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Exam 1 > CVD > Flashcards

CVD Flashcards

1
Q

Use QRISK to assess:

A

CV risk for 1• prevention up to 84yrs

CV risk in Type 2 DM

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2
Q

Do not use QRISK:

A

Type 1 DM

pre-existing CVD

Family history: lipid abnormality/ hypercholesterolaemia

> 85yrs

ALL HIGH RISK

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3
Q

Underestimation of risk:

A

Underlying med conditions/treatment increasing CV risk eg HIV

Pt treated with anti hypertensives or lipid modification therapy or recently stopped smoking.

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4
Q

Smoking status

A

Stopped in previous 5 years = smoker

Use clinical judgement

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5
Q

Pack years

A

Pack-year = 20/day for one year

Pack year no. = Packs per day * years as smoker

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6
Q

Provide info w/o framing

A

For every 100 people like you, about 20 will have a heart attack or stroke in the next 10 years, but 80 will not.

If all 100 take a statin for 10 years, 15 will still have a heart attack or stroke regardless of whether they take a statin or not.

However, for 5 of the 100, taking a statin will prevent them from having a heart attack or stroke.

I can’t tell you if you are one of the 5 who will benefit or one of the 95 who will not get any benefit.

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7
Q

RRR

ARR

NNT

A

Relative risk reduction

Absolute risk reduction

Number needed to treat

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8
Q

RRR ARR NNT equation

A

RRR = 30%

Pt with 20% 10yr risk => 14%

ARR = 20 - 14 = 6%

NNT = 100/ARR = 100/6 = 17
1 of 17 will benefit from taking statin

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9
Q

Thromboembolic disease is caused by

A

Caused by blood clots

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10
Q

Types of Thromboembolic diseases

A

Arterial Thrombosis

Venous Thrombosis

inherited/Acquired

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11
Q

Heart anatomy

O2 rich

Side?

In

Out

A

Left heart

In: left and right pulmonary veins
Return blood from left lung

Left atrium

Atrioventricular valve

Left ventricle

Aortic semilunar valve

Out: Aorta
to upper body/ systemic circulation
To lower body (below)

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12
Q

Heart anatomy

O2 poor blood

Side

In

Out

A

Right

In: superior vena cava
Blood from head, upper limbs
Inferior vena cava
Blood from trunk, legs

Right atrium

Right atrioventricular valve

Right ventricle

Pulmonary semilunar valve

Out: Right/left pulmonary arteries
Lungs

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13
Q

Heart anatomy
O2 rich side
Out?

A

Left heart

Out: Aorta
to upper body/ systemic circulation
To lower body (below)u

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14
Q

Heart anatomy
O2 poor side
Out?

A

Right heart

Out: Right/left pulmonary arteries
Lungs

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15
Q

Heart anatomy
O2 poor side
In?

A

Right

In: superior vena cava
Blood from head, upper limbs

Inferior vena cava
Blood from trunk, legs

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16
Q

Heart anatomy
O2 rich side
In?

A

Left heart

In: left and right pulmonary veins
Return blood from left lung

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17
Q

Prevent back-flow

A

Papillary muscles contract with ventricles to prevent back flow

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18
Q

Diastole

A

Isovolumetric ventricular relaxation

AV valves closed
Aortic and pulmomary valves closed

AV valves open -
Ventricular filling - blood flows into ventricles
Aortic and pulmonary valves stay closed

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19
Q

ORBIT bleeding risk score

A

Age >74 years Yes+1

Bleeding history
Any history of GI bleeding, intracranial bleeding, or hemorrhagic stroke
Yes+2

GFR <60 mL/min/1.73 m2
Yes+1

Treatment with antiplatelet agents
Yes+1

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20
Q

first-line treatment strategy for atrial fibrillation

A

Rate control

except:
• whose atrial fibrillation has a reversible cause
• who have heart failure thought to be primarily caused by atrial fibrillation
• with new-onset atrial fibrillation
• with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
• for whom a rhythm-control strategy would be more suitable based on clinical judgement.

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21
Q

initial rate-control monotherapy to people with atrial fibrillation

A

standard beta-blocker (that is, a beta-blocker other than sotalol)

or a rate-limiting calcium-channel blocker (diltiazem or verapamil)

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22
Q

If monotherapy doesnt control AF pt symptoms

A
  • a beta-blocker
  • diltiazem
  • digoxin

Do not offer amiodarone for long-term rate control.

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23
Q

NSR - arrythmia

A

Normal sinus rhythm

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24
Q

arrythmia

A

abnormal heart rate or rhythm

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25
Q

where arrythmia

A

ventricular and supra ventricular

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26
Q

SUPRAVENTRICULAR

A

 Above the AV node (atrial arrythmias)
 At the AV junction  Within AV node

anywhere other than ventricle

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27
Q

VENTRICULAR

A

Within the ventricles

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28
Q

BRADYCARDIA

A

 slow HR 

< 60 bpm

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29
Q

TACHYCARDIA

A

 fast HR

 > 100 bpm

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30
Q

arrythmia Symptoms:

A 
 Dizzy/ light headed 
 Palpitations
 Chest pain
 Fatigue
 Occasionally lose consciousness Small no leads to cardiac arrest

2º to sudden drop in bp and blood flow due to circulation problems from arryhthmia.

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31
Q

arrythmia Diagnosis

A

ECG

Upwards deflection = electrical activity away from heart.

downwards = towards heart

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32
Q

arrythmia Management

A

can be caused by hypo/hyperthyroidism, electrolyte imbalances eg K, Mg. and dysfunction of cardiac vessel

 Underlying disease
 Drug therapy
 Non-Pharmacological: 
 Electrical cardioversion
 Radiofrequency ablation / cryoablation 
 Pacemakers
 Defibrillators
33
Q

Vaughan Williams classification of antiarrhythmic drugs

A

Class I: block sodium channels  Ia (quinidine, procainamide, disopyramide) Increases AP
 Ib (lignocaine) decreases AP
 Ic (flecainide) AP

Class II: ß-adrenoceptor antagonists (atenolol, sotalol)

Class III: prolong AP and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol)

Class IV: Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil)
[Others: Digoxin, adenosine]

34
Q

BRADYCARDIAS

A

Sinus bradycardia:
 SA node fires at a slow rate

Sinus node disease:
 SA node fails to generate electrical impulse - Mainly idiopathic (fibrosis of conduction tissue)
-Some 2o AMI or cardiomyopathies

AV node disease: “Heart block”
 Failure of AV node to conduct electrical impulse to ventricles
-Frequently idiopathic
- Also 2o AMI, congenital defects, infection, surgery (valve) & drugs which slow down heart(ß-blockers, digoxin, verapamil)

35
Q

Management bradycardia

A

acute treatment: atropine, increases heart rate. might need one-off stat dose to pt.

 Underlying cause (stop drugs, treat disease eg hypothyroidism)

chronically and long-term-
Permanent Pacemaker (PPM):
 inserted in “skin-pocket” below collar bone
 leads from pace maker inserted into heart & sense electrical activity within heart
 deliver small electrical impulses to myocardial tissue if detect inappropriate rhythm
36
Q

TACHYCARDIAS supra and ventricular

A 
Supraventricular arrhythmias:
 Atria:
-Sinus tachycardia
-Sinus node re-entry tachycardia
- **Atrial fibrillation**
- Atrial flutter
- Atrial tachycardia

AV junction:
-AV junctional
tachycardias
-Wolff-Parkinson White Syndrome

Ventricular tachycardias:

  • Ventricular ectopics
  • Torsades de pointes
  • Ventricular fibrillation
37
Q

Sinus Tachycardia (ST):

A

 HR but normal rhythm
 normal response to exercise
 infection (infection increases heart rate, drop in bp increases heart rate.),  bp, anaemia, thyrotoxicosis, hypovolaemia (loss of blood), shock, PE
 S/E: nicotine, ß2-agonists, levothyroxine, salbutamol, aminophylline

38
Q

Atrial flutter:

A

 Less frequent than AF, but similar underlying causes
 Re-entry circuit within the R atrium
 -> rapid atrial rhythm (about 300bpm)
 ECG has “saw tooth pattern”
 Ventricles usually beat once for every 2-4 atrial flutter waves
 Stasis of blood in atria - need for anticoagulation

39
Q

Ventricular Tachycardias (VT):

A

 Occasional palpitations from extra ventricular beats (“ectopics”) common
 Frequent/ runs of ectopic beats more serious
 VT defined as when five or more ventricular beats
occur consecutively
 Possible causes:
 AMI, IHD (Ischeamic Heart disease), cardiomyopathies, myocarditis, valvular disease

40
Q

Torsades de pointes

A

 due to QT prolongation - increases risk of ventricular arrythmias occuring

 Causes:
 Congenital - heriditory
 Hypokalaemia / hypomagnesaemia

 Drugs:
 Antiarhythmics (Class IA or III)  Erythromycin & clarithromycin  Tricyclic antidepressants
 Cisapride
 Terfenadine & astemizole  Haloperidol
 Lithium
 Phenothiazines
41
Q

Aspiring stat dose

A

Patients with large disabling strokes should receive aspirin 300mg OD for 14 days before being converted onto an appropriate long􏰀term antithrombotic.

42
Q

NG tube

A

Nasogastric tube

43
Q

Dyspepsia for pt GB who has 2 week course aspirin

A

Mr GB has a history of dyspepsia and has now be given a 2 week course of aspirin. NICE NG128, indicates the use of a PPI for any patient who has previously suffered with dyspepsia with aspirin. Discuss with Dr and ask them to prescribe a PPI, i.e. lansoprazole 15mg OD orodispersible.

44
Q

Patient is newly diagnosed with AF (time of onset unclear). They should be started on

A

Ask the Dr to prescribe bisoprolol (cardioselective) 5mg OD. Monitor BP and pulse, increase dose if HR not controlled.

45
Q

After initial 14 days of aspirin 300mg, patient should be initiated on

A

long-term antithrombotic treatment with an anticoagulant to reduce the risk of another stroke due to the AF.

Ask Dr to prescribe warfarin or a DOAC (suggest name and starting dose, i.e. Warfarin 2mg OD and monitor INR).

46
Q

apixaban

A

anticoagulant

47
Q

anticoagulant drugs

A

Apixaban 􏰀 Swallowed with water, with or without food. Can be crushed.

Edoxaban 􏰀 Can be taken with or without food. Can be crushed.

Dabigatran 􏰀 Do not crush. The oral bioavailability may be increased by 75% after a single dose. Can be taken with or without food.

Rivaroxaban 􏰀 Should be taken with food. Tablet can be crushed.

48
Q

CCB

A

Amlodipine, Lisinopril, bendroflumethiazide, atorvastatin, warfarin 􏰀 can be crushed and dispersed in water.

49
Q

why pt cannot receive remaining med?

A

Following a stroke, a patient is at high risk of suffering issues with their ability to swallow due to the stroke affecting areas of the brain that control that process. For this reason all stroke patients are made􏰆 􏰂nil b􏰇 mouth􏰄 until the􏰇 have had their s􏰈allo􏰈 assessed b􏰇 a member of the SALT or SLT 􏰀 speech and language therapist. The SALT will then decide on how the patient can receive food, fluids and medication.

50
Q

Acute med for GB pt stroke

A

Following diagnosis of stroke with conformation of ischaemia (through imaging), the appropriate first line treatment can be provided. Within the 4.5 hour window, it may be appropriate to give a patient thrombol􏰇sis 􏰈ith alteplase􏰆 ho􏰈ever Mr GB􏰄s collapse was 6 hours previous so this treatment would not be appropriate.
The first 􏰀line treatment here would therefore be 􏰀 Aspirin 300mg STAT (this had been prescribed for Mr GB).

51
Q

statin in acute stroke stages

A

• CI with haemorrage

52
Q

acute stroke caused by AF

A
  • AF causes the stasis of blood in the heart due to the disordered pumping of the atria, • allows the blood to clot, clot pumped out of the heart to the brain.
  • NICE CG 180, the first line pharmacological treatment for rate or rhythm control in AF is a beta-blocker.
53
Q

anticoagulation in acute stroke?

A

no - incase of haemorrhagic stroke

54
Q

CHA2 DS2-VASc assessment tool

A

NICE recommends anyone with CHA2DS2VASc of 2 or more (1 or more if male) should be considered for anticoagulation eg DOAC

male patients with a score of 1 or more and female patients with a score of 2 or more indicate that anticoagulation should be initiated.
It is also important to consider that patients risk of bleeding, this is done using the
HASBLED assessment tool; here increasing points indicate that the patient is at increased risk of bleeding. Clinicians use this and their clinical judgement to determine whether the patient is still appropriate to be started on anticoagulation.

55
Q

obese pt, then what?

A

Patient is obese. Obesity increases your risk of stroke and MI.
A – Discuss healthy diet – 5+ fruit and vegetables per day, decreased saturated fat and cholesterol intake, appropriate exercise – mobilisation around the house, gardening, cleaning as appropriate to the patient’s ability. Discuss weight loss.

56
Q

NICE guidelines, what is the first line drug treatment for someone with a ventricular rate of 130bpm

A

Standard beta-blocker e.g. bisoprolol 2.5mg od & titrate according to response

57
Q

complications of AF

A

Thromboembolism - Stasis of blood within atria predisposes to cerebral and systemic thromboembolism. Sluggish atrial blood flow also allows partial activation of the clotting cascade. AF increases risk of stroke 5 fold, 25% of all ischaemic strokes are caused by underlying AF

Heart failure

Exacerbation of angina – Mr GH

58
Q

If monotherapy does not work, ventricular rate 100bpm

A

If monotherapy does not work, consider combination therapy with 2 from:
- Beta-blockers - Diltiazem(CCB}
- Digoxin
(digoxin only appropriate for monotherapy if sedentary but can be used for add on therapy)
Suggest add in diltiazem (and therefore stop amlodipine – also a CCB but not rate limiting)

59
Q

Left atrial appendage

A

Left atrial appendage occlusion – left atrial appendage is a small muscular sac in the wall of left atrium (function not known) – 80-90% of all non-valvular strokes in AF patients occur as a result of blood clots formed in left atrial appendage.
Watchman device can be inserted to seal it off (parachute shaped, self-expanding device) Will continue anticoagulants for up to 6 months after procedure

60
Q

Digoxin mono or combination therapy - when?

A

In AF, monotherapy if sedentary but can be used for add on therapy.

61
Q

AF first line

A

standard BB eg bisoprolol 2.5mg and titrate according to response.

62
Q

AF second like if ventricular rate not controlled

A

monotherapy to combination therapy. 2 of BB, diltiazem, digoxin.

63
Q

BP ideal

A

<140/90 inc. DM11

64
Q

BP >80 years

A

<150/90

65
Q

BP in terms of hyperthyroidism

A

increases.

66
Q

Orthopnea

A

harder to breath when lying down.

67
Q

harder to breathe when lying down is:

A

orthopnea

68
Q

Fluid overload

A

IV diuretic furosemide 80mg OD/BD

69
Q

Thromboprophylaxis required

A

dalteparin SC 5000IU OD or enoxaparin s/c 40mg od

70
Q

Furosemide dose

A

40mg BD IV to 80mg BD IV. 4mg/min to prevent ototoxicity.

71
Q

Furosemide dose if 80mg BD IV not effective, then?

A

240mg IV infusion over 24hrs.

72
Q

Furosemide 240mg IV infusion over 24hrs not work, then?

A

Add metolozone (unlicensed)

73
Q

Low pulse, continue digoxin? In HF, AF.

A

Stop. Control AF with BB.

74
Q

Coughing due to ACEi, then?

A

Consider change to ARB if ACEI cause and unable to tolerate (e.g. Candesartan, Losartan, Valsartan + details of dose)

75
Q

Counselling on new drugs

A

counsel on indication, dose, frequency & side-effects

76
Q

Avoid OTC in HF new drugs

A

NSAIDs, sodium containing antacids

77
Q

NSAIDs in HYP

A

risk of fluid retention and increased BP so avoid if possible

78
Q

Alteplase for stroke within?

A

4.5hr of pt symptoms

Exam 1 (11 decks)

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