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MPharm Y3S1 > CVD Clinical > Flashcards

CVD Clinical Flashcards

1
Q

What must you include on a discharge letter?

A

Changes to a patients meds (existing meds changed/stopped and new meds started with reasons)
Length of intended treatment
Monitoring requirements
Any new allergies or adverse effects identified

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2
Q

What is primary CV risk?

A

CV risk reduction with aim of preventing CVD in those at risk of developing it e.g DM (not yet established CVD)

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3
Q

What is secondary CV risk?

A

CV risk reduction in those with established CVD (e.g MI) to reduce the risk of further CV events/deterioration in CV function

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4
Q

What are the 3 tools for estimation of CV risk?

A

Framingham equations
Assign
Qrisk

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5
Q

What is the framingham estimation of CVD risk based on?

A

Age
Gender
BP
Smoking
Cholesterol (TC:HDL ratio)

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6
Q

Describe the Framingham heart study:

A

5209 men and women ages 30-62 from Framingham
Baseline and follow up every 2 years
Now study 2nd/3rd/4th generation etc

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7
Q

What are the limitations of the Framingham heart study?

A

Doesn’t take into account other risk factors :
-ethnicity, FH, BMI, socioeconomic factors so underestimation
Framingham based equations for risk reflect risks of CVD in 1960s-1980s in a North American cohort (over-estimate of UK population)

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8
Q

What is the Assign tool for developing CV risk?

A

Does include social deprivation and FH
Score risk factors 1-99
High risk is a score more than 20
Approved by Scottish guidelines
Computer based online system

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9
Q

What does the QRISK assessment tool include?

A

Ethnicity, treated HT, social deprivation, BMI, FH, other conditions (e.g AF, DM, CKD STAGE 3/4/5, RA)
Newer- migraine, corticosteroids, systemic lupus erythematosus, atypical antipsychotics ED, severe mental illness

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10
Q

What does CVD include?

A

Fatal and non fatal stroke
TIA (transischemic attacks), MI and angina

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11
Q

What is the process for identifying people for CVD risk?

A

Review estimates on ongoing basis for all over 40s
Prioritise for full formal risk assessment if; over 10 year risk CVD is greater than 10%

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12
Q

What is the full formal risk assessment process?

A

Tool only provides an approximation
Use QRISK3 to assess CV risk for PRIMARY prevention for ages 25-84 years
Use QRISK to assess CV risk in type TWO diabetes aged 25-84

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13
Q

What are the criteria for people who can’t be assessed using QRISK and why?

A

T1D
eGFR < 60ml/min and/ or albuminuria
Risk of familial hypercholesterolaemia/ other inherited lipid abnormiality
Over 85 years (especially if smoke/HT)
These are all automatically considered high risk

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14
Q

Why might there be an underestimation of CVD risk using QRISK3?

A

If there are underlying medical conditions which increase CVD risk e.g HIV, severe mental illness, autoimmune disorders
In patients already treated with antihypertensives or lipid modifying therapy or recently stopped smoking
If taking treatment which causes dyslipidaemia e.g immunosuppressives

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15
Q

What is the process for determining smoking status?

A

Patients who have stopped smoking in previous 5 years should be considered as smokers for CV risk
Risk from smoking more than 5 years ago depends on lifetime exposure and risk will lie somewhere-use clinical judgement

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16
Q

What are pack years?

A

A pack year is smoking 20 cigarettes a day for 1 year
So 1 pack has 20 cigarrettes

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17
Q

How would you calculate pack years?

A

Nº pack years= (nºcigarettes smoked per day x nº years smoked)/ 20
OR
Nº pack years= packs smoked per day x years as a smoker

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18
Q

What should be the process before offering statins?

A

Discuss benefits of lifestyle changes (may need support)
Optimise management of other modifiable risk factors e.g BP/BG

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19
Q

What information should you give to patients when informing them about statins?

A

ABSOLUTE RISK (not relative risk)
Likely benefits
Likely harms

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20
Q

What is the absolute risk reduction (ARR)?

A

Risk of developing CVD over a period of time taking into account their previous risk
e.g If relative risk reduction of statin is 30%, take 30% away from their original risk if they have a 20% 10 year risk, their ARR is 6% decrease

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21
Q

What is relative risk reduction (RRR)?

A

Compare between 2 groups, those treated/not treated
Makes data look better

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22
Q

What is the number needed to treat (NNT)?

A

Number needed to treat with statin to prevent one person from stroke/MI
e.g if NNT is 17, means 17 people need to be treated for one person to see benefit

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23
Q

How do you calculate NNT?

A

100/ARR

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24
Q

Would aspirin be used for primary prevention of CVD?

A

No not routinely offered for PRIMARY
Secondary is different

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25
Q

What is the lifestyle advice to reduce cholesterol?

A

Healthy eating
Cardioprotective diet (decreased saturated fats)
Physical activity (150mins a week of moderate exercise)
BMI (18.5-24.9)- weight management
Alcohol consumption
Smoking cessation

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26
Q

What are the baseline assessments before starting a statin?

A

Smoking status
Alcohol consumption
BP
BMI
Lipid profile: total cholesterol, non HDL, HDL and triglycerides
Diabetes status
Renal function
LFTs: transaminase level (alanine aminotransferase or aspartate aminotransferase)
TSH-hypothyroidism, known to increase cholesterol levels and myopathy SEs

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27
Q

What are the guidelines/treatment for primary prevention for people with and without T2D?

A

If 10 year QRISK3 10% or more:
-atorvastatin 20mg daily
Don’t rule out if less than 10% if patient has an informed preference to take or concern risk may be underestimated
If 85 or older consider atorvastatin 20mg OD

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28
Q

What are the guidelines/ treatment for primary prevention for people with T1D?

A

Offer atorvastatin 20mg daily for all T1D when:
-40 years or older
-DM 10 years or more
Established nephropathy
Other CVD risk factors

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29
Q

What are the guidelines/ treatment for secondary prevention for people with and without T2D?

A

Atorvastatin 80mg OD
Lifestyle at the same time
Lower dose if:
-drug interactions
-high risk ADRs
-patient preference

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30
Q

What are the guidelines/ treatment for primary and secondary prevention in a patient with CKD?

A

Atorvastatin 20mg OD
If target reduction not achieved and eGFR 30 or more then increase dose
If eGFR less than 30 then agree higher dose with renal specialist

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31
Q

What are the Fluvastatin doses and their intensity?

A

20mg=low
40mg=low
80mg=medium

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32
Q

What is statin intensity?

A

Ability to decrease cholesterol levels (%)
20-30%= low
31-40%= medium
Above 40%= high intensity

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33
Q

What are the pravastatin doses and their intensity?

A

10mg=low
20mg=low
40mg=low

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34
Q

What are the simvastatin doses and their intensity?

A

10mg=low
20mg=medium
40mg=medium
80mg=high (not recommend due to muscle toxicity)

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35
Q

What are the atorvastatin doses their intensity?

A

10mg= medium
20mg= high
40mg=high
80mg=high

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36
Q

What are the rosuvastatin doses and their intensity?

A

5mg=medium
10mg=high
20mg=high
40mg=high

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37
Q

What are the aim for % reduction when taking statins?

A

Aim for 40% reduction in non-HDL cholesterol
HDL cholesterol (good) more than 1mmol/L

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38
Q

What are the follow up monitoring requirements for taking statins?

A

At 3 months:
Total cholesterol, HDL and non-HDL cholesterol
LFTs (AST/ALT):
-if more than 3x the upper limit of normal, discontinue and recheck in 1 month
-if less than 3 times the upper limit of normal, continue statin and recheck in 1 month
Creatine Kinase, CK (enzyme released when muscle damage):
-only if develop symptoms of stain related muscle toxicity
Then again at 12 months and then annually
If up titration of dose needed then recheck after 3 months again

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39
Q

What should occur if after the follow up (after 3 months), a greater than 40% reduction in non-HDL is not achieved?

A

Discuss adherence and timing of dose
Optimise adherence to diet and lifestyle measures
Consider increasing the dose if started on less than atorvastatin 80mg and the person is judged to be at a higher risk because of the co-morbidities, risk score or using clincal judgement

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40
Q

What are the main side effects of statins?

A

Stain associated muscle symptoms:
Stain Related Muscle Toxicity (SRM)
-symmetrical pain and/or weakness
-large proximal muscles, nearer to centre of body e.g arms, shoulders, hips
-worsened on exercise
-elevated CK
-resolve with discontinuation

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41
Q

What are the other side effects of statins?

A

GI disturbance- diarrhoea (early stages, tends to resolve)
Hepatotoxicity
New onset T2D- shouldn’t stop statin as benefits outweigh risk
Neurocognitive and neurological impairment e.g dementia (conflicted evidence)
Intracranial haemorrhage- (conflicted evidence)
Sleep disturbances e.g nightmares

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42
Q

What are the strategies to over come intolerance in statins?

A

Therapy with a lower dose statin is better than no statin
De-challenge- stop initially to see resolvement
Re-challenge at lower dose of same high intensity statin
Change statin (hydrophilic e.g rosuvastatin instead of lipophilic e.g atorvastatin as less likely to cross into other tissues)
Consider alternative day/twice weekly dosing
Consider alternatives e.g ezetimibe, PC5K9, bempedoic acid, inclisiran

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43
Q

Name the 2 types of thrombosis in thromboembolic disease:

A

Arterial thrombosis
Venous thrombosis

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44
Q

What are the types of arterial thrombosis?

A

Acute myocardial infarction (AMI)
Transient Ischemia attack (TIA)
Cerebral vascular infarcts/ accidents (CVAs)

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45
Q

What are the types of venous thrombosis?

A

DVT
Pulmonary embolism (PE)

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46
Q

What is an inherited/ acquired thromboembolic disease?

A

Thrombophilia- genetic susceptibility of clotting

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47
Q

What are the causes of arterial thrombosis?

A

Occurs as a result of rupture of atherosclerotic plaque
Platelet deposition and vessel occlusion
White thrombi

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48
Q

What are the causes of venous thrombosis?

A

Often occurs in normal vessels
Majority of deep vein in leg
Red thrombi- bulkier, fibrin rich

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49
Q

What is CHD?

A

CHD is a condition in which the vascular supply to the heart is impeded by atheroma (fatty plaques), thrombosis or spasm so decrease in blood flow

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50
Q

What is the problem with inadequate blood supply?

A

Causes decrease O2 supply to the heart so ischaemic chest pain (IHD-ischaemic heart disease) and depending on extent can cause:
-stable angina (exercise induced)
-acute coronary syndrome (ACS)/MI+ unstable angina
-sudden death

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51
Q

Describe the epidemiology of CHD:

A

Main cause of death
Accounts for more 1/5 deaths in males
1/6 deaths in females
About 4% UK population have symptoms of CHD
More common in males (until women reach menopause) and then increases with age
About 124000 AMI a year of which about 15-20% die
In UK, S.Asians have around 45% risk of death and Black African/ Caribbean have around 50% decreased risk of death

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52
Q

What is the aetiology of atherosclerosis?

A

Complex inflammatory process initiated due to injury or dysfunction of the endothelium
Results in increase permeability to oxidised lipoproteins which are taken up by macrophages to lipid laden foam cells
Results in production of fatty streaks (seen under microscope)
SM cells migrate and proliferate and secrete collagen, proteoglycans, elastin and GPs
Results in fibrous cap-> plaque
Results in narrowing of BVs in blood flow and result in repute of plaque so clot

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53
Q

What are the main risk factors for CHD/ atherosclerosis?

A

Non-modifiable:
-age
-gender
-FH
Modifiable:
-smoking
-diet
-central abdominal obesity
-hypertension
-hyperlipidemia

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54
Q

What are the other risk factors for CHD/ atherosclerosis?

A

DM
Sedentary lifestyle
Ethnicity
Alcohol
Stress

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55
Q

Describe the pathophysiology of atherosclerosis:

A

Imbalance between O2 demand and supply
O2 demand:
-HR, contractility, systolic wall tension
O2 supply:
-coronary blood flow, O2 carrying capacity of blood

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56
Q

What is stable angina?

A

Narrowing of coronary arteries due to atheromatous plaques
-chest pain typically provoked by exercise, stress, heavy meals or extremes in temp (as excess demand on heart and blood supply not enough to treat demand)
-relieved by rest (decrease demand) or sublingual GTN
-“demand ischaemia”
-narrowed coronary arteries unable to meet increase O2 demand

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57
Q

What are the clinical symptoms of stable angina?

A

Central crushing chest pain
May radiate to jaw, neck, back or arms
‘constricting’,’choking’, ‘heavy weight’, ‘burning’, ‘stabbing’
Induced by exercise etc and relieved by rest
Lack of ECG and cardiac enzyme changes

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58
Q

What is the symptom control management for stable angina?

A

SL GTN for acute angina- tab or spray under tongue
Antianginals:
1st line-BBs, CCBs
Add on: long lasting nitrate, ivabradine, ran-laziness, nicoradnil

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59
Q

What is the secondary prevention for management for stable angina?

A

Lifestyle changes (smoking/weight loss/diet/excerise etc)
Antiplatelet (aspirin)
Statins (atorvastatin 20-80mg)

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60
Q

Name the different forms of Acute Coronary Syndromes (ACS):

A

MI:
-ST elevated MI (STEMI)
-Non-ST elevated MI (NSTEMI)
Unstable angina (troponin +ve ACS)

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61
Q

What are differential diagnosis of ACS?

A

History of ischamic chest pain- could be gastric
ECG changes
Increased cardiac enzymes

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62
Q

What are the first tests that a patient is undergone when they present in hospital for ischaemic chest pain?

A

12 lead ECG
Cardiac enzymes
Other enzymes

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63
Q

Describe what an ECG would show if a patient has ACS?

A

ST elevation NOT seen in:
-NSTEMI
-Unstable angina
Sometimes other ECG changes:
STEMI:
-left bundle branch block (LBBB)
NSTEMI:
-T wave inversion/ ST segment depression
-Q wave changes

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64
Q

Name and describe cardiac enzymes which can aid diagnosis in ACS:

A

Troponin T and Troponin I
Highly specific to cardiac muscle cells
Released when cardiac muscles damaged, release after 2-4 hours and peaks at 12 hrs, can persist up to 7 days
Standard troponin assays- repeated after 10-12 hrs
High sensitivity troponin assays- repeated after 3 hrs (enables to rule out early NSTEMI, as no change on ECG, if not raised then not an NSTEMI)

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65
Q

Describe the results of cardiac enzymes to indicate what diagnosis of ACS it is if at all?

A

STEMI/NSTEMI means increase troponin levels of more than 99th percentile cut off/ upper reference limit (varies according to specific assay used)
Unstable angina, some changes in troponin level but doesn’t meet criteria for MI
< 0.4ng/ml means ACS unlikely
Size of troponin increase is equal to size of infarct- more cells damaged

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66
Q

What other causes can increase the level of troponin?

A

PE
HF
Myocarditis
CKD
Sepsis

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67
Q

Name other enzymes that can rise in a STEMI/NSTEMI:

A

Creatine Kinase (CK)
Aspartate Transaminase (AST) and Lactatedehydrogenase (LDH)
Not used on own as not specific enough

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68
Q

Describe the use of CK tests in ACS:

A

Peaks within 24 hours
Normal within 48 hours
Also in skeletal muscle and brain
CK-MB, cardiac specific isoform

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69
Q

Describe the use of AST and LDH tests in ACD:

A

Non specific
Released from other parts of the body
AST can be released in liver disease
Not used routinely
LDH peaks at 3-4 days and remains increased for up to 10 days, can be useful in late presentation

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70
Q

What is a MI?

A

Thrombosis (blood clots) forms at site of rupture of atheromatous plaques, blocks instead or reduces blood supply
Leads to prologued and severe ischaemia
Leads to death of cardiac muscle cells (release of enzymes)
STEMI= damage to full thickness of cardiac muscle
NSTEMI= damage to partial thickness of cardiac muscles
Both still full blockage

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71
Q

Describe unstable angina:

A

Supply ischaemia
Results in decrease of coronary blood flow and decrease oxygen supply due to thrombus formation
Leads to a partial blockage (UA) and complete blockage (STEMI/NSTEMI)
Thrombus forms as a result of plaque rupture and activation and aggregation of platelets

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72
Q

What is the main the clinical features of STEMI/NSTEMI?

A

Severe chest pain, sudden onset, often at rest and constant- not relieved by rest or GTN
20% of AMI have no symptoms- silent MIs are more common in elderly and DM

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73
Q

What are the other clinical features of STEMI/NSTEMI?

A

Sweating
Restlessness
Breathlessness
Pale
N&V
Grey

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74
Q

What are the clinical features of UA?

A

Sudden deterioration in angina symptoms
Often at rest, not relieved by rest of GTN
No ECG changes, small increase in troponin

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75
Q

What is the immediate treatment for a STEMI?

A

Oxygen (if indicated)- releives ischaemia
Diamorphine
-pain relief
-anxiolytic (anxious)
-vasodilation
Antiemetic (e.g cyclizine, metoclopramide)
Aspirin
-300mg STAT asap
Clopidogrel (or Ticagrelor or Prasugrel)
-300mg STAT (or 180mg or 60mg)
PPCI

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76
Q

Which antiplatelet should you offer when someone is having a STEMI?

A

With no reperfusion therapy, just medical management offer ticagrelor
With PCI offer prasugrel if not taking an anticoagulant, offer clopidogrel if already taking an anticoagulant

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77
Q

What does PPCI stand for?

A

Primary Percutaneous Coronary Intervention

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78
Q

What is the purpose of PPCI and when should it be administered when a patient has a STEMI?

A

Thrombolysis
Repurfusion- break down clot and limit damage
Optimal time:
“call to needle”-1 hour
“door to needle”- 30mins
After 6 hours the damage is irreversible

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79
Q

Name examples of PPCI drugs:

A

Streptokinase
Alterplase
Tenecteplase
Reletplase
Activates plasminogen to plasmin which breaks down fibrin in the clot

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80
Q

What are the CI of PPCI?

A

CVA (Cerebral vascular accident- stroke)
Surgery
Peptic ulcer
Uncontrolled HT
If more than 6 hrs of onset of symptoms

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81
Q

What are the SEs of PPCIs?

A

Haemorrhage, stroke, repercussion arrythmias, allergy to streptokinase as antigenic

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82
Q

What should occur after having PPCI?

A

Heparin for the first 48 hrs after thrombolysis

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83
Q

What are the complications of STEMI?

A

Arrthymias
LVF- left ventricular HF

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84
Q

What is the secondary prevention for STEMIs?

A

5 Gold standard medicines they need to be on:
DAPT (Dual Antiplatelet Therapy):
-Aspirin +ticagrelor/clopidogrel/prasugrel for 12 months , aspirin for life
B blocker- review at 12 months, continue if also HF
ACEi
Statin - Atorvastatin 80mg OD
Lifestyle changes

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85
Q

What is the immediate treatment for a NSTEMI or UA?

A

Oxygen
Diamorphine
Aspirin
Clopidogrel (or ticagrelor or prasugrel)
Fondaparinux- until stable
NO THROMBOLYSIS OR PPCI

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86
Q

Describe the use of Fondaparinux for the treatment of NSTEMI/UA:

A

Injection
Inhibitor of factor Xa- prevent formation of new blood clots

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87
Q

What are the further treatments/ investigations that need to be done to someone who presents with an NSTEMI or UA?

A

Further treatment depends on prediction of 6 month risk of mortality if further CV events
Use GRACE scoring system (Global Registry of Acute Cardiac Events)
If intermediate/high risk >3% they will have an angiogram and PCI
If low risk <3% conservative management (no angiogram/PCI)

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88
Q

What is the secondary prevention for NSTEMIs and UA?

A

Same as STEMI-same 5:
DAPT (Dual Antiplatelet Therapy):
-Aspirin +ticagrelor/clopidogrel/prasugrel for 12 months , aspirin for life
B blocker- review at 12 months, continue if also HF
ACEi
Statin - Atorvastatin 80mg OD
Lifestyle changes

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89
Q

What is an angiography?

A

Thin radiopaque tube (catheter into coronary circulation- normally in wrist/groin)
X-ray contrast material injected into coronary artery
Allows observation of severity of narrowing (stenosis) due to atherosclerotic plaque (looks pale due to reduction in blood flow)
In MI identifies exactly where blood clot present

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90
Q

What are surgical interventions when a patient has a ACS?

A

PCI:
-angioplasty
-stenting
-Coronary Artery Bypass Graft (CABG)

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91
Q

Describe an angioplasty:

A

Balloon mounted on tip of very thin Cather inserted through obstruction and inflated so compressed plaque
As balloon is deflated and removed
Restenosis common (the plaque can collapse back down again)

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92
Q

Describe stenting:

A

Wire mesh (tubular) inserted with balloon to keep stenosis open
Balloon will then be removed
Bare metal stent (BMS)-endothelisation- BV walls over grow the stent so restenosis
Drug Eluting stent (DES)- elutes anti-proliferative drug (e.g tacrolimus, Paclitaxel), stops overgrowth of stent by wall tissue

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93
Q

What is an in-stent thrombosis?

A

Both angioplasty and stents can damage vessel wall so increases clotting

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94
Q

What should a patient be on after they have surgical interventions due to an ACS?

A

Long term aspirin and 12 months clopidogrel/ticagrelor/prasugrel

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95
Q

Describe what is a drug eluting balloon?

A

Balloon covered with anti-proliferative drug e.g paclitaxel
Released into vessel walls during inflation
Lipophilic so absorbed into vessel wall
No problem of in-stent stenosis
Not as good as stents when to preventing restenosis but better than plain angioplasty

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96
Q

What is primary PCI and when should it be used?

A

Gold standard treatment for STEMI (instead of using thrombolysis)
Better outcomes and less people CI compared to thrombolysis
Patient taken straight to angiosuite for angiogram then angioplasty (with or without stenting)
Clot is removed during procedure
“Call to balloon time”= 120mins
“Door to balloon time”= 30 mins

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97
Q

Describe what CABG is:

A

Veins grafted to by-pass stenosis in coronary artery
Vein usually taken from leg and grafter either side of stenosis- can bypass up to 4

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98
Q

What type of heart failure (HF) can you get?

A

Right, left or both sided HF

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99
Q

How does the heart work?

A

Two pumps working together
-deoxygenated blood from muscles and organs enters right side
-heart pumps the blood to the lungs to be oxygenated, takes up O2 and eliminates CO2
-Oxygen rich blood enters left side if heart which are then pumped through arteries to organs and tissues

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100
Q

What is stroke volume (SV)?

A

The volume of blood ejected during systole

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101
Q

What is the CO, mean HR, SV and ejection fraction (EF) of blood in a normal healthy person?

A

CO around 5L/min
Mean HR around 70bpm
SV around 70ml
Filled ventricle is 130ml so EF more than 50% of ventricle contents

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102
Q

What is HF?

A

The ability of the heart to function as a pump is impaired
Unable to sustain an adequate delivery of blood so O2 and nutrients don’t get to tissues

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103
Q

What is the incidence of HF?

A

Common condition increases with age
Average annual incidence:
0.3-2% of overall population
3-5% >65 yrs
8-16% >75 yrs
Often from complications of the conditions in the elderly

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104
Q

What is the mortality rate in HF and why?

A

High- 50% dead in 5 years:
-recurrent pump failure
-sudden cardiac death
-recurrent MI

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105
Q

What is the correlation between HF and AF?

A

10% with HF will have AF as a contributory factor

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106
Q

Name and describe the 2 main groups of the aetiology of HF:

A

Pump failure- damage to the heart muscle so decrease in myocardial contractility
Overloading- extra workload on the heart:
-decrease force and velocity of contraction and delayed relaxation
-excessive after load (pressure overload)
-excessive pre load (volume overload)

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107
Q

What is after load?

A

The pressure that the chamber of the heart has to generate in order to eject blood out of the chamber (into circulation) aka total peripheral resistance

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108
Q

What is preload?

A

Volume of blood present in a ventricle of the heart, after passive filling and atrial contraction aka left ventricular end diastolic volume (amount of stretch of left ventricle)
Volume of blood coming into the heart

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109
Q

What is pump failure?

A

Damage to the heart
-leads to systolic failure so failure of the heart to contract
Can occur acutely* after MI or progressively (chronically) from diffuse fibrosis of myocardial tissue

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110
Q

What are the causes of pump failure?

A

Ischaemic HD
MI
Cardiomyopathy (heart muscle disease-malfunctioning muscle)
Arrhythmias
Viruses and infection
Inflammation
Excessive alcohol consumption
Diffuse fibrosis- formation of excessive connective tissue- stiff heart muscle

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111
Q

What is overloading?

A

Overwork and overstretch of the cardiac muscle
-can cause structural and biochemical abnormalities in cells
Can lead to:
-decrease force, velocity of contraction and delayed relaxation
Effects are usually irreversible

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112
Q

What are the main causes of overloading?

A

Excessive after load
Excessive preload

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113
Q

What can cause excessive after load?

A

If systemic vascular resistance is high
If pulmonary vascular resistance is high
Valve dysfunction

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114
Q

Describe how high systemic vascular resistance can cause excessive after load:

A

E.g hypertension
Raised after load on the left ventricle and cause it to fail

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115
Q

Describe how high pulmonary vascular resistance can cause excessive after load:

A

E.g pulmonary hypertension secondary to chronic lung disease
-right ventricular failure (cor pulmonale)

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116
Q

Describe how valve dysfunction can cause excessive after load:

A

Stenosis of incompetence (valve disease/ dysfunction)

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117
Q

What can cause excessive pre load?

A

Uncommon cause of failure
Hypervolaemia is usual cause
-fluid retention e.g secondary to renal failure
-excessive IV infusions
-polycythaemia (over production of RBCs so increase volume of blood)
-drugs e.g NSAIDs, steroids

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118
Q

What are other causes of overloading?

A

Excessive demand
-anaemia
-hyperthyroidism or thyrotoxicosis (increase metabolic rate to increase demand)
-valve dysfunction
-bradycardia or tachycardia
-widespread vasodilation e.g septic shock, CO increased to increase BP

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119
Q

What are precipitating factors which cause HF?

A

Anything that increases myocardial workload:
-arrhythmias
-obesity
-anaemia
-infective endocarditis
-hyperthyroidism
-pulmonary infection
-pregnancy
-change in therapy including poor compliance e.g diuretics can increase urine output so not ideal

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120
Q

What is acute HF?

A

Rapid onset e.g after MI
Contractility immediately drops:
-CO falls

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121
Q

What is compensated acute HF?

A

CVS initiates compensation in order to maintain CO and peripheral perfusion

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122
Q

What is decompensated acute HF?

A

If MI is very severe, extensive damage to heart muscle
CO dramatically drops
There is no cardiac reserve, CVS unable to compensate and is overwhelmed

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123
Q

What is chronic HF?

A

Same as acute but decline is progressive rather than a sudden fall
Patients can remain in compensated failure indefinitely:
-severe stress can drive them into decompensation e.g infection, fluid overload, exertion or anaemia

124
Q

What is Starling’s law?

A

The greater the volume of blood entering the heart during diastole, the greater the volume of blood ejected during systolic contraction

125
Q

What is a normal heart function considered to be like in Starling’s law?

A

Achieved by an increase stretching of muscle fibres and increase force of contraction

126
Q

What is a failed heart function considered to be like in Starling’s law?

A

As the heart starts to fail, the over stretched muscle is unable to respond to the increase in preload, so decrease in CO and initial compensatory process leads to decompensatory process

127
Q

What is compensation in HF?

A

Not just a reduction in CO and tissue perfusion
The heart adapts to respond to changes:
-cardiac enlargement
-arterial constriction
-increase sympathetic drive
-salt and water retention

128
Q

Describe cardiac enlargement as a compensatory method in HF:

A

Progressive alteration of ventricular size, shape and function
-cardiac muscle stretched from increase residual volume after contraction
-muscle ineffectual
-responsible for significant impairment of the heart as a pump

129
Q

Name and describe an example of cardiac enlargement:

A

Left ventricular hypertrophy (LVH)
Enlargement and thickening of left ventricular wall

130
Q

Describe arterial constriction as a compensatory method in HF:

A

When CO is decreased:
-arteries constrict to divert blood to organs from skin and GIT (non essential)
BUT can also raise systemic vascular resistance so increase after load on the heart

131
Q

Describe increased sympathetic drive as a compensatory method in HF:

A

Failing heart and decreased tissue perfusion -> stimulates the sympathetic NS via baroreceptors
-exposes the heart to catecholamines with +ve inotropic and chronotropic effects so increases levels of noradrenaline, angiotensin, aldosterone and vasopressin
Promotes excessive stimulation of the heart and widespread vasoconstriction
Increase contractility

132
Q

What does a §+ve chronotrophic mean?

A

Increase force of contraction

133
Q

What does a +ve ionotrophic mean?

A

Increase rate of contraction

134
Q

Describe salt and water retention as a compensatory method in HF:

A

Decreased CO so decreased renal perfusion so releases renin (activates RAS system)
Renin leads to formation of angiotensin I and II so vasoconstriction, leads to adrenal aldosterone release

135
Q

How does aldosterone play a role in the salt and water retention in HF?

A

Retains salt and water at distal renal tubule so expands blood volume and increases pre load
Promotes the release of Atrial Natriuretic Peptide (ANP)- vasodilator to counteract the increase in pre load

136
Q

What are the 3 major clinical symptoms of HF?

A

Exercise limitation (fatigue)
Shortness of breath (SOB)
Oedema

137
Q

Why is exercise limitation a symptom of HF?

A

Due to decreased CO, impaired oxygenation and decrease blood flow to exercising muscles

138
Q

Why is SOB a symptom of HF?

A

‘Back pressure’ from failing heart causes fluid to accumulate in lungs- oxygenated blood coming from lungs to left side of heart, if left side faults then back log
Mostly occurs when exercising or lying down (gravitational forces)
Can be accompanied with a cough

139
Q

Why is oedema a symptom of HF?

A

Swelling of ankles and feet (gravitational forces)
Due to retention of salt and water

140
Q

What are the clinical features of HF a result from?

A

Hypoperfusion (forward component)
Congestion/odema (backward component)
Both conditions co-exist , cause different features and may vary accordingly to which side of the heart is affected

141
Q

What is hypoperfusion?

A

Decrease in perfusion (either side)
Impaired blood flow ahead of the heart (leaving the failing heart) or the chamber affected

142
Q

What is congestion/ odema?

A

Lack of blood entering a failing heart, increase in pressure in veins draining into the heart

143
Q

Describe the symptoms of hypo perfusion:

A

Effects independent of which side fails
Peripheral vasoconstriction (decrease in blood supply going away from the heart)
-fatigue and exercise intolerance (lack of O2 and nutrient to tissues)
-cold and pale extremities
-fluid and electrolyte retention
-tachycardia and tachypnoea (increase in HR and BR)

144
Q

Describe the symptoms of congestion/ odema in right sided HF:

A

(Receives deoxygenated to lungs)
*peripheral odema (swollen ankles)
-hepatomegally (enlargement of liver)
-raised jugular venous pressure
-peripheral cyanosis
-fluid and electrolyte retention

145
Q

Describe the symptoms of congestion/ odema in left sided HF:

A

More common and usually more serious
-pulmonary oedema
*dyspnoea (SOB)
-orthopnoea (SOB lying down)- due to redistribution of fluid to lungs occurs due to abdominal pressure-increases nº pillows
-paroxysmal nocturnal dyspnoea (PND)
-cough/wheeze
-central cyanosis
-tiredness
-breathlessness

146
Q

Name the different New York Heart Association classification of HF symptoms:

A

NYHA class I, II, III, IV

147
Q

Describe the NYHA class I:

A

No limitations, ordinary physical activity doesn’t cause fatigue, breathlessness or palpitations

148
Q

Describe the NYHA class II:

A

Mild HF
Slight limitation of physical activity
Such patients are comfortable at rest
Ordinary physical activity results in fatigue, palpitation, breathlessness or angina pectoris e.g walking up the stairs

149
Q

Describe the NYHA class III:

A

Moderate HF
Marked limitation of physical activity
Although patients are comfortable at rest, less than ordinary physical activity will lead to symptoms e.g walking to the toilet

150
Q

Describe the NYHA class IV:

A

Severe HF
Inability to carry on any physical activity without discomfort
Symptoms of congestive cardiac failure are present even at rest with any physical activity
Increase discomfort is experienced

151
Q

What are the physical investigations of HF?

A

Raised jugular vein
Lung sounds
Swelling of ankles and legs

152
Q

Describe how a raised jugular vein can be a sign of AF:

A

Vein in the side of the neck in somebody with HF becomes visible due to venous distension
e.g Jugular Venous Pressure (JVP) of 5cm- can see it for a length of 5cm above level of sternum
The more visible, the greater the accumulation of fluids

153
Q

Describe how lung sounds can be a sign of AF:

A

Crackles at bases (crepitations)
-represents HF with pulmonary oedema

154
Q

What are the tests to assess HF?

A

Natriuretic Peptides
*Echocardiography

155
Q

Describe the test of Natriuretic peptides in HF:

A

BNP (BrainNP)
*NTproBNP (N terminal- more stable)
Secreted from ventricle in somebody who has HF due to compensatory process

156
Q

Describe the echocardiography test in HF:

A

Gold standard test
See heart in motion and assess performance as a pump
Measure ejection fraction (EF)

157
Q

Name and describe the different ejection fraction results:

A

HFrEF- HF with Reduced EF (≤40%)
HFpEF- HF with Persevered EF (≥50%)
HRmrEF- HF with MidRange EF (41-50%)

158
Q

What are other investigations/tests carried out in HF?

A

Chest X-ray (size of hear and lung consolidation)
HR and rhythm and sounds
ECG (AF)
BP
Blood tests (anaemia, RF, thyroid disease)

159
Q

What are the aims of treatment in HF?

A

Decrease morbidity
-relieve symptoms
-improve exercise tolerance
Decrease mortality

160
Q

What are the targets of drug therapy depending on the cause?

A

Disease of the myocardium:
-increase inotropy
OR
Excessive load
-decrease pre/after load

161
Q

What is the initial treatment in acute HF?

A

IV diuretics, E.G furosemide 80mg BD

162
Q

What is the function of diuretics in HF?

A

Decrease pre load
Decrease symptoms: pulmonary and peripheral oedema
Decrease hospital admission and increase exercise performance

163
Q

Describe the use of thiazide diuretics in HF:

A

Less potent, used for mild HF
e.g bendroflumethiazide up to 5mg OM (2.5mg in hypertension)
Not effective at eGFR <20ml/min

164
Q

Describe the use of loop diuretics in HF:

A

Mainstay of treatment
Most common
Potent
e.g furosemide, bumetanide
Can use high doses
Can use IV (furosemide)

165
Q

Describe Metolazone in HF:

A

Atypical thiazide diuretic
Effective in reduced renal function
Used in combo with loop diuretics in resistant HF
STAT doses 2.5/5mg (normally sufficient)
Short term 2.5-5mg OD for 2-3 days
Long term maintenance (severe HF) 2.5/5mg 2-3 times a week on top of daily loop diuretic

166
Q

What are the pharmaceutical care issues of using diuretics?

A

Hypotension
Dehydration
Renal impairment
Electrolyte disturbance
Rate of admin of IV furosemide

167
Q

Name the first line treatments for HF:

A

ACEi/ARBs
B blockers
Aldosterone antagonists (aka MRAs- mineralocorticoid receptor antagonists) e.g spironlactone

168
Q

Describe the use of ACEi first line for HF:

A

Decrease preload and after load
Improve symptoms and long term survival
Lots of evidence
Start low dose then up titrate

169
Q

Describe the use of ARBs first line for HF:

A

Alternative in patients intolerant to ACEi
Evidence for improvement in long term survival but not as good as ACEis

170
Q

Describe the use of B blockers first line for HF:

A

Joint first line with MRAs and ACEi
Only BBs licensed for HF:
Decrease preload and after load
Caution: can cause worsening of symptoms initially “start low, go slow” up titrate

171
Q

Name the B blockers licensed in HF:

A

-bisoprolol -carvediol -nebivolol

172
Q

Describe the use of aldosterone antagonists first line for HF:

A

Joint first line with BB and ACEi
Low dose-some diuretic effect
Block action of aldosterone development in LVF
Long term survival and hospital admission

173
Q

Name examples of MRAs:

A

Spironlactone
Eplerenone

174
Q

Name the add on therapies for HF:

A

Hydralazine/ nitrates
Ivabradine
ARNIs
Digoxin
SGLT2i

175
Q

Describe the use of Hydralazine/ nitrates for add on therapies for HF:

A

For patients intolerant/ CI to ACEis/ARBs
Add on therapy (especially if African or Caribbean origin)
Trials used isosorbide dinitrate- now use isosorbide mononitrate)

176
Q

Describe the use of ivabradine for add on therapies for HF:

A

Lowers HR- needs to be above 75bpm
Selectively and specifically inhibits if channels in SA node
LVEF less than 35%

177
Q

Describe the use of ARNIs for add on therapies for HF:

A

Sacubitril and Valsartan (Entresto)
Sacubitril- nepriysin inhibitor (stops degradation of atrial and brain natriuretic peptide)
Valsartan- ARB
Need to stop ACEi/ARB 36 hrs before as 2 ARBs- this decreases chance of severe reaction e.g angioedema
LVEF less than 35%
ESC recommends it joint first line

178
Q

Describe the use of digoxin for add on therapies for HF:

A

Improves symptoms, exercise tolerance and hospital admissions but not mortality

179
Q

Describe the use of SGLT2i for add on therapies for HF:

A

e.g Dapagliflozin, Empagliflozin
Whether diabetic or not
ESC recommends it joint first line

180
Q

What is an arrhythmia?

A

An abnormality in the heart rate, and/or abnormality in the rhythm
-can be regularly irregular
-can be irregularly irregular

181
Q

What is the normal rhythm of the heart called?

A

Sinus rhythm=NSR

182
Q

Where can cardiac arrhythmias occur?

A

Supraventricular
Ventricular

183
Q

Describe where the supra ventricular cardiac arrhythmias occur:

A

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

184
Q

Describe where the ventricular cardiac arrhythmias occur:

A

Within the ventricles

185
Q

What effect on the heart rate can cardiac arrhythmias have?

A

Bradycardia (slow HR) <60bpm
Tachycardia (fast HR) >100bpm

186
Q

What are the symptoms of cardiac arrhythmias?

A

Dizzy/ light headed
Palpitations- can feel heart beat
Chest pain
Fatigue
Can also be asymptomatic
Occasionally in severe cardiac arrhythmias decrease in consciousness, small number cardiac arrest (secondary to sudden drop in BP and blood flow)

187
Q

What is the main diagnosis for cardiac arrhythmias?

A

ECG
In ECG paper-large square= 0.25 secs
small square=0.04 secs
Upwards reflection- electrical activity away from the heart
Downwards- towards the heart

188
Q

What are the main management options for cardiac arrhythmias?

A

Treat the underlying disease e.g identify thyroid, electrolyte imbalance, cardiomyopathy
Drug therapy
Non-pharmacological treatment

189
Q

What is the non-pharmacological treatment for cardiac arrhythmias?

A

Electrical cardio version
Radio frequency ablation/cryoablation
Pacemakers
Defibrillators

190
Q

Name types of bradycardia:

A

Sinus bradycardia
Sinus node disease
AV node disease

191
Q

Describe sinus bradycardia:

A

SA node fires at a slow rate

192
Q

Describe sinus node disease:

A

SA node fails to generate electrical impulse
-mainly idiopathic (fibrosis of conduction tissue)
-some 2º AMI or cardiomyopathies

193
Q

Describe AV node disease:

A

‘Heart block’
Failure of AV node to conduct electrical impulse to ventricles
-frequent idiopathic
-also due to AMI, congenital defects, infection, surgery (valve and drugs which decrease HR e.g BB, Digoxin, verapamil)

194
Q

What is the management for bradycardic patients?

A

Acute- Atropine (increase HR, one off STAT)
Underlying cause (stop drugs, treat disease e.g hypothyroidism)
Permanent pacemaker (PPM)

195
Q

Describe the use of PPMs:

A

Inserted into ‘skin pocket’ below collar bone
Leads inserted into heart and sense electrical activity within the heart
Delivery small electrical impulses to myocardial tissue if detect inappropriate rhythm e.g slow
Each patient has individual threshold, it monitors HR constantly and if drops below threshold then the pacemaker will send impulses

196
Q

Name different types of supra ventricular arrhythmias (tachycardia) and where they occur:

A

Atria:
-sinus tachycardia
-sinus node re-entry tachycardia
*AF
-atrial flutter
-atrial tachycardia
AV junction:
-AV junctional tachycardias
-Wolff-Parkinson White syndrome

197
Q

Name different types of ventricular tachycardias and where they occur:

A

-ventricular ectopics
-Torsades de Pointes
-ventricular fibrillation (most serious-> cardiac arrest)

198
Q

Describe a sinus tachycardia (ST):

A

Increased HR but normal rhythm
Normal response to exercise
Infection, decreased BP, anaemia, thyrotoxicosis, hypovolaemia (loss of blood), shock, PE
SE: nicotine, B2 agonist, levothyroxine, salbutamol, aminophylline

199
Q

Describe an atrial flutter:

A

Less frequent than AF, but similar underlying causes
Re-entry circuit within the right atrium-> rapid atrial rhythm around 300bpm
ECG= saw tooth pattern
Ventricles usually beat once for every 2-3 atrial flutter
Stasis of blood in atria->need for anticoagulation

200
Q

Describe Wolff-Parkinson white syndrome:

A

Accessory pathway conducts electrical pulse direct from atria to ventricles (bypass AV node)
Ventricular rate up to 600bpm
Serious, life threatening

201
Q

Describe ventricular tachycardias (VT):

A

Occasional palpitations from extra ventricular beats
‘ectopics’ common
Frequent/ runs of ectopic beats, more serious
VT defined as five or more ventricular beats occur consecutively

202
Q

What are the possible causes of VT?

A

AMI
IHD
Cardiomyopathies
Myocarditis
Valvular disease

203
Q

Describe Torsades de pointes:

A

Due to QT prolongation- extension between Q and T wave

204
Q

What can cause Torsades de pointes?

A

Congenital (hereditary)
Hypokalaemia/magnesmia
Drugs:
-Antiarrythmics (class IA or III)
-Erythromycin/clarithromycin
-Tricyclic antidepressants
-Cisapride
-Terfenadine and astemxizole
-Haloperidol
-Lithium
-Phenothiazines

205
Q

Describe ventricular fibrillation (VF):

A

Rapid and uncoordinated contraction of the ventricular tissue
Severely compromised cardiac output (as can’t effectively pump blood through)
Lose consciousness within 10-20 secs
Most common cause of death due to AMI- needs treatment of defibrillation

206
Q

Describe Direct Current Cardioversion (DCCV) is used for as a treatment for cardiac arrhythmias:

A

Cardioversion= process of restoring hearts normal rhythm
Used typical for AF and atrial flutter
Chemical cardioversion=drugs

207
Q

Describe how DCCV works:

A

Application of controlled electric shock across chest wall
-override disordered conduction
-allow SA node to regain control of HR
-pt briefly anaesthetised

208
Q

What is a problem with DCCV and how is this overcome?

A

Increase risk of thromboembolism so needs anticoagulation for a min of 3 weeks before and 4 weeks afterwards as doesn’t always stay

209
Q

Describe radio frequency ablation/cryoablation as a treatment for cardiac arrhythmias:

A

Need exact location of point responsible for generating arrhythmia
Catheter with electrode at tip guided into heart to appropriate points
RF energy/ freezing destroys tissue and disrupts conduction pathway
=90% success rate, prevents need for long term drug therapy

210
Q

Describe defibrillation as a treatment for cardiac arrhythmias:

A

Delivery of electric shock to the myocardium via the chest wall, as patient in cardiac arrest
Needs to be given ASAP
Used in conjunction with cardiopulmonary resuscitation (CPR)

211
Q

Describe internal cardioversion defibrillators (ICDs) as a treatment for cardiac arrhythmias:

A

Implanted into high risk patients with resistant VTs
Monitor rate and rhythms
Initially deliver rapid rate impulses (faster than arrhythmia) to try to regain control and then slow down
If falls, deliver internal electric shock
Unpleasant for pt
Higher voltage than DCCV

212
Q

Describe the epidemiology of AF:

A

Most common causing supra ventricular tachycardia
About 1 in 20 over 65 years in UK
7% of UK admissions
5x increase risk of stroke
Less common in women than men but women respond to treatment less well and have an increased risk of mortality

213
Q

What are the cardiac risk factors for AF?

A

HT, IHD, structural heart diseases

214
Q

What are the non cardiac risk factors for AF?

A

DM, thyrotoxicosis, increased alcohol, COPD

215
Q

Describe the pathophysiology of AF:

A

Irregular, rapid atrial rate (300-600bpm) secondary to chaotic conduction within atria
Acute- less 48 hrs
Chronic- more 48 hrs

216
Q

Name and describe the different types of chronic AF:

A

Paroxysmal- intermittent or self terminating
Persistent- successfully converted by treatment
Permanent- failed or unsuitable treatment

217
Q

Why is there an increased risk of thromboembolism in AF patients?

A

Stasis of blood within atria predisposed to cerebral and systemic thromboembolism
Sluggish atrial blood flow allows partial activation of the clotting cascade
Ventricular rate 100-180bpm

218
Q

What are the common symptoms of AF?

A

Some asymptomatic
SOB
Dizziness
Fatigue
Palpitations

219
Q

What are the complications of AF?

A

HF
Angina
Thromboembolism

220
Q

What is the management of AF?

A

Stroke prevention
Rate control
Rhythm control

221
Q

What have you got to assess in a AF patient in regards to stroke?

A

Assess stroke risk:
-CHA2DS2VASc stroke risk score
-consider anticoagulant >1men >2 women
Assess bleeding risk:
-ORBIT score to assess risk of bleeding in people who are starting or have started anticoagulation

222
Q

What is the anticoagulation treatment in patients with AF?

A

DOACs - first line
Apixiban, Rivaroxiban, Edoxaban, Dapigatran
Warfarin if DOAC is CI/not tolerated

223
Q

What is another treatment in patients with AF to decrease stroke risk?

A

Left atrial appendage occlusion
Alternative only if anticoagulation not tolerated or CI

224
Q

What would be the reasons why first line heart rate control in AF wouldn’t be appropriate?

A

Reversible cause e.g infection
HF caused by AF as can worsen HF
New onset of AF (within 48 hrs)

225
Q

What is the treatment for heart rate control in AF?

A

First line strategy
Standard BB e.g bisoprolol or rate limiting CCB e.g diltiazem, verapamil
Digoxin- only if sedentary lifestyle as doesn’t control exercise induced AF
If mono therapy doesn’t control, combine 2 of BB, diltiazem or digoxin

226
Q

What is the treatment for rhythm control in AF?

A

used when rate control isn’t successful or still symptomatic
1st line= cardioversion
2nd line= drug therapy

227
Q

Name and describe the drug therapy in rhythm control in AF:

A

First line: Standard B blocker (+ve as gives both rhythm and rate control)
Others: Dronedarone
Amiodarone (2nd line especially in HF as can make it worse so CI)

228
Q

What is the treatment for paroxysmal AF (PAF)?

A

“Pill in the pocket” (e.g flecanide) treat attacks only
If frequent, aim to reduce frequency/prevent paroxysms by rate/rhythm control
Not digoxin (increase frequent/rapid and persistant paroxysms)
Abstinence from alcohol/ caffeine
Antithrombotic- needs to be considered as when have paroxysms have increased risk of stroke

229
Q

What are alternative treatments for AF when all other treatments have failed/ unsuitable?

A

Non pharmacological:
-left atrial ablation: RF ablation a point in left atrium where arrhythmia generated
-pace and ablate: RF ablation of AV node + pacemaker

230
Q

What is the most common cause of bradycardia arrhythmia?

A

Heart block

231
Q

What is the most common cause of tachycardia arrhythmia?

A

Atrial Fibrillation

232
Q

What are key medications to look out for when a patient has heart block?

A

Warfarin/ anticoagulants- stop these as patients will have a PPM (surgery)
Rate controlling CCB e.g diltiazem- as can make bradycardia worse
B blockers e.g even eye drops as in elderly enough can get into systemic circulation

233
Q

What would the rhythm of an ECG be like in heart block and why?

A

Normally a P wave for every QRS complex = 1:1 ratio
Regular P wave (because always getting contraction of atria) but not always a QRS complex (but not always reciprocal contraction of the ventricles)

234
Q

What is first degree heart block?

A

1:1 ratio of P waves to QRS complexes but abnormally long PR interval
Conduction though AV node is delayed
May develop into 2nd or 3rd degree heart block

235
Q

What is second degree heart block?

A

Not all P waves results in a QRS complex
At risk of developing complete heart block (3rd degree)
Atrial contraction not always followed by ventricular contraction
May follow a pattern e.g 2:1 ratio where alternative P waves not conducted

236
Q

What is third degree heart block?

A

Complete heart block
No conduction through AV node- so not QRS
Atrial contraction continues due to SA node- so P waves present
Ventricular contraction due to automatic rhythm of AV node (escape rhythm- which is automatic) but much slower so medical emergency- they won’t immediately die but the escape rhythm can’t be maintained

237
Q

What is the pre med for a dual chamber pace maker insertion?

A

Flucloxacillin IV 1g STAT
Co-dydramol IV STAT

238
Q

What is the medication used during the procedure of a dual chamber pace maker insertion?

A

Gentamicin 80mg STAT injected into the pocket

239
Q

Describe the doses of Amiodarone in rhythm control therapy:

A

200mg TDS 1 week then 200mg BD for 1 week then 200mg OD maintenance
Half life up to 40-50 days so need a loading dose as takes a while to have an effect
Unlicensed alternative dose: 400mg TDS for 3 days then 200mg OD maintenance

240
Q

What are the doses of Digoxin in rate control therapy?

A

500mcg x2 STAT doses 6 hours apart
125mcg OD maintenance

241
Q

What are the side effects of amiodarone and therefore monitoring parameters?

A

Bradycardia
Phototoxicity (need high factor spf)
Slate grey skin
Taste disturbances
Corneal micro deposits-glow (get pt to report any eye sign changes)
Liver dysfunction (initially then every 3 months to monitor)
Thyroid dysfunction (hypo more common)
Pulmonary toxicity (report any breathing problems)

242
Q

What are the SEs of digoxin?

A

N&V as narrow therapeutic index so chance of toxicity if these symptoms
Blurred vision
Anorexia
Bradycardia

243
Q

Describe a major interaction between rhythm control and rate control therapy and what should be changed?

A

Amiodarone causes increased levels of digoxin (can double levels) as inhibits Pgp mediated transport of digoxin
Reduce digoxin by 50% if continued use in combo- can use full dose short term, interaction can take 1-4 weeks to occur
Often stop digoxin once ventricular rate is reduced so not often an issue

244
Q

What is a VTE and name the different sub types?

A

Thromboembolic event occurring within the venous system
-DVT= in deep veins
-Pulmonary embolism (PE)= lungs
The vessel is often normal (in MI/stroke it often contains plaques)

245
Q

What’s the epidemiology of DVT?

A

1 in 1000 people have DVT per year
Higher incidence in hospitals
Fatality range of between 1-5%
More common in males
Patients over 40

246
Q

What is the aetiology of DVT?

A

Stagnation (slow) blood flow- areas around the valves of the legs
Hypercoagulability - increase risk of clotting (may be inherited)
Vascular injury
Endothelial injury:
-collagen exposure
-platelet aggregation
-thrombus

247
Q

What are the risk factors for developing DVT?

A

Age, obesity, varicose veins, long haul flights (or other transport longer than 4hrs)
Immobility (best rest more than 4 days)
Pregnancy and puerperium (6wks post pregnancy)
Previous VTE (5x greater increase)
Male sex

248
Q

What are the predisposing conditions of getting a VTE?

A

Trauma or surgery (especially to pelvis, hip or lower limb)
Malignancy (+chemo/radiotherapy)
CCF (congested cardiac failure), recent AMI
Infection
Hormone therapy (COCs, HRT, tamoxifen)
Inherited acquired disorders (thrombophilias)
Vasculitis

249
Q

What are the clinical features of VTE?

A

60% in calf veins (distal DVTs)
Some asymptomatic
Unilateral leg swelling
Tenderness, warmth, redness
Superficial veins
Calf pain
Oedema

250
Q

Describe the Wells clinical score as a diagnosis for VTE:

A

If alternative diagnosis (as likely or greater probability than DVT)
Total above score:
-high probability ≥ 3
-moderate probability 1 or 2
-low probability 0- allows to see whether need for further diagnostic tests

251
Q

What are the clinical parameters for the Wells clinical score?

A

Active cancer
Paralysis or recent immobilisation
Bedridden for more than 3 days/major surgery in past 4 weeks
Entire leg swelling
Localised tenderness along distribution of deep venous system
Calf swelling of more than 3cm compared to asymptomatic leg
Pitting oedema
Previous DVT
Collateral superficial veins (non varicose)

252
Q

Describe the breakdown of a thrombus formation?

A

Thrombus formation
Fibrinolytic response
Plasmin generation
Fibrin breakdown
Release of fibrin degradation products (predominantly D dimer)

253
Q

Describe a blood test to test for DVT:

A

D-dimer assay- fibrin degradation product
High -ve predictive value (a low D dimer + a low Wells means a good indicative of -ve DVT)

254
Q

What are the disadvantages of the D-dimer test to diagnose a DVT?

A

Not as good as positive predictive values as false positives can be present
Increase in trauma, recent surgery, haemorrhage, cancer, sepsis, pregnancy
False positives common in elderly
Affected by heparin use, important to check levels before heparin treatment as can decrease D dimer levels

255
Q

Name the diagnostic imaging used to absolutely diagnose a VTE:

A

Venography
Duplex ultrasonography (doplus)
Magnetic resonance imaging (MRI)

256
Q

Describe venography as a diagnostic imaging tool for VTE:

A

Previously gold standard diagnostic test
Not routinely used now as invasive (as cancelation and injection of radioactive material)

257
Q

Describe doplus as a diagnostic imagine tool for VTE:

A

Produce an image of blood flow through limbs
Non-invasive
High sensitivity

258
Q

Describe MRI as a diagnostic imagine tool for VTE:

A

Not widely available
Expensive

259
Q

What are other possible diagnosis’ instead of a VTE?

A

Physical trauma
-tear in calf muscle, sprain, haematoma, tendon rupture fracture
Cellulitis
Ruptured Baker’s cyst- fluid filled swelling at back of knee, rupturing giving calf pain and swelling
Oedema

260
Q

What is the management for VTE?

A

Identify and treat any underlying cause
Prevent damage to valves of veins
Allow normal circulation to limbs
*Prevent PE
Immediate management with injectable anticoagulant

261
Q

What is the first line injectable anticoagulant used in a VTE and why?

A

Heparin
Prevents extension of the thrombus and further complications

262
Q

How does unfractionated heparin (UFH) work?

A

Intrinsic pathway
Binds to Antithrombin III and inhibits factor Xa to thrombin
IV/SC admin

263
Q

What are the SEs of UFH?

A

Haemorrhage
Thrombocytopenia (monitor platelets if more than 5 days)
Hyperkalaemia (due to effect on aldosterone)
Osteoporosis, alopecia (in extended period)

264
Q

What is the blood test monitoring requirements when using UFH?

A

Activated partial thromboplastin time (APTT)
Therapeutic and toxic monitoring
Measurement of how long to clot

265
Q

What is the normal APTT for someone not having UFH?

A

30-40 secs

266
Q

How do you calculate the APTT ratio?

A

Pts APTT at a given time/ APTT reference value

267
Q

What is the target APTT and APTT ratio for someone using UFH, and what should be the consequences if someone is out of range?

A

APTT: 80-100 secs
APTT: 1.5-2.5 secs
If below, increase heparin by rate of infusion
If above, then reduce rate of heparin infusion

268
Q

Name examples of Low Molecular Weight Heparin (LMWH):

A

Enoxaparin
Tinzaparin

269
Q

How does LMWH work?

A

Less effect on thrombin, more effect on factor Xa

270
Q

What are the benefits of using LMWH instead of UFH?

A

Don’t have to monitor APTT as more predicable (there is a specific anti-Xa assay if needed- not routine)
Longer half life- SC OD admin (no infusion)
Decrease risk of thrombocytopenia and osteoporosis

271
Q

Name 3 coumarins:

A

Warfarin
Acenocoumarol (nicoumaione)
Phenindione

272
Q

How does warfarin work?

A

Extrinsic pathway
Inhibits metabolism of vit K and affects the activation of factors II,VII,IX and X
Onset 8-12 hours, but full effect not seen for 48-72 hrs (hence always overlapped with heparin)

273
Q

What are the monitoring requirements for warfarin?

A

Baseline: clotting screen, Hb, platelets, LFTs, INR, signs of bleeding

274
Q

What is prothrombin time (PT) and international normalised ratio (INR)?

A

Reference range: 10-14 secs
Relates to changes in extrinsic or common pathways
Expressed as a reference to standard prep
Normal INR= 1-1.2

275
Q

What are the loading dose schedules for warfarin normally?

A

e.g Day 1 10mg, Day 2 10mg, Day 3 INR

276
Q

In which circumstances is the dose of warfarin decreased?

A

Increased PT, LFTs, CFF, parental feeding
Elderly, weight less than 60kg
Other drugs which may potentiate INR

277
Q

Describe Dabigatrin etexilate:

A

Direct thrombin inhibitor
Treatment of VTE prophylaxis of VTE post surgery
Doesn’t require TDM
Haemorrhage
Duration dependant on indication

278
Q

Describe Rivaroxaban/ edoxaban/ apixiban:

A

Direct inhibitors of activated factor X
Treatment of VTE + prophylaxis of VTE post surgery
Doesn’t require DTM
Nausea and haemorrhage
Duration depends on indication

279
Q

Describe the management of VTE and what it does:

A

Compression stockings:
-assist calf muscle pump
-decrease venous hypertension
-decrease venous valvular reflux
-decrease leg oedema
-aids microcirculation
-prevents venous ischaemia

280
Q

Describe the epidemiology of PE:

A

1 in 1000 people per year in the UK
2nd most common cause of unexpected death after IHD
Increase frequency with increased age
High mortality rate (32%)

281
Q

What are adverse prognostic factors instead of PE?

A

Clinically major embolism
Cancer
Congestive cardiac failure (CCF)
Previous or current DVT

282
Q

Describe the pathophysiology of PE?

A

Blood clot of thrombus formed in the venous system (can be anywhere but normally in calf veins)
Break free and embolism to lung
Normally multiple clots
Lower lobes more common
Obstruct pulmonary artery system:
-increase pulmonary artery pressure
-right heart failure
-infarction of lung tissue

283
Q

Describe the main clinical symptoms of PE:

A

Acute onset chest pain
General malaise
Dyspnoea/ SOB
Haemoptysis (coughing up blood)

284
Q

Describe the other clinical symptoms of PE:

A

Cough, wheeze, tachypnea (RR>16/min)
Abdominal pain, anxiety, cardiac arrhythmias
Syncope (loss of consciousness)

285
Q

Name the examinations and tests used for diagnosis of PE:

A

Chest X-ray
V/Q scan (gold standard)
Non specific but will contribute:
Laboratory tests
ECG
Sometimes used when other tests inconclusive:
Computed tomographic pulmonary angiography (CTPA)
Pulmonary angiography

286
Q

Describe a chest X ray for diagnosis for PE:

A

Can look normal initially, after 24 hrs:
-pleural effusion
-elevated diaphragm
-westermark sign (collapse of pulmonary BVs)

287
Q

Describe a V/Q scan for diagnosis for PE:

A

Use of radiocactive isotopes made by pharmacy
IV Technetum-99, labelled human albumin
Inhalation of Xenon- 133 gas
Perfusion and ventilation-provide images of these- decrease in perfusion in blood clot but normal ventilation in PE
High sensitivity

288
Q

Describe laboratory tests for diagnosis for PE:

A

Decreases in atrial oxygen saturations (PaO2)
Increase in WCC
Increase in ESR
Increase in D-dimer levels

289
Q

Describe ECG tests for diagnosis for PE:

A

Often normal
Sometimes tachycardia

290
Q

Describe CTPA for a diagnosis for PE:

A

100% sensitive and 100% specific for large central embolic (very accurate) but invasive + expensive
Able to see small clots

291
Q

Describe pulmonary angiography:

A

Injecting contrast media into main pulmonary artery
+ve result shows obstruction to pulmonary artery blood flow
Ideal diagnostic tool but invasive (risky)

292
Q

What are other possible diagnosis’ of PE?

A

Acute coronary syndrome (ACS)
Pneumonia
CCF
AF
Acute anaemia
COPD/ asthma

293
Q

Describe the management for PE:

A

Supportive therapy- pain relief
Immediate coagulation- as DVT
Fibrinolytics (only in massive PE)

294
Q

Name examples of fibrinolytic drugs:

A

Urokinase
Streptokinase
Alteplase
Reteplase

295
Q

How do fibrinolytic drugs work?

A

Thrombolytics
-activating plasminogen to breakdown of formed fibrin
Increased risk of haemorrhage

296
Q

What are the CI of thrombolytics?

A

Recent surgery, ‘active bleeding sites’
Renal/ liver disease
History of stroke

297
Q

Name conditions when the risk of VTE is increased by 10 fold:

A

Hospitalised patients after trauma, surgery or immobilising medical illness
Pregnant and puerperal women

298
Q

What should occur if a patient is on oestrogen containing contraceptive if they are to have major surgery?

A

Stop 4 weeks before

299
Q

What are risk factors in someone with increased VTE risk needing prophylaxis?

A

Active cancer/ cancer treatment
Age over 60
Critical care admission
Dehydration
Known thrombophilias
Obesity- BMI over 30
One or more significant medical co-morbidities:
-heart disease, endocrine or respiratory pathologies, acute infectious diseases, inflammatory conditions)
Personal history of first degree relative with history or VTE
Use of HRT/oestrogen containing contraceptive
Varicose veins with phlebitis

300
Q

What types of surgery are high risk?

A

*Orthopaedic surgery
Cardiac
Vascular
Urological
Thoracic
Gynaecological
Neurosurgery

301
Q

When are patients at high risk for VTE when anaesthetised for surgery?

A

If under general anaesthetic for more than 90 mins or 60 mins if in the lower limb
Thrombosis after surgery occurs within first 72 hours but can be longer

302
Q

What are factors that can increase bleeding risk?

A

Active bleeding
Acquired bleeding disorders (liver failure)
Concurrent use of anticoagulants
Lumbar puncture/ epidural/ spinal anaesthesia within previous 4 hours or expected within next 12 hours
Acute stoke
Thrombocytopenia (platelets less than 75x10^9/L)
Uncontrolled systolic hypertension (230/120)
Untreated inherited bleeding disorders

303
Q

What is the type of mechanical prophylaxis for VTE?

A

Thigh length graduated compression stockings
From admission until usual level of mobility

304
Q

What are the type of pharmacological prophylaxis for VTE?

A

LMWH (e.g Daltrparin, enoxaparin), Fondaparinux
High risk surgery e.g hip, need 4 weeks worth of thromboprophylaxis + cancer

305
Q

What are the doses of Dalteparin?

A

SC 5000IU OD

306
Q

What are the doses of Enoxaparin?

A

SC 40mg OD

MPharm Y3S1 (13 decks)

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