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Y5 Cardiovascular System > List I - Act Core Conditions > Flashcards

List I - Act Core Conditions Flashcards

1
Q

What is a cardiac arrest?

A
  • Electrical problem with the heart
  • Person will be unconscious, unresponsive
  • Wont be breathing normally
  • Without immediate treatment the person will die
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2
Q

What are the reversible causes of cardiac arrest?

A
  • Hypoxia
  • Hypovolaemia
  • Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic
  • Hypothermia
  • Thrombosis (coronary or pulmonary)
  • Tension pneumothorax
  • Tamponade - cardiac
  • Toxins
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3
Q

What are the heart rhythms associated with cardiac arrest divided into?

A
  • Shockable - VF and pVT

* Non-shockable - asystole and PEA

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4
Q

How should shockable rhythms be managed?

A
  1. Confirm cardiac arrest
  2. Call resuscitation team
  3. Perform uninterrupted chest compressions while applying AED pads
  4. Plan actions before pausing CPR for rhythm analysis
  5. Stop chest compressions; confirm VF/pVT from ECG (brief 5 seconds)
  6. Resume chest compressions immediately; warn to stand clear and remove o2 delivery device
  7. Choose energy setting of at least 150J for the first shock, same or higher for subsequent shocks
  8. Ensure the person giving compressions is the only person touching the patient
  9. Warn everyone to stand clear, when clear, give the shock
  10. After the shock, immediately restart CPR using a ratio of 30:2 starting with chest compressions
  11. Continue CPR for 2 min
  12. Pause briefly to check the monitor
  13. If VF/pVT, repeat steps 6-12 above and deliver a second shock
  14. If VF/pVT persists, repeat steps 6-8 above and deliver a third shock. Resume chest compressions immediately. Give adrenaline 1 mg IV and amiodarone 300 mg IV while performing a further 2 min CPR. Withhold adrenaline if there are signs of return of spontaneous circulation during CPR
  15. Repeat this 2 min CPR - rhythm/pulse check - defibrillation sequence if VF/pVT persists
  16. Give further adrenaline 1 mg IV after alternate shocks (i.e. approximately every 3-5 min)
  17. If organised electrical activity compatible with cardiac output is seen, seek evidence of ROSC (signs of life, central pulse and end tidal CO2 if available)
    - ROSC, start post-resuscitation care
    - No signs of ROSC, continue CPR and switch to the non-shockable algorithm
  18. If asystole is seen, continue CPR and switch to the non-shockable algorithm
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5
Q

How should non-shockable rhythms be managed?

A
  1. Start CPR 30:2
  2. Give adrenaline 1 mg IV
  3. Continue CPR 30:2 until the airway is secured - then continue chest compressions without pausing during ventilation
  4. Recheck the rhythm after 2 min

If electrical activity compatible with a pulse is seen, check for a pulse and/or signs of life:

  • If pulse and/or signs of life are present, start post resuscitation care
  • If no pulse and/or no signs of life are present (PEA or asystole):
  • Continue CPR
  • Recheck the rhythm after 2 min and proceed accordingly
  • Give further adrenaline 1 mg IV every 3-5 minutes (during alternate 2 min loops of CPR)

If VF/pVT at rhythm check:
- Change to shockable side of algorithm

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6
Q

How is shock administration different when witnessed in a monitored patient (e.g. in a coronary care unit) ?

A
  • Up to 3 quick successive (stacked) shocks are recommended rather than 1 shock followed by CPR
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7
Q

What is a myocardial infarction (heart attack)?

A
  • Problem with the blood flow to the heart muscle
  • Acute MI is when the blood flow to the heart is abruptly cut off causing tissue damage
  • Usually the result of a blockage in one or more of the coronary arteries
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8
Q

What is the role of the ECG in a person suspected of having a myocardial infarction?

A
  • To determine if a person is having an ischaemic event
  • Signs of an acute MI include:
  • Hyperacute T waves but often only for a few minutes
  • ST elevation may then develop
  • T waves typically become inverted within the first 24 hours, can last for days to months
  • Pathological Q waves develop after several hours to days - change usually persists indefinitely
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9
Q

What is the definition of ST elevation?

A
  • New ST elevation at the J-point in two contiguous lead with the cut off points:

> =0.2 mV in men or >= 0.15 mV in women in leads V2-V3 and/or >=0.1 mV in other leads

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10
Q

What is the initial management of a patient with ST elevevation MI?

A

In the absence of contraindications, all patients should be given:

  • Oxygen 15L NRBM if there is signs of hypoxia, aiming for 94-98%
  • IV morphine 2.5-5mg and anti-emetic cover such as metoclopramide 10mg or cyclizine if LVF is not compromised
  • Aspirin 300mg chewed or dispersed in water
  • Clopidogrel (P2Y12-receptor antagonist) or ticagrelor
  • Glycoprotein IIb/IIIa inhibitors eptifibatide and tirofiban can be used in to reduce the risk of immediate vascular occlusion in intermediate and high risk patients (NSTEMI/unstable angina - GRACE score >3% +/- PCI 96 mins)
  • Heparin or a LMWH or fondaprinux (in patients who cannot have PCI within 90 minutes they need another thrombolytic drug alongside)
  • Beta blockers (with LV dysfunction diltiazem or verapamil)
  • ACEi or ARB in patients with no contraindications
  • All patients should be closely monitored for hyperglycaemia; those with diabetes or raised blood glucose concentration should receive insulin
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11
Q

What is acute left ventricular failure?

A
  • Rapid onset of symptoms (SOB/chest pain, etc) due to abnormal cardiac function
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12
Q

What are the causes of ALVF?

A
  • Cardiac - ACS, acute decompensation of existing HF, acute heart valve disease, arrhythmia, malignant HTN, myocarditis, cardiac tamponade, high out-put failure, fluid overload
  • Respiratory - ARDS, neurogenic (head injury)
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13
Q

How common is ALVF?

A
  • 13% of inpatients admitted with ACS
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14
Q

What is the pathophysiology of ALVF?

A
  • Reduced cardiac output
  • Poor perfusion
  • Increased pulmonary capillary wedge pressure
  • Severe pulmonary oedema
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15
Q

What are the symptoms and signs of acute decompensated HF - leading to ALVF?

A

Symptoms - Mild SOB without evidence of pulmonary oedema/cardiogenic shock
Signs - JVP potentially raised

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16
Q

What are the symptoms and signs of pulmonary oedema - leading to ALVF?

A

Symptoms - Chest x-ray confirmed severe SOB, orthopnoea, pink frothy sputum
Signs - Sat up/forward, cyanosis/pale, diffuse lung crepitations, pink frothy sputum, cardiac wheeze, gallop rhythm
* Cardiogenic shock - tachycardia, hypotension, reduced urine output

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17
Q

What are the differential diagnoses for ALVF?

A
  • Hypertensive HF
  • Aortic dissection
  • PE
  • Pneumonia
  • Asthma
  • COPD
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18
Q

What are the blood investigations of ALVF?

A
  • FBC low Hb (precipitator)
  • U and E (raised creatinine)
  • LFT (deranged)
  • Troponin I raised if MI
  • Plasma BNP (high negative predictive value)
  • ABG (type I respiratory failure) low O2, low CO2
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19
Q

What are the imaging investigations for ALVF?

A
  • Chest x-ray
  • Aveolar oedema (Bat wings)
  • Kerley B lines (interstitial oedema)
  • Cardiomegaly (if chronic HF)
  • Upper lobe diversion
  • Pleural effusion
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20
Q

What are the special tests for ALVF?

A
  • ECG - MI/arrhythmia
  • Swan-Ganz - pulmonary artery floatation catheter
  • Measure CO and PCWP in those with severe HF requiring ionotropic support
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21
Q

What is the approach to the management of a patient with ALVF?

A
  • A to E assessment
  • A - maintain/sit up
  • B - SpO2, RR, CXR, ABG, NRBM 15L/min O2
  • C - HR, BP, JVP, ECG, IV access for bloods
  • D - GCS/AVPU - brief history
  • Management
  • Diamorphine 2.5-5mg IV slowly
  • Furosemide 40-80 mg IV slowly
  • GTN 2 puffs/0.3 mg tablets (NOT if SBP <90)
  • More furosemide if worsening
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22
Q

What is the ongoing management for patients with ALVF?

A
  • Monitor for:
  • Cyanosis
  • HR
  • BP
  • JVP
  • UO
  • RR
  • ABG
  • Once improving monitor:
  • Daily weights
  • Pulse/BP (every 6hrs)
  • Repeat chest x-ray
  • Change to oral furosemide/bumetanide
  • Add thiazide if on large dose loop diuretic
  • ACEi (if LVF or hydralazine and nitrate if ACEi CI)
  • Consider beta blocker and spironolactone
  • Consider digoxin +/- warfarin
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23
Q

What are the potential complications of ALVF?

A
  • Type 1 respiratory failure
  • Cardiogenic shock
  • Cardio-respiratory arrest
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24
Q

What is the clinical threshold standard for suspecting hypertension?

A
  • Systolic bp above or equal to 140mmHg
  • Diastolic bp above or equal to 90mmHg
  • Or both
  • Diagnosis is confirmed with ambulatory bp monitoring (ABPM) or home bp monitoring (HBPM)
  • Measure BP in both arms
  • If the difference in readings in both arms is >15mmHg repeat the measurements
  • If the difference remains >15mmHg on the second measurement, check BP in the arm with the higher reading
  • If clinical BP is >140/90 or higher take a second reading
  • Record the lower of the last 2 readings
  • If the clinical BP is between 140/90 and 180/120 offer ambulatory BP monitoring (ABPM - 2 per hour during waking hours, use average of 14 measurements) to confirm the diagnosis of hypertension (HBPM - 1 in morning x 2 < 1 min apart and same in evening - continue for at least 4 days, ideally 7 days) if the person is not able to tolerate ABPM
  • While waiting for diagnosis of hypertension carry out the following:
  • Investigations for target organ damage - e.g. CKD, CVD, etc
  • QRISK2
  • ECG
  • U and E
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25
Q

What are the different stage classifications of hypertension?

A
  • Stage one - 140/90mmHg to 159/99 and subsequent ABPM daytime average or HBPM at least 135/85mmHg to 149/94
  • Stage two - 160/100mmHg to 179/119 and subsequent ABPM daytime average or HBPM at least 150/95mmHg or higher
  • Stage 3 - Severe hypertension - clinic systolic at least 180mmHg or diastolic at least 120mmHg
  • Accelerated hypertension - clinic bp higher than 180/120mmHg or higher (often over 220/120) with signs of papilloedema and/or retinal haemorrhage
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26
Q

When should a patient be referred for same day specialist care for hypertension?

A
  • Clincal BP higher than 180/120mmHg and higher with signs of papilloedema and/or retinal haemorrhage (accelerated hypertension)
  • Life threatening symptoms such as new onset confusion, chest pain, signs of heart failure or AKI
  • Suspected phaeochromocytoma (labile or postural hypotension, headache, palpitations, pallor and diaphoresis
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27
Q

What are the risk factors for hypertension?

A
  • Age - increasing age
  • Sex - up to 65 years women tend to have lower bp than men, 65 to 74 years women have a higher blood pressure
  • Ethnicity - black african and carribean at greater risk
  • Genetic - 40% variability explained by genetics
  • Social deprivation - 30% increased risk for those socially deprived in England
  • Lifestyle - smoking, alcohol, salt, obesity, inactivity
  • Anxiety and emotional stress - raise bp due to increased adrenaline and cortisol
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28
Q

Why is it important to manage hypertension?

A
  • Increases the risk of developing many other diseases including:
  • Heart failure
  • Coronary artery disease
  • Stroke
  • Chronic kidney disease
  • Peripheral arterial disease
  • Vascular dementia
  • At least half of all heart attacks and strokes are associated with hypertension
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29
Q

How does the risk increase with increasing blood pressure?

A
  • Each 2 mmHg rise in systolic blood pressure is associated with a 7% increased risk of mortality from ischaemic heart disease and 10% increased risk of mortality from stroke
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30
Q

How does correction of high blood pressure reduce health risks?

A

Major study found that every 10mmHg reduction in blood pressure resulted in:

  • 17% reduction in coronary heart disease
  • 27% reduction in stroke
  • 28% reduction in heart failure
  • 13% reduction in all cause mortality
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31
Q

How should ABPM be conducted to confirm a diagnosis of hypertension?

A
  • At least 2 measurements per hour taken during the person’s usual waking hours (e.g. 08:00 - 22:00)
  • Use the average value of atleast 14 measurements taken during the person’s usual waking hours to confirm hypertension
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32
Q

How should HBPM be conducted to confirm a diagnosis of hypertension?

A
  • Each BP recording two consecutive measurements are taken at least 1 minute apart with the person seated
  • BP is recorded twice daily, ideally morning and evening
  • BP recording continues for at least 4 days, ideally 7 days - discard the measurements taken on the first day and use the average value of all the remaining measurements
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33
Q

How can risk of a patient developing CVD in 10 years be estimated?

A
  • Using the QRISK2
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34
Q

How should stage one hypertension be managed?

A
  • Offer antihypertensive drug treatment to people aged under 80 years with stage 1 hypertension who have one or more of the following:
  • Target organ damage
  • Established CVD
  • Renal disease
  • Diabetes
  • 10 year CVD risk equivalent to 10% or greater
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35
Q

How should stage two hypertension be managed?

A
  • Offer antihypertensive drug treatment to people of any age with stage 2 hypertension
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36
Q

How should severe hypertension be managed?

A
  • Consider starting antihypertensive drug treatment immediately
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37
Q

How should accelerated hypertension by managed?

A
  • Consider referring for same day specialist care
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38
Q

What are the NICE recommended drug options for managing hypertension in a patient under 55?

A
  • Step 1 - ACEi or low cost ARB
  • Step 2 - ACEi or ARB + calcium channel blocker (can use thiazide diuretic)
  • Step 3 - ACEi or ARB + CCB + thiazide like diuretic
    (thiazide = indapamide)
  • Step 4 - Resistant hypertension- check potassium (<4.5 = spironolactone, >4.5 = alpha or beta blocker)
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39
Q

What are the NICE recommended drug options for managing hypertension in a patient over 55 or black African or Caribbean?

A
  • Step 1 - Calcium channel blocker
  • Step 2 - Calcium channel blocker + ACEi or ARB (can use thiazide diuretic)
  • Step 3 - CCB + ACEi or ARB + thiazide like diuretic
    (thiazide = indapamide)
  • Step 4 - Resistant hypertension (<4.5 = spironolactone, >4.5 = alpha or beta blocker)
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40
Q

When should antihypertensive medication be offered for hypertension?

A
  • Stage two - 160/100mmHg and subsequent ABPM daytime average or HBPM at least 150/95mmHg
  • Offer lifestyle advice as well
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41
Q

How should BP be measured in clinic?

A
  • Measure BP in both arms
  • If different by 15mmHg repeat the measurements
  • If the difference remains >15mmHg on the second measurement, measure subsequent BP in the arm with the higher reading
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42
Q

If the BP measured in clinic is 140/90mmHg or higher, what is the next step?

A
  • Take a second measurement during the consultation

* If the second measurement is substantially different from the first, take a third measurement

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43
Q

Which measurement should be recorded as the clinical BP?

A
  • Record the lower of the last 2 measurements
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44
Q

What does the QRISK3 calculate?

A
  • Calculates a persons risk of developing of developing a heart attack or stroke over the next 10 years
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45
Q

What information is required to calculate the QRISK3?

A
  • Age
  • Gender
  • Ethinicity
  • Post code?
  • Smoking status
  • Diabetes status
  • Angina or heart attack in a 1st degree relative <60
  • CKD stage 3, 4, 5
  • Atrial fibrillation
  • On BP treatment
  • Do you have migraines
  • Rheumatoid arthritis
  • SLE
  • Severe mental illness
  • Atypical antipsychotic
  • Regular steroids
  • Diagnosis of ED
  • Cholesterol/HDL ratio
  • Systolic BP
  • StDev two most recent sys BP
  • BMI
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46
Q

How is ABPM measured?

A
  • 2 measurements per hour
  • Taken during usual waking hours 08:00 to 22:00 use the average value of at least 14 measurements to confirm diagnosis of hypertension
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47
Q

How is HBPM measured?

A

Ensure that for each BP recording:

  • 2 consecutive measurements are taken at least 1 minute apart with the person seated
  • BP is recorded twice daily, ideally morning and evening
  • BP recording continues for at least 4 days ideally 7 days
  • Discard measurements taken on the first day and use the average value of all the remaining measurements to confirm a diagnosis of hypertension
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48
Q

How is a diagnosis of hypertension confirmed differently in clinic compared to ABPM or HBPM?

A
  • Clinic BP 140/90 or higher

* ABPM daytime average or HBPM average of 135/85 or higher

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49
Q

How often should a persons BP be measured if hypertension is not diagnosed?

A
  • At least every 5 years - more often if the persons clinical BP is close to 140/90
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50
Q

How often should BP be measured for people with type 2 diabetes?

A
  • At least annually - without previously diagnosed hypertension or renal disease
  • Offer and reinforce preventative lifestyle advice
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51
Q

How should cardiovascular risk and target organ damage be assessed in people with hypertension?

A
  • CVD risk - QRISK2
  • Test for the presence of protein in the urine by sending for ACR and urine dip for haematuria
  • Take a blood sample for HbA1c, U and E’s, creatinine, eGFR, total cholesterol and HDL cholesterol
  • Examine fundi for presence of retinopathy
  • Arrange for 12 lead ECG
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52
Q

How is a patient with stage 1 hypertension managed initially (ABPM/HBPM >=135/85mmHg?

A
  • Treat if <80 years AND any of the following apply:
  • Target organ damage
  • Established CV disease
  • Renal disease
  • Diabetes
  • 10 year CV risk equivalent to 10% or greater
  • Consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated risk below 10%
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53
Q

What are the targets for hypertension when treatment has started?

A
  • Clinic BP
  • Age <80 years
  • 140/90 mmHg
  • Age >80 years
  • 150/90 mmHg
  • ABPM/HBPM
  • Age <80 years
  • 135/85 mmHg
  • Age >80 years
  • 145/85 mmHg
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54
Q

How is BP measured in children?

A
  • Correct cuff size is 2/3 length of the upper arm
  • 4th Korotoff sound is used to measure the diastolic BP until adolescence, when the 5th Korotkoff sound can be used
  • Results should be compared with normal values for age
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55
Q

What is the most common cause of hypertension in younger children?

A
  • Secondary hypertension - renal parenchymal disease accounts for up to 80%
  • Causes of hypertension in children
  • Renal parenchymal disease
  • Renal vascular disease
  • Coarctation of the aorta
  • Phaeochromocytoma
  • Congenital adrenal hyperplasia
  • Essential or primary hypertension (more common as children become older)
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56
Q

What are the secondary causes of hypertension in adults?

A
  • Between 5-10% of people with hypertension have primary hyperaldosteronism, including Conn’s syndrome (most common causes of secondary hypertension)
  • Renal disease accounts for a large proportion of other causes of secondary hypertension:
  • Glomerulonephritis
  • Pyelonephritis
  • Adult polycystic kidney disease
  • Renal artery stenosis
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57
Q

Which endocrine disorders (other than hyperaldosteronism) can result in increased BP?

A
  • Phaeochromocytoma
  • Cushing’s syndrome
  • Liddle’s syndrome
  • Congenital adrenal hyperplasia (11-beta hydroylase deficiency)
  • Acromegaly
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58
Q

Which drugs can lead to hypertension?

A
  • Steroids
  • Monoamine oxidase inhibitors
  • COCP
  • NSAID’s
  • Leflunomide
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59
Q

What other causes of hypertension are there?

A
  • Pregnancy

* Coarctation of the aorta

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60
Q

Which conditions of hypokalaemia are associated with hypertension?

A
  • Cushing’s syndrome
  • Conn’s syndrome (primary hyperaldosteronism)
  • Liddle’s syndrome
  • 11-beta hyroxylase deficiency (congenital adrenal hyperplasia - 10% of the condition)
  • Anti-ulcer drug carbenoxolone
  • Liquorice excess
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61
Q

What are the conditions of hypokalaemia without hypertension?

A
  • Diuretics
  • GI loss e.g. diarrhoea, vomiting
  • Renal tubular acidosis (type 1 and 2)*
  • Bartter’s syndrome
  • Gitelman syndrome
  • Type 4 renal tubular acidosis is associated with hyperkalaemia
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62
Q

In which group is isolated systolic hypertension more common in?

A
  • Elderly - around 50% of people aged 70 years and older

* Treated in the same way as standard hypertension

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63
Q

What is chronic cardiac failure?

A
  • Syndrome where cardiac output CO and BP fail to maintain adequate circulation for bodily metabolic demands despite satisfactory filling pressure (so excludes conditions causing poor venous return like low BP)
  • CCF - R and L HF fluid overload
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64
Q

What are the main symptoms of heart failure?

A
  • Shortness of breath
  • Swollen ankles, feet, stomach and around the lower back area
  • Fatigue or weakness
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65
Q

What are the most common causes of heart failure?

A
  • Myocardial infarction - can cause long term damage to the heart muscle which can lead to reduced function
  • High blood pressure - can put extra strain on the heart which over time can lead to damage
  • Cardiomyopathy - disease of the heart muscle, can be inherited
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66
Q

What are the other possible causes of heart failure?

A
  • Damaged or diseased valves
  • Congenital heart problems
  • Abnormal rhythm - arrhythmia
  • Viral infection - endocarditis
  • Cancer treatment - chemotherapy toxicity
  • Excessive alcohol consumption
  • Thyroid disease
  • Anaemia
  • Pulmonary hypertension - can damage the right side of the heart
  • Amyloidosis - build up of abnormal proteins in heart, liver and kidneys and can lead to dysfunction (cardiac amyloidosis) ‘stiff heart syndrome’ tends to make the ventricles stiff
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67
Q

What is the process of diagnosing heart failure?

A
  • Detailed history
  • Perform a clinical examination
  • Establish if the patient has had a previous MI
  • MI+ = <2 weeks specialist assessment and doppler echocardiography
  • MI- = Measure serum natriuretic peptides, high levels as above within 2 weeks, raised level as above but within 6 weeks
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68
Q

What is the purpose of the assessment of heart failure?

A
  • To establish:
  • Heart failure with left ventricular systolic dysfunction
  • Heart failure with preserved ejection fraction
  • Unlikely heart failure
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69
Q

What is the management for patients with heart failure with preserved ejection fraction?

A
  • Manage the comorbid conditions in line with NICE guidance
  • High blood pressure
  • Ischaemic heart disease
  • Diabetes mellitus
  • Offer rehabilitation and education
  • Offer diuretics for congestion and fluid retention
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70
Q

What is the management for patients with heart failure with left ventricular systolic dysfunction?

A
  • Offer both ACEi and beta blockers as first line treatment
  • Consider ARB if ACEi not suitable
  • Consider hydralazine in combination with nitrate if intolerant of ACEi and ARBs
  • If symptoms persist seek specialist advice
  • Second line treatments consider:
  • Aldosterone antagonist (MRA)
  • Examples include spironolactone and eplerenone
  • ARB
  • Hydralazine in combination with nitrate
  • Third line - only initiated by a specialist
  • Ivabradine - criteria sinus rhythm >75/min and a left ventricular fraction <35%
  • Sacubitril-valsartan - criteria left ventricular fraction <35%
  • Considered in heart failure with reduced ejection fraction who are symptomatic on ACEi or ARB’s, initiated following ACEi or ARB wash out period
  • Digoxin - strongly indicated if there is AF
  • Hydralazine in combination with nitrate
  • Indicated in Afro-Caribbean patients
  • Cardiac resynchronisation therapy
  • Indications include a widened QRS e.g. LBBB complex on ECG
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71
Q

What are the important features of history when suspecting heart failure?

A
  • Breathlessness - on exertion, at rest, on lying flat (orthopnoea), nocturnal cough, or waking from sleep (paroxysmal nocturnal dyspnoea)
  • Fluid retention (ankle swelling, bloated feeling, abdominal swelling, or weight gain)
  • Fatigue, decreased exercise tolerance, or increased recovery time after exercise
  • Light headedness or history of syncope
    Risk factors:
  • Coronary artery disease including previous MI, hyptertension, AF and diabetes mellitus
  • Drugs, including alcohol
  • Family history of heart failure or sudden cardiac death under age 40
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72
Q

What are the important features to examine for in heart failure?

A
  • Tachycardia (>100) and pulse rhythm
  • Laterally displaced apex beat, heart murmurs, third or fourth heart sounds (gallop rhythm)
  • Hypertension
  • Raised JVP
  • Enlarged liver
  • Tachpnoea, basal crepitations, pleural effusions
  • Dependent oedema (legs, sacrum) ascites
  • Obesity
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73
Q

How should a person with suspected heart failure be initially managed?

A
  • Review the patients medication and stop or reduce any drugs that may cause or worsen heart failure
  • If the symptoms are severe, start a loop diuretic such as
  • Furosemide 20-40mg daily
  • Bumetanide 0.5-1.0mg daily
  • Torasemide 5-10mg daily
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74
Q

How should the patient be investigated if there is suspected heart failure?

A
  • Arrange admission if the patient has severe symptoms
  • For pregnant women (or given birth within 6 months) with suspected heart failure, arrange emergency admission or seek immediate specialist advice
  • Measure NT-proBNP
    >2000pg/mL - refer to be seen within 2 weeks for specialist assessment and echocardiography
    400-2000pg/mL - refer to be seen within 6 weeks for specialist assessment and echocardiography
    <400pg/mL be aware that a diagnosis of heart failure is less likely
  • Arrange 12 lead ECG
  • Consider other tests to identify possible aggravating factors and to exclude other presentations:
  • Chest x-ray
  • Blood tests - U&Es, eGFR, FBC, TFT, LFT, HbA1c, fasting lipids
  • Urine dip for blood and protein
  • Lung function tests (peak flow and/or spirometry)
  • Manage and arrange for any underlying causes
  • Refer patients with valve disease for specialist assessment
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75
Q

What can reduce the levels of natriuretic peptides?

A
  • BMI >35
  • Drugs - diuretics, ACEi, ARBs, beta-blockers and aldosterone antagonists (such as spironolactone
  • African-Carribean family origin
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76
Q

What can increase the levels of natriuretic peptides?

A
  • Age >70 years
  • LV hypertrophy
  • RV overload
  • Hypoxia
  • Pulmonary hypertension
  • CKD
  • Sepsis
  • COPD
  • Diabetes mellitus
  • Liver cirrhosis
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77
Q

What are the differentials with similar presentation to heart failure?

A
  • COPD
  • Asthma
  • Pulmonary embolism
  • Lung cancer
  • Anxiety
    Conditions causing peripheral oedema such as:
  • Prolonged inactivity or venous insufficiency causing dependent oedema
  • Nephrotic syndrome
  • Drugs (CCB - dihydropyridines - amlodipine or nifedipine - or NSAIDs)
  • Hypoalbuminaemia
  • Pelvic tumour
  • Obesity
  • Severe anaemia or thyroid disease
  • Bilateral renal artery stenosis
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78
Q

Which additional tests should be done for patients with heart failure to evaluate possible aggravating factors and/or alternative diagnoses?

A
  • Chest x-ray
  • Blood tests
  • Renal function profile
  • Thyroid function profile
  • Liver function profile
  • Lipid profile
  • HbA1c
  • FBC
  • Urinalysis
    Peak flow or spirometry
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79
Q

When reviewing the results of NT-proBNP how should they be interpreted?

A

Be aware that:

  • NT -proBNP level less than 400ng/litre (47 pmol/litre) in an untreated person makes a diagnosis of heart failure less likely
  • Level of serum natriuretic peptide does not differentiate between heart failure with reduced ejection fraction and heart failure with preserved ejection fraction
  • All patients with a NT -proBNP level less than 400ng/litre (47 pmol/litre) should be reviewed for alternative causes
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80
Q

How should patients with heart failure caused by valve disease be managed?

A
  • Refer people with heart failure caused by valve disease for specialist assessment and advice regarding follow up
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81
Q

What should be included in the first consultation for a person with newly diagnosed heart failure?

A
  • MDT with extended first consultation, followed by a second consultation to take place within 2 weeks if possible. At each consultation:
  • Discuss the person’s diagnosis and prognosis
  • Explain heart failure terminology
  • Discuss treatments
  • Address the risk of sudden death, including any misconceptions about that risk
  • Encourage the person and their family or carers to ask any questions they have
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82
Q

What is the New York Heart Failure Classification system?

A
  • System of classifying the extent of heart failure
  • Rated 1 - 4
  • 1 - No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnoea (SOB)
  • 2 - Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea
  • 3 - Marked limited physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpation, or dyspnoea
  • 4 - Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases
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83
Q

Which drug is recommended by NICE for people with NYHA class 2 to 4 stable chronic heart failure with systolic dysfunction and 75 BPM or more and already on standard therapy (beta blocker, ACEi and aldosterone antagonists and with LVEF <35% or less?

A
  • Ivabadine - can be recommended after a stabilisation period of 4 weeks on optimised standard therapy with ACEi, beta blockers and aldosterone antagonists
  • Should be started by a heart failure specialist with access to MDT
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84
Q

What is the indication for prescribing sacubitril valsartan in heart failure?

A
  • NYHA class 2 to 4
  • LVEF <35% or less
  • Already taking a stable dose of ACEi or ARBs
  • Started by a specialist
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85
Q

What is the indication for digoxin in heart failure?

A
  • Recommended for worsening or severe heart failure with reduced ejection fraction despite first line treatment for heart failure
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86
Q

When should digoxin levels be taken to assess for toxicity or adherence?

A
  • 8 to 12 hours after the last dose

* Digoxin levels should not be monitored routinely

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87
Q

How should heart failure be treated for people with reduced ejection fraction in people with CKD?

A

For patients with eGFR of 30 ml/min/1.73m2 or above

  • Offer standard treatment ACEi etc
  • For patients with eGFR of 45 ml/min/1.73m2 or below consider lower doses and/or slower titration of dose of ACE inhibitors or ARBs, MRA and digoxin
  • eGFR <30 - specialist heart failure MDT should consider liasing with a renal physician
  • Monitor response to titration of medicines closely in people who have heart failure with reduced ejection fraction and CKD taking into account the increased risk of hyperkalaemia
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88
Q

Which pharmacological treatments can be used to manage all types of heart failure?

A
  • Diuretics
  • routinely for the relief of congestive symptoms and fluid retention
  • people with preserved ejection fraction should usually be offered low to medium dose loop diuretics (<80mg furosemide per day)
  • Calcium channel blockers
  • Avoid verapamil and diltiazem in people with heart failure with reduced ejection fraction
  • Amiodarone
  • With specialist consultation, requires review at 6 months, liver and thyroid function tests and a review of side effects per 6 months
  • Anticoagulants
  • People with heart failure and atrial fibrillation
  • History of thromboembolism
  • Vaccinations
  • Annual flu vaccine
  • Pneumococcal vaccine only once
  • Contraception in women of child bearing age
  • Specialist shared care between cardiologist and obstetrician if pregnancy occurs
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89
Q

Which further lifestyle factors should be screened for/managed for all patients with heart failure?

A
  • Depression
  • Lifestyle advice
  • Salt and fluid restriction only in patients with dilutional hyponatraemia, advise to avoid salt substitutes that contain potassium
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90
Q

When are people in end stage heart failure?

A
  • People who are regarded as being at risk of dying within the next 6-12 months due to their heart failure
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91
Q

What are the common symptoms of end stage heart failure?

A
  • Pain
  • Breathlessness
  • Persistent cough
  • Fatigue
  • Limitation of physical activity
  • Depression and anxiety
  • Constipation
  • Loss of appetite and nause
  • Oedema
  • Insomnia
  • Cognitive impairment
92
Q

How can the trajectory of end stage heart failure be predicted?

A

Can be difficult but indicators include:

  • Frequent hospital admissions
  • Poor response to treatment and severe breathlessness at rest NYHA 4
  • Presence of cachexia
  • Low serum albumin
  • Progressive deterioration in eGFR and hypotension limiting the use of drug treatments
  • Acute deterioration and increasing frequency hospital admissions from comorbid conditions such as chest infection
  • Poor quality of life and dependence on others for most activities of daily living
  • People who are clinically judged to be close to the end of life
93
Q

Which guidelines and framework can be used for people with a chronic/life limiting condition including heart failure to estimate prognosis and optimise the care of people nearing the end of life who are looked after by primary care teams?

A
  • Prognostic Indicator Guidelines

* Gold Standards Framework

94
Q

How should a person with end stage heart failure be managed?

A
  • Liaise with cardiologist and make sure all treatment options have been considered (including deactivation of implantable cardioverter-defibrillator if appropriate)
  • Explore the goals and provide realistic explanation of the situation to the person
  • Involve the MDT - community nurses, heart failure nurses, palliative care team, occupational therapists, physiotherapists, dietetics, out of hours services and hospice care
  • Review medication and provide symptom relief
  • Ensure the person has an advance care plan in place (if they wish)
  • Discussion of advance decisions
95
Q

What does the medication and symptom review include in a person with end stage heart failure?

A
  • Breathlessness - optimise standard treatment, consider an opioid, a benzodiazepine and/or home oxygen
  • Pain - chest pain is often due to cardiac ischaemia, this can be relieved by morphine and nitrates
  • Anxiety and depression
  • Insomnia
  • Constipation, nausea and loss of appetite
96
Q

What should the advance care plan include in a patient with a life limiting condition including heart failure?

A
  • Anticipatory prescribing medication to manage symptoms and when, who, and how to call for help when there is a crisis or acute exacerbation
  • Needs for psychological and spiritual care
  • Care of the family (before and after a persons death)
  • Information on prognosis in a sensitive, open and honest manner
  • Preferred place of care and death
  • Whether resuscitation should be attempted of they were to have a life threatening deterioration - make this information available to out of hours services and ambulance services
  • Discuss advance directives/decisions if they wish - allows the person to specify (before they have lost capacity to decide) what treatments they would want and would not consent to
97
Q

What advice and information should you give to a person with confirmed heart failure?

A
  • Advise the person about reporting symptoms of worsening heart failure - increasing breathlessness, fatigue, ankle swelling or abdominal swelling and rapid weight gain
  • Advise to seek urgent medical advice if symptoms deteriorate
  • Consider advising the person to monitor their weight at home same time of day
  • Advise to seek medical advice if they have rapid weight gain (>2kg in 3 days)
  • Advise to limit salt intake - <6g salt per day
  • People with severe symptomatic heart failure limit fluid intake to 1.5 to 2L per day to relieve symptoms, or consider a weight based fluid restriction such as 30 mL/kg body weight or 35mL/kg body weight for those over 85kg
  • Do not severely restrict fluid or it will risk dehydration
  • Smoking cessation if relevant
  • Alcohol consumption - recommended levels
  • Physical activity levels - regular low intensity for people with stable heart failure
  • Nutritional status
  • BMI <18.5 refer for dietetic advice
  • BMI >30 give advice on maintaining a healthy weight
  • Sexual activity - can continue normal sexual activity as long as it does not provoke undue symptoms
98
Q

What is the advice regarding driving for a person with heart failure?

A
  • Persons responsibility to inform the DVLA
  • Group 1 - cars and motorbikes, driving can continue as long as there are no symptoms that may distract the drivers attention (no need to inform DVLA)
  • Group 2 - lorries and buses - disqualified if symptomatic, re-licensing may be permitted if left ventricular ejction fraction is >40%
99
Q

When should primary care refer a patient with heart failure to specialist MDT or cardiology service?

A
  • Severe heart failure NYHA class 4
  • Heart failure that does not respond to treatment in primary care or can no longer be managed in the home setting
  • Heart failure resulting from valvular heart disease
  • Left ventricular ejection fraction of 35% or less
  • Consider referral if they also have a comorbidity such as CKD or COPD
  • Refer women with heart failure and reduced ejection fraction who are planning to get pregnant for specialist pre-conceptual advice and refer women who are pregnant for specialist management
  • Women who wish to conceive should be advised to continue contraception until they have seen an obstetrician and cardiologist for pre-conceptual advice
100
Q

How should a patient with heart failure be followed up?

A
  • All require regular follow up and monitoring
  • Delivered by - MDT which may include: heart failure nurse, pharmacist
  • Frequency of follow up is individualised according to severity and stability of symptoms, treatment and comorbidities
  • Should be short (days to 2 weeks) if the clinical condition or drugs have changed and at least every 6 months if the condition is stable
  • Monitor NT-pro-BNP levels depending on local availability in people of <75 years age
101
Q

What symptoms and signs should be monitored for in patients with heart failure at follow up?

A
  • Ask about palpitations, SOB, oedema, syncopal and presyncopal symptoms
  • If the person has syncope or presyncope (unless clearly due to postural hypotension) refer to cardiologist as this may be due to ventricular tachycardia, particularly in people who have reduced ejection fraction
  • Check the persons pulse rate and rhythm and examine the heart - ECG if arrhythmia suspected
  • Assess fluid status
  • Assess the persons functional capacity according to NYHA classification
  • Assess cognitive status and psychological needs including anxiety and depression
  • Provide a self management plan
  • Assess nutritional status
  • Review the persons medications
  • Ensure the person has been offered a supervised group exercise based heart failure rehabilitation programme
  • Ensure immunisations are up to date
  • Monitor serum urea, electrolytes and eGFR every 6 months
  • Consider referral if indicated
  • Provide women of child bearing age advice about contraception and pregnancy
102
Q

What does a fluid status assessment consist of in a patient with heart failure?

A

Assess fluid status by checking for the following:

  • Changes in body weight
  • Oedema (abdomen, sacrum, genitalia and ankles)
  • Raised JVP
  • Fine lung crepitations
  • Hepatomegaly (liver engorgement)
  • Postural drop in blood pressure (decrease of >20mmHg suggests hypovolaemia)
103
Q

What are the recommended doses for ARB’s (AIIRA’s) for heart failure?

A
  • Candesartan
  • Initial dose - 4 mg once per day
  • Target dose - 32 mg once a day
  • Losartan
  • Initial dose - 12.5 mg once a day
  • Target dose - 150 mg once a day
  • Valsartan
  • 40 mg twice a day
  • Target dose 160 mg twice a day
104
Q

What are the adverse reactions of AIIRA’s?

A
  • Hypotension
  • Worsening renal function
  • Hyperkalaemia
  • Monitor U and E’s and renal function after starting, each dose increase and every 3-6 months
  • AIIRA’s not recommended in breast feeding or pregnancy
105
Q

What are some important drug interactions of AIIRA’s?

A
  • Aliskiren - direct renin inhibitor is not recommended with DBM or eGFR<60
  • ACEi - use with is not recommended
  • Risk of hyperkalaemia with trimethoprim
  • Many more
106
Q

How should the dose be titrated for AIIRA’s?

A
  • Measure eGFR, U and E’s, BP before prescribing
  • If the person has CKD and potassium >5mmol/l do not start treatment with an AIIRA
  • Start a low dose as recommended, titrate the dose up at short intervals (2 weeks) until the target dose or highest tolerated is reached
  • Measure renal function and BP after each upward titration
  • Do not increase if there is worsening renal function or hyperkalaemia
  • Once treatment is stable, measure renal function and serum electrolytes at least every month for 3 months and then at least every 6 months and at any time if the person becomes unwell
  • Advise the person that if they develop diarrhoea or vomiting while taking an AIIRA they should maintain their fluid intake and stop the AIIRA for 1-2 days until they recover
107
Q

What are the recommended doses for ACEi for heart failure?

A
  • Captopril
  • Initial dose - 6.25 mg to 12.5 mg, two to three times per day
  • Target dose - 50 mg x 3 a day
  • Enalapril
  • Initial dose - 2.5 mg twice a day
  • Target dose - 10 mg to 20 mg twice a day
  • Fosinopril
  • 10 mg once a day
  • Target dose 40 mg once a day
108
Q

What are the adverse reactions of ACEi’s?

A
  • Hypotension
  • Worsening renal function
  • Hyperkalaemia
  • Monitor U and E’s and renal function after starting, each dose increase and every 3-6 months
  • Cough - if intolerable consider switching to AIIRA
  • Angio-oedema
  • Rash
  • Gastrointestinal symptoms - taste disturbance, nausea, vomiting
  • Pancreatitis
  • Respiratory symptoms
  • Hypoglycaemia
  • Blood disorders
109
Q

What are some important drug interactions of ACEi’s?

A
  • Alcohol - increases hypotensive effect
  • Aldosterone antagonists - risk hyperkalaemia and hypotension
  • Many more
110
Q

How should the dose be titrated for ACEi’s?

A
  • Measure eGFR, U and E’s, BP before prescribing
  • If the person has CKD and potassium >5mmol/l do not start treatment with an AIIRA
  • Start a low dose as recommended, titrate the dose up at short intervals (2 weeks) until the target dose or highest tolerated is reached
  • Measure renal function and BP after each upward titration
  • Do not increase if there is worsening renal function or hyperkalaemia
  • Once treatment is stable, measure renal function and serum electrolytes at least every month for 3 months and then at least every 6 months and at any time if the person becomes unwell
  • Advise the person that if they develop diarrhoea or vomiting while taking an ACEi they should maintain their fluid intake and stop the ACEi for 1-2 days until they recover
111
Q

What are the recommended doses for beta blockers for heart failure?

A
  • Bisoprolol
  • Initial dose - 1.25 mg once per day with food
  • Target dose - 10 mg a day
  • Increase from 1.25 mg to 2.5 mg to 3.75 mg to 5 mg at 1-week intervals. After taking 5mg once a day for 4 weeks, increase to 7.5 mg and after another 4 weeks, increase to 10 mg.
  • Cardedilol
  • Initial dose - 3.125 mg twice a day with food
  • Target dose - 25 mg to 50 mg twice a day
  • Severe heart failure or weighs less the 85kg, target dose is 25 mg x 2 per day
  • Titrate by doubling every two weeks
  • Nebivolol (for people >70 years)
  • 1.25 mg once a day
  • Target dose 100 mg once a day
  • Increase dose from 1.25 mg to 2.5
112
Q

What are the adverse reactions of beta blockers?

A
  • Deteriorating symptoms of heart failure (such as symptoms of fluid overload and fatigue)
  • Hypotension
  • Bradycardia
113
Q

What are some important drug interactions of beta blockers?

A
  • Antipsychotics and antidepressants - risk of hypotension
  • Baclofen - hypotensive effect
  • Verapamil - risk bradycardia in concurrent use
114
Q

How should the dose be titrated for beta blockers?

A
  • Should only be started once the person is stable (without fluid overload or hypotension)
  • Advise there may be an initial worsening of symptoms and this will be temporary, will improve over 3-6 months
  • See dosing for target doses and titration
  • Monitor heart rate, BP and clinical status after each dose increase
  • Consider halfing dose if HR decreases to 50 beats per minute or less
115
Q

What are the recommended doses for diuretics for heart failure?

A
  • Bumetanide
  • Starting dose - 0.5 mg in the elderly - 1 mg
  • 1-5 mg usual daily dose
  • Furosemide
  • Starting dose - 20-40 mg
  • 20-120 mg usual daily dose
  • Torasemide
  • Starting dose - 5-10 mg
  • 10-20 mg usual daily dose
116
Q

What are the adverse reactions of diuretics for heart failure?

A
  • Mild GI upset
  • Hyperglycaemia
  • Acute urinary retention
  • Electrolyte and water imbalance
  • Metabolic alkalosis - risk increases with higher doses
117
Q

What are some important drug interactions of diuretics?

A
  • Increased risk of ototoxicity with aminoglycosides or vancomycin
  • Enhanced hypotensive effect with MAOI’s
  • Many more
118
Q

How should the dose be titrated for beta blockers?

A
  • Measure eGFR, U and E’s, BP before prescribing
  • Recheck renal function, serum electrolytes and blood pressure 1–2 weeks after starting treatment.
  • Titrate the dose up or down according to symptoms
119
Q

What is the mortality of chronic cardiac failure?

A
  • 82% within 6 years after diagnosis
120
Q

What vaccinations should be offered to a patient with heart failure?

A
  • Annual flu vaccine
  • One off pneumococcal vaccine
  • Those with asplenia, splenic dysfunction or CKD need a booster every 5 years
121
Q

How should DVT be managed?

A
  • Same day assessment and referral if DVT is suspected in a woman who is pregnant or has given birth within the past 6 weeks
  • For all others use the two-level Wells score to assess the probability
122
Q

How is the two level Wells score worked out?

A
  • Score one point for each of the following:
  • Active cancer (treatment ongoing, within last 6 weeks, or palliative)
  • Paralysis, paresis or recent plaster immobilisation of the legs
  • Recently bed ridden for 3 days or more, or major surgery within the last 12 weeks requiring general or regional anaesthesia
  • Localised tenderness (back of the calf)
  • Entire leg is swollen
  • Calf swelling by more than 3 cm compared with asymptomatic leg
  • Pitting oedema confined to the symptomatic leg
  • Collateral superficial veins (non-varicose)
  • Previous documented DVT
  • Subtract two points if an alternative cause is considered at least as likely as DVT
  • Alternative causes:
  • Physical trauma
  • Cardiovascular disorders
  • Ruptured Baker’s cyst
  • Cellulitis
  • Dependent oedema
  • Lymphatic obstruction
  • Septic arthritis
  • Cirrhosis
  • Nephrotic syndrome
  • Compartment syndrome
123
Q

After performing the two level Wells Score - how is the score interpreted?

A
  • Two points or more - DVT is likely

* Unlikely if the score is one point or less

124
Q

What is the next step in management if the person is likely to have a DVT according to the Wells score (2 or more)?

A
  • Refer for a proximal leg vein USS to be carried out within 4 hours
  • If a leg vein USS cannot be carried out within 4 hours of being requested:
  • Take a blood sample for D-dimer testing
  • Give an interim 24-hour dose of parenteral anticoagulant (apixaban or rivaroxaban)
  • Arrange for a proximal leg vein USS (to be carried out within 24 hours of being requested)
125
Q

What is the next step in management if the person is unlikely to have a DVT according to the Wells score (one point or less)?

A
  • Offer D-dimer testing:
  • If the D-dimer test is positive, refer for a proximal leg vein USS to be carried out within 4 hours
  • If a leg vein USS cannot be carried out within 4 hours of being requested:
  • Take a blood sample for D-dimer testing
  • Give an interim 24-hour dose of parenteral anticoagulant (apixaban or rivaroxaban)
  • Arrange for a proximal leg vein USS (to be carried out within 24 hours of being requested)
  • If the D-dimer test is negative, consider an alternative diagnosis to explain symptoms
126
Q

How should a person with confirmed DVT be followed up?

A
  • Maintenance therapy with an oral anticoagulant (warfarin, apixaban, dabigatran, edoxaban, or rivaroxaban) following acute treatment
  • Ensure adequate monitoring - specialists will decide on choice and duration of treatment - usually 3 months
  • For warfarin the INR target is 2.5 to keep within the range of 2.0-3.0
  • DOACs do not require monitoring
  • Ensure that people with an unprovoked DVT are investigated appropriately for the possibility of undiagnosed cancer and have been offered testing for thrombophilia
  • Advise the person:
  • How to use anticoagulants
  • About the duration of treatment and any monitoring requirements
  • About possible adverse effects and interactions associated with anticoagulation treatment
127
Q

What is an provoked DVT?

A
  • Associated with a transient risk factor such as significant immobility, surgery, trauma, and pregnancy or puerperium
  • COCP and HRT are also considered to be provoking risk factors
  • These risk factors can be removed therefore risk of recurrence can be reduced
128
Q

What is an unprovoked DVT?

A
  • Occurring in the absence of a transient risk factor
  • May have no identifiable risk factor or a risk factor that is persistent and not easily correctable (such as active cancer or thrombophilia)
  • Because these factors cannot be removed the person is at an increased risk of recurrence
129
Q

For people who are diagnosed with unprovoked DVT who are not already known to have cancer, which investigations should be offered according to NICE guidelines?

A
  • Physical examination (guided by the person’s full history)

Other investigations now not indicated

  • Chest x-ray
  • Blood tests (FBC, calcium and LFTs)
  • Urinalysis
  • Consider an abdomino-pelvic CT scan (and a mammogram for women) in all people aged over 40 years of age with a first unprovoked DVT who do not have signs or symptoms of cancer based on initial investigations
130
Q

For people who are diagnosed with unprovoked DVT who are planned to have their anticoagulation stopped, how should they be investigated for thrombophilia?

A

Not standard

  • Consider testing for anti-phospholipid antibodies
  • Consider testing for hereditary thrombophilia people who have had an unprovoked DVT and who have a first degree relative who has had DVT
131
Q

If LMWH is used (NICE now recommend DOACs for treatment and prevention) to treat people with a confirmed DVT, how should this be done?

A
  • Start treatment as soon as possible
  • Offer a vitamin K antagonist within 24 hours
  • Ensure that the LMWH is continued for at least 5 days or until the INR is 2 or above for at least 24 hours
  • VKA is continued for at least 3 months
  • Tinzaparin should be adminsitered subcutaneously
  • Recommended dose for DVT is 175 units / kg once daily
  • Contraindicated in:
  • Acute bacterial endocarditis
  • Current (or history) of heparin induced thrombocytopenia
  • Active bleeding
132
Q

What is post-thrombotic syndrome?

A
  • Chronic venous hypertension causing limb pain, swelling, hyperpigmentation, dermatitis, ulcers, venous gangrene and lipodermatosclerosis
  • Affects up to 50% of people usually within 2 years of DVT of the lower limbs and can be debilitating
133
Q

What is heparin induced thrombocytopenia (HIT)?

A
  • May occur 5-7 days after the initial exposure to heparin but can occur in less than one day in people previously exposed to heparin
  • Incidence is low in people treated with LMWH
134
Q

What are the key changes to the NICE guidelines 2020 in relation to VTE?

A
  • DOAC’s are now recommended first line for most people with VTE
  • Routine cancer screening is no longer recommended following VTE diagnosis
135
Q

When performing the Well’s score and the result is DVT is unlikely - how should the D-dimer be interpreted?

A
  • Age adjusted cut offs should be used for patients >50 years
136
Q

In which situations should LMWH now be used in place of DOAC’s for confirmed VTE?

A
  • Renal impairment is severe e.g. <15/min
  • Use LMWH, unfractionated heparin or LMWH followed by VKA i.e. warfarin
  • Antiphospholipid syndrome (especially triple positive)
  • LMWH followed by VKA i.e. warfarin
137
Q

How long should patients with confirmed VTE remain on anti-coagulation?

A
  • At least 3 months

* After this period depends if the DVT was provoked or unprovoked

138
Q

What does provoked mean in terms of DVT?

A
  • Due to an obvious precipitating factor
  • E.G. Immobilisation following major surgery
  • Implication is that this event was transient and the patient is no longer at increased risk
139
Q

What does unprovoked mean in terms of DVT?

A
  • Absence of an obvious precipitating factor
  • I.E. Possibility that there are unknown factors e.g. mild thrombophilia etc
  • Makes the patient at more risk of further clots
140
Q

How is anti-coagulation time managed for a provoked DVT?

A
  • 3 months
141
Q

How is anti-coagulation time managed for an unprovoked DVT?

A
  • 6 months

* Should also be balanced with HASBLED score according to NICE

142
Q

What is the approach to thrombophilia screening for a patient with an unprovoked DVT?

A
  • Not offered if the patient will be on life long warfarin
  • Consider testing for antiphospholipid antibodies if unprovoked DVT or PE
  • Consider testing for hereditary thrombophilia in patients who have an unprovoked DVT or PE and who have a first degree relative who has had DVT or PE
143
Q

What is acute limb ischaemia?

A
  • Any sudden reduction or worsening of limb perfusion with potential threat to limb viability (revascularise <4-6h to save the limb)
144
Q

What other presentations fall within the same spectrum as acute limb ischaemia and are part of peripheral arterial disease?

A
  • Intermittent claudication
  • Critical limb ischaemia
  • Acute limb threatening ischaemia
145
Q

How is acute limb ischaemia classified in terms of onset?

A
  • Acute - ischaemia <14 days
  • Acute on chronic - worsening symptoms/signs <14 days
  • Chronic - stable for >14 days
146
Q

How is acute limb ischaemia classified in terms of severity?

A
  • Incomplete - limb unthreatened
  • Complete - threatened
  • Irreversible - not viable
147
Q

What are the features of critical limb ischaemia?

A
  • 1 or more of the following:
  • Rest pain in foot for more than 2 weeks
  • Ulceration
  • Gangrene
148
Q

What level of ABPI is suggestive of critical limb ischaemia?

A
  • <0.5 ABPI
149
Q

What is ABPI?

A
  • Ratio of the systolic blood pressure in the lower leg to that in the arms
  • Lower BP in the legs (result ABPI <1) indicates peripheral arterial disease (PAD)
150
Q

How are ABPI levels further interpreted in acute limb ischaemia?

A
  • 1 = normal
  • 0.6-0.9 = claudication
  • 0.3-0.6 = rest pain
  • <0.3 = impending
151
Q

What are the causes of ALI?

A
  • Thrombus 60%
  • Embolus 30% - Left atrial 80% of emboli
  • AF
  • Prosthetic valves
  • Atrial myxoma
  • RhD
  • Others
  • Left ventricle
  • Prosthetic bypass grafts
  • Aneurysm
  • Paradoxical embolism via patent foramen ovale
  • Graft/angioplasty occlusion 15%
  • Others 10%
  • Trauma
  • Iatrogenic injury
  • Popliteal aneurysm
  • Aortic dissection
152
Q

What are the risk factors for thrombus formation?

A
  • Dehydration
  • Hot weather
  • DM
  • Infection
  • Gastroenteritis
  • Low BP
  • Immobility
  • Malignancy
  • Hyperviscosity
  • Polycythemia
  • Thrombocytosis
  • Thrombophilia
  • Protein C or S deficiency
  • Activated protein C resistance
  • Factor V leiden
  • Anti-phospholipid syndrome
153
Q

How common is acute limb ischaemia?

A
  • Common surgical emergency
  • > 75 yrs
  • M:F = 1:1
  • Often presents over <24-48 hrs
154
Q

What is the pathophysiology of acute limb ischaemia?

A
  • Artery bifurcations are most commonly affected (usually aorto-iliac or popliteal)
155
Q

What are the symptoms of acute limb ischaemia?

A
  • 7 P’s
  • Pain - worse on limb raised (absent if complete)
  • Pallor - mottled/cyanosed
  • Pulseless - also in chronic
  • Perishingly cold - not always
    • Paraesthesia - high risk (later anaesthesia)
    • Paralysis - high risk (may be irrevesible after 4-6 hrs)
  • Pistol shot onset
156
Q

What are the signs of acute limb ischaemia?

A
  • Long CRT>2’s
  • Skin changes - marble white (arterial spasm +/- red when dependent
  • Light mottling (blue purple, blanches on pressure)
  • Fixed mottling - darker, non-blanching as blood coagulates: irreversible
  • Blistering or liquifaction (gangrene)
  • Pallor grades
  • 0 none
  • 1 in >60s when 60 degrees
  • 2 >30s
  • 3 <30s
  • 4 When horizontal
  • Embolic - often when clear demarcation between normal and ischaemic skin
  • Look for underlying cause - irregular pulse, abnormal heart sounds/valve clicks
157
Q

What is the classification system for acute limb ischaemia?

A
  • Rutherford Classification
  • I - Viable, not immediately threatened, CRT intact
  • IIa and IIb - Threatened, salvageable if treated - emergency if IIb
  • III - Irreversible, primary amputation needed
158
Q

What are the differential diagnoses for acute limb ischaemia?

A

Acute painful limb

  • Limb threatening
  • Acute limb ischaemia
  • Compartment syndrome
  • MI
  • Spinal cord compression
  • Septic arthritis
  • Necrotising fasciitis
  • Gangrene
  • Sickle cell crisis
  • Others
  • Gout/cellulitis (may be red when dependent)
  • DVT (improved with raised legs)
  • Trauma (joint/muscle/bone)
159
Q

What are the blood investigations for ALI?

A
  • FBC - raised PCV / low plts predispose to thrombosis, clotting screening and group and save
  • U and E’s - raised CK and K+
  • CRP
  • Lipids
  • Glucose
    Others
  • D-Dimer
160
Q

What are the urine investigations for ALI?

A
  • MSU dipstick (myoglobinuria muscle damage)
161
Q

What are the radiological investigations for ALI?

A
  • Chest x-ray - cardio-megaly (heart failure, left ventricular aneurysm), dilated thoracic aorta (embolic source)
  • Angiography - if thrombosis in situ is suspected as cause to define site/extent of lesion, but if embolic cause is strongly suspected - no need for angiography - go straight for embolectomy
162
Q

What special tests can be done for ALI?

A
  • ABPI
  • Claudication 0.6-0.9
  • Rest pain 0.5-0.6
  • Critical limb ischaemia <0.5
  • Impending gangrene <0.3
  • ECG - AF / previous MI
163
Q

What is the immediate approach to the management of ALI?

A
  • A to E assessment - call for senior help
  • A - Sit up and maintain airway
  • B - SpO2 and RR 15L O2 NRBM
  • C - Peripheral pulses, HR, BP, JVP, IV access (NBM), bloods
  • D - GCS, PEARL, BM
  • E - temperature
  • Management
  • Analgesia - Morphine 10 mg IV and metoclopramide 10 mg
  • Fluids - IV NaCl to correct hypovolaemia
  • Brief history and check clerking notes
  • Examination - CVS, RS, abdominal, limbs, MSK, neurological
  • Check pulses with doppler if available
  • Forced alkaline diuresis - if renal impairment IV fluids/diuretics may reduce renal injury from Mb-uria
  • Unfractionated heparin
164
Q

What is the surgical management of ALI?

A
  • Embolic cause
  • Embolectomy - fogarty catheter
  • Local thrombolysis - t-PA
  • Thrombotic cause
  • Urgent angiography
  • Thrombolysis <6hrs
  • Monitor on HDU/vascular ward
  • Repeat angiography at 8-12hrs
  • Surgical bypass
  • Angioplasty
  • Post procedure
  • Anti-coagulation
  • Unfractionated heparin IVI
  • Look for the cause - embolic TTE/USS (aorta, popliteal, femoral)
165
Q

What are the complications of ALI?

A
  • Extensive tissue death/necrosis if not treated <6 hrs
  • Gangrene - wet (clostridium - gram stain the pus/necrotic tissue/blood cultures - benzylpenicillin 2.4g/4 hr IV, clindamycin 600mg/6 hr IV, metronidazole 500mg/6-8 hrs IV - surgical debridement
  • Limb loss/amputation - from permanent muscle necrosis
  • Distal embolisation, metabolic - rhabdomyolysis, hyperkalaemia, ARF, sepsis
  • Post surgery - reperfusion injury, compartment syndrome
166
Q

What is the mortality of acute limb ischaemia?

A
  • 22% (amputation rate 16%)
167
Q

What are the preventative measures for peripheral arterial disease?

A
  • Advise and offer assistance to patients who smoke to stop smoking
  • Optimise management of comorbidities
  • Hypertension
  • Diabetes mellitus
  • Obesity
  • Exercise - NICE recommend a supervised exercise programme for all patients with peripheral arterial disease prior to other interventions
  • Medications
  • Statin 80mg Atorvastatin is recommended
  • Aim for cholesterol of <4-5, LDL <2-2.5 reduce risk of CVS by 33%
  • Clopidogrel first line anti-platelet
168
Q

What is superficial thrombophlebitis?

A
  • Inflammation and thrombosis of vein (can progress to DVT)
169
Q

What are the risk factors for superficial thrombophlebitis?

A
  • IV cannula
  • Varicose veins
  • IVDU
  • Previous thrombophlebitis/DVT
  • DVT risk factors
170
Q

What are the symptoms/signs of superficial thrombophlebitis?

A
  • Gradual onset tenderness over vein
  • Swelling, tenderness, redness
  • Red, tender, warm with a hard palpable vein/varicosity
171
Q

What are the differentials for a superficial thrombophlebitis?

A
  • DVT
  • Superficial migratory thrombophlebitis
  • Paraneoplastic of intra-abdominal malignancy (Trousseu’s sign)
172
Q

What is Trousseau’s sign?

A
  • Carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
  • Wrist flexion and fingers drawn together
173
Q

What are the investigations for superficial thrombophlebitis?

A
  • As per DVT if suspected DVT

* Compression Doppler USS to exclude DVT if suspected

174
Q

What is the approach to the management of superficial thrombophlebitis?

A
  • Conservative
  • Patient education - keep active, hot flannel over vein, raise the limb (reduce swelling)
  • Medical
  • Prophylaxis - remove and re-site the cannula, elevate limb, exercise, compression stockings
  • Medications - NSAID’s - ibuprofen 400mg/6hr po (max 2.4g/24hr), LMWH only if suspected DVT
175
Q

What are the risks of superficial thrombophlebitis?

A
  • Infection
  • DVT (extension)
  • PE
  • Malignancy/vasculitis - if recurs, superficial migratory thrombophlebitis
176
Q

What are the preventative measures for superficial thrombophlebitis?

A
  • Infection control guidelines - inspect the cannula sites daily
  • Look at cannula site
  • Cannula dressing - loose/contaminated - replace
  • Check it still flushes
  • Replace cannula every 72 hrs
  • VIP score (Visual Infusion Phlebitis)
177
Q

What is cannula related thrombophlebitis?

A
  • IV cannula incorrectly sited such that fluid/drugs leak into SC tissue cannot be infused/injected into vein
  • Or removable of cannula leads to phelebitis from drugs/infection etc
178
Q

What are the causes of cannula related thrombophlebitis?

A
  • Poor/non-sterile cannula insertion technique
179
Q

What are the symptoms/signs of cannula related thrombophlebitis?

A
  • Symptoms - pain, erythema, swelling

* Signs - pain, erythema, swelling, induration, palpable venous cord, pyrexia

180
Q

What can be used to assess for a manage cannula related thrombophlebitis?

A
  • Visual Infusion Phlebitis score
    0) IV site healthy, no phlebitis, observe cannula
    1) 1 of pain/erythema, possible phlebitis, observe cannula
    2) 2 of pain/erythema/swelling, early stages of phlebitis, re-site cannula
    3) All of pain along cannula path/erythema/induration, medium stage phlebitis, re-site cannula, consider treatment
    4) All 3 plus palpable venous cord, advance stage phlebitis/start of thrombophlebitis, re-site cannula, consider treatment
    5) All 4 plus pyrexia, advanced stage thrombophlebitis, initiate therapy, re-site cannula
181
Q

What are the differentials for cannula related thrombophlebitis?

A
  • Swelling/erythema
  • Angioedema
  • Cellulitis
  • Superficial thrombophlebitis
  • Gout
  • Lymphoedema
182
Q

If no improvement - what are the investigations for cannula related thrombophlebitis?

A
  • Blood cultures
  • USS of swelling to exclude collection
  • Swab for MC and S if purulent discharge/infection suspected
183
Q

What is the management of cannula related thrombophlebitis?

A
  • Conservative
  • Patient education - keep active, hot flannel over vein, raise thumb to reduce swelling
  • Medical
  • Prophylaxis - remove/re-site cannula if VIP >2 (ideally other arm)
  • Elevate affected limb
  • Medication - analgesia: NSAID’s (ibuprofen 400 mg/6 hrs po max 2.4g/24h)
  • Anti-biotics - if infection related VIP >3 flucloxacillin 250mg /6 hrs po
  • Surgical
  • Only if discussed with surgeons in light of USS
184
Q

What are the possible complications of cannula related thrombophlebitis?

A
  • Bruising
  • Infiltration
  • Extravasation
  • Superficial thrombophlebitis
  • Infection
185
Q

How can cannula related thrombophlebitis be prevented?

A
  • Inspect cannula sites daily
  • Look at cannula site
  • Check it still flushes
  • Replace cannula every 72 hrs
  • Monitor using VIP score
186
Q

What is heart block?

A
  • Atrioventricular block or heart block
  • Impaired electrical conduction between the atria and ventricles
  • 3 types of heart block 1st, 2nd, 3rd degree
187
Q

What are the features of 1st degree heart block?

A
  • PR interval >0.2 seconds (normal = <0.2 s (3-5 small squares))
  • Asymptomatic first degree heart block is relatively common and does not need treatment
188
Q

What are the features of 2nd degree heart block?

A
  • Type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
  • Type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
189
Q

What are the features of 3rd degree (complete) heart block?

A
  • No association between the P waves and QRS complexes
190
Q

What is a bundle branch block?

A
  • Partial conduction block below the bundle of his
191
Q

What is a bifasicular block?

A
  • RBBB plus L bundle hemi-block (L bundle has anterior/posterior fasicles)
192
Q

What is a trifasicular block?

A
  • Bifasicular block plus 1st degree heart block
193
Q

What are the causes of 1st/2nd degree heart block?

A
  • Variant
  • Athletes
  • Sick sinus syndrome
  • IHD
  • Acute carditis
  • Drugs (digoxin, beta-blockers)
194
Q

What are the causes of a 3rd degree (complete) heart block?

A
  • Idiopathic (fibrosis)
  • Congenital
  • IHD
  • Aortic valve calcification
  • Cardiac surgery/trauma
  • Drugs (digoxin toxicity, beta-blockers, CCB, amiodarone)
  • Infiltration (abscesses, granulomas, tumours, parasites)
  • Neuromuscular
195
Q

What are the causes of a RBBB?

A
  • Isolated RBBB
  • PE
  • Cor pulmonale
196
Q

What are the causes of a LBBB?

A
  • IHD
  • HTN
  • Cardiomyopathy
  • Idiopathic fibrosis
197
Q

What is the pathophysiology of heart block?

A
  • 1st: benign rhythm from delay in AVN/bundle of his conduction
  • 2nd: Mobitz II more serious than I
  • 3rd: ventricle usually develops escape rhythm at 30-40 bpm with wide QRS as ‘new’ pacemaker originates in ventricular tissue (takes longer to conduct through myocardium by myocyte-myocyte transmission rather than specialised conducting tissue
  • BBB wide QRS from delayed conduction
198
Q

What are the symptoms/signs of heart block?

A

Symptoms

  • Asymptomatic
  • Dizzy on standing
  • Palpitations
  • SOB +/- chest pain
  • Stokes-Adams attacks (LOC with 3rd)

Signs

  • Bradycardia
  • Raised JVP (cannon waves in 3rd)

Worrying signs in 3rd

  • Features of heart failure
  • Bradycardia
  • Hypotension
  • Reduced GCS
199
Q

What are the differential diagnoses for heart block?

A
  • Sinus bradycardia
  • MI
  • Drugs - digoxin, vasovagal, low T4, hypothermia, Cushing’s reflex, sleep, physical fitness
  • Others
  • Heart blocks
  • Rate controlled AF
  • Digoxin effect/toxicity
200
Q

What are the blood investigations for 3rd degree heart block?

A
  • FBC
  • Clotting screen if considering pacing
  • U and E
  • Cardiac markers
  • Digoxin level
201
Q

What are the special tests to investigate heart block?

A
  • ECG
  • 3rd - complete dissociation of P waves and QRS (narrow QRS: proximal lesion may respond to atropine, broad QRS: distal lesion, unlikely to respond), may be signs of MI
  • RBBB (MoRroW): QRS >0.12s, RSR in V1 (dominant R), inverted T waves in V1-V4, deep wide S wave in V6
  • Bifasicular block - RBBB plus LAD (if anterior hemiblock) RAD (if L posterior hemiblock)
  • LBBB (WiLliaM): QRS >0.12, notched R wave in V6, no septal Q waves, inverted T waves in I, aVL, V5-V6 (if LBBB - cannot comment on ST segment /T wave)
  • With pacemaker - fusion beat (combined native depolarisation and pacemaker impulse)
202
Q

What is the approach to the management of complete (3rd degree) heart block?

A
  • Call senior help and ARREST team
  • A - lay flat/legs elevated
  • B - 15L O2 via NRBM, SpO2, RR
  • C - HR, BP, JVP, ECG, defibrillator if dizzy/GCS <15/SBP <90, IV access for bloods
  • D - GCS
  • Titrate 500mg atropine IV every 2-3 mins (until HR improves max 3mg)
  • 20ml flush
  • Treat underlying cause
  • Consider pacing
203
Q

What are the indications for temporary pacing in heart block?

A
  • Sinus bradycardia
  • Post anterior MI (with 2/3 bi/trifasicular block), suppress drug resistant SVT/VT
  • Special situations - during cardiac surgery, GA, EPS, drug OD (digoxin, beta blocker, verapamil
204
Q

What are the indications for permanent pacemaker in heart block?

A
  • 3rd degree heart block
  • Mobitz II
  • Persistent AV block post MI
  • Sinus bradycardia (sick sinus syndrome)
  • Drug resistant SVT/VT
205
Q

What is the procedure for a pacemaker?

A
  • Pre-procedure
  • FBC, clotting, HBsAg
  • IV access
  • Consent for procedure under local anaesthetic
  • NBM from midnight in case GA needed
  • Consider pre-meds - prophylactic flucloxacillin and benzylpenicillin (20mins before and 1 and 6 h after)
  • Post procedure
  • Check wound
  • Chest x-ray (screen position/pneumothorax)
  • Check pace maker function/ECG
  • 1 week check for wound haematoma/dehiscence
  • Problems
  • Failure - if apical HR >6bpm
206
Q

What are the complications of heart block?

A
  • 3rd degree
  • Asystole risk
  • PEA (always check pulse)
  • Pacemaker syndrome (single chamber pacing)
  • Retro-grade conducation to atria (contract in ventricular systole, retrograde flow in pulmonary veins, reduced CO, SOB, palpitations, malaise, syncope
  • Pacemaker tachycardia (dual chamber)
  • Short circuit between electrodes
  • Artificial WPW - treatment - use single chamber pacing
207
Q

What are the DVLA rules relating to hypertension?

A
  • Can drive unless treatment causes unacceptable side affects, no need to notify DVLA
  • If group 2 entitlement - disqualifies from driving if resting BP consistently 180mmHg systolic or more and/or 100 mmHg diastolic or more
208
Q

What are the DVLA rules for driving after angioplasty (elective)?

A
  • 1 week off driving
209
Q

What are the DVLA rules for driving after CABG?

A
  • 4 weeks off driving
210
Q

What are the DVLA rules for driving after ACS?

A
  • 4 weeks off driving, 1 week if successfully treated by angioplasty
211
Q

What are the DVLA rules for driving after angina?

A
  • Driving must cease if symptoms occur at rest/at the wheel
212
Q

What are the DVLA rules for driving after pacemaker insertion?

A
  • 1 week off driving
213
Q

What are the DVLA rules for driving after implantable cardioverter-defibrillator (ICD)?

A
  • If implanted for sustained ventricular arrhythmia - cease driving for 6 months
  • If implanted prophylactically then cease driving for 1 month
  • Having an ICD results in permanent bar for Group 2 drivers
214
Q

What are the DVLA rules for driving after catheter ablation for an arrhythmia?

A
  • 2 days off driving
215
Q

What are the DVLA rules for driving with an aortic aneurysm?

A
  • 6cm or more - notify DVLA
  • Licensing will be permitted subject to annual review
  • Aortic diameter of 6.5cm or more disqualifies patients from driving
216
Q

What are the DVLA rules for driving after heart transplant?

A
  • Do not drive for 6 weeks

* No need to notify DVLA

217
Q

What is postural hypotension?

A
  • Defined as a fall of systolic BP >20 mmHg on standing
    or diastolic BP fall >10 mmHg on standing (or on sitting from lying if severe)
  • Important cause of falls in the elderly
218
Q

What are the causes of postural hypotension?

A
  • Hypovolaemia - dehydration, anaemia, vasovagal
  • Autonomic dysfunction: diabetes, Parkinson’s, multi-system atrophy, Guillain-Barr, syphilis, ageing
  • Drugs: diuretics, anti-hypertensives, L-dopa, phenothiazines, antidepressants, sedatives, antipsychotics
  • Alcohol
  • Endocrine - Addison’s, hypopituitarism (reduced ACTH)
219
Q

What is the pathophysiology of postural hypotension?

A
  • Autonomic nervous system
  • Fails to prevent hypotension on standing
  • Unlike neurocardiogenic syncope the BP start immediately on standing, not after a delay and there is never any absolute bradycardia
220
Q

What are the symptoms/signs of postural hypotension?

A
  • Symptoms
  • Unsteadiness/dizziness +/- LOC when standing, falls, collapse
  • Signs
  • SBP drop >20 or DBP drop >10 on standing for 3-5 mins
  • Measure BP in both arms lying and standing
221
Q

What are the differential diagnoses for postural hypotension?

A
  • Falls/collapse
  • Serious
  • MI
  • Arrhythmias
  • Shock
  • Sepsis
  • CVA
  • Seizure
  • Hypoglycaemia
  • Hypoxia
  • PE
  • Common
  • Postural hypotension
  • Mechanical fall e.g. tripping
  • Syncope (vasovagal, cardiac, neurological, situational, micturation/carotid sensitivity/cough
  • Ataxia
222
Q

What are the appropriate investigations for postural hypotension?

A
  • Investigate the cause of syncope/collapse

* Falls clinic - special equipment available to monitor patient under various tilts

223
Q

What is the conservative approach to managing postural hypotension?

A
  • Identify any precipitants
  • Medication review
  • Stop if possible or change
  • Optimise medical conditions
  • DM control, autonomic neuropathy
  • Lifestyle
  • Immediate - down if feeling faint, get out of chairs slowly, hold onto something on standing
  • Physical measures
  • Leg crossing, squatting, elastic abdo binders/graduated leg stockings to improve venous circulation (check DP pulse present), careful exercise
  • Diet
  • Eat little/more often (if post prandial dizziness)
  • Reduce carbohydrate/alcohol
  • Increase salt intake 150mmol Na+/day
  • Night time
  • Head raised in bed to increase renin release
  • Reduce fluid loss
  • Increase standing BP
  • Referral - falls clinic
224
Q

What is the medical approach to postural hypotension?

A
  • 1st line
  • Fludrocortisone up to 0.3 mg /24 h only if tolerated (retains fluid)
  • Monitor weight (caution in CCF/low albumin)
  • Worsens oedema/high BP
  • 2nd line
  • Sympathomimetics (midodrine/ephedrine)
  • Pyridostigmine (if detrusor under activity too)
  • Erythropeitin
  • 1/2 Cafergot suppository (caffeine 50 mg plus ergotamine 1mg)
  • Desmopressin
  • Octreotide
225
Q

What are the risks/complications of postural hypotension?

A
  • Falls - bone/soft tissue injury, intracranial bleed, fracture NOF

Y5 Cardiovascular System (3 decks)

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