Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M E D > c a r d i o > Flashcards

c a r d i o Flashcards

1
Q

what are the causes of bradycardia

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how are bradycardias classified

A
  1. Sinus bradycardia
  2. First degree heart block: PR > 200ms
  3. Second degree heart block
     Wenkebach / Mobitz I
     Mobitz II
  4. Complete heart block
     Junctional: narrow QRS @ ~50bpm
     Ventricular: broad QRS @ ~40bpm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

management of bradycardias if asymptomatic

A

If asymptomatic and rate >40: no Rx needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

management of bradycardias if symptomatic or rate less than 40bpm

A
  1. Rx underlying cause: e.g. drugs, MI
  2. Medical
     Atropine 0.6–1.2g (max 3g) IV  Isoprenaline IVI
  3. Pacing: External
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what’s the elective management for bradycardias

A

permeant pacing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are signs of bradycardia

A

signs may indicate instability: Systolic BP < 90 mmHg, HR < 40 bpm, poor perfusion, and poor urine output, ventricular arrhythmias requiring suppression or heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

sinus node dysfunction can lead to…

A

sinus bradycardia, sick sinus syndrome (tachy-brady), sinus arrest alone or as part of vasovagal syncope.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what ECG changes confirm sinus bradycardia

A

There is a slow rate but every QRS is preceded by a p wave.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is 1st degree HB characterised by

A

PR interval greater than 0.2s

no specific treatment required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pt with 1st degree AV block on digoxin.. you should check for..

A

check for toxicity - remember drugs is a cause of bradycardias - digoxin can cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is second degree AV block characterised by

A

progressive lengthening of PR interval followed by failure of the atrial impulse to conduct to the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

when does second degree AV block occur

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the management for second degree HB

A

No specific therapy is indicated. Higher degrees of AV block should be looked for if patients present with syncope or dizziness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is second degree AV block Mobitz type II characterised by

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how is second degree Mobitz type II managed

A

In the absence of a recent acute coronary event, permanent pacing should be arranged (if drugs have been excluded).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

complete/ third degree AV block is characterised by

A

no conduction from the atria to the ventricles and therefore AV dissociation. There is no relationship between the P waves and QRS complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where can complete AV block occur

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe the treatment of severe hyperkalaemia cause complete AV block and in haemodyamically unstable pt

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is third degree heart block managed

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe the pathology behind AF

A

LA loses refractoriness before the end of atrial systole.

 → recurrent, uncoordinated contraction @ 300-600bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why af can trigger HF

A

Atrial contraction responsible for ~25% of CO

often triggers heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the common causes of AF

A

IHD
 Rheumatic heart disease
 Thyrotoxicosis
 Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are other cause of AF

A 
 Alcohol
 Pneumonia
 PE
 Post-op
 Hypokalaemia
 RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the sx associated with AF

A 
Asympto
 Chest pain
 Palpitations
 Dyspnoea
 Faintness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what clinical signs are associated with AF

A

Irregularly irregular pulse
 Pulse deficit: difference between pulse and HS
 Fast AF → loss of diastolic filling → no palpable pulse
 Signs of LVF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what investigations are required

A

ECG
 FBC, U+E, TFTs, Trop
 Consider TTE: structural abnormalitie

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

is an echo done in suspected AF

A

Perform if suspected structural heart disease (on the basis of symptoms or examination finding of a murmur or signs of heart failure).

  1. Where a rhythm control strategy (cardioversion) is being considered
  2. Baseline echocardiogram required to inform long term management
28
Q

cardiac monitoring in paroxysmal AF - how is it done

A

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.

29
Q

what are the types of AF

A 
acute - less than 48 hrs
paroxysmal - self limiting, 7 days our less
persistent - more than 7 days 
permenant - all the time 
atrial flutter
30
Q

what are the 3 principles of management in AF

A
  1. Anticoagulation to prevent stroke
  2. Rate control
  3. Rhythm control
31
Q

what does the CHA2DS2VaSc score assess and what do the scores relate to

A

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

32
Q

what score is used to assess bleeding risk

A

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:

33
Q

what are DOACs and why are they preferred

A

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)

34
Q

How do DOACS work

A

inhibit factor Xa (apixiban, rivaroxaban and edoxaban) or direct thrombin inhibitor (dabigatran) to reduced thromboembolic events.

35
Q

describe rate control in AF

A

REFER TO WORKBOOK FLOW CHART

page 36

36
Q

describe rate control in AF, how does it work

A

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

37
Q

what is SVT

A

rate greater than 100bpm
QRS width less than 120ms

narrow complex tachycardia

38
Q

ddx for SVT

A 
Sinus tachycardia
2. Atrial
 AF
 Atrial flutter
 Atrial tachycardia
3. AV nodal re-entry tachycardia
4. AV re-entry tachycardia
39
Q

describe the physiology behind SVT management

A

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

40
Q

rapid broad complex tachycardia after STEMI is nearly always

A

VT

41
Q

How is VT with broad QRS signal following STEMI managed

A

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.

42
Q

what is the first line treatment of SVT in haemodynically stable pts

A

vagal manoeuvres - breath holding and valsava manoeuvre

43
Q

how do you do the valsalva manoeuvre

A

having the patient bear down as though having a bowel movement or blowing hard into a syringe to move the plunger)

44
Q

how do vagal manoeuvres act in svt

A

all slow conduction in the AV node and can potentially interrupt the re-entrant circuit.

45
Q

how is the carotid sinus massage done. what must be done before and why?

how long to wait before trying other side

A

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

46
Q

what can be used if SVT not terminated by vagal manoeuvres

A
  1. 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
47
Q

what are the SE of adenosine, when managing SVT

A

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.

48
Q

If the tachycardia continues despite successful induction of at least some degree of AV blockade, the rhythm is almost certainly…

A

atrial tachycardia or flutter

AVRT is excluded and AVNRT is unlikely

49
Q

synchronised cardioversion following sedation is used in

A

starting at 150J

can be used immediately in patients who are hypotensive, have pulmonary oedema, have chest pain with ischaemia, or are otherwise unstable.

50
Q

what are the commonest bacterial causes of IE

A

streptococci viridans -

staph aureus - IVDU

51
Q

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

A

staphlococci esp coagulase negative

52
Q

‘Late’ prosthetic valve infections are commonly due to

A

viridans streptococci, Staphylococcus aureus and coagulase- negative staphylococci.

53
Q

Lx in IE

A

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
54
Q

what is the major diagnostic criteria for IE

A

major vs minor

major = endocardial involvement, positive blood cultures, positive echo findings, new valve regurgitation, dehiscence of prosthesis

55
Q

describe the minor diagnostic criteria for IE

A

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

56
Q

what is the management for IE

A

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

57
Q

what should be monitored in IE

A

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

58
Q

when is surgery indicated in IE

A

moderate to severe cardiac failure due to valve compromise
valve dehiscence
valve obstruction
paravalvular abscess

59
Q

management of HTN urgency or emergency

A
  1. sodium nitroprusside
  2. labetalol
  3. GTN
  4. Esmolol
60
Q

oral regime for HTN urgency

A

amlodipine
diltiazem
lisinopril

61
Q

control of phaechro HTN

A

alpha and beta blockers

commonly use phenoxybenzamine then use beta

never start with beta adrenergic blocker first

62
Q

aortic stenosis murmur describe it

A

ejection systolic murmur radiating to neck or carotid

63
Q

where to listen for aortic stenosis murmur

A

2nd ICS right side

64
Q

aortic regurgitation murmur

A
  1. early diastolic murmur

left sternal edge

65
Q

aortic regurgitation associated with and managed by

A

collapsing pulse, De Musset’s sign = head bobbing

ACEi to reduce after load + surgery if indicated

66
Q

mitral regurgitation murmur is

A

pan systolic blowing murmur hears over mitral area 5th ICS midclavicular line radiates to axilla

M E D (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions