CVD Flashcards
Use QRISK to assess:
CV risk for 1• prevention up to 84yrs
CV risk in Type 2 DM
Do not use QRISK:
Type 1 DM
pre-existing CVD
Family history: lipid abnormality/ hypercholesterolaemia
> 85yrs
ALL HIGH RISK
Underestimation of risk:
Underlying med conditions/treatment increasing CV risk eg HIV
Pt treated with anti hypertensives or lipid modification therapy or recently stopped smoking.
Smoking status
Stopped in previous 5 years = smoker
Use clinical judgement
Pack years
Pack-year = 20/day for one year
Pack year no. = Packs per day * years as smoker
Provide info w/o framing
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.
RRR
ARR
NNT
Relative risk reduction
Absolute risk reduction
Number needed to treat
RRR ARR NNT equation
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
Thromboembolic disease is caused by
Caused by blood clots
Types of Thromboembolic diseases
Arterial Thrombosis
Venous Thrombosis
inherited/Acquired
Heart anatomy
O2 rich
Side?
In
Out
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)
Heart anatomy
O2 poor blood
Side
In
Out
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
Heart anatomy
O2 rich side
Out?
Left heart
Out: Aorta
to upper body/ systemic circulation
To lower body (below)u
Heart anatomy
O2 poor side
Out?
Right heart
Out: Right/left pulmonary arteries
Lungs
Heart anatomy
O2 poor side
In?
Right
In: superior vena cava
Blood from head, upper limbs
Inferior vena cava
Blood from trunk, legs
Heart anatomy
O2 rich side
In?
Left heart
In: left and right pulmonary veins
Return blood from left lung
Prevent back-flow
Papillary muscles contract with ventricles to prevent back flow
Diastole
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
ORBIT bleeding risk score
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
first-line treatment strategy for atrial fibrillation
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.
initial rate-control monotherapy to people with atrial fibrillation
standard beta-blocker (that is, a beta-blocker other than sotalol)
or a rate-limiting calcium-channel blocker (diltiazem or verapamil)
If monotherapy doesnt control AF pt symptoms
- a beta-blocker
- diltiazem
- digoxin
Do not offer amiodarone for long-term rate control.
NSR - arrythmia
Normal sinus rhythm
arrythmia
abnormal heart rate or rhythm
where arrythmia
ventricular and supra ventricular
SUPRAVENTRICULAR
Above the AV node (atrial arrythmias)
At the AV junction Within AV node
anywhere other than ventricle
VENTRICULAR
Within the ventricles
BRADYCARDIA
slow HR
< 60 bpm
TACHYCARDIA
fast HR
> 100 bpm
arrythmia Symptoms:
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.
arrythmia Diagnosis
ECG
Upwards deflection = electrical activity away from heart.
downwards = towards heart
arrythmia Management
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
Vaughan Williams classification of antiarrhythmic drugs
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]
BRADYCARDIAS
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)
Management bradycardia
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
TACHYCARDIAS supra and ventricular
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
Sinus Tachycardia (ST):
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
Atrial flutter:
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
Ventricular Tachycardias (VT):
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
Torsades de pointes
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
Aspiring stat dose
Patients with large disabling strokes should receive aspirin 300mg OD for 14 days before being converted onto an appropriate longterm antithrombotic.
NG tube
Nasogastric tube
Dyspepsia for pt GB who has 2 week course aspirin
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.
Patient is newly diagnosed with AF (time of onset unclear). They should be started on
Ask the Dr to prescribe bisoprolol (cardioselective) 5mg OD. Monitor BP and pulse, increase dose if HR not controlled.
After initial 14 days of aspirin 300mg, patient should be initiated on
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).
apixaban
anticoagulant
anticoagulant drugs
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.
CCB
Amlodipine, Lisinopril, bendroflumethiazide, atorvastatin, warfarin can be crushed and dispersed in water.
why pt cannot receive remaining med?
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 sallo 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.
Acute med for GB pt stroke
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 thrombolsis ith alteplase hoever Mr GBs 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).
statin in acute stroke stages
• CI with haemorrage
acute stroke caused by AF
- 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.
anticoagulation in acute stroke?
no - incase of haemorrhagic stroke
CHA2 DS2-VASc assessment tool
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.
obese pt, then what?
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.
NICE guidelines, what is the first line drug treatment for someone with a ventricular rate of 130bpm
Standard beta-blocker e.g. bisoprolol 2.5mg od & titrate according to response
complications of AF
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
If monotherapy does not work, ventricular rate 100bpm
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)
Left atrial appendage
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
Digoxin mono or combination therapy - when?
In AF, monotherapy if sedentary but can be used for add on therapy.
AF first line
standard BB eg bisoprolol 2.5mg and titrate according to response.
AF second like if ventricular rate not controlled
monotherapy to combination therapy. 2 of BB, diltiazem, digoxin.
BP ideal
<140/90 inc. DM11
BP >80 years
<150/90
BP in terms of hyperthyroidism
increases.
Orthopnea
harder to breath when lying down.
harder to breathe when lying down is:
orthopnea
Fluid overload
IV diuretic furosemide 80mg OD/BD
Thromboprophylaxis required
dalteparin SC 5000IU OD or enoxaparin s/c 40mg od
Furosemide dose
40mg BD IV to 80mg BD IV. 4mg/min to prevent ototoxicity.
Furosemide dose if 80mg BD IV not effective, then?
240mg IV infusion over 24hrs.
Furosemide 240mg IV infusion over 24hrs not work, then?
Add metolozone (unlicensed)
Low pulse, continue digoxin? In HF, AF.
Stop. Control AF with BB.
Coughing due to ACEi, then?
Consider change to ARB if ACEI cause and unable to tolerate (e.g. Candesartan, Losartan, Valsartan + details of dose)
Counselling on new drugs
counsel on indication, dose, frequency & side-effects
Avoid OTC in HF new drugs
NSAIDs, sodium containing antacids
NSAIDs in HYP
risk of fluid retention and increased BP so avoid if possible
Alteplase for stroke within?
4.5hr of pt symptoms
