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ZERO TO FINALS A.S. > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is atherosclerosis, what vessels does it affect and what causes it ?

A

A combination of atheromas (fatty deposits in artery walls) and sclerosis (the process of hardening or stiffening of the blood vessel walls). Atherosclerosis affects medium and large arteries. It is caused by chronic inflammation and activation of the immune system in the artery wall. This causes deposition of lipids in the artery wall followed by the development of fibrous atheromatous plaques.

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2
Q

What do atheromatous plaques cause (three things) ?

A
  • Stiffening of the artery walls leading to HTN and strain on the heart trying to pump blood against resistance
  • Stenosis of the artery leading to reduced blood flow (e.g. in angina)
  • Plaque rupture results in a thrombus that can block a distal vessel and cause ischaemia (e.g. a coronary syndrome where a coronary artery becomes blocked).
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3
Q

Name 3 non-modifiable RF’s of atherosclerosis ?

A

Age
Family History
Male sex

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4
Q

Name 7 modifiable RF’s of atherosclerosis ?

A

Smoking
Alcohol consumption
Poor diet (high sugar and trans-fat low in fruit and veg and omega 3)
Low exercise
Obesity
Poor sleep
Stress

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5
Q

Name 5 co-morbidities that increase risk of atherosclerosis ?

A

Diabetes
HTN
CKD
Inflammatory conditions such as RA
Atypical antipsychotic medications

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6
Q

Name 6 end results of atherosclerosis

A

Angina
MI
TIA
Strokes
PVD
Chronic mesenteric ischaemia

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7
Q

What is the difference between primary and secondary prevention of CVD?

A

Primary - for patients that have never had a CV event
Secondary - for patients that have developed angina, MI, TIA, stroke or PVD already.

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8
Q

What is meant by optimising modifiable risk factors in terms of preventing CVD (four points) ?

A

Advice on diet, exercise and weight loss
Stop smoking
Stop drinking alcohol
Optimise treatment of co-morbidites

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9
Q

As part of primary prevention a QRISK3 score should be performed. What is that?

A

Calculates the % risk that a pt will have a MI or stroke in the next ten years.

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10
Q

In regards to the QRISK3 score when should a statin be started? + What statin/dose?

A

When they have more than a 10% risk.
Atorvastatin 20mg at night.
NICE recommend that lipids are measured at 3 months incase the dose needs to be increased (aim of greater than 40% reduction in non-HDL cholesterol).
NICE also recommend that LFTS are checked at 3 and 12 months as they can cause a raise in AST and ALT (They don’t usually need to be stopped unless the rise is more than 3 times the upper normal limit).

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11
Q

What should patients with CKD or type 1 diabetes for more than 10 years be offered?

A

Atorvastatin 20mg OD

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12
Q

What are the four A’s of secondary prevention of CVD?

A 
Aspirin (plus a second antiplatelet such as clopidogrel for 12 months). 
Atorvastatin 80mg. 
Atenolol (or other B blocker - commonly bisoprolol) titrated to maximum tolerated dose. 
ACE inhibitor (commonly ramipril) titrated to maximum tolerated dose.
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13
Q

Name 3 notable side effects of statins?

A

Myopathy (check creatine kinase in patients with muscle pain or weakness)
Type 2 diabetes
Haemorrhagic stroke (very rarely)

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14
Q

What is angina?

A

The narrowing of the coronary arteries resulting in reduced blood flow to the myocardium. During times of high demand e.g. exercise, there is an insufficient supply blood to meet the demand. This causes the symptoms of angina, typically constricting chest pain +- radiation to the jaw or arms.

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15
Q

What is the difference between stable and unstable angina?

A

Stable - when symptoms are always relieved by rest or GTN spray
Unstable - when the symptoms come on randomly whilst at rest. It is a type of ACS.

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16
Q

What is the gold standard investigation for diagnosing angina?

A

CT coronary angiography

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17
Q

What 8 baseline investigations should patients with angina have ?

A

Physical exam (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to starting an ACEi and other medications)
LFTs (prior to starting statins)
Lipid profile
TFTs
HbA1C and fasting glucose (for diabetes)

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18
Q

What are the four principles of angina management ?

A

RAMP
Refer to cardiology (urgently if unstable)
Advise them about the diagnosis, management and when to call an ambulance
Medical treatment
Procedural or surgical interventions

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19
Q

What are the 3 aims to the medical management of angina ?

A

Immediate symptomatic relief
Long term symptomatic relief
Secondary prevention of CVD

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20
Q

Discuss the immediate symptomatic relief of angina ?

A

GTN spray is used prn
Causes vasodilation
Instruct patient to take GTN when symptoms start, then repeat after 5 mins if required. If there is still pain 5 minutes after the repeat dose - call an ambulance.

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21
Q

Long term symptomatic relief of angina ?

A

Use either or both if symptoms are not controlled on one:

  • B blocker (e.g. bisoprolol 5mg OD)
  • CCB (e.g. amlodipine 5mg OD)
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22
Q

What other options for the long term symptomatic relief of angina may be considered by a specialist ?

A

Long acting nitrates e.g. isosorbide mononitrate
Ivabradine
Nicorandil
Ranolazine

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23
Q

4 A’s of secondary prevention of angina ?

A

Aspirin (i.e. 75mg OD)
Atorvastatin 80mg OD
ACEi
Already on B blocker for symptomatic relief

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24
Q

What are the two main procedural/ surgical interventions of angina ?

A

PCI with coronary angioplasty
CABG

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25
Q

What is PCI with coronary angioplasty ?

A

PCI with coronary angioplasty is offered to all patients with proximal or extensive disease on CT coronary angiography. A catheter is inserted into the brachial or femoral artery which is fed up into the coronary arteries under X ray guidance. Contrast is used to see the areas of stenosis. This can be treated with balloon dilation followed by the insertion of a stent

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26
Q

What is a CABG ?

A

The chest is opened along the sternum. A graft vein is taken from the pts leg (usually great saphenous vein) and sewing it onto the affected coronary artery to bypass the stenosis.

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27
Q

What four areas does the RCA supply ?

A

Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area

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28
Q

What two areas does the circumflex artery supply?

A

Left atrium
Posterior aspect of left ventricle

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29
Q

What two areas does the LAD artery supply?

A

Anterior aspect of left ventricle
Anterior aspect of the septum

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30
Q

When a pt presents with possible ACS symptoms what should you do ?

A

Perform an ECG

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31
Q

What two ECG changes would indicate a STEMI ?

A

ST elevation in leads consistent with an area of ischaemia
or
New left BBB

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32
Q

What three ECG changes could indicate a NSTEMI ?

A

T wave inversion in a specific region
Pathological Q waves
ST depression - This suggests a deep infarct and is a late sign

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33
Q

If there are no ECG changes in someone with suspected ACS what else should you check

A

Troponin

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34
Q

Name six symptoms of ACS ?

A

N+V
Sweating and clamminess
Feelings of impending doom
Shortness of breath
Palpitations
Pain radiating to the jaw or arms

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35
Q

If someone has ACS how long should symptoms last for ?

A

Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina.

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36
Q

What type of patients may not experience typical chest pain during an acute coronary syndrome ?

A

Diabetic patients. They can experience a “silent MI”

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37
Q

Left coronary artery - heart area and leads?

A

Anterolateral
I, aVL, V3-6

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38
Q

LAD - heart area and leads?

A

Anterior
V1-4

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39
Q

Circumflex artery - heart area and leads?

A

Lateral
I, aVL, V5-6

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40
Q

RCA - heart area and leads?

A

Inferior
II, III, aVF

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41
Q

What are troponins ?

A

Proteins found in cardiac muscle

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42
Q

A diagnosis of ACS typically requires what ?

A

Serial troponins e.g. at baseline and 6 or 12 hours after the onset of symptoms

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43
Q

Why is a rise in troponin consistent with myocardial ischaemia ?

A

As troponin is released from ischaemic heart muscle

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44
Q

What is meant by troponins are non specific in relation to ACS ?

A

Raised troponin does not automatically mean ACS

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45
Q

Name five causes of raised troponins besides ACS ?

A

Chronic renal failure
Sepsis
Myocarditis
PE
Aortic dissection

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46
Q

In the event of an ACS you should perform all the normal investigations you would normally arrange for stable angina plus what three other investigations and why ?

A

Chest Xray - to investigate for pulmonary oedema and other causes of chest pain
Echocardiogram - after the event to assess the functional damage to the heart
CT coronary angiogram - to assess for coronary artery disease

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47
Q

Patients with a STEMI presenting within 12 hours of onset should be discussed urgently with the local cardiac centre for what two procedures?

+

Other management of STEMI and NSTEMI ?

A 
Primary PCI (if available within 2 hours of presentation) 
Thrombolysis (if PCI not available within 2 hours)
  • Immediate dual antiplatelet therapy (DAPT; aspirin plus Ticagrelor, Prasugrel, or Clopidogrel) and pain relief. Paramedics usually give the Aspirin and opiates. Oxygen should be avoided and nitrates are useless for MI.
  • Anticoagulation for 24-72hrs; Heparin, Fondapariux or similar
  • Both STEMI and NSTEMI should have angiography and if possible stenting; STEMI immediately, NSTEMI within 72hrs or sooner if complications
  • Secondary prevention; DAPT for a year then Aspirin alone, Statin, Betablocker for a year, ACE inhibitor, and treatment of any complication (heart failure, arrhythmia, etc).

Cardiac rehabilitation; exercise, education, diet, smoking cessation

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48
Q

What is thrombolysis and name some thrombolytic agents ?

A

It involves injecting a fibrinolytic medication that rapidly dissolves clots.

Examples = alteplase, streptokinase and tenecteplase

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49
Q

What is the treatment for an acute NSTEMI ?

A

BATMA

Beta blocker - unless contraindicated
Aspirin - 300mg stat dose
Ticagrelor - 180mg stat dose (clopidogrel 300mg is an alternative)
Morphine - titrate to control pain
Anticoagulant: LMWH at treatment dose

Give oxygen only if oxygen saturations are dropping (i.e. <95%)

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50
Q

What score is used to assess for PCI in NSTEMI ?

A

GRACE score

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51
Q

What does a GRACE score show ?

A

6 month risk of death or repeat MI after having an NSTEMI
<5% = low risk
5-10% = medium risk
>10% = high risk

If the patient is medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

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52
Q

Complications of MI ?

A

DREAD

Death
Rupture of the heart septum or papillary muscles
oEdema (heart failure)
Arrhythmia and aneurysms
Dressler’s syndrome

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53
Q

What is dresslers’s syndrome (post-myocardial infarction syndrome) ?

A

It usually occurs 2-3 wks following an MI. It is caused by a localised immune response and causes pericarditis .

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54
Q

How does dressler’s syndrome present and name two complications ?

A

Pleuritic chest pain, low grade fever and pericardial rub on auscultation

Pericardial effusion and rarely a pericardial tamponade

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55
Q

How can a diagnosis of dressler’s syndrome be made ?

A

ECG - global ST elevation and T wave inversion
Echocardiogram - pericardial effusion
Inflammatory markers - CRP, ESR

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56
Q

What is the management of dressler’s syndrome ?

A

NSAIDS (aspirin, ibuprofen)
In more severe cases - steroids (prednisolone)
Pt may need pericardiocentesis to remove fluid from around the heart

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57
Q

Secondary prevention medical management of MI ?

A

6 A’s

Aspirin 75mg OD
Another antiplatelet e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg OD
ACEi (e.g. ramipril titrated as tolerated to 10mg OD)
Atenolol (or other B blocker titrated as high as tolerated)
Aldosterone antagonist for those with CHF (i.e. eplerenone titrated to 50mg OD)

Dual antiplatelet therapy duration will vary following PCI procedures depending on the type of stent that was inserted

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58
Q

Secondary prevention lifestyle advice of MI ?

A

Stop smoking
Reduce alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions e.g. HTN, diabetes

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59
Q

What is acute left ventricular failure

A

When the left ventricle is unable to adequately move blood through the left side of the heart and out into the body.

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60
Q

What does acute LVF cause, how does this happen ?

A

Pulmonary oedema (when lung tissue and alveoli become full of interstitial fluid)

There is a backlog of blood from the left ventricle that increases the amount of blood in the LA, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid into the surrounding tissues and are unable to reabsorb it. This interferes with normal gas exchange in the lungs causing shortness of breath, reduced oxygen saturation and the other S+S.

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61
Q

Name four triggers for acute LVF ?

A

Iatrogenic (e.g. aggressive IV fluids in frail elderly pt with impaired LV function)
Sepsis
MI
Arrhythmias

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62
Q

How does acute LVF present and what type of respiratory failure does it cause ?

A

Rapid onset breathlessness. This is exacerbated by lying flat and improves on sitting up.

Type 1 respiratory failure

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63
Q

Three symptoms of acute LVF ?

A

SOB
Looking and feeling unwell
Cough with frothy white or pink sputum

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64
Q

What signs would you see on examination of acute LVF (six) ?

A

Increased RR
Decreased oxygen sats
Tachycardia
3rd heart sound
Bilateral basal crackles “sounding wet” on auscultation
Hypotension in severe cases (cardiogenic shock)

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65
Q

In someone presenting with acute LVF there may also be S+S relating to the underlying cause, name three examples ?

A

Chest pain in ACS
Fever in sepsis
Palpitations with arrhythmias

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66
Q

If a patient with acute LVF also has right sided HF what might you also find on examination ?

A

Raised JVP
Peripheral oedema in the ankles, legs and sacrum

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67
Q

Work up for acute LVF ?

A

History
Clinical exam
ECG - to look for ischaemia and arrhythmias
ABG
CXR
Routine bloods for infection, kidney function, BNP and consider troponin if suspect MI
Echocardiogram

If the clinical presentation is acute LVF then initiate treatment before having the diagnosis confirmed by BNP or echo. Pts can deteriorate quickly.

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68
Q

What is B-type natriuretic peptide (BNP) ?

A

A hormone that is released from the ventricles when the myocardium is stretched beyond normal range. A high BNP blood test result indicates that the heart is overloaded.

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69
Q

What is the action of BNP ?

A

It causes the smooth muscle in blood vessels to relax which reduces systemic vascular resistance. It also acts on the kidneys as a diuretic. Both of these effects make it easier for the heart to pump blood around the body.

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70
Q

Name five causes of a high blood BNP level other than HF ?

A

Tachycardia
Sepsis
PE
Renal impairment
COPD

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71
Q

Why is echocardiography useful in investigation acute LVF ?

A

It assesses the function of the LV and identifies any structural abnormalities in the heart. The mean measure of LV function is the ejection fraction. Above 50% is considered normal.

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72
Q

Cardiomegaly may be seen on the CXR of a pt with acute LVF, how is it defined ?

A

When the cardiothoracic ratio is more than 0.5 - when the diameter of the widest part of the heart is more than half the diamter of the widest part of the lung fields

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73
Q

Upper lobe venous diversion may also be seen on the CXR of a pt with acute LVF, what is that ?

A

Normally when stand erect the lower lobe veins contain a lot more blood than the upper lobes which remain relatively small. In LVF the backlog of blood causes the upper lobes to fill up and become engorged. This is visible as increased prominence and diameter of the upper lobe vessels on CXR.

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74
Q

Name 3 other CXR findings as a result of fluid leaking from oedematous lung tissue ?

A

Bilateral pleural effusions
Fluid in interlobar fissures
Fluid in the septal lines (Kerley lines)

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75
Q

Management of acute LVF ?

A

Pour SOD
Pour away (stop) their IV fluids
Sit up - sit the patient upright as gravity takes fluid in the lungs to the bases leaving the upper lungs clear for better gas exchange
Oxygen - if the pts sats are falling below 95%
Diuretics - e.g. IV furosemide 40mg stat

Also monitor fluid balance

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76
Q

Other management options to consider in severe acute pulmonary oedema or cardiogenic shock ?

A

IV opiates - opiates such as morphine act as vasodilators but are not routinely recommended
Non-invasive ventilation - Would try CPAP first. Then if this doesn’t work the pt may need full intubation and ventilation.
Inotropes - For example an infusion of noradrenalin. Inotropes strengthen the force of heart contractions and improve HF however they need close titration and monitoring so by this point you would need to send the pt to a the local coronary unit, high dependency unit or ICU.

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77
Q

What is chronic heart failure ?

A

Basically just the chronic version of acute heart failure. Is either caused by impaired LV contraction (systolic heart failure) or impaired LV relaxation (diastolic heart failure).

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78
Q

Key features that patients with CHF present with (five) ?

A
  • Breathlessness worsened by exertion
  • Cough. They may produce frothy white/ pink sputum.
  • Orthopnoea. This s the sensation of SOB when lying flat, relieves by sitting or standing. Ask them how many pillows they use at night.
  • Paroxysmal nocturnal dyspnoea
  • Peripheral oedema
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79
Q

What is PND ?

A

A term used to describe the experience that pts have of suddenly waking at night with a severe attack of SOB

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80
Q

Diagnosis of CHF ?

A

Clinical presentation
BNP blood test specifically the N-terminal pro-B-type natriuretic peptide (NT-proBNP)
Echocardiogram
ECG

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81
Q

Name 4 causes of CHF ?

A

Ischaemic heart disease
Valvular heart disease (commonly aortic stenosis)
HTN
Arrhythmias (commonly AF)

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82
Q

Overall management of CHF ?

A
  • Refer to specialist (NT-proBNP > 2000ng/litre warrans an urgent referral)
  • Careful discussion and explanation of the condition
  • Medical management
  • Surgical treatment in severe aortic stenosis or mitral regurgitation
  • HF specialist nurse input for advice and support

Additional information:

  • Yearly flu and pneumococcal vaccine
  • Stop smoking
  • Optimise treatment of co morbidities
  • Exercise as tolerated
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Not at all
2
3
4
5
Perfectly
83
Q

Medical treatment of CHF ?

A

(ABAL)
ACEi (e.g. ramipril titrated as tolerated up to 10mg OD)
B blocker (e.g. bisoprolol titrated as tolerated up to 10mg OD)
Aldosterone antagonist - when symptoms not controlled with A and B (spironolactone or epelerone)
Loop diuretics (e.g. furosemide 40mg OD)

Extra details on medical treatment:

  • An ARM can be used instead of ACEi if they are not tolerated e.g. candesartan
  • Avoid ACEi in patients with valvular heart disease until initiated by specialist
  • Pts should have their U&Es monitored closely whilst on diuretics, ACEi and aldosterone antagonists as all three medications can cause electrolyte disturbances.
84
Q

What is cor pulmonale ?

A

Right sided HF caused by respiratory disease. Pulmonary HTN results in the right ventricle not being able to pump blood out of the ventricle and into the pulmonary arteries due to the increased pressure and resistance. This leads to back pressure of blood in the right atrium, vena cava and the systemic venous system.

85
Q

Name 5 causes of cor pulmonale ?

A

COPD is the most common cause
PE
Interstitial lung disease
Cystic fibrosis
Primary pulmonary HTN

Note: Lung diseases that cause hypoxia over a long period of time can lead to cor pulmonale as hypoxia causes an increase in resistance in the pulmonary circulation leading to an increase in the pressure etc etc.

86
Q

Presentation of cor pulmonale ?

A

Often pts with early cor pulmonale are asymptomatic. The main PC is SOB. Unfortunately SOB is also caused by the chronic lung diseases that cause CP. Pts may also present with peripheral oedema, increased breathlessness on exertion, syncope or chest pain.

87
Q

Signs of cor pulmonale (7) ?

A

Hypoxia
Cyanosis
Raised JVP
Peripheral oedema
Third heart sound
Murmurs
Hepatomegaly

88
Q

Management of cor pulmonale ?

A

Involves treating the symptoms and the underlying cause. Long term oxygen therapy is often used.

89
Q

What is essential (primary) hypertension ?

A

HTN that has developed on its own without a secondary cause. Accounts for 95% of HTN.

90
Q

Secondary cause of HTN ?

A

ROPE
Renal disease - most common cause of secondary HTN. If the BP is very high or doesn’t respond to treatment consider renal artery stenosis.
Obesity
Pregnancy induced HTN/ pre-eclampsia
Endocrine - most endocrine conditions can cause HTN but primarily consider hyperaldosteronism (Conn’s syndrome). A simple test for this is a renin:aldosterone ratio blood test.

91
Q

Five complications of HTN ?

A

Ischaemic heart disease
Cerebrovascular accident i.e. stroke or haemorrhage
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure

92
Q

Diagnosis of HTN ?

A

Can be made based on several readings in the clinic, 24 hour ambulatory blood pressure or home readings.

The latest thinking is that home readings taken by the patient at different times throughout the day are the gold standard.

Stage 1 HTN, Clinic reading > 140/90, Home reading >135/85
Stage 2 HTN, Clinic reading > 160/100, Home reading >155/95

93
Q

Initial management of HTN ?

A

Investigate for possible causes and end organ damage.

Advice on lifestyle including diet, reducing salt intake to under 6g per day, stopping smoking and taking regular exercise

94
Q

Medical management of HTN

A

Step 1: Aged less than 55 and non-black use an ACEi. Aged over 55 or black use CCB.
Step 2: Non-black use A+C. If black then use ARB instead of ACEi.
Step 3: ACEi + CCB + Thiazide like diuretic
Step 4 : ACEi + CCB + Thiazide like diuretic + Diuretic

For step 4 if the serum potassium is more than 4.5 mmol/L then the added diuretic is a higher dose thiazide diuretic e.g. indapamide. If the serum potassium is below 4.5 then the added diuretic is a potassium sparring diuretic e.g. spironolactone (this is helpful when thiazide diuretics are causing hypokalaemia).

IMPORTANT: Monitor U&Es regularly when using ACEi + diuretic

95
Q

Treatment targets for HTN ?

A

< 80 years, systolic target < 140, diastolic target < 90
>80 years, systolic target < 150, diastolic target < 90

Note: These are likely to be lowered when the next set of guidelines are released. The last set for HTN was in 2011.

96
Q

Treatment for HTN in diabetic pts ?

A

First line treatment = ACEi in everyone except:

  • Women with child bearing potential = CCB
  • Black pts: ACEi + CCB
97
Q

What is a 3rd heart sound (S3) ?

A

Heard roughly 0.1 seconds after S2. Think of it as rapid ventricular filling causing the chordae tendineae to pull to their full length and twang like a guitar string. Can be normal in young healthy people (15-40) as the heart functions so well that the ventricles allow rapid filling. Can indicate HF in older patients as the ventricles and chordae are stiff and weak so they reach their limit much faster than normal. Picture tight hamstrings in an older pt sharply tightening as they start to bend over.

98
Q

What is a 4th heart sound (S4) ?

A

Always abnormal and rare to hear. It occurs just after atrial contraction and immediately before the systolic S1 and is caused by the atria contracting forcefully in an effort to overcome an abnormally stiff or hypertrophic ventricle.

99
Q

Which side of the stethoscope should you use for high and low pitched sounds ?

A 
Bell = low pitched (church bell) 
Diaphragm = high pitched
100
Q

What are the 4 valve areas + surface markings of each ?

A

Mitral - 5th ICS mid-clavicular line
Tricuspid - 5th ICS left sternal border
Pulmonary - 2nd ICS left sternal border
Aortic - 2nd ICS right sternal border

101
Q

Where is Erb’s point and what is it the best area for ?

A

3rd ICS left sternal border. Best area for listening to S1&S2.

102
Q

What special manoeuvres can be used to emphasise certain murmurs (say which murmurs) ?

A
  • Patient on their left hand side (mitral stenosis)
  • Patient sat up, leaning forward and holding exhalation (aortic regurgitation)
103
Q

Mnemonic for assessing a murmur ?

A

SCRIPT
Site - Where is the murmur the loudest?
Character - soft/blowing/crescendo/decrescendo/crescendo-decrescendo
Radiation
Intensity - What grade is the murmur?
Pitch
Timing - Is it systolic or diastolic?

104
Q

What are the murmur grades

A
  1. Difficult to hear
  2. Quiet
  3. Easy to hear
  4. Easy to hear with palpable thrill
  5. Can hear with stethoscope barely touching chest
  6. Can hear with stethoscope off the chest
105
Q

Script for describing a murmur ?

A

“This pt has a soft/harsh/blowing, Grade …, systolic/ diastolic murmur, heard loudest in the aortic/ mitral/ tricuspid/ pulmonary area, that does not/ radiates to the carotids/ left axilla. It is high/ low pitched and has a crescendo/ decrescendo/ c+d shape. This is suggestive of a diagnosis of mitral stenosis / aortic stenosis”

106
Q

Valvular heart disease can cause hypertrophy (thickening both outwards and into the chamber) or dilation (thinning and expanding) of the myocardium in different heart areas. This affects the chamber immediately before the pathological wave. Give 4 examples

A

Mitral stenosis causes left atrial hypertrophy
Aortic stenosis causes left ventricular hypertrophy

Mitral regurgitation causes left atrial dilation
Aortic regurgitation causes left ventricular dilation
(blood leaking back stretches the heart muscle resulting in dilation)

107
Q

2 causes of mitral stenosis ?

A

Rheumatic fever
Infective endocarditis

108
Q

Describe what you would hear upon auscultating someone with mitral stenosis ?

A
  • Mid-diastolic, low pitched “rumbling” murmur due to a low velocity of blood flow.
  • There will be a loud S1 due to the thick valves requiring a large systolic fore to shut, then shutting suddenly.
  • You can palpate a tapping apex beat, due to loud S1.
109
Q

2 conditions mitral stenosis is associated with?

A

Malar flush - due to the back-pressure of blood in the pulmonary system causing a rise in CO2 and vasodilation
AF - Due to the LA struggling to push blood through the stenotic mitral valve causing strain, electrical disruption and resulting fibrillation

110
Q

5 causes of mitral regurgitation ?

A
  • Idiopathic weakening of valve with age
  • Ischaemic heart disease
  • Infective endocarditis
  • Rheumatic fever
  • Connective tissue disorders such as Marfan syndrome or Ehlers Danlos syndrome
111
Q

Describe what you would hear upon auscultating someone with mitral regurgitation and what does it result in ?

A
  • Pan systolic, high pitched “whistling” murmur
  • The murmur radiates to the left axilla

It results in CCF because the leaking valve causes a reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart. Therefore you may hear a 3rd heart sound.

112
Q

2 causes of aortic stenosis ?

A
  • Age related idiopathic calcification
  • Rheumatic fever
113
Q

Describe what you would hear upon auscultating someone with aortic stenosis and can you name a couple of other signs of it ?

A
  • Ejection systolic, high pitched murmur
  • Crescendo-decrescendo character as blood flow is slowest at the start and end and fastest in the middle
  • Radiates to carotids
  • Slow rising pulse and narrow pulse pressure
  • Pts may complain of exertional syncope due to difficulty maintaining good flow to the brain
114
Q

2 causes of aortic regurgitation ?

A

Idiopathic age related weakness
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

115
Q

Describe what you would hear upon auscultating someone with aortic regurgitation and what other signs might be there ?

A
  • Early-diastolic, soft murmur
  • Is also associated with a Corrigan’s pulse (AKA collapsing pulse). A Corrigan’s pulse is a rapidly appearing and disappearing pulse at the carotids as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve an into the ventricles.
  • Can cause a “Austin-Flint” murmur. This is heard at the apex and is an early diastolic “rumbling” murmur due to blood flowing back through the aortic vlave and over the mitral valve causing it to vibrate.
116
Q

What does aortic regurgitation result in ?

A

Heart failure due to a back pressure of blood waiting to get through the left side of the heart.

117
Q

Pts that have had a valve replacement will have a scar. What is the most common scar and name a less common one too ?

A

Midline sternotomy
Lateral thoracotomy

118
Q

What are the two categories of valves and the lifespans of each ?

A

Bioprosthetic - Around ten years
Mechanic - Well over twenty years but require lifelong anticoagulation with warfarin. The INR target range with mechanical valves is 2.5 to 3.5.

119
Q

Three types of mechanic heart valve ?

A

Starr Edwards valve - no longer being implanted, high risk of thrombus formation
Tilting disc valve - single tilting disk
St Jude valve - two tilting metals discs, least risk of thrombus formation

120
Q

Three major complications from mechanical heart valves ?

A

Thrombus formation
Infective endocarditis (infection in prosthesis)
Haemolysis causing anaemia (as blood gets churned in the valve)

121
Q

Mechanical valves cause a click, which valves replace each heart sound ?

A

A click replaces S1 for metallic mitral valve
A click replaces S2 for metallic aortic valve

122
Q

What is transcatheter aortic valve implantation (TAVI) and what patients is it used for ?

A

A treatment for severe aortic stenosis. Usually in pts that are high risk for an open valve replacement operation. It involves local or general anaesthetic, inserting a catheter into the femoral artery and feeding a wire under Xray guidance to the location of their aortic valve, then inflating a balloon to stretch the stenosed aortic valve and implanting a bioprosthetic valve in the location of the aortic valve.

Open surgery is still the first line option for younger fitter pts.

123
Q

Do pts that have a TAVI typically require warfarin ?

A

Not typically as the valve is bioprosthetic.

124
Q

Pathophysiology of atrial fibrillation and name 4 effects ?

A

Disorganised electrical activity overrides the normal organised activity from the SA node meaning the contraction of the atria is uncoordinated, rapid and irregular. This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles resulting in:

  • Irregularly irregular ventricular contractions
  • Tachycardia
  • HF due to poor filling of the ventricles during diastole
  • Risk of stroke
125
Q

Why does AF increase stroke risk ?

A

There is a tendency for blood to collect in the atria and form blood clots. These can become emboli and travel to the brain and block cerebral arteries causing an ischaemic stroke.

126
Q

How does AF present, name four presenting symptoms ?

A

Patients are often asymptomatic and AF is incidentally picked when when attending for other reasons.

Presenting symptoms can be:

  • Palpitations
  • SOB
  • Syncope (dizziness or fainting)
  • Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
127
Q

What are the two differential diagnoses for an irregularly irregular pulse, how can they be differentiated (two ways) ?

A

AF and ventricular ectopics

Can be differentiated:

  • Using an ECG
  • Ventricular ectopics disappear when the heart rate gets over a certain threshold. Therefore a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.
128
Q

3 signs of AF on an ECG ?

A
  • Absent P waves
  • Narrow QRS complex tachycardia
  • Irregularly irregular ventricular rhythm
129
Q

Valvular AF ?

A

Pts with AF who also have moderate to severe mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology itself has lead to the AF.

130
Q

Non-valvular AF ?

A

AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis.

131
Q

Most common causes of AF ?

A

mrs SMITH
Sepsis
Mitral valve pathology (stenosis or regurgitation)
Ischaemic heart disease
Thyrotoxicosis
Hypertension

132
Q

Two principles to treating AF ?

A

Rate or rhythm control
Anticoagulation to prevent stroke

133
Q

What is the premise behind rate control of AF ?

A

In AF atrial contractions are not coordinated so the ventricles have to fill up by suction and gravity. This is considerably less efficient. The higher the HR the less time is available for the ventricles to fill with blood, reducing the cardiac output. The aim is to get the HR below 100 to extend the time during diastole when the ventricles can fill with blood.

134
Q

NICE guidelines (2014) suggests all patients with AF should have rate control as first line unless (four reason)?

A
  • Reversible causes for their AF
  • Their AF is of new onset (within the last 48 hours)
  • Their AF is causing heart failure
  • They remain symptomatic despite being effectively rate controlled
135
Q

Options for rate control (three) ?

A
  1. B blocker is the first line
  2. CCB (e.g. diltiazem, not preferable in HF)
  3. Digoxin (only in sedentary people. It needs monitoring and there is a risk of toxicity)
136
Q

Rhythm control can be offered to patients when ?

A
  • There is a reversible cause for their AF
  • Their AF is of new onset (within the last 48hrs)
  • Their AF is causing HF
  • They remain symptomatic despite being effectively rate controlled
137
Q

Aim of rhythm control of AF and how is this done ?

A

To return the pt to a normal sinus rhythm. This can be done through a single cardioversion event that puts the pt back into a normal sinus rhythm or long term medical rhythm control that sustains a normal rhythm.

138
Q

How would you decide between giving immediate cardioversion or delayed cardioversion to a candidate for rhythm control?

A
  • Immediate if the AF has been present for less than 48 hrs or they are severely haemodynamically unstable.
  • Delayed cardioversion if the AF has been present for more than 48 hrs and they are stable.
139
Q

In delayed cardioversion how long should pts be anticoagulated for, why and what else should they have whilst waiting for cardioversion?

A

A minimum of 3 wks prior to cardioversion.

Anticoagulation is essential because during the 48 hrs prior to cardioversion they may have developed a blood clot in the atria and reverting them back to sinus rhythm carries a high risk of mobilising that clot and causing a stroke. They should have RATE CONTROL whilst waiting for cardioversion.

140
Q

What’re the two options for cardioversion ?

A

Pharmacological or electrical

141
Q

First line drugs for pharmacological cardioversion of AF ?

A
  • Flecanide
  • Amiodarone (the drug of choice in pts with structural heart disease)
142
Q

What is electrical cardioversion ?

A

The aim is to rapidly shock the heart back into sinus rhythm. This involves sedation or a general anaesthetic and using a cardiac defibrillator machine to deliver controlled shocks in an attempt to restore sinus rhythm.

143
Q

Drugs used for long term medical rhythm control of AF ?

A
  • B blockers are first line for rhythm control
  • Dronedarone is second line for maintaining normal rhythm where pts have had successful cardioverison
  • Amiodarone is useful in pts with HF or LV dysfunction.
144
Q

What is paroxysmal AF and should these pts be anticoagulated ?

A

When the AF comes and goes in episode, usually not lasting more than 48hrs.

They should be anticoagulated on their CHADSVASc score like any other AF pt.

145
Q

What is the “pill in the pocket” approach for pts for paroxysmal AF and what conditions need to be met ?

A

This is where pts take a pill to terminate their AF only when they feel symptoms of AF starting. To be appropriate for this approach they need to have infrequent episodes without any underlying structural heart disease.

146
Q

Which drug is the usual treatment for a “pill in the pocket” approach for AF and when should you avoid this drug ?

A

Flecanide. Avoid in atrial flutter as it can cause 1:1 AV conduction and resulting in a significant tachycardia.

147
Q

Without anticoagulation pts with AF have around a 5% risk of stroke each year (depending on CHADSVASC score), what is the risk with anticoagulation ?

A

About 1-2%

148
Q

What is the INR ?

A

Is a calculation of how the prothrombin time of the pt compares with the prothrombin time of normal healthy adult. For example an INR of 2 indicates that the pt has a prothrombin time twice that of a normal healthy adult.

149
Q

Being started on warfarin is a reasonably large undertaking. It requires close monitoring of their INR and frequent dose adjustments to keep the INR in range. It is given once a day and usually at 6pm in hospital so that an INR can be obtained prior to the dose. What is the target INR for AF ?

A

2-3

150
Q

Which system metabolises warfarin in the liver ?

A

Cytochrome P450 system

151
Q

What needs to happen when starting new medications in a pt already on warfarin and why ?

A

INR needs close monitoring and the warfarin dose needs adjusting accordingly as the INR will be affected by other drugs that influence the activity of the P450 system such as antibiotics.

152
Q

What else can affect INR in a patient on warfarin ?

A
  • Many foods, particularly those that contain vitamin K such as leafy green vegetables
  • Those that affect P450 such as cranberry juice and alcohol
  • This means it is important to monitor INR more closely when the pt changes medications or their diet.
153
Q

What is the half life of warfarin and what can be using to reverse its effects ?

A
  • 1 to 3 days
  • Vitamin K
154
Q

NOvel AntiCoagulants (NOACS) or Direct acting Oral AntiCoagulants (DOACS) are currently on patent making them expensive. For example it costs £27 for apixaban versus £1 for warfarin per month. What offsets this cost ?

A

The cost of monitoring warfarin is much higher than apixaban. Also NOACS will be coming off patient over the next few years.

155
Q

Their is no way to reverse the effects of NOACS however they have a lower bleeding risk and relatively short half life compared to warfarin. Name 4 advantages of NOACS over warfarin ?

A
  • No monitoring is required
  • No major interaction problems
  • Equal or slightly better than warfarin at preventing strokes in AF
  • Equal or slightly less risk of bleeding than warfarin
156
Q

What tool is used for assessing whether a pt with AF should be started on anticoagulants ?

A

CHA2DS2VASc score

157
Q

What does the CHA2DS2VASc mnemonic stand for and when should anticoagulation be offered ?

A

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

1 : consider anticoagulation
>1 : offer anticoagulation

158
Q

What tool is used for establishing a patient’s risk of a major bleed whilst on anticoagulation or as a monitoring tool in patients with a high risk of bleeding + what does it stand for ?

A

HAS-BLED
H - Hypertension
A - Abnormal renal and liver function
S - Stroke
B - Bleeding
L - Labile INRs (whilst on warfarin)
E - Elderly
D - Drugs or alcohol

The easiest way to calculate the HAS-BLED score is with an online calculator that will provide a risk of bleeding based on their score.

159
Q

What are the two shockable and two non-shockable cardiac arrest rhythms ?

A

Shockable:

  • Ventricular fibrillation
  • Ventricular tachycardia

Non-shockable:

  • Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
  • Asystole (no significant electrical activity)
160
Q

Tachycardia treatment summary in an unstable patient ?

A
  • Consider up to 3 synchronised shocks
  • Consider an amiodarone infusion
161
Q

Tachycardia treatment summary in a stable patient ?

A

Narrow complex (QRS < 0.12s)

  • Atrial fibrillation - rate control with B blocker or diltiazem (CCB)
  • Atrial flutter control rate with a B blocker
  • Supraventricular tachycardias - treat with vagal manoeuvres and adenosine

Broad complex (QRS > 0.12s)

  • Ventricular tachycardia or unclear - amiodarone infusion
  • If known SVT with bundle branch block- treat as normal SVT
  • If irregular may be variation of AF - seek expert help
162
Q

What is atrial flutter ?

A

It is caused by a “re-entrant rhythm” in either atrium. This is where the electrical signal circulates in a self perpetuating loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300 bpm. The signal makes its way into the ventricles every second lap due to the long refractory period of the AV node, causing 150 bpm ventricular contraction. It gives the “sawtooth appearance” on the ECG with P wave after P wave.

163
Q

Name four conditions associated with atrial flutter ?

A
  • HTN
  • Ischaemic heart disease
  • Cardiomyopathy
  • Thyrotoxicosis
164
Q

Treatment of atrial flutter ?

A

Treatment is similar to AF:

  • Rate/rhythm control with B blockers or cardioversion
  • Treat the reversible underlying condition
  • Radiofrequency ablation of the re-entrant rhythm
  • Anticoagulation based on CHA2DS2VASc score
165
Q

What is a supraventricular tachycardia ?

A

They are caused by the electrical signal re-entering the atria from the ventricles. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in a fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

166
Q

What is paroxysmal SVT ?

A

Describes a situation where SVT reoccurs and remits in the same pt over time.

167
Q

What are the three main types of SVT ?

A
  • “AV nodal re-entrant tachycardia” is when the re-entry point is back through the AV node
  • “AV re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome)
  • “Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. The ectopic electrical activity causes an atrial rate of > 100bpm.
168
Q

Acute management of stable pts with SVT ?

A

When managing SVT take a stepwise approach trying each step to see whether it works before moving on. Make sure they are on continuous ECG monitorig.

  • Valsalva manoeuvre - ask the pt to blow hard against resistance, for example into a plastic syringe.
  • Carotid sinus massage - massage the carotid on one side gently with two fingers
  • Adenosine
  • An alternative to adenosine is verapamil
  • Direct current cardioversion may be required if the treatment above fails
169
Q

What is adenosine ?

A

It works by slowing cardiac conduction primarily through the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm.

170
Q

How is adenosine given ?

A

It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway .

171
Q

Why can adenosine be scary for pts and/or doctors ?

A

It will often cause a brief period of asystole or bradycardia however it is quickly metabolised and sinus rhythm should return.

172
Q

Key points on administering adenosine (four) ?

A
  • Avoid if patient has asthma, COPD, heart failure, heart block or severe hypotension
  • Warn the pt about the scary feeling of dying or impending doom when injected
  • Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)
  • Initially 6mg, then 12mg and further 12mg if no improvement between doses.
173
Q

Long term management of pts with paroxysmal SVT ?

A

Options are:

  • Medication (B blockers, CCB, amiodarone)
  • Radiofrequency ablation
174
Q

What is Wolff-Parkinson-White syndrome ?

A

Caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the AV node. The extra pathway that is present in WPW syndrome is often called the Bundle of Kent.

175
Q

Definitive treatment of WPW syndrome ?

A

Radiofrequency ablation of the accessory pathway

176
Q

ECG changes seen on someone with WPW syndrome (three) ?

A
  • Short PR interval (<0.12 seconds)
  • Wide QRS complex (>0.12 seconds)
  • “Delta wave” (a slurred upstroke on the QRS complex).
177
Q

Most antiarrhythmic medications are contraindicated in pts with WPW that develop AF or atrial flutter, why is this ?

A

If a pt has a combination of AF or atrial flutter and WPW there is a risk that the chaotic electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia. Most antiarrhythmic medications increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway.

178
Q

What is radiofrequency ablation ?

A

Catheter ablation is performed in an electrophysiology laboratory, often called a “cath lab”. It involves local or general anaesthetic, inserting a catheter into the femoral veins and feeding a wire through the venous system under Xray guidance to the heart. Once in the heart it is placed against different areas to test the electrical signals at that point to try and find the location of any abnormal electrical pathways. The operator may try and induce the arrhythmia to make the abnormal pathway easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity

179
Q

Radiofrequency ablation can be curative for certain cases of arrhythmia caused by abnormal electrical pathways including what diseases ? (name four)

A
  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardias
  • WPW syndrome
180
Q

What is torsades de pointes ?

A

It is a type of polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”, describing the ECG characteristics. It looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes get progressively smaller than larger then smaller and so on. It occurs in pts with a prolonged QT interval which is an ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction. Waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of the heart myocytes. These abnormal spontaneous depolarisations prior to repolarisation are known as “afterdepolarisations”. These afterdepolarisations spread throughout the ventricles leading to a ventricular contraction prior to proper repolarisation occurring. When this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation it is called torsades de pointes.

When a pt develops torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest

181
Q

Causes of prolonged QT ?

A
  • Long QT syndrome (inherited)
  • Medications such as antipsychotics, citalopram, flecanide , sotalol, amiodarone and macrolide antibiotics
  • Electrolyte disturbances such as hypokalaemia, hypomagnesaemia and hypocalcaemia
182
Q

Acute management of Torsades de Pointes ?

A
  • Correct the cause (electrolyte disturbances or medications)
  • Magnesium infusion (even if they have a normal magnesium)
  • Defibrillation if VT occurs
183
Q

Long term management of prolonged QT syndrome (four points) ?

A
  • Avoid medications that prolong the QT interval
  • Correct electroyte disturbances
  • B blockers (not sotalol)
  • Pacemaker or implantable defibrillator
184
Q

What are ventricular ectopics ?

A

Premature ventricular beats caused by random electrical discharges from outside the atria. Pts often present complaining of random brief palpitations (“an abnormal beat”).

185
Q

How common are ventricular ectopics ?

A

They are relatively common at all ages and in healthy pts however they are more common in pts with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure)

186
Q

How can ventricular ectopics be diagnosed ?

A

On an ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG

187
Q

What is bigeminy ?

A

This is where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.

188
Q

Management of ventricular ectopics (3 bullet points) ?

A
  • Check bloods for anaemia, electrolyte disturbances and thyroid abnormalities
  • Reassurance and no treatment in otherwise healthy people
  • Seek expert advice in pts with background heart conditions or other concerning features or findings such as chest pain, syncope, murmur or family history of sudden death
189
Q

What is a first degree heart block + what ECG changes would you see ?

A

It’s when there is delayed atrioventricular conduction through the AV node. Despite this every atrial impulse leads to a ventricular contraction, meaning every p waves results in a QRS complex. On an ECG this presents as a PR interval greater than 0.2 seconds (5 small or 1 big square)

190
Q

What is a second degree heart block ?

A

It’s when some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes.

There are three patterns of second degree heart block:

  • Wenckebach’s phenomenon (Mobitz Type 1)
  • Mobitz Type 2
  • 2:1 Block
191
Q

What is Wenckebach’s phenomenon (Mobitz Type 1) + what ECG changes would you see ?

A

This is where the atrial impulses become gradually weaker until they don’t pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats.

On an ECG this will appear as an increasing PR interval until the P wave no longer conducts to the ventricles. This culminates in an absent QRS complex after a p wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle then repeats itself.

192
Q

What is Mobitz type 2 + what ECG changes would you see ?

A

This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of p waves to QRS complexes, for example 3 p waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal. There is a risk of asystole with Mobitz Type 2.

193
Q

What is a 2:1 block ?

A

This is where there 2 p waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. This can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which.

194
Q

What is a Third Degree Heart Block ?

A

This is referred to as a complete heart block. There is no observable relationship between p waves and QRS complexes. There is a significant risk of aystole.

195
Q

Treatment for bradycardias and AV node blocks if pt stable ?

A

Observe

196
Q

Treatment for bradycardias and AV node blocks if pt unstable or risk of aystole ?

A

Fist line:
-Atropine 500mcg IV

No improvement:

  • Atropine 500mcg IV (repeated up to 6 doses for a total to 3mg)
  • Other inotropes (such as noradrenalin)
  • Transcutaneous cardiac pacing (using a defibrillator)
197
Q

Treatment for bradycardias and AV node blocks in pts with high risk of aystole ?

A
  • Temporary transvenous cardiac pacing - using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
  • Permanent implantable pacemaker - when available
198
Q

What type of medication is atropine and name 4 side effects ?

A

It is an antimuscarinic medication that works by inhibiting the parasympathetic nervous system.

  • Pupil dilation
  • Urinary retention
  • Dry eyes
  • Constipation
199
Q

What are pacemakers ?

A

They deliver controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve the heart function. They consist of a pulse generator (the little pacemaker box) and pacing leads that carry electrical impulses to the relevant part of the heart. The box is implanted under the skin (most commonly the left anterior chest wall or axilla) and the wires are implanted into the relevant chambers of the heart.

Modern pacemakers have a computer that monitors the natural electrical activity and tailors its function to that. Basically if it is already working perfectly, no intervention is provided by the pacemaker. The batteries last around 5 years.

200
Q

Do pacemakers interact with day to day electrical activities and what may they be a contraindication for ?

A

In short no. They may be a contraindication for MRI (due to powerful magnets) and electrical interventions such as TENS machines and diathermy in surgery. Many modern pacemakers are MRI compatible.

201
Q

What is one of the most important tasks on a cremation form regarding pacemakers ?

A

Pacemakers need to be removed prior to cremation. They can cause significant damage if burned.

202
Q

5 indications for a pacemaker?

A
  • Symptomatic bradycardias
  • Mobitz type 2 AV block
  • Third degree heart block
  • Severe heart failure (biventricular pacemakers)
  • Hypertrophic obstructive cardiomyopathy (ICDs)
203
Q

What is a single-chamber pacemaker ?

A

They have leads in a single chamber either the RA or the RV. They are placed in the RA if the AV conduction in the pt is normal and the issue is with the SA node. This way they stimulate depolarisation in the RA and this electrical activity then passes to the LA and through the AV node to the ventricles in the normal way. They are placed in the right ventricle if the AV conduction in the pt is abnormal and they stimulate the ventricles directly.

204
Q

What is a dual-chamber pacemaker ?

A

They have leads in both the RA and RV. This allows the pacemaker to synchronise the contractions of both the atria and ventricles

205
Q

What is a biventricular (triple-chamber) pacemaker ?

A

They have leads in the RA, RV and LV. These are usually in pts with HF. The objective is to synchronise the contractions in these chambers to try to optimise heart function. They are also called cardiac resynchronisation therapy (CRT) pacemakers.

206
Q

What are implantable cardiac defibrillators (ICDs) ?

A

They continually monitor the heart and apply a defibrillator shock to cardiovert the pt back into sinus rhythm if they identify a shockable arrhythmia.

207
Q

What ECG changes would you see with single-chamber and dual chamber pacemakers ?

A

The pacemaker intervention can be seen as a sharp vertical line on all leads of the ECG trace. A line before the p wave indicates a lead in the atria. A line before each QRS complex indicates a lead in the ventricles.

Therefore:

  • A line before either the P or QRS but not the other indicates a single-chamber pacemaker
  • A line before both the P and QRS indicates a dual-chamber pacemaker.

ZERO TO FINALS A.S. (13 decks)

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