c a r d i o Flashcards
what are the causes of bradycardia
DIVISIONS
drugs = ABCD
ischaemia or infarction = inferior MI
Vagal hypertonia = athletes, vasovagal syncope, carotid sinus syndrome
Infection = viral myocarditis, RF, infective endocarditis
Sick sinus syndrome
Infiltration = restrictive or dilated cardiomyopathy = MD, amyloid
O - hypothyroidism, hypokalaemia or hyper, hypothermia
Neuro = increased ICP
septal defect - primum ASD
surgery or catheterisation
how are bradycardias classified
- Sinus bradycardia
- First degree heart block: PR > 200ms
- Second degree heart block
Wenkebach / Mobitz I
Mobitz II - Complete heart block
Junctional: narrow QRS @ ~50bpm
Ventricular: broad QRS @ ~40bpm
management of bradycardias if asymptomatic
If asymptomatic and rate >40: no Rx needed
management of bradycardias if symptomatic or rate less than 40bpm
- Rx underlying cause: e.g. drugs, MI
- Medical
Atropine 0.6–1.2g (max 3g) IV Isoprenaline IVI - Pacing: External
what’s the elective management for bradycardias
permeant pacing
what are signs of bradycardia
signs may indicate instability: Systolic BP < 90 mmHg, HR < 40 bpm, poor perfusion, and poor urine output, ventricular arrhythmias requiring suppression or heart failure.
sinus node dysfunction can lead to…
sinus bradycardia, sick sinus syndrome (tachy-brady), sinus arrest alone or as part of vasovagal syncope.
what ECG changes confirm sinus bradycardia
There is a slow rate but every QRS is preceded by a p wave.
what is 1st degree HB characterised by
PR interval greater than 0.2s
no specific treatment required
pt with 1st degree AV block on digoxin.. you should check for..
check for toxicity - remember drugs is a cause of bradycardias - digoxin can cause
what is second degree AV block characterised by
progressive lengthening of PR interval followed by failure of the atrial impulse to conduct to the ventricles
when does second degree AV block occur
occurs in young fit pts with high vagal tone - can see during night if monitored
It can occur quite frequently following inferior MI and rarely proceeds to complete heart block.
what is the management for second degree HB
No specific therapy is indicated. Higher degrees of AV block should be looked for if patients present with syncope or dizziness.
what is second degree AV block Mobitz type II characterised by
characterised by a constant PR interval followed by sudden failure of a P wave to be conducted to the ventricles.
ECG of second degree heart block with 2 p waves for every QRS.
how is second degree Mobitz type II managed
In the absence of a recent acute coronary event, permanent pacing should be arranged (if drugs have been excluded).
complete/ third degree AV block is characterised by
no conduction from the atria to the ventricles and therefore AV dissociation. There is no relationship between the P waves and QRS complexes
where can complete AV block occur
This block can occur above the AV node at the His region (narrow complex escape and usually well tolerated such as congenital complete heart block) or beneath the AV node with broad complex escape (not well tolerated). In can also be intermittent therefore look for ECGs with trifascicular or bifascicular block (RBBB, left axis deviation with or without prolonged PR interval) and alternating LBBB and RBBB.
describe the treatment of severe hyperkalaemia cause complete AV block and in haemodyamically unstable pt
severe hyperkalaemia (can be treated with IV calcium chloride - 10 ml of 10% solution over 3-5 minutes). In the haemodynamically unstable patient, atropine can be administered (600 μg to a maximum of 3 mg). Isoprenaline administered at a rate of 5 μg/min can be tried.
how is third degree heart block managed
Urgent permanent pacing is indicated, and should be considered within 24 hours, in all patients except those with a reasonable likelihood of recovery of conduction - such as in patients with a recent coronary event.
describe the pathology behind AF
LA loses refractoriness before the end of atrial systole.
→ recurrent, uncoordinated contraction @ 300-600bpm
Why af can trigger HF
Atrial contraction responsible for ~25% of CO
often triggers heart failure
What are the common causes of AF
IHD
Rheumatic heart disease
Thyrotoxicosis
Hypertension
What are other cause of AF
Alcohol Pneumonia PE Post-op Hypokalaemia RA
what are the sx associated with AF
Asympto Chest pain Palpitations Dyspnoea Faintness
what clinical signs are associated with AF
Irregularly irregular pulse
Pulse deficit: difference between pulse and HS
Fast AF → loss of diastolic filling → no palpable pulse
Signs of LVF
what investigations are required
ECG
FBC, U+E, TFTs, Trop
Consider TTE: structural abnormalitie
is an echo done in suspected AF
Perform if suspected structural heart disease (on the basis of symptoms or examination finding of a murmur or signs of heart failure).
- Where a rhythm control strategy (cardioversion) is being considered
- Baseline echocardiogram required to inform long term management
cardiac monitoring in paroxysmal AF - how is it done
If paroxysmal (intermittent) AF is suspected, further cardiac monitoring is recommended. Short term cardiac monitoring with a 24 hour cardiac monitor is considered the first line investigation, and is universally available to clinicians without requiring Cardiology input.
The AliveCor app/cardiac monitor is also available in primary care where repeated snap shots of rhythm over time can increase diagnostic yield.
what are the types of AF
acute - less than 48 hrs paroxysmal - self limiting, 7 days our less persistent - more than 7 days permenant - all the time atrial flutter
what are the 3 principles of management in AF
- Anticoagulation to prevent stroke
- Rate control
- Rhythm control
what does the CHA2DS2VaSc score assess and what do the scores relate to
quantify risk of stroke or systemic embolism
The score estimate an adjusted stroke rate per year
score of 2 or more = significant risk = anticoag
score of 1 in men - intermediate = consider anticoagulant consider bleeding risk
score of - - low risk = no anticoagulation required
score 1 or 0 in women is low = no anticoagulants
what score is used to assess bleeding risk
HAS-BLED
It estimates the rate of major bleeds per 100 patient years
a) Uncontrolled hypertension (SBP>160mmHg)
b) Poor INR control (“labile INR”), as measured by time-in-therapeutic range (TTR)
c) Concurrent medication (aspirin, NSAIDs)
d) Harmful alcohol consumption (>14 units per week)
score is not intended to withhold anticoagulation, but to inform discussions and enable identification and optimisation of reversible risk factors for bleeding, including:
what are DOACs and why are they preferred
direct oral anticoagulants
They do not require regular testing of levels compared to the INR monitoring of warfarin. There are no restrictions on food or alcohol.
lower rates of bleeding to warfarin (brain and GIT)
How do DOACS work
inhibit factor Xa (apixiban, rivaroxaban and edoxaban) or direct thrombin inhibitor (dabigatran) to reduced thromboembolic events.
describe rate control in AF
REFER TO WORKBOOK FLOW CHART
page 36
describe rate control in AF, how does it work
slow the heart response to AF by slowing conduction at the Av node to reduce ventricular conduction and therefore heart rate.
look at diagram in work book
what is SVT
rate greater than 100bpm
QRS width less than 120ms
narrow complex tachycardia
ddx for SVT
Sinus tachycardia 2. Atrial AF Atrial flutter Atrial tachycardia 3. AV nodal re-entry tachycardia 4. AV re-entry tachycardia
describe the physiology behind SVT management
SVT most people have AVNRT or AVRT
these arrhythmias depend on AV nodal contraction and therefore can be terminated by transiently blocking AV nodal conduction
rapid broad complex tachycardia after STEMI is nearly always
VT
How is VT with broad QRS signal following STEMI managed
sustained VT who are haemodynamically compromised cardioversion is indicated (synchronised 150 – 200 joule shock with a biphasic defibrillator).
Suppression can be achieved with β-blockers
. Amiodarone can be tried (300 mg IV over a few minutes, followed by 900 mg over 24 hours).
An alternative is lidocaine (50 - 100 mg over 3 - 5 minutes), which may be repeated after 5 minutes. No more than 200 - 300 mg should be given in one hour.
what is the first line treatment of SVT in haemodynically stable pts
vagal manoeuvres - breath holding and valsava manoeuvre
how do you do the valsalva manoeuvre
having the patient bear down as though having a bowel movement or blowing hard into a syringe to move the plunger)
how do vagal manoeuvres act in svt
all slow conduction in the AV node and can potentially interrupt the re-entrant circuit.
how is the carotid sinus massage done. what must be done before and why?
how long to wait before trying other side
Carotid massage is another vagal manoeuvre that can slow AV nodal conduction. Massage the carotid sinus for several seconds on the non-dominant cerebral hemisphere side. This manoeuvre is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this manoeuvre. Do not perform carotid massage on both sides simultaneously. Wait at least 10 seconds before trying the other side
what can be used if SVT not terminated by vagal manoeuvres
- intravenous adenosine or calcium channel blockers. Adenosine is a short-acting drug that blocks AV node conduction; it terminates 90% of tachycardias due to AVNRT or AVRT. It is given as a rapid IV bolus followed by a saline flush
what are the SE of adenosine, when managing SVT
Adenosine has a very short half-life. It may produce chest discomfort (which the patient should be warned about), transient hypotension and flushing. It should be avoided in patients with significant reversible airways disease. The crash trolley should be next to the patient when administering this drug in the unlikely event of significant bradyarrhythmia or more rarely tachyarrhythmia.
If the tachycardia continues despite successful induction of at least some degree of AV blockade, the rhythm is almost certainly…
atrial tachycardia or flutter
AVRT is excluded and AVNRT is unlikely
synchronised cardioversion following sedation is used in
starting at 150J
can be used immediately in patients who are hypotensive, have pulmonary oedema, have chest pain with ischaemia, or are otherwise unstable.
what are the commonest bacterial causes of IE
streptococci viridans -
staph aureus - IVDU
IE occurring ‘early’ (up to 1 year) after the implantation of prosthetic heart valves is thought to be due to perioperative contamination and is mainly caused by
staphlococci esp coagulase negative
‘Late’ prosthetic valve infections are commonly due to
viridans streptococci, Staphylococcus aureus and coagulase- negative staphylococci.
Lx in IE
key investigations = blood cultures (at least 3 cultures over hours, at 3 different sites) and echocardiogram (ToE more sensitive TTE)
● Full blood count ● ESR and CRP ● U&Es ● Liver function tests ● Urine dipstick analysis and MSU for microscopy/culture ● Chest X-ray ● ECG
what is the major diagnostic criteria for IE
major vs minor
major = endocardial involvement, positive blood cultures, positive echo findings, new valve regurgitation, dehiscence of prosthesis
describe the minor diagnostic criteria for IE
predisposing valve or cardiac abnormality
IVDU
pyrexia more than 38
embolic phenomenon
vasculitic phenomenon
blood cultures with organism grown but not meeting major criteria
echo findings suggestive but not meeting major criteria
what is the management for IE
IV Abx via tunnelled central venous line
streptococci = benzylpenicillin or vancomycin if pen allergy plus gentamicin
enterococci = amoxicillin or vancomycin if pen allegory and gentamicin
staph = fluclox or vancomycin if pen allergic or MRSA plus gentamicin
what should be monitored in IE
echocardiogram once weekly to assess vegetation size and to look for complications - valve destruction, abscess intracardiac
ECG twice a week to look for conduction disturbance
when is surgery indicated in IE
moderate to severe cardiac failure due to valve compromise
valve dehiscence
valve obstruction
paravalvular abscess
management of HTN urgency or emergency
- sodium nitroprusside
- labetalol
- GTN
- Esmolol
oral regime for HTN urgency
amlodipine
diltiazem
lisinopril
control of phaechro HTN
alpha and beta blockers
commonly use phenoxybenzamine then use beta
never start with beta adrenergic blocker first
aortic stenosis murmur describe it
ejection systolic murmur radiating to neck or carotid
where to listen for aortic stenosis murmur
2nd ICS right side
aortic regurgitation murmur
- early diastolic murmur
left sternal edge
aortic regurgitation associated with and managed by
collapsing pulse, De Musset’s sign = head bobbing
ACEi to reduce after load + surgery if indicated
mitral regurgitation murmur is
pan systolic blowing murmur hears over mitral area 5th ICS midclavicular line radiates to axilla
