -lood pressure should -e controlled to atarget systolic of 100120 mmhg /hilst a/aiting intervention

8ype +

• Conservative management

• ed rest

• (educe bood pressure abetao to prevent progression

An intraluminal tear has formed a 'Hap'

that can -e clearly seen in the ascending

aorta. 8his is a Stanford type A

dissection

Stanford type dissection& seen in the

descending aorta +endovascular repair

of type aortic dissection may have a

role in the future

=eart -loc6

8ypes of heart -loc6

5irst degree heart boc$




, interval 3 0.2 seconds

1econd degree heart boc$ 8ype 1 <o-itJ I& 7enc6e-ach! progressive prolongation of the ,

interval until a dropped -eat occurs

8ype 2 <o-itJ II! , interval is constant -ut the , /ave is often notfollo/ed -y a S comple%

+hird degree compete heart boc$ 8here is no association -et/een the , /aves and S comple%es;eatures

Syncope

=eart failure

egular -radycardia #0@0 -pm!

7ide pulse pressure

KD, cannon /aves in nec6

Daria-le intensity of S1

o

o

EC"

sho/ing third degree complete! heart -loc6

+++Complete heart -loc6 secondary to a right coronary artery CA! infarction. 8he

atrioventricular node is supplied -y the posterior interventricular artery& /hich in

the maBority of patients is a -ranch of the right coronary artery. In the remainder of

patients the posterior interventricular artery is supplied -y the left circumHe% artery.




Cardiac tamponade

;eatures

• $yspnoea

• aised KD,& /ith an a-sent M descent this is due to the limited rightventricular 9lling

• 8achycardia

• =ypotension

• <uVed heart sounds

• ,ulsus parado%us

• Fussmaul's sign much de-ate a-out this!

• EC" electrical alternans

8he 6ey di5erences -et/een constrictive pericarditis and cardiac tamponadeare summarised in the ta-le -elo/

"ardiac

tamponade

"onstricti)e pericarditis

7P A-sent M

descent

U Q M present

Pusus paradoxus ,resent A-sent

Gussmau6s sign are ,resent

"haracteristic features ,ericardial calci9cation on

CU

A commonly used mnemonic to remem-er the a-sent M descent in cardiactamponade is tamponade O tampa%




heumatic fever criteria

heumatic fever develops follo/ing an immunological reaction to recent 2L /ee6s

ago! treptococcus pyogenes infection. $iagnosis is -ased on evidence of recentstreptococcal infection accompanied -y

• 2 maBor criteria

• 1 maBor /ith 2 minor criteria

Evidence of recent streptococcal infection

• AS48 3 200iuml

• =istory of scarlet fever

• ,ositive throat s/a-

• Increase in dnase titre

<aBor criteria

• Erythema marginatum

• Sydenham's chorea

• ,olyarthritis

• Carditis endo& myo or peri!




• Su-cutaneous nodules

<inor criteria

•

aised ES or C,

• ,yre%ia

• Arthralgia not if arthritis a maBor criteria!

• ,rolonged , interval

• Erythema marginatum is seen in around 10* of children /ith rheumatic

fever. It is rare in adults

•

Infective endocarditis

odi:ed Du$e criteria

Infective endocarditis diagnosed if

• ,athological criteria positive& or

• 2 maBor criteria& or

• 1 maBor and # minor criteria& or

• @ minor criteria

Pathoogica criteria

,ositive histology or micro-iology of pathological material o-tained at




autopsy or cardiac surgery valve tissue& vegetations& em-olic fragments orintracardiac a-scess content!

aor criteria

,ositive -lood cultures

• 8/o positive -lood cultures sho/ing typical organisms consistent /ithinfective endocarditis& such as treptococcus viridans and the =ACEFgroup& or

• ,ersistent -acteraemia from t/o -lood cultures ta6en 3 12 hours apartor three or more positive -lood cultures /here the pathogen is lessspeci9c such as taph aureus and taph epidermidis& or

• ,ositive serology for Co$iella -urnetii& :artonella species or Chlamydia

psittaci& or

• ,ositive molecular assays for speci9c gene targets

Evidence of endocardial involvement

• ,ositive echocardiogram oscillating structures& a-scess formation& ne/valvular regurgitation or dehiscence of prosthetic valves!& or

• Ne/ valvular regurgitation

inor criteria

• ,redisposing heart condition or intravenous drug use

• <icro-iological evidence does not meet maBor criteria

• ;ever 3 #GWc

• Dascular phenomena maBor em-oli& splenomegaly& clu--ing& splinter

haemorrhages& Kane/ay lesions& petechiae or purpura

• Immunological phenomena glomerulonephritis& 4sler's nodes& othspots

nfecti)e endocarditis= prophyaxis




8he 200G guidelines from NICE have radically changed the list of proceduresfor /hich anti-iotic prophyla%is is recommended

NICE recommends the follo/ing procedures do not re:uire prophyla%is

• $ental procedures

• pper and lo/er gastrointestinal tract procedures

• "enitourinary tract this includes urological& gynaecological ando-stetric procedures and child-irth

• pper and lo/er respiratory tract this includes ear& nose and throatprocedures and -ronchoscopy

8he guidelines do ho/ever suggest

• Any episodes of infection in people at ris6 of infective endocarditisshould -e investigated and treated promptly to reduce the ris6 ofendocarditis developing

• If a person at ris6 of infective endocarditis is receiving antimicro-ialtherapy -ecause they are undergoing a gastrointestinal orgenitourinary procedure at a site /here there is a suspected infection

they should -e given an anti-iotic that covers organisms that causeinfective endocarditis

nfecti)e endocarditis= prognosis and management

,oor prognostic factors

1taph aureus infection see beow

Prosthetic )a)e especiay 6eary6# acHuired during surgery

"uture negati)e endocarditis

3ow compement e)es




<ortality according to organism

• Staphylococci #0*

• o/el organisms 1@*

• Streptococci @*

Current anti-iotic guidelines source ritish National ;ormulary!

1cenario 1uggested antibiotic therapy

nitia bind therapy Native valveAmo%icillin& consider adding lo/

dose gentamicin

If penicillin allergic& <SA orsevere sepsisDancomycin Q lo/dosegentamicin

If prosthetic valveDancomycin Q rifampicin Q lo/dose gentamicin

,ati)e )a)e endocarditis caused by

staphyococci

;luclo%acillin

If penicillin allergic or <SADancomycin Q rifampicin

Prosthetic )a)e endocarditis causedby staphyococci

;luclo%acillin Q rifampicin Q lo/dose gentamicin

If penicillin allergic or <SADancomycin Q rifampicin Q lo/dose gentamicin

ndocarditis caused by fuy-sensiti)estreptococci e.g. iridans

enJylpenicillin

If penicillin allergicDancomycin Q lo/dosegentamicin

ndocarditis caused by ess sensiti)estreptococci

enJylpenicillin Q lo/dosegentamicin




If penicillin allergicDancomycin Q lo/dosegentamicin

Indications for surgery

• Severe valvular incompetence

• Aortic a-scess often indicated -y a lengthening , interval!

• Infections resistant to anti-ioticsfungal infections

• Cardiac failure refractory to standard medical treatment

• ecurrent em-oli after anti-iotic therapy

,rosthetic heart valves

8he most common valves /hich need replacing are the aortic and mitralvalve. 8here are t/o main options for replacement -iological -ioprosthetic!or mechanical.

Bioogica bioprosthetic )a)es echanica )a)es

Fsuay bo)ine or porcine in

origin

aor disad)antage is structura

deterioration and caci:cation

o)er time. ost oder patients

> / years for aortic )a)es

and > L0 years for mitra )a)esrecei)e a bioprosthetic )a)e

3ong-term anticoaguation not

usuay needed. arfarin may be

gi)en for the :rst ' months

8he most common type no/

implanted is the -ileaHet valve. all

andcage valves are rarely used

no/adays

<echanical valves have a lo/ failure

rate

<aBor disadvantage is the increased

ris6 of throm-osis meaning long

term anticoagulation is needed.

Aspirin is normally given in addition

unless there is a contraindication.




depending on patient factors.

3ow-dose aspirin is gi)en ong-

term.

8arget IN

• Aortic 2.0#.0

• <itral 2.@#.@

;ollo/ing the 200G NICE guidelines for prophyla%is of endocarditis anti-iotics

are no longer recommended for common procedures such as dental /or6.

=eart failure $iagnosis

NICE issued updated guidelines on diagnosis and management in 2010. 8hechoice of investigation is determined -y /hether the patient has previouslyhad a myocardial infarction or not.

,revious myocardial infarction

• Arrange echocardiogram /ithin 2 /ee6s

No previous myocardial infarction

• <easure serum natriuretic peptides N,!

• If levels are 'high' arrange echocardiogram /ithin 2 /ee6s

• If levels are 'raised' arrange echocardiogram /ithin L /ee6s




1erum natriuretic peptides

type natriuretic peptide N,! is a hormone produced mainly -y the leftventricular myocardium in response to strain. Dery high levels are associated/ith a poor prognosis.

B,P ,tprobnp

?igh e)es 3 )00 pgml 11L

pmollitre!

3 2000 pgml 2#L

pmollitre!

(aised

e)es

100)00 pgml 2(11L

pmollitre!

)002000 pgml )2#L

pmollitre!

,orma

e)es

100 pgml 2( pmollitre! )00 pgml ) pmollitre!

;actors /hich alter the N, level

Increase N, levels $ecrease N, levels

?eft ventricular hypertrophy

Ischaemia

8achycardia

ight ventricular overload

=ypo%aemia including pulmonary

em-olism!

"; L0 mlmin

Sepsis

C4,$$ia-etes

Age 3 0

?iver cirrhosis

4-esity

$iuretics

ACE inhi-itors

eta-loc6ers

Angiotensin 2 receptor -loc6ers

Aldosterone antagonists

=eart failure NM=A classi9cation

8he Ne/ Mor6 =eart Association NM=A! classi9cation is /idely used toclassify the severity of heart failure

NM=A Class I

• No symptoms




• No limitation ordinary physical e%ercise does not cause undue fatigue&dyspnoea or palpitations

NM=A Class II

• <ild symptoms

• Slight limitation of physical activity comforta-le at rest -ut ordinaryactivity results in fatigue& palpitations or dyspnoea

NM=A Class III

• <oderate symptoms

• <ar6ed limitation of physical activity comforta-le at rest -ut less thanordinary activity results in symptoms

NM=A Class ID

• Severe symptoms

• na-le to carry out any physical activity /ithout discomfort symptomsof heart failure are present even at rest /ith increased discomfort /ith

any physical activity

=eart failure drug management

A num-er of drugs have -een sho/n to improve mortality in patients /ithchronic heart failure




A" inhibitors 1A# 1<3D# "<,1,1F1

1pironoactone (A31

Beta-boc$ers "B1

?ydraaIine with nitrates ?5+-!

No longterm reduction in mortality has -een demonstrated for loop diureticssuch as furosemide.

NICE issued updated guidelines on management in 2010& 6ey points include

5irst-ine treatment for a patients is both an A"-inhibitorand a beta-boc$er

• Secondline treatment is no/ either an aldosterone antagonist&

angiotensin II receptor -loc6er or a hydralaJine in com-ination /ith anitrate

f symptoms persist cardiac resynchronisation therapy ordigoxinM shoud be considered

• $iuretics should -e given for Huid overload

• 45er annual inHuenJa vaccine

• 45er oneo5++ pneumococcal vaccine

+++ Pumonary oedema /ith -ilateral course crac6les and coughproductive of /hite sputum. 8he patient has signs of right sided heart failure/ith raised KD, and peripheral oedema. 8hey also have a history of <I andhypertension that are t/o ris6 factors for heart failure.

NICE guidance on Acute =eart ;ailure 201) states that a patient /ho hasfailed medical management of pulmonary oedema /ith severe dyspnoeashould -e considered for C,A,. I,A, is not used in acute pulmonaryoedema.




=eart failure acute management

<anagement options in acute heart failure include

<xygen

Diuretics

<piates

asodiators

notropic agents

"PAP

Ftra:tration

echanica circuatory assistance= e.g. ntra-aortic baooncounterpusation or )entricuar assist de)ices

• NICE recommend that all heart failure patients should ta6e -oth anACEinhi-itor and a -eta-loc6er

• Consideration should -e given to discontinuing -eta-loc6ers in theshortterm.

• oth naapri and Bisoproo have -een sho/n to improveprognosis in patients /ith heart failure. Enalapril ho/ever /ould also-e -etter at treating the hypertension. NICE guidelines recommend the

introduction of an ACE inhi-itor prior to a -eta-loc6er in patients /ithchronic heart failure.




• oth "ar)edio and Bisoproo have -een sho/n to reduce mortalityin sta-le heart failure. 8he other -eta-loc6ers have no evidence -aseto support their use.

• D*<N,!has also not -een proven to reduce mortality in patients /ithheart failure. It may ho/ever improve symptoms due to its inotropic

properties. $igo%in is strongly indicated if there is coe%istent atrial9-rillation

• erapamil is contraindicated in patients /ith heart failure.

• 8he follo/ing drugs have all -een sho/n to reduce mortality inpatients /ith left ventricular failure

• ACEinhi-itors

• eta-loc6ers

•

Angiotensin receptor -loc6ers

• Aldosterone antagonists

• =ydralaJine and nitrates

•

=eart failure nondrug management

Cardiac resynchronisation therapy

• ;or patients /ith heart failure and /ide S

• iventricular pacing

• Improved symptoms and reduced hospitalisation in NM=A class IIIpatients

E%ercise training

1 eferenceshttps///.nice.org.u6guidancecg10G 8he $igitalis Investigation "roup. 8he E5ect of $igo%in on <ortality and <or-idity in ,atients /ith=eart ;ailure. N Engl K <ed. 1((##L@2@@##




• Improves symptoms -ut not hospitalisationmortality

+++In symptomatic heart failure patients /ho are on optimal medical therapy&there are several treatment options to improve mortality. Cardiacresynchronisation therapy is indicated in patients /ith left ventriculardysfunction& eBection fracture #@* and S duration 3120ms. AnImplanta-le cardiac de9-rillator IC$! is indicated in patients /ith previoussustained ventricular tachycardia& eBection fraction #@* and symptoms no/orse than class III of of the Ne/ Mor6 =eart Association functionalclassi9cation.

$igo%in reduces hospitalisation -ut not mortality in heart failure. Increasingthe furosemide dose may help /ith symptomatic relief from Huid overload-ut has no e5ect on mortality. =eart transplantation and ventricular assistdevices /ould not -e an option in a patient of this age.

=ttp///.nice.org.u6guidanceta#1)resourcesguidanceimplanta-lecardioverterde9-rillatorsandcardiacresynchronisationtherapyforarrhythmiasandheartfailurerevie/ofta(@andta120pdf

http///.nice.org.u6guidanceta#1)resourcesguidanceimplanta-lecardioverterde9-rillatorsandcardiacresynchronisationtherapyforarrhythmiasandheartfailurerevie/ofta(@andta120pdf

Dalvular =eart $isease

Aortic stenosis

<ost common cause

• Mounger patients L@ years -icuspid aortic valve




• 4lder patients 3 L@ years calci9cation

;eatures of severe aortic stenosis

• Narro/ pulse pressure

• Slo/ rising pulse

• $elayed ES<

• Softa-sent S2

• S)

• 8hrill

• $uration of murmur

• ?eft ventricular hypertrophy or failure

Causes of aortic stenosis

Degenerati)e caci:cation most common cause inoder patients > / years

Bicuspid aortic )a)e most common cause in youngerpatients @ / years

• 7illiam's syndrome supravalvular aortic stenosis!

• ,ostrheumatic disease

• Su-valvular =4C<

<anagement

• If asymptomatic then o-serve the patient is general rule

• If symptomatic then valve replacement




• If asymptomatic -ut valvular gradient 3 @0 mmhg and /ith featuressuch as left ventricular systolic dysfunction then consider surgery

• alloon valvuloplasty is limited to patients /ith critical aortic stenosis/ho are not 9t for valve replacement

• Aortic stenosis management AD if symptomatic& other/ise cuto5 isgradient of @0 mmhg.

• No action should -e ta6en at present as if patient is currentlyasymptomatic. If the aortic valve gradient 3 @0 mmhg or there isevidence of signi9cant left ventricular dysfunction then surgery issometimes considered in selected asymptomatic patients

• ?eft ventricular systolic dysfunction /ill result in a decreased Ho/rateacross the aortic valve and hence a :uieter murmur.

• $ilated cardiomyopathy is associated /ith the development of mitral

regurgitation& not aortic regurgitation

• In general& aortic valve replacement is indicated in symptomaticpatients /ith severe aortic stenosis. 8he presence of symptoms isassociated /ith a mortality of 2# years. 8he triad of symptoms isdyspnoea& chest pain and syncope. Dalve replacement inasymptomatic patients is more controversial.

Aortic regurgitation

;eatures

• Early diastolic murmur

• Collapsing pulse

• 7ide pulse pressure

• <iddiastolic Austin;lint murmur in severe A due to partial closureof the anterior mitral valve cusps caused -y the regurgitation streams

Causes due to valve disease!

• heumatic fever

• Infective endocarditis




• Connective tissue diseases e.g. AS?E

• icuspid aortic valve

Causes due to aortic root disease!

• Aortic dissection

• Spondylarthropathies e.g. An6ylosing spondylitis!

• =ypertension

• Syphilis

•

<arfan's& Ehler$anlos syndrome

7hilst some patients /ith acromegaly have mitral valve prolapse <D,! it isnot a common association. It should -e remem-ered that the prevalence of<D, in a standard population is around @10*

<itral valve prolapse

<itral valve prolapse is common& occurring in around @10 * of thepopulation. It is usually idiopathic -ut may -e associated /ith a /ide varietyof cardiovascular disease and other conditions

Associations

• Congenital heart disease ,$A& AS$

• Cardiomyopathy

• 8urner's syndrome

• <arfan's syndrome& ;ragile U

• 4steogenesis imperfecta

• ,seudo%anthoma elasticum




• 7ol5,ar6inson 7hite syndrome

• ?ong8 syndrome

• Ehlers$anlos Syndrome

• ,olycystic 6idney disease

;eatures

• ,atients may complain of atypical chest pain or palpitations

• <idsystolic clic6 occurs later if patient s:uatting!

• ?ate systolic murmur longer if patient standing!

• Complications mitral regurgitation& arrhythmias including long 8!&em-oli& sudden death

In this age group hypertrophic o-structive cardiomyopathy /ould -e a morecommon cause of the murmurrecurrent collapse than aortic stenosis.

=4C< features

=ypertrophic o-structive cardiomyopathy =4C<! is an autosomadominant disorder of muscle tissue caused -y defects in the genesencoding contractile proteins. 8he most common defects involve a mutationin the gene encoding Xmyosin heavy chain protein or myosin -inding

protein C. 8he estimated prevalence is 1 in @00.

;eatures

• 4ften asymptomatic




• $yspnoea& angina& syncope

• Sudden death most commonly due to ventricular arrhythmias!&

arrhythmias& heart failure

• Ker6y pulse& large 'a' /aves& dou-le ape% -eat

• EBection systolic murmur increases /ith Dalsalva manoeuvre anddecreases on s:uatting

Associations

• ;riedreich's ata%ia

• 7ol5,ar6inson 7hite

Echo mnemonic < SA< AS=

• <itral regurgitation <!

• Systolic anterior motion SA<! of the anterior mitral valve leaHet

• Asymmetric hypertrophy AS=!

EC"

• ?eft ventricular hypertrophy

• ,rogressive 8 /ave inversion

• $eep /aves

• Atrial 9-rillation may occasionally -e seen




EC" sho/ing typical changes of =4C< including ?D= and 8 /ave inversion

$ilated cardiomyopathy

$ilated cardiomyopathy $C<! -asics

• $ilated heart leading to systolic Q diastolic! dysfunction

• All ) cham-ers a5ected -ut ?D more so than D

• ;eatures include arrhythmias& em-oli& mitral regurgitation

• A-sence of congenital& valvular or ischaemic heart disease

Causes often considered separate entities

• Alcohol may improve /ith thiamine

• ,ostpartum

• =ypertension

4ther causes




• Inherited see -elo/!

• Infections e.g. Co%sac6ie & =ID& diphtheria& parasitic

• Endocrine e.g. =yperthyroidism

• In9ltrative+ e.g. =aemochromatosis& sarcoidosis

• Neuromuscular e.g. $uchenne muscular dystrophy

• Nutritional e.g. F/ashior6or& pellagra& thiamineselenium de9ciency

• $rugs e.g. $o%oru-icin

Inherited dilated cardiomyopathy

• Around a third of patients /ith $C< are thought to have a geneticpredisposition

• A large num-er of heterogeneous defects have -een identi9ed

• 8he maBority of defects are inherited in an autosomal dominant fashionalthough other patterns of inheritance are seen

+these causes may also lead to restrictive cardiomyopathy

+++ =aemochromatosis is more commonly associated /ith restrictivecardiomyopathy -ut a dilated pattern may also -e seen. 8here is a 6no/nassociation -et/een 7ilson's disease and cardiomyopathy -ut this ise%tremely rare and not often clinically signi9cant

7ol5,ar6inson 7hite

7ol5,ar6inson 7hite 7,7! syndrome is caused -y a congenital accessoryconducting path/ay -et/een the atria and ventricles leading to aatrioventricular reentry tachycardia AD8!. As the accessory path/ay doesnot slo/ conduction A; can degenerate rapidly to D;




,ossi-le EC" features include

• Short , interval

• 7ide S comple%es /ith a slurred upstro6e 'delta /ave'

• ?eft a%is deviation if rightsided accessory path/ay+

• ight a%is deviation if leftsided accessory path/ay+

EC" sho/ing short , interval associated /ith a slurred upstro6e delta

/ave!. Note the nonspeci9c S88 changes /hich are common in 7,7 andmay -e mista6en for ischaemia. 8he left a%is deviation means that this istype 7,7& implying a rightsided path/ay

;urther e%ample sho/ing a characteristic delta /ave




$i5erentiating -et/een type A andtype

• 8ype A leftsided path/ay!dominant /ave in D1

• 8ype rightsided path/ay!no dominant /ave in D1

Associations of 7,7

• =4C<

• <itral valve prolapse

• E-stein's anomaly

• 8hyroto%icosis

•Secundum AS$

<anagement

• $e9nitive treatment radiofre:uency a-lation of the accessory path/ay

• <edical therapy sotalol++& amiodarone& Hecainide

+in the maBority of cases& or in a :uestion /ithout :uali9cation& 7ol5

,ar6inson7hite syndrome is associated /ith left a%is deviation

++sotalol should -e avoided if there is coe%istent atrial 9-rillation as

prolonging the refractory period at the AD node may increase the rate of




transmission through the accessory path/ay& increasing the ventricular rate

and potentially deteriorating into ventricular 9-rillation

,ulmonary em-olism investigation

7e 6no/ from e%perience that fe/ patients around 10*! present /ith the

medical student te%t-oo6 triad of peuritic chest pain# dyspnoea and

haemoptysis. ,ulmonary em-olism can -e diPcult to diagnose as it can

present /ith virtually any cardiorespiratory symptomsign depending on it's

location and siJe.

1o which features ma$e pumonary emboism more i$eyO

8he ,I4,E$ study1 in 200 loo6ed at the fre:uency of di5erent symptoms

and signs in patients /ho /ere diagnosed /ith pulmonary em-olism.

8he relative fre:uency of common clinical signs is sho/n -elo/

+achypnea respiratory rate >!/2min - 9/%

"rac$es - 8%




+achycardia heart rate >!002min - 44%

5e)er temperature >'L.8" - 4'%

It is interesting to note that the 7ell's criteria for diagnosing a ,E use

tachycardia rather than tachypnoea.

&0!& ," guideines

All patients /ith symptoms or signs suggestive of a ,E should have a historyta6en& e%amination performed and a chest %ray to e%clude other pathology.If a ,E is still suspected a t/olevel ,E 7ells score should -e performed

Clinical pro-a-ility simpli9ed scores ,E li6ely more than ) points ,E unli6ely ) points or less

f a P is 6i$ey6 more than 4 points arrange an immediate

computed tomography pumonary angiogram "+PA. f there is a

deay in getting the "+PA then gi)e ow-moecuar weight heparin

unti the scan is performed.

f a P is 6uni$ey6 4 points or ess arranged a D-dimer test. f this

is positi)e arrange an immediate computed tomography pumonary

angiogram "+PA. f there is a deay in getting the "+PA then gi)eow-moecuar weight heparin unti the scan is performed.

f the patient has an aergy to contrast media or rena impairment a

2C scan shoud be used instead of a "+PA.


Clinical feature ,oin

ts

"inica signs and symptoms of D+ minimum of eg sweing

and pain with papation of the deep )eins

#

An aternati)e diagnosis is ess i$ey than P #

?eart rate > !00 beats per minute 1.@

mmobiisation for more than ' days or surgery in the

pre)ious 4 wee$s

1.@

Pre)ious D+2P 1.@

?aemoptysis 1

aignancy on treatment# treated in the ast / months# or

paiati)e

1



"+PA or 2C scanO

8he consensus vie/ from the ritish 8horacic Society and NICE guidelines is

as follo/s

• Computed tomographic pulmonary angiography C8,A! is no/ the

recommended initial lungimaging modality for nonmassive ,E.Advantages compared to D scans include speed& easier to performoutofhours& a reduced need for further imaging and the possi-ility ofproviding an alternative diagnosis if ,E is e%cluded

• If the C8,A is negative then patients do not need further investigationsor treatment for ,E

• Dentilationperfusion scanning may -e used initially if appropriatefacilities e%ist& the chest %ray is normal& and there is no signi9cant

symptomatic concurrent cardiopulmonary disease.

?a-elled C8,A sho/ing a large saddleem-olus

;urther C8,A again sho/ing a saddleem-olus




EC" from a patient /ith a ,E. Sho/s a sinus tachycardia and a partial

S1#8# the S /ave is not particularly convincing.

EC" of a patient /ith a ,E. It sho/s some of the EC" features that may -e

associated /ith ,E sinus tachycardia& S1& 8# and 8 /ave inversion in the

precordial leads!. 4ther features such as the left a%is deviation are atypical.

1ome other points

$dimers




• Sensitivity O (@(G*& -ut poor speci9city

EC"

• 8he classic EC" changes seen in ,E are a large S /ave in lead I& a large /ave in lead III and an inverted 8 /ave in lead III 'S1#8#'.=o/ever this change is seen in no more than 20* of patients

• ight -undle -ranch -loc6 and right a%is deviation are also associated/ith ,E

• Sinus tachycardia may also -e seen

D scan

• Sensitivity O (G* speci9city O )0* high negative predictive value&i.e. If normal virtually e%cludes ,E

• 4ther causes of mismatch in D include old pulmonary em-olisms& AD

malformations& vasculitis& previous radiotherapy

• C4,$ gives matched defects

C8,A

• ,eripheral em-oli a5ecting su-segmental arteries may -e missed

,ulmonary angiography

• 8he gold standard

• Signi9cant complication rate compared to other investigations

1. Clinical Characteristics of ,atients /ith Acute ,ulmonary Em-olism$ata

from ,I4,E$ II! Am K <ed. 4ct 200 12010! G1G( .




,ulmonary Em-olism management

The NICE guidelines of 2012 rovided some clarit! on ho" long atients should beanticoagulated for after a ulmonar! embolism #$E%& 'elected oints are listed belo"&

(o" molecular "eight hearin #()*% or fondaarinu, should be given initiall! after a $E isdiagnosed& An e,cetion to this is for atients "ith a massive $E "here thrombol!sis is being

considered& In such a situation unfractionated hearin should be used&

• A vitamin antagonist #i&e& *arfarin% should be given "ithin 2. hours of the diagnosis

• The ()* or fondaarinu, should be continued for at least / da!s or until the

international normalised ratio #IN% is 2&0 or above for at least 2. hours "hichever islonger i&e& ()* or fondaarinu, is given at the same time as "arfarin until the IN is

in the theraeutic range

• *arfarin should be continued for at least months& At months NICE advise that

clinicians should 3assess the ris4s and benefits of e,tending treatment3

• NICE advise e,tending "arfarin be!ond months for atients "ith unprovoked $E& This

essentiall! means that if there "as no obvious cause or rovo4ing factor #surger! traumasignificant immobilit!% it ma! iml! the atient has a tendenc! to thrombosis and should

be given treatment longer than the norm of months

• 5or atients "ith active cancer NICE recommend using ()* for 6 months

Thrombol!sis

• Thrombol!sis is no" recommended as the first-line treatment for massive $E "here there

is circulator! failure #e&g& !otension%& 7ther invasive aroaches should be considered

"here aroriate facilities e,ist




$eep vein throm-osis diagnosis and management

DiagnosisNICE pu-lished guidelines in 2012 relating to the investigation andmanagement of deep vein throm-osis $D8!.If a patient is suspected of having a $D8 a t/olevel $D8 7ells score should-e performed

+wo-e)e D+ es score

"inica feature Poin

ts

Acti)e cancer treatment ongoing# within / months# or

paiati)e

1

Paraysis# paresis or recent paster immobiisation of the

ower extremities

1

(ecenty bedridden for ' days or more or maor surgery

within !& wee$s reHuiring genera or regiona anaesthesia

1

3ocaised tenderness aong the distribution of the deep

)enous system

1

ntire eg swoen 1

"af sweing at east ' cm arger than asymptomatic side 1

Pitting oedema con:ned to the symptomatic eg 1

"oatera super:cia )eins non-)aricose 1

Pre)iousy documented D+ 1

An aternati)e diagnosis is at east as i$ey as D+ 2

Clinical pro-a-ility simpli9ed score $D8 li6ely 2 points or more

$D8 unli6ely 1 point or less

If a $D8 is 'li6ely' 2 points or more! A pro%imal leg vein ultrasound scan should -e carried out /ithin )

hours and& if the result is negative& a $dimer test If a pro%imal leg vein ultrasound scan cannot -e carried out /ithin )

hours a $dimer test should -e performed and lo/molecular /eight




heparin administered /hilst /aiting for the pro%imal leg veinultrasound scan /hich should -e performed /ithin 2) hours!

If a $D8 is 'unli6ely' 1 point or less!

,erform a $dimer test and if it is positive arrange

A pro%imal leg vein ultrasound scan /ithin ) hours

If a pro%imal leg vein ultrasound scan cannot -e carried out /ithin ) hourslo/molecular /eight heparin should -e administered /hilst /aiting for thepro%imal leg vein ultrasound scan /hich should -e performed /ithin 2)hours!

anagement?o/ molecular /eight heparin ?<7=! or fondaparinu% should -e giveninitially after a $D8 is diagnosed.

• A vitamin F antagonist i.e. 7arfarin! should -e given /ithin 2) hoursof the diagnosis

• 8he ?<7= or fondaparinu% should -e continued for at least @ days or

until the international normalised ratio IN! is 2.0 or a-ove for at least2) hours& /hichever is longer& i.e. ?<7= or fondaparinu% is given atthe same time as /arfarin until the IN is in the therapeutic range

• 7arfarin should -e continued for at least # months. At # months& NICEadvise that clinicians should 'assess the ris6s and -ene9ts of e%tending

treatment'

• NICE add 'consider e%tending /arfarin -eyond # months for patients

/ith unprovoked pro%imal $D8 if their ris6 of D8E recurrence is highand there is no additional ris6 of maBor -leeding'. 8his essentiallymeans that if there /as no o-vious cause or provo6ing factor surgery&trauma& signi9cant immo-ility! it may imply the patient has a tendencyto throm-osis and should -e given treatment longer than the norm of #months. In practice most clinicians give L months of /arfarin forpatients /ith an unprovo6ed $D8,E

•;or patients /ith active cancer NICE recommend using ?<7= for Lmonths

5urther in)estigations and thrombophiia screening

As -oth malignancy and throm-ophilia are o-vious ris6 factors for deep veinthrom-osis NICE ma6e recommendations on ho/ to investigate patients /ith




unprovo6ed clots.

45er all patients diagnosed /ith unprovo6ed $D8 or ,E /ho are not already6no/n to have cancer the follo/ing investigations for cancer

•A physical e%amination guided -y the patient's full history! and

• A chest Uray and

• lood tests full -lood count& serum calcium and liver function tests!and urinalysis.

Consider further investigations for cancer /ith an a-dominopelvic C8 scanand a mammogram for /omen! in all patients aged over )0 years /ith a9rst unprovo6ed $D8 or ,E

8hrom-ophilia screening

• Not o5ered if patients /ill -e on lifelong /arfarin i.e. 7on't altermanagement!

• Consider testing for antiphospholipid anti-odies if unprovo6ed $D8 or,E

• Consider testing for hereditary throm-ophilia in patients /ho have had

unprovo6ed $D8 or ,E and /ho have a 9rstdegree relative /ho hashad $D8 or ,E

Angiotensinconverting enJyme inhi-itors

Angiotensinconverting enJyme ACE! inhi-itors are no/ the esta-lished 9rstline treatment in younger patients /ith hypertension and are alsoe%tensively used to treat heart failure. 8hey are 6no/n to -e less e5ective intreating hypertensive AfroCari--ean patients. ACE inhi-itors are also used totreat dia-etic nephropathy and have a role in secondary prevention of

ischaemic heart disease.

<echanism of action

• Inhi-it the conversion angiotensin I to angiotensin II




Sidee5ects

• Cough occurs in around 1@* of patients and may occur up to a yearafter starting treatment. 8hought to -e due to increased -rady6inin

levels

• Angioedema may occur up to a year after starting treatment

• =yper6alaemia

• ;irstdose hypotension more common in patients ta6ing diuretics

Cautions and contraindications

• ,regnancy and -reastfeeding avoid

• enovascular disease signi9cant renal impairment may occur inpatients /ho have undiagnosed -ilateral renal artery stenosis

• Aortic stenosis may result in hypotension

• ,atients receiving highdose diuretic therapy more than G0 mg offurosemide a day! signi9cantly increases the ris6 of hypotension

• =ereditary of idiopathic angioedema

<onitoring

• rea and electrolytes should -e chec6ed -efore treatment is initiatedand after increasing the dose

• A rise in the creatinine and potassium may -e e%pected after startingACE inhi-itors. Accepta-le changes are an increase in serumcreatinine& up to #0*+ from -aseline and an increase in potassium up

to @.@ mmoll+.

+enal Association F& Clinical Fno/ledge Summaries :uote @0* /hich

seems rather high. SI"N advise that the fall in egfr should -e less than 20*.




8he NICE CF$ guidelines suggest that a decrease in egfr of up to 2@* or a

rise in creatinine of up to #0* is accepta-le

++ ,atients /ith -ilateral renovascular disease e.g. enal artery stenosis!

may develop an acute 6idney inBury AFI! if ACE inhi-itors are administered.

8his is -ecause elevated angiotensin II levels constrict the e5erent arteriolemore than the a5erent arteriole /ithin the 6idney& /hich normally helps to

maintain glomerular capillary pressure and 9ltration. emoving this

constriction -y -loc6ing angiotensin II formation can cause an a-rupt fall in

glomerular 9ltration rate.

NICE advise the follo/ing '*er people aged under ;; years an AC6inhi-itor or a lo5cost A':. f an AC6 inhi-itor is prescri-ed and is nottolerated (for e$ample! -ecause of cough)! o*er a lo5cost A':.'

p to 1@* of patients /ho are started on an ACE inhi-itor develop a drycough. =er symptoms are interfering /ith sleep and have persisted no/ forfour /ee6s. It is therefore appropriate to s/itch her to an angiotensin IIreceptor -loc6er.

Angiotensin II receptor -loc6ers




Angiotensin II receptor -loc6ers are generally used in situations /herepatients have not tolerated an ACE inhi-itor& usually due to the developmentof a cough.

E%amples

• Candesartan

• ?osartan

• Ir-esartan

?i6e ACE inhi-itors they should -e used /ith caution in patients /ithrenovascular disease. Sidee5ects include hypotension and hyper6alaemia.

<echanism

• loc6 e5ects of angiotensin II at the A81 receptor

Evidence -ase

• Sho/n to reduce progression of renal disease in patients /ith dia-eticnephropathy

•

Evidence -ase that losartan reduces CDA and I=$ mortality inhypertensive patients

,atients /ith aortic stenosis are at ris6 of profound hypotension /ith ACEinhi-itors.

endroHumethiaJide is a /ea6 diuretic that is commonly copresecri-ed /ithACE inhi-itors. 8he ris6 of hypotension relates to highdose loop diuretics& fore%ample furosemide G0mg -d.

,atients /ith chronic 6idney disease stage 2 have& -y de9nition& a glomerular

9ltration rate of 3 L0 mlmin1.# mR. It is unli6ely that this /ill have asigni9cant e5ect on the ris6 of sidee5ects.




8ricyclic overdose

4verdose of tricyclic antidepressants is a common presentation toemergency departments. Amitriptyline and dosulepin dothiepin! areparticularly dangerous in overdose.

Early features relate to anticholinergic properties dry mouth& dilated pupils&agitation& sinus tachycardia& -lurred vision.

;eatures of severe poisoning include

•

Arrhythmias

• SeiJures

• <eta-olic acidosis

• Coma

EC" changes include

• Sinus tachycardia

• 7idening of S

• ,rolongation of 8 interval

7idening of S 3 100ms is associated /ith an increased ris6 of seiJures/hilst S 3 1L0ms is associated /ith ventricular arrhythmias

<anagement

• ID -icar-onate may reduce the ris6 of seiJures and arrhythmias insevere to%icity

• Arrhythmias class 1a e.g. uinidine! and class Ic antiarrhythmics e.g.;lecainide! are contraindicated as they prolong depolarisation. Class III




drugs such as amiodarone should also -e avoided as they prolong the8 interval. esponse to lignocaine is varia-le and it should -eemphasiJed that correction of acidosis is the 9rst line in managementof tricyclic induced arrhythmias

•Intravenous lipid emulsion is increasingly used to -ind free drug andreduce to%icity

• $ialysis is ine5ective in removing tricyclics

$igo%in and digo%in to%icity

$igo%in is a cardiac glycoside no/ mainly used for rate control in themanagement of atrial 9-rillation. As it has positive inotropic properties it issometimes used for improving symptoms -ut not mortality! in patients /ithheart failure.echanism of action

• $ecreases conduction through the atrioventricular node /hich slo/sthe ventricular rate in atrial 9-rillation and Hutter

• Increases the force of cardiac muscle contraction due to inhi-ition ofthe NaQF Q atpase pump. Also stimulates vagus nerve

Digoxin toxicity,lasma concentration alone does not determine /hether a patient hasdeveloped digo%in to%icity. 8he N; advises that the li6elihood of to%icityincreases progressively from 1.@ to # mcgl.

5eatures

• "enerally un/ell& lethargy& nausea Y vomiting& anore%ia& confusion&

yello/green vision

• Arrhythmias e.g. AD -loc6& -radycardia!

Precipitating factors




• Classically hypo6alaemia+

• Increasing age

• enal failure


• =ypomagnesaemia& hypercalcaemia& hypernatraemia& acidosis

• =ypoal-uminaemia

• =ypothermia

• =ypothyroidism

• $rugs amiodarone& :uinidine& verapamil& diltiaJem& spironolactonecompetes for secretion in distal convoluted tu-ule therefore reducee%cretion!& ciclosporin. Also drugs /hich cause hypo6alaemia e.g. 8hiaJides and loop diuretics

anagement

• $igi-ind

• Correct arrhythmias

• <onitor potassium

+hyper6alaemia may also /orsen digo%in to%icity& although this is very smallprint

Amiodarone

Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial&nodal and ventricular tachycardias. 8he main mechanism of action is -y-loc6ing potassium channels /hich inhi-its repolarisation and henceprolongs the action potential. Amiodarone also has other actions such as-loc6ing sodium channels a class I e5ect!

8he use of amiodarone is limited -y a num-er of factors




• ?ong halflife 20100 days!

• Should ideally -e given into central veins causes throm-ophle-itis!

• =as proarrhythmic e5ects due to lengthening of the 8 interval

• Interacts /ith drugs commonly used concurrently e.g. $ecreases

meta-olism of /arfarin

• Numerous longterm adverse e5ects see -elo/!

<onitoring of patients ta6ing amiodarone

• 8;8& ?;8& YE& CU prior to treatment

• 8;8& ?;8 every L months

Adverse e5ects of amiodarone use

• 8hyroid dysfunction

• Corneal deposits

• ,ulmonary 9-rosispneumonitis

• ?iver 9-rosishepatitis

• ,eripheral neuropathy& myopathy

• ,hotosensitivity

• 'Slategrey' appearance

• 8hrom-ophle-itis and inBection site reactions

• radycardia




Calcium channel -loc6ers

Calcium channel -loc6ers are primarily used in the management ofcardiovascular disease. Doltagegated calcium channels are present inmyocardial cells& cells of the conduction system and those of the vascularsmooth muscle. 8he various types of calcium channel -loc6ers have varyinge5ects on these three areas and it is therefore important to di5erentiatetheir uses and actions.

xampes ndications Q notes 1ide-eEects and

cautions

erapami Angina& hypertension&

arrhythmias

=ighly negatively inotropic

Should not -e given /ith -eta

-loc6ers as may cause heart

-loc6

=eart failure&

constipation&

hypotension&

-radycardia&

Hushing

DitiaIem Angina& hypertension

?ess negatively inotropic than

verapamil -ut caution should still

-e e%ercised /hen patients have

heart failure or are ta6ing -eta

-loc6ers

=ypotension&

-radycardia& heart

failure& an6le

s/elling

,ifedipine#

amodipine#

feodipine

dihydropyridin

es

=ypertension& angina& aynaud's

A5ects the peripheral vascular

smooth muscle more than the

myocardium and therefore do not

result in /orsening of heart failure

;lushing&

headache& an6le

s/elling




+++ 8he N; /arns that shortacting formulations of nifedipine are associated

/ith large variations in -lood pressure and may cause reHe% tachycardia

eta-loc6ers

eta-loc6ers are an important class of drug used mainly in the managementof cardiovascular disorders.

Indications

• Angina

• ,ostmyocardial infarction

• =eart failure -eta-loc6ers /ere previously avoided in heart failure -ut

there is no/ strong evidence that certain -eta-loc6ers improve -othsymptoms and mortality

• Arrhythmias -eta-loc6ers have no/ replaced digo%in as the ratecontrol drug of choice in atrial 9-rillation

• =ypertension the role of -eta-loc6ers has diminished in recent yearsdue to a lac6 of evidence in terms of reducing stro6e and myocardialinfarction.

• 8hyroto%icosis

• <igraine prophyla%is

• An%iety

E%amples

• Atenolol

• ,ropranolol one of the 9rst -eta-loc6ers to -e developed. ?ipidsolu-le therefore crosses the -lood-rain -arrier




Sidee5ects

• ronchospasm

• Cold peripheries

• ;atigue

• Sleep distur-ances& including nightmares

Contraindications

• ncontrolled heart failure

• Asthma

• Sic6 sinus syndrome

• Concurrent verapamil use may precipitate severe -radycardia

<<< :eta5-lockers com-ined ith verapamil can potentially cause profound

-radycardia and asystole.

eta-loc6er overdose

;eatures

• radycardia

• =ypotension=eart failure

• Syncope

• <anagementIf -radycardic then atropineIn resistant cases glucagon may -e used

=aemodialysis is not e5ective in -eta-loc6er overdose

"astric lavage should only -e attempted if at all! if patients present

/ithin 12 hours of ta6ing the overdose.




,rescri-ing in pregnant patients

Dery fe/ drugs are 6no/n to -e completely safe in pregnancy. 8he list -elo/largely comprises of those 6no/n to -e harmful. Some countries havedeveloped a grading system see the lin6.

Anti-iotics

• 8etracyclines

• Aminoglycosides

• Sulphonamides and trimethoprim

• uinolones the N; advises to avoid due to arthropathy in someanimal studies




4ther drugs

• ACE inhi-itors& angiotensin II receptor antagonists

• Statins

• 7arfarin

• Sulfonylureas

• etinoids including topical!

• Cytoto%ic agents

8he maBority of antiepileptics including valproate& car-amaJepine andphenytoin are 6no/n to -e potentially harmful. 8he decision to stop suchtreatments ho/ever is diPcult as uncontrolled epilepsy is also a ris6

+++ NICE are very clear on this point4*er antihypertensive drug treatment to

omen of child5-earing potential in line ith the recommendations on &anagement

of pregnancy ith chronic hypertension4

Natriuretic peptide

8here are t/o types of natriuretic peptide that can -e measured in serum B-type natriuretic peptide B,P and ,-termina pro-B,P ,+-probnp!.N8pro-np is the inactive prohormone of N, and is released from the leftventricle in response to ventricular strain. It acts to increase renal e%cretionof /ater and sodium& and rela% vascular smooth muscle causing vasodilation.




N, should -e measured in patients /ith suspected heart failure /ho havenot had a previous myocardial infarction. 8he serum level helps to determinethe li6elihood of heart failure and thus the need for specialist assessmentand echocardiography. 8he value helps dictate the level of urgency of the

referral given high N; levels 3)00! carry poor prognosis. In these cases 2/ee6 /ait for urgent echocardiography and specialist assessment is advised.

Although elevated levels of N, do not con9rm the diagnosis of heart failure&normal levels rule the diagnosis out highly sensitivity -ut varyingspeci9city!.

NICE suggest that N, measurements are not necessary in people /ithsuspected heart failure /ho have had a previous myocardial infarction. 8hesepatients re:uire urgent referral& echocardiography and specialist assessment

-ecause if heart failure is present this carries a poor prognosis.

Increased N, levels 3)00! are not on their o/n diagnostic of heart failure&and may -e elevated as a result of left ventricular hypertrophy& myocardialischaemia& atrial 9-rillation& pulmonary hypertension& hypo%ia& pulmonaryem-olism& right ventricular strain& chronic o-structive pulmonary disease&liver failure& sepsis& dia-etes& and renal impairment. In addition& levels tendto -e higher in /omen& and in people older than 0.

=eart failure is unli6ely if N, levels are lo/ 100!. =o/ever& aldosteroneantagonists& ACE inhi-itors& angiotensinII receptor antagonists& -eta

-loc6ers and diuretics can all falsely lo/er N, levels& as can o-esity.

B-type natriuretic peptide

type natriuretic peptide N,! is a hormone produced mainly -y the leftventricular myocardium in response to strain.

7hilst heart failure is the most o-vious cause of raised N, levels any cause

of left ventricular dysfunction such as myocardial ischaemia or valvulardisease may raise levels. aised levels may also -e seen due to reducede%cretion in patients /ith chronic 6idney disease. ;actors /hich reduce N,levels include treatment /ith ACE inhi-itors& angiotensin2 receptor -loc6ersand diuretics.

E5ects of N,




• Dasodilator

• $iuretic and natriuretic

• Suppresses -oth sympathetic tone and the reninangiotensin

aldosterone system

"inica uses of B,P

$iagnosing patients /ith acute dyspnoea

• A lo/ concentration of N, 100pgml! ma6es a diagnosis of heart

failure unli6ely& -ut raised levels should prompt further investigation tocon9rm the diagnosis

• NICE currently recommends N, as a helpful test to rule out adiagnosis of heart failure

,rognosis in patients /ith chronic heart failure

• Initial evidence suggests N, is an e%tremely useful mar6er of

prognosis

"uiding treatment in patients /ith chronic heart failure

• E5ective treatment lo/ers N, levels

Screening for cardiac dysfunction

• Not currently recommended for population screening




Cardiac imaging noninvasive techni:ues e%cludingechocardiography

8he a-ility to image the heart using noninvasive techni:ues such as <I& C8and radionuclides has evolved rapidly over recent years.

,ucear imaging

8hese techni:ues use radiotracers /hich are e%tracted -y normal

myocardium. E%amples include

• 8hallium

• 8echnetium ((mtc! sestami-i a coordination comple% of theradioisotope technetium((m /ith the ligand metho%yiso-utyl isonitrile<II!& used in '<II' or cardiac Single ,hoton Emission Computed 8omography S,EC8! scans

• ;luorodeo%yglucose ;$"! used in ,ositron Emission 8omography ,E8!scans

8he primary role of S,EC8 is to assess myocardial perfusion and myocardialvia-ility. 8/o sets of images are usually ac:uired. ;irst the myocardium atrest follo/ed -y images of the myocardium during stress either e%ercise orfollo/ing adenosine dipyridamole!. y comparing the rest /ith stressimages any areas of ischaemia can classi9ed as reversi-le or 9%ed e.g.;ollo/ing a myocardial infarction!. Cardiac ,E8 is predominately a researchtool at the current time

<"A

• <ulti "ated Ac:uisition Scan& also 6no/n as radionuclide angiography

• adionuclide technetium((m! is inBected intravenously

• 8he patient is placed under a gamma camera




• <ay -e performed as a stress test

• Can accurately measure left ventricular eBection fraction. 8ypically used

-efore and after cardioto%ic drugs are used

"ardiac "omputed +omography "+

Cardiac C8 is useful for assessing suspected ischaemic heart disease& usingt/o main methods

• Calcium score there is 6no/n to -e a correlation -et/een the amountof atherosclerotic pla:ue calcium and the ris6 of future ischaemicevents. Cardiac C8 can :uantify the amount of calcium producing a'calcium score'

• Contrast enhanced C8 allo/s visualisation of the coronary arterylumen

If these t/o techni:ues are com-ined cardiac C8 has a very high negativepredictive value for ischaemic heart disease.

"ardiac (

Cardiac <I commonly termed C<! has -ecome the gold standard forproviding structural images of the heart. It is particularly useful /henassessing congenital heart disease& determining right and left ventricularmass and di5erentiating forms of cardiomyopathy. <yocardial perfusion canalso -e assessed follo/ing the administration of gadolinium. Currently C<provides limited data on the e%tent of coronary artery disease.

,lease also see the ritish =eart ;oundation lin6 for an e%cellent summary.




$D?A cardiovascular disorders

8he guidelines -elo/ relate to carmotorcycle use unless speci9cally stated.

;or o-vious reasons& the rules relating to drivers of heavy goods vehicles

tend to -e much stricter

Speci9c rules

• =ypertension can drive unless treatment causes unaccepta-le sidee5ects& no need to notify $D?A. If "roup 2 Entitlement the dis:uali9esfrom driving if resting , consistently 1G0 mmhg systolic or moreandor 100 mm =g diastolic or more

• Angioplasty elective! 1 /ee6 o5 driving

• CA" ) /ee6s o5 driving

• Acute coronary syndrome ) /ee6s o5 driving& 1 /ee6 if successfullytreated -y angioplasty

• Angina driving must cease if symptoms occur at restat the /heel




• ,acema6er insertion 1 /ee6 o5 driving

• Implanta-le cardioverterde9-rillator IC$! if implanted for sustained

ventricular arrhythmia cease driving for L months. If implantedprophylatically then cease driving for 1 month. =aving an IC$ results in

a permanent -ar for "roup 2 drivers

• Successful catheter a-lation for an arrhythmia 2 days o5 driving

• Aortic aneurysm of Lcm or more notify $D?A. ?icensing /ill -epermitted su-Bect to annual revie/. An aortic diameter of L.@ cm ormore dis:uali9es patients from driving

• =eart transplant $D?A do not need to -e noti9ed

=eart failure is one of the adverse signs indicating the need for urgent

synchronised $C cardioversion

Documents

Cardiovascular System _ PLAB_Passmed _Theory