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Yr 5 conditions > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the reversible causes of cardiac arrest?

A

4 Hs: Hypovolaemia, hypoxia, hypothermia, hypo/hyperkalaemia (and other metabolic disturbances)
4 Ts: Thrombosis (coronary or pulmonary), Tension pneumothorax, Tamponade - cardiac, toxins

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2
Q

What are the ‘shockable rhythms’ in cardiac arrest for which a defibrillator can be used?

A

Ventricular fibrillation

Pulseless ventricular tachycardia

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3
Q

In the shockable rhythms, when should shocks be administered via the defibrillator?

A

As soon as it’s recognised that the rhythm is shockable and then every after every 2-minute cycle of CPR (as long as the rhythm remains to be VF/pulseless VT

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4
Q

How often should adrenaline be administered in cardiac arrest with shockable rhythms?

A

After the 3rd shock then after every alternate cycle (i.e. every 3-5 mins thereafter)

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5
Q

How often should adrenaline be administered in cardiac arrest with non-shockable rhythms?

A

Adrenaline 1mg 1:10000 should be given as soon as possible. Should be treated with 2 minutes of CPR prior to reassessment of the rhythm

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6
Q

What additional drug can be given in shockable rhythm cardiac arrest?

A

Amiodarone 300mg iv after the 3rd shock

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7
Q

STEMI is diagnosable based on ECG changes (and confirmed with troponin results), what ECG changes are diagnostic of STEMI?

A

ST elevation in at least 2 anatomically contiguous leads or new Left bundle branch block

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8
Q

Regarding coronary artery occlusion, how does STEMI differ from NSTEMI or unstable angina?

A

STEMI - indicates complete occlusion of an artery

NSTEMI/unstable angina - indicates partial occlusion

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9
Q

Which 3 patient groups are most likely to have a ‘silent MI’ - MI without chest pain?

A

The elderly
Women
Diabetics

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10
Q

What will an ECG show in NSTEMI?

A 
Non-specific changes
T-wave inversion
Hyper-acute T waves
ST depression
(these changes can also be seen in unstable angina but more likely that the ECG will be normal)
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11
Q

How is unstable angina distinguishable from NSTEMI?

A

Only through troponin results which will be negative in unstable angina but raised in NSTEMI

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12
Q

Changes in which ECG leads indicate a blockage in the right coronary artery supplying the inferior part of the heart?

A

Leads II, III, aVF

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13
Q

Changes in which ECG leads indicate a blockage in the left anterior descending artery supplying the anterior part of the heart?

A

Leads V1-V4

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14
Q

Changes in which ECG leads indicate a blockage in the left circumflex artery supplying the lateral part of the heart?

A

Leads I, aVL, V5, V6

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15
Q

What is the acute management of ACS?

A

M - morphine 5-10mg iv and metaclopramide 10mg iv
O - oxygen (if sats <94%)
N - Nitrates (GTN spray sublingually)
A - Aspirin 300mg po
T - Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)

A LMWH may also be given, particularly in NSTEMI

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16
Q

What are the definitive management options for STEMI?

A

Contact local coronary care unit for:
Percutaneous coronary intervention (PCI) - if available within 2 hours
Thrombolysis - with e.g. tenecteplase if PCI not available within 2 hours

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17
Q

What scoring system can be used to calculate whether a patient with NSTEMI should receive PCI?

A

Grace score.

If > 5%, PCI advised

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18
Q

What 5 drugs form the secondary prevenatative pharmacological measures in ACS?

A 
B - Beta-blocker e.g. bisoprolol 10mg
A - Aspirin 75mg
S - Statin e.g. atorvastatin 80mg
I - Inhibitor of ACE e.g. ramipril 10mg
C - Clopidogrel 75mg or ticagrelor 60mg bd
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19
Q

What are the complications of MI?

A 
D – Death/cardiac arrest
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
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20
Q

What is Dressler’s syndrome?

A

An autoimmune reaction against antigenic proteins formed as the myocardium recovers after MI, causing pericarditis that typically occurs around 2-6 weeks after an MI. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

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21
Q

How does stable angina (aka angina pectoris) differ from ACS?

A

Stable angina is usually brought on by exertion as opposed to coming on at rest in ACS, and in stable angina, symptoms are usually relieved after resting for up to 5 mins or with GTN spray - this is not the case in ACS.

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22
Q

What is the Gold Standard diagnostic investigation for angina pectoris?

A

CT coronary angiogram - highlights any stenosis of the coronary arteries

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23
Q

What percentage narrowing of a coronary artery diameter is considered significant?

A

> 70%

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24
Q

How is stable angina managed?

A

GTN spray to be used PRN when chest pain comes on.
Aspirin and atorvastatin.
Beta-blocker or rate-limiting calcium channel blocker if B-blocker not tolerated/contraindicated. If Sx not controlled with monotherapy and intolerant of other drug, consider adding a long acting nitrates (e.g. isosorbide mononitrate)/Ivabradine/Nicorandil/Ranolazine
If necessary, consider procedural/surgical intervention with PCI or CABG.

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25
Q

What is the classical appearance on ECG of atrial flutter?

A

‘Sawtooth’ appearance

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26
Q

How is atrial flutter managed?

A

Rate/rhythm control with beta blockers or cardioversion.
Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis).
Radiofrequency ablation of the re-entrant rhythm - curative for most patients.
Anticoagulation based on CHA2DS2VASc score.

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27
Q

What may be seen on an X-ray of someone with pulmonary oedema (as a result of heart failure)?

A 
A - alveolar oedema (bat wing opacities)
B - Kerley B lines
C - cardiomegaly
D - dilated upper lobe vessels
E - pleural effusion
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28
Q

Heart failure is the end-stage of nearly all cardiovascular diseases, therefore identifying its cause and slowing the progression of the disease process is important. What are some causes of heart failure?

A

IHD and HTN (most common causes).
Valvular diseaes (e.g. mitral regurg, aortic stenosis, tricuspid regurg, ASD/VSD).
Arrhythmias.

Others:
Pericardial effusion/pericarditis.
Drugs (B-blockers/CCBs/alcohol/cocaine)
Cardiomyopathies.
Severe anaemia.
Pulmonary hypertenison.
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29
Q

What additional heart sound may be heard in someone with heart failure?

A

‘Gallop’ S3

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30
Q

What are the cut offs for NT-proBNP for referring someone with suspected heart failure for echocardiogram, which will confirm the diagnosis?

A

> 2,000 – require urgent referral to cardiology for an echocardiogram (<2 weeks)
400 – 2,000 – require referral to cardiology for an echocardiogram (<6 weeks)
<400 – heart failure is unlikely and consider an alternative diagnosis

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31
Q

What classification system is commonly used to categorise severity of heart failure?

A 
New York Heart Association [NYHA] Classification of Heart Failure.
Class I (no limitation of function) to class IV (severe limitation, Sx may be present at rest)
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32
Q

What is the cut off for left ventricular ejection fraction (LVEF) for having heart failure with reduced ejection fraction (HFrEF)?

A

LVEF less than 40%.

LVEF is at least 40% in heart failure with preserved ejection fraction (HFpEF).
40-49% is classed as heart failure with mid-range ejection fraction (HFmrEF). 50+% is considered normal.

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33
Q

What is the management of heart failure?

A

Lifestyle measures: smoking cessation, lose weight if overweight, meditteranean diet, salt restriction, restricted fluid intake, reduce alcohol, cardiac rehab exercise.
Pharmacological: ACE-i and beta-blocker. Diuretic (furosemide commonly used). Consider adding Spironolactone if ACE-i and beta-blocker ineffective at controlling Sx.
Other: annual flu and pneumococcal vaccine, depression screen, treat other co-morbidities.
Surgery: may be required in cases of severe aortic stenosis or mitral regurgitation.

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34
Q

What is classed as stage 1 HTN?

A

BP in surgery/clinic is ≥140/90 mm Hg and ambulatory blood pressure monitoring (ABPM) or home blood pressure monitoring (HBPM) ranges from 135/85 mm Hg to 149/94 mm Hg.

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35
Q

What is classed as stage 2 HTN?

A

BP in surgery/clinic is ≥160/100 mm Hg but less than 180/120 mm Hg and ABPM or HBPM is ≥150/95 mm Hg.

36
Q

What is classed as stage 3 or severe HTN?

A

Systolic BP in surgery/clinic is 180 mm Hg or higher or diastolic BP is 120 mm Hg or higher.

37
Q

When is a diagnosis of hypertension confirmed?

A

A clinic blood pressure of 140/90 mm Hg or higher; and

ABPM daytime average or HBPM average of 135/85 mm Hg or higher.

38
Q

When should anti-hypertensive medication be offered to patients?

A

Anyone under 80 who has stage 2 HTN;

Anyone under 80 who has stage 1 HTN and evidence of target organ damage/established cardiovascular disease/renal disease/diabetes/estimated 10-year risk of cardiovascular disease of 10% or more.
OR
Anyone under 60 with persistent stage 1 HTN and CV risk < 10%

39
Q

When should specialist referral be made for patients with HTN?

A

Those under 40 to look for secondary causes
and
those whose HTN is not being controlled with 3 anti-hypertensives

40
Q

What is the target BP for HTN patients under 80?

A

<140/90

41
Q

What is the target BP for HTN patients over 80?

A

<150/90

42
Q

What is the target BP for HTN patients with diabetes mellitus?

A

<130/80

43
Q

What is malignant hypertension (aka hypertensive crisis)?

A

HTN that comes on suddenly with SBP of >200 mmHg and / or DBP of >130 mmHg PLUS signs of target organ damage.
End-organ damage may be encephalopathy, dissection, pulmonary oedema, nephropathy, eclampsia, papilloedema and/or angiopathic haemolytic anaemia. Accelerated hypertension needs urgent (same-day) assessment and immediate treatment to reduce the BP within minutes to hours.

44
Q

What are the 4 grades of hypertensive retinopathy?

A

Grade 1: increased tortuosity, silver-wiring
Grade 2: AV nipping
Grade 3: cotton-wool spots (areas of infarction), exudates, flame haemorrhages
Grade 4: papilloedema (optic disc swelling)

45
Q

How does the Wells’ score for PE influence management of potential PE?

A

Score of 2+: Treat with LMWH and do proximal leg USS, if USS negative, do d-dimer and if this is positive, repeat the USS 7 days later.
Score 1 or less: do D-dimer test, if negative, DVT highly unlikely. If positive, offer proximal leg USS

46
Q

What is the ‘gold standard’ investigation for DVT but is rarely used in clinical practice?

A

Contrast venography - iv catheter is placed in a dorsal vein of the foot and contrast medium is infused into the vein.

47
Q

How long should anticoagulation be continued for in patients with a provoked DVT (e.g. post-op)?

A

3 months then reasses

48
Q

How long should anticoagulation be continued for in patients with a unprovoked DVT?

A

6 months then reassess

49
Q

How long should anticoagulation be continued for in patients with recurrent DVTs?

A

Lifelong

50
Q

In patients who have an ‘unprovoked’ DVT, what additional tests should be performed?

A 
Investigate for cancer with: 
History and examination
Chest X-ray
Bloods (FBC, calcium and LFTs)
Urine dipstick
CT abdomen and pelvis in patients over 40
Mammogram in women over 40
51
Q

What are the 6 Ps of acute limb ischaemia?

A 
Pain
Pallor
Pulseless
Paralysis
Paraesthesia
Perishing cold
52
Q

How is critical limb ischaemia treated?

A

Urgent referral to vascular team
Analgesia
Urgent revascularisation by: Angioplasty and stenting or bypass surgery.
Intra-arterial thrombolysis is an option if it is thought this will be safer than surgery

53
Q

What is superficial thrombophlebitis?

A

It occurs when a superficial vein (usually the great saphenous vein of the leg or its tributaries) becomes inflamed and the blood within it clots

54
Q

How is superficial thrombophlebitis managed?

A

Topical NSAID cream to help relieve the Sx (redness and tenderness over the vein).
If it associated with extensive varicose veins, excise the affected vein.
LMWH (for 1 month) may be beneficial in some, especially if the risk of it extending into the deep veins is high.

55
Q

How may cannula-related phlebitis present?

A

A small lump may appear days or weeks after the cannula has been removed and it can take months to resolve completely.
Long-term cannulae can predispose to septic phlebitis.

56
Q

What does complete heart block look like on ECG?

A

No relationship between p waves and QRS complexes; both are occuring at their own pace.
(Ventricular contraction ~20-40bpm)

57
Q

How is complete heart block managed?

A

Atropine 500mcg iv repeated doses if necessary up to a total of 3mg
If no improvement, Temporary transvenous cardiac pacing.
Long-term: Permanent implantable pacemaker when available

58
Q

How much of a BP drop is considered sufficient to be classed as postural hypotension?

A

> 20 systolic /10 diastolic mm Hg within three minutes of standing

59
Q

What are the features of AF on ECG?

A

Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm

60
Q

What compenents make up the CHA2DS2VASc score?

A 
C – Congestive heart failure
H – Hypertension                                      
A2 – Age >75 (Scores 2)
D – Diabetes
S2 – Stroke or TIA previously (Scores 2)
V – Vascular disease                                 
A – Age 65-74
S – Sex (female)

Score >1 = offer anticoagulation (DOAC or warfarin) - after assessing bleeding risk with HASBLED score

61
Q

What is the first line option for rate control in AF?

A

A beta-blocker (e.g. bisoprolol)

If contra-indicated (i.e. asthma etc.) use a rate-limiting CCB such as diltiazem or verapamil (BUT NOT IN HEART FAILURE)

62
Q

In what situations should rate-control not be offered as first line treatment option for AF?

A

AF has a reversible cause (e.g. infection, alcohol intoxication).
Presence of heart failure thought to be primarily caused by AF.
New-onset AF (i.e. <48 hours).

63
Q

What is classed as 1st degree heart block?

A

PR interval greater than 0.20 seconds (5 small or 1 big square)

64
Q

What is the difference between Mobitz type 1 (Wenkebach) and Mobitz type 2 2nd degree heart block?

A

In Wenckebach’s phenomenon (Mobitz Type 1), there is a gradual distancing between the p wave and QRS complex until a QRS complex is dropped and then the cycle resets
In Mobitz type 2 2nd degree heart block, PR interval is normal except for every 2 or 3 p waves for which there is no ventricular beat - can result in asystole

65
Q

How are heart blocks with a risk of asystole (Mobitz type 2 and 3rd degree heart block) managed?

A

Atropine 500mcg IV repeated up to 6 doses (3mg)
Transcutaneous cardiac pacing (using a defibrillator)

When available, permanent implantable pacemaker

66
Q

What are the ECG features of ventricular tachycardia?

A

QRS is broad
T waves difficult to identify
No p waves
Regular QRS (~200bpm)

67
Q

What arrhythmia are patients with a prolonged QT interval at particular risk of?

A

Torsades de Pointes - a polymorphic VT

68
Q

What are the ECG features of Wolff-Parkinson-White synrome?

A

Short PR interval (< 0.12 seconds)
Wide QRS complex (> 0.12 seconds)
“Delta wave” which is a slurred upstroke on the QRS complex

69
Q

What is the management approach to someone presenting with SVT?

A

Ensure continuous cardiac monitoring.
Valsalva manoeuvre.
Carotid sinus massage.
Adenosine - fast IV bolus 6mg, then 12mg and further 12mg as required.
An alternative to adenosine is verapamil (calcium channel blocker)
Direct current cardioversion may be required if the above treatment fails

70
Q

What are the long-term management options for someone with paroxysmal SVT?

A

Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation

71
Q

What should the patient be warned of before administering adenosine?

A

They may experience an impending sense of doom/feel as if they are going to die

72
Q

If a patient has a tachyarrhythmia and is haemodynamically unstable, what treatment should be given?

A

Direct current (DC) cardioversion

73
Q

What sort of murmur may be heard with mitral regurgitation?

A

Pan-systolic, high pitched “whistling” murmur due to high velocity blood flow through the leaky valve.
The murmur radiates to left axilla. You may hear a third heart sound

74
Q

What is the most common cause of mitral regugitation in the developed world?

A

Idiopathic degeneration (with aging)

75
Q

What is the most common cause of mitral stenosis?

A 
Rheumatic fever
(Infective endocarditis is also an important cause)
76
Q

What may be heard on heart auscultation in a patient with mitral stenosis?

A

Loud first heart sound with an opening snap in early diastole.
A mid-diastolic low pitched “rumbling” murmur due to a low velocity of blood flow, best heard, with the patient in the left lateral position, with the bell of the stethoscope

77
Q

How is the pulse pressure described in aortic stenosis?

A

Narrow pulse pressure

There may also be a slow-rising pulse

78
Q

What kind of murmur is heard in aortic stenosis?

A

Crescendo-decrescendo systolic ejection murmur

Radiates to the carotids

79
Q

What kind of murmur is heard in aortic regurgitation and how should the patient be sat to best hear this?

A

Early diastolic, soft murmur.

Best heard in the aortic area, with the patient sitting forward and at end of expiration

80
Q

Which arrhythmia is genetically linked with Hypertrophic Obstructive Cardiomyopathy (HOCM)?

A

Wolff-Parkinson-White syndrome

81
Q

Which valve is most commonly affected by infective endocarditis?

A

Mitral valve

Followed by aortic

82
Q

What is the most common organism responsible for infective endocarditis?

A

Staph aureus

83
Q

How many blood cultures should be taken when investigating infective endocarditis (in subacute or chronic presentation)?

A

3 sets of blood cultures should be taken from peripheral sites with at least 6 hours between them prior to commencing antimicrobial therapy

N.B. in the acute presentation, 2 sets of blood cultures should be taken at different times within 1 hour prior to commencement of empirical therapy.

84
Q

What imaging investigation should be performed for everyone with suspected IE?

A

Echocardiogram

85
Q

What are the cut-offs for the results of ABPI when assessing peripheral vascular disease?

A

> 0.9 is normal
0.6 – 0.9 is mild disease
0.3 – 0.6 is moderate to severe disease
<0.3 is severe disease to critical ischaemic

(an ankle SBP of 80 and an arm SBP of 100 gives a ratio of 0.8)

86
Q

At what size should an AAA be considered for surgical repair?

A

> 5.5cm

Below this, annual USS monitoring of AAA and modification of CV risk factors tends to be the management option

Yr 5 conditions (16 decks)

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