Cardiology Flashcards

1
Q

Outline the two main disease processes involved in atherosclerosis? (2)

A
  • Atheromatous plaque formation
  • Scarring and stiffenening of the aterial walls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between atherosclerosis and arteriosclerosis

A
  • Atherosclerosis affects the large and medium-sized arteries
  • Arteriosclerosis affects the smaller arterioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three main components to the aetiology of atherosclerosis

A
  • Endothelial damage
  • Chronic inflammation
  • Activation of the immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three main outcomes of untreated atherosclerosis

A
  • Stiffening of the vessels walls leading to hypertension
  • Stenosis of the vessel walls causing stable angina and/or periperal vascular disease
  • Plaque rupture leading to thrombus formation and the development of an acute coronary syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the non-modifiable risk factors of cardiovascular disease

A
  • Age
  • Family history
  • Male sex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the modifiable risk factors for cardiovascular disease

A
  • Smoking
  • Alcohol consumption
  • Poor diet
  • Lack of exercise
  • Poor sleep
  • Stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which co-morbidities can increase the risk of developing cardiovascular disease

A
  • Diabetes (both T1DM and T2DM)
  • Hypertension
  • CKD
  • Inflammatory conditions (RA)
  • Atypical antipsycotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which conditions can cardiovascular disease lead to if left untreated

A
  • Stable angina
  • Acute coronary syndromes (unstable angina, STEMI and NSTEMI)
  • Stroke
  • Transient ischaemic attack
  • Peripheral vascular disease
  • Chronic mesenteric ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the first port-of-call in the prevention of a patient developing cardiovascular disease

A

Optimise the modifiable risk factors

  • Inform patient about diet, excercise, smoking etc.
  • Optimise treatment for underlying co-morbidities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between primary and secondary prevention of cardiovascular disease

A

Primary prevention - prevents CVD from developing in the first instance

Secondary prevention - prevents reoccurance and/or progression of cardiovascular disease following and ischaemic event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most important step in the primary prevention of cardiovascular disease

A

Perform a Q-RISK3 score - a prediction of the likelihood of an ischaemic event over the next 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

If a patients’ Q-RISK3 score is greater than 10, what does this mean

A

This means that there is a greater that 10% chance of the patient having an ischaemic event over the next 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

If a patients’ Q-RISK3 score is greater than 10, what primary prevention is indicated

A

Q-RISK3 >10; commence atorvastatin (20mg) taken once a day at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What dose of statin is indicated in the primary prevention of a patient with a Q-RISK3 score greater than 10?

A

20mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is the primary prevention of cardiovascular disease treatment different in patients with CKD or T1DM lasting greater than 10 years?

A

These patients should be started on atorvastatin 20mg regardless of Q-RISK3 score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the aim of statin treatment in the primary prevention of cardiovascular disease

A

To reduce non-HDL cholesterol by 40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What monitoring is required in patients treated with a statin in the primary prevention of cardiovascular disease

A

3 monthly lipid profiling to ensure that a 40% reduction is acheived

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the mainstay treatments given in the secondary prevention of cardiovascular disease

A

The Four A’s

  • Aspirin
  • Atorvastatin
  • Atenolol (or bisoprolol)
  • ACE-I (usually ramipril)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the treatment dose of statin given to patients in the secondary prevention of cardiovascular disease

A

80mg (this is compared to 20mg in primary prevention)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the main side effects of statins?

A
  • Myopathy
  • T2DM
  • Haemorrhagic stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

A patient on statins presents with muscle ache and pains as well as weakness. What investigation should be carried out?

A

Creatine kinase blood test to look for rhabdomyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is meant by angina?

A

Angina refers to cardiac-related chest pain that occurs as a result of a narrowing of the coronary arteries that reduces the blood and oxygen supply to the myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the difference between stable and unstable angina?

A

Stable angina - cardiac chest pain that only presents on exertion and which are relieved by GTN

Unstable angina - cardiac chest pain that presents spontaneously at rest and occurs as a result of atheromatous plaque rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the symptoms of angina

A

Constricting chest pain +/- radiation to the jaw/left arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the gold standard investigation for angina
CT coronary angiography
26
What investigations are most appropriate when investigating angina
- Physical exam - ECG; looking for old ischaemic changes, rule out PE and other causes of chest pain - FBC; looking for signs of anaemia - U&Es; indicating renal function prior to commencing ACE-I - LFTs; indicating liver function prior to commencing statin - Lipid profile; indicating modifiable risk factors and potential benefits of statin therapy - TFTs; hypo- and/or hyperthyroidism can be related to angina - HbA1C; looking for diabetes which is an optimisible disease risk factor
27
Outline the management techniques for angina
" **_R_eferra**l – to cardiology **_A_dvice** – advise patient about diagnosis, management and when to **_M_edical treatment** – symptomatic relief and secondary prevention of subsequent cardiovascular disease **_P_rocedural/surgical treatment –** either PCI or CABG "
28
What are the three main aims in the medical management of angina
- Immediate symptomatic relief - Further symptomatic prevention - Secondary prevention - Procedural/surgical intervention
29
Outline the immediate symptomatic relief strategies in the treatment of angina
GTN Spray - GTN + Rest (5mins) - No symptomatic relief --\> repeat - Still no pain relief after repeat --\> ambulance
30
Outline the further symptomatic prevention strategies in the treatment of angina
"- **β-blocker** (bisoprolol or atenolol, 5mg) **_OR_** **Ca2+ channel blocker** (amlodipine, 5mg) - Combine **β-blocker _AND_ CCB** if symptoms persist - Further persistance o Long-acting nitrates - **isosorbide mononitrate** o Funny current (If) blockers - **ivabradine** o K+ channel activators - **nicorandil** (also NO donor) o Late Na+ current blockers - **ranolazine** "
31
Outline the secondary prevention strategies in the treatment of angina
" **The Four A’s** - Aspirin (75mg) - Atorvastatin (80mg) - Atenolol (or bisoprolol) - ACE-I (usually ramipril) "
32
What are the two options for procedural/surgical intervention in the treatment of angina
- Percutaneous coronary intervention (PCI) with coronary angioplasty - Coronary artery bypass grafting (CABG)
33
When is PCI considered in patients with angina?
Offered to patients with proximal (left main stem) or extensive disease indicated by the CTCA
34
When is CABG considered in patients with angina?
Offered to patients with extremely severe stenosis
35
What is the acute cause of an acute coronary syndrome
Thrombus formation usually as a result of atheromatous plaque rupture
36
What are the key types of acute coronary syndrome
- Unstable angina - NSTEMI - STEMI
37
Why are thrombi that occur in acute coronary syndromes treated differently to those that occur in DVT or PE?
- **Thrombi** that occur in fast flowing **arterial vessels** consist mostly of **platelets** and are as such treated with **anti**_platelets_**** (DAPT; aspirin + ticagrelor/prasugrel/clopidogrel) - **Thrombi** that occur in slower flowing **venous vessels** consist mostly of **fibrin**, hence are treated with **anti**_coagulants_**** (clotbusters, DOACs, LMWH and Vitamin K antagonists)
38
Which areas of the heart are supplied by the right coronary artery (RCA)
- Right atrium - Right ventricle - Inferior aspect of left ventricle - Posterior septal area
39
Which areas of the heart are supplied by the circumflex artery?
- Left atrium - Posterior aspect of left ventricle
40
Which areas of the heart are supplied by the left anterior descending artery (LAD)?
- Anterior aspect of left ventricle - Anterior aspect of septum
41
What is the first port-of-call in the diagnosis of a patient presenting with the symtoms of an acute coronary syndrome?
Perform an ECG and look for new ischaemic changes
42
How is a STEMI diagnosed from an ECG
" * *_Primary Features;_** - ST segment elevation - New LBBB (left axis deviation, QRS \> 0.12s, W/negative deflection in V1, M/positive deflection in V6) **Secondary Features** - (may be present alongside primary features, if in isolation, consider NSTEMI) - ST depression (reciprocal changes) - T wave inversion "
43
What is the definition of a STEMI?
- ST elevation - New LBBB
44
If an ECG carried out on a patient with symptoms of an acute coronary syndrome reveals no ST elevation and/or new LBB, what is the next appropriate investigation?
Perform troponin blood test
45
What is the definition of NSTEMI
- No ST elevation - Raised troponin - AND/OR other ischaemic ECG changes (ST depression, T wave inversion or pathological Q waves)
46
If troponin levels are normal and there are no pathological changes on the ECG of a patient presenting with the symptoms of an ACS, what are the likely diagnoses
- Unstable angina - Musculoskeletal chest pain (costochrondritis, pectoralis tear etc.)
47
What are the symptoms of an acute coronary syndrome
**Central, constricting chest pain** that may be **associated** with - Nausea/vomiting - Sweating and clamminess - Sense of impending doom - SOB - Palpitations - Pain radiating to jaw or arms
48
What features of the symptoms of ACS are important in order to diagnose ACS?
**- Duration**; must persist for longer than 20mins **- Relief**; not relieved by GTN and/or rest
49
What is meant by a silent MI
This occurs in diabetic patients where peripheral neuropathy prevents the patient from experiencing the classical chest pain associated with an acute coronary syndrome
50
What ischaemic ECG changes are important to look out for in NSTEMI
- ST depression - T wave inversion - Pathological Q waves
51
When using troponin blood tests to diagnose acute coronary syndromes, what do we need to ensure
**Multiple troponins have been carried out** - Baseline on admission/indication - + 6hrs after symptoms developed - + 12hrs after symptoms developed
52
What can be said about the specificity and sensitivity of troponin blood tests
- Highly sensitive - hence accurate in detecting raised levels - Highly non-specific - hence raised troponins does NOT confirm ACS
53
What are the non-ACS causes of myocardial ischaemia and hence raised troponin levels
- Chronal renal failure - Sepsis - Myocarditis - Aortic dissection - Pulmonary embolism
54
What investigations should be carried out in a patient suspected to be suffering from an acute coronary syndrome
- Physical exam - ECG - FBC - U&Es - LFTs - Lipid profiling - TFTs - HbA1C
55
What imaging should be carried out for patients suspected of suffering from an acute coronary syndrome
- CXR; to assess for non-cardiac causes - Echocardiogram; after the event to assess functional damage - CT coronary angiogram; to assess for coronary artery disease
56
What are the two key treatment options in patients presenting with STEMI and under what conditions should these be used?
- Primary Percutaneous Coronary Intervetnion (PCI) - if available within two hours of presentation - Thrombolysis - if PCI not available within two hours of presentation
57
Outline the steps of PCI used in the treatment of STEMI
- Catheter inserted into femoral/brachial artery - Guided up to coronary arteries under X-ray - Contrast injected to identify occlusion - Balloon inflated to widen the vessel and/or clot aspirated - Stent inserted to maintain open vessel - Drugs may be eluted to prevent restenosis
58
Outline the treament options for thrombolysis in patients presenting with a STEMI where PCI is not available within 2hrs
- Streptokinase - Alteplase - Tenecteplase
59
What is the acute treatments used for patients presenting with an NSTEMI
"**_(O)BATMAN_** - **_B_eta blocker** (atenolol or bisoprolol) unless contraindicated (asthma, CCF, pregnancy) - ****_A_**spirin 300mg** stat dose - ****_T_**icagrelor 180mg** (or clopidogrel 300mg) - ****_M_**orphine** (titrated up to control pain) - ****_A_**nticoagulant;** LMWH such as **enoxaparin** **1mg/kg** twice daily for 2-8 days (or tinzaparin/dalteparin) - **_N_**itrates (GTN); to relieve CA spasm **NB**: Consider **O2 therapy if SpO2\< 95%** "
60
What tool can be used to assess the need for PCI in NSTEMI
**GRACE Score** - gives a 6 month risk of death or repeat MI after having and NSTEMI
61
How can the GRACE score be used to guide PCI options in patients with NSTEMI
**_GRACE Score;_** - \<5% - Low Risk - no need for PCI - 5-10% - Medium Risk - consider PCI - \>10% - High Risk - proceed with PCI within four days
62
What are the potential complications of MI?
"**_DREAD;_** - ****_D_**eath** - ****_R_**upture** of heart septum/papillary muscle - ****_E_**dema** secondary to heart failure - ****_A_**rrhythmia** and aneurism - ****_D_**ressler's** syndrome "
63
What is Dressler's syndrome?
- Also known as post-MI syndrome - Occurs 2-3 weeks after MI - Localised immune response - Causes **pericarditis** - Pleuritic chest pain, pericardial rub - Can cause pericardial effusion and pericardial tamponade
64
How can Dressler's syndrome be diagnosed
- ECG changes; **global ST elevation**, T wave inversion - Echocardiogram; reduced ejection fraction from effusion/tamponade - Raised inflammatory markers; CRP and ESR
65
How can Dressler's syndrome be managed
- NSAIDs; aspirin or ibuprofen - Steroids; prednisolone (more severe cases) - Pericardiocentesis
66
Outline the medical management used in the secondary prevention of MI
"**_The Six A's_** (not to be confused with the four A's for CVD) - **_A_spirin 75mg**; once daily - ****_A_**ntiplatelet**; clopidogrel/ticagrelor for up to **12 months** - ****_A_**tenolol** (or bisoprolol); dose titrated as **high as tolerated** - ****_A_**torvostatin 80mg**; once daily - ****_A_**CE Inhibitor** (ramipril); titrated **upto 10mg** once daily - ****_A_**ldosterone Antagonist** (**eplerenone**); used in **patients** in **heart failure** secondary to the MI, titrated up to **50mg** once daily "
67
Outline the lifestyle management used in the secondary prevention of MI
- Smoking cessation - Reduced EtOH consumption - Mediterranean diet - Cardiac rehabilitation; specific cardiac exercise regimes - Optimisation of other medical conditions; DM and HTN
68
What are the different classifications of MI
Type 1 **-** **traditional** MI due to an acute coronary event Type 2 **-** ischaemia **secondary** to increased demand or **reduced supply of oxygen** (e.g. secondary to severe anaemia, tachycardia or hypotension) Type 3 **-** **sudden cardiac death** or cardiac arrest suggestive of an ischaemic event Type 4 **-** MI **associated** with **PCI/coronary stunting/CABG**
69
What is meant by acute left ventricular failure (LVF)?
Acute LVF occurs when the left ventricular is unable to adequately move blood through the left side of the heart causing a backlog
70
What is the result of acute LVF
Backlog of blood into the left atrium, pulmonary veins and lungs leading to subsequent pulmonary oedema
71
What happens as a result of pulmonary oedema
- Impaired gas exchange - Decreased SpO2 - SOB
72
Outline some of the causes of acute left ventricular failure?
" * *_AIMS;_** - **_I_atrogenic**; due to fluid overload from IVF administration in elderly patients - ****_S_**epsis** - ****_M_**I** - ****_A_**rrhythmias** "
73
What is the typical presentation of acute LVF?
- Rapid onset breathlessness - Type 1 respiratory failure (**PaO2 \< 8kPa** with normal or low PaCO2) - SOB - Looking and feeling unwell - Cough; frothy, white/pink sputum
74
What signs should be looked for when examining a patient in acute LVF?
* *_Primary Features;_** - Increased respiratory rate - Reduced SpO2 - Tachycardia - 3rd Heart Sound (S3) - Bibasal crackles on auscultation - Hypotension in severe cases (cardiogenic shock) **_Secondary Features (underlying cause);_** - Chest pain --\> ACS - Fever --\> sepsis - Palpitations --\> arrhythmia
75
What clinical signs may be seen in acute LVF that has backed up and caused right sided heart failure?
- Raised JVP - Peripheral oedema
76
What should be considered first when reviewing a patient that has suddenly begun to desaturate
- Assess fluid balance - Likely fluid overload - Renal function (CKD/AKI)
77
What investigations should be carried out in a patient expected of being in acute LVF?
- History - Clinical exam - ECG; looking for arrhythmia/ischaemia as underlying cause - **Echocardiogram** - ABG; looking for type 1 respiratory failure or raised lactate in sepsis - CXR; looking for pulmonary oedema and to assess for cardiomegaly - Bloods; FBC, CRP, U&Es - Special Tests; **B-type natriuretic peptide** (BNP) and/or troponin if MI suspected
78
When shoudl treatment be initiated in a patient presenting with signs of acute LVF?
**Commence treatment before diagnosis confirmed** with echocardiogram or BNP (i.e. as soon as acute LVF suspected)
79
What can be said about the sensitivity and specificity of B-type natriuretic peptide (BNP) testing?
- Highly **sensitive**; hence if **not raised**, acute **LVF** can be **ruled out** - Highly **non-specific**; hence **if raised**, acute **LVF** can**not** be **ruled out**, however other causes need to be investigated
80
Other than acute LVF, what else can cause raised BNP levels?
- Tachycardia - Sepsis - Pulmonary embolism - Renal impairment - COPD
81
When carrying out an echocardiogram in suspected acute LVF, which value is important for conffering the diagnosis
**_Ejection Fraction;_** - \>50%; normal - \<50%; pathological
82
When carrying out a CXR in suspected actue LVF, which parameters are important to measure?
"**_Cardiothoracic Ratio;_** - Cardiothoracic ratio = width of widest part of heart field/width of widest part of lung fields - Cardiomegaly is present when the cardiothoracic ratio \>0.5 **_Upper Lobe Venous Diversion;_** - Increased prominence and diameter of the upper lobe vessels ![]() **_Fluid Leakage;_** - Bilateral pleural effusions - Fluid in interlobar fissures - Fluid in septal lines (Kerley lines) "
83
Outline the management for acute left ventricular failure (LVF)
"**_Pour SOD_** **- **_P_**our**; stop IV fluids and monitor fluid balance, may need to fluid restrict - **_S_it** patient upright - ****_O_**xygen** (if SpO2 \< 95% and falling); be cautious in COPD - ****_D_**iuretics;** furosemide 40mg IV "
84
Outline the management of severe acute LVF causing pulmonary oedema or cardiogenic shock?
- IV Opiates; morphine acts as a vasodilator - NIV; CPAP, potential escalation to ITU for intubation and mechanical ventilation - Inotropes; noradrenaline
85
What are the two subtypes of chronic heart failure?
- Systolic Heart Failure; impaired ventricular contraction - Diastolic Heart Failure; impaired ventricular relaxation
86
What are some of the key symptoms a patient in chronic heart failure will present with?
- **Breathlessness;** worsened on exertion - **Cough**; may be productive with frothy white/pink sputum - **Orthopnoea**; SOB that is worsened upon lying flat - **Paroxysmal noctural dyspnoea**; suddenly awaking at night with severe SOB and cough - **Peripheral oedema**
87
What causes paroxysmal noturnal dyspnoea (PND)?
- Fluid settling across large area of lungs upon being supine - Respiratory cente in medulla less responsive during sleep (hence more severe hypoxia before awakening( - Less adrenaline circulation resulting in decreased cardiac output
88
How is chronic heart failure diagnosed?
- Clinical presentation - BNP blood test; specifically N-terminal pro-B-type natriuretic peptide (NT-proBNP) - Echocardiogram - ECG
89
What are the main causes of chronic heart failure?
- Ischaemic heart disease (IHD) - Valvular heart disease; most often **aortic stenosis** - Hypertension (HTN) - Arrhythmias; most often **atrial fibrillation**
90
Outline the immediate management steps for chronic heart failure?
- Referral; to specialist (NT-proBNP \>2000ng/L is urgent) - Discussion; with the patient as to the chronic nature of the condition - Medical management; ABAL - Surgical management; used in severe aortic stenosis or mitral regurgitation - Specialist nurse; consult heart failure nurse for input
91
Outline the long-term management steps for chronic heart failure?
- Yearly flu and pneumococcal vaccination - Smoking cessation - Optimisation of co-morbidities - Exercise as tolerated
92
Outline the first-line medical treatment of chronic heart failure?
"**_ABAL;_** - ****_A_**CE Inhibitor/ARB; ramipril** titrated as tolerated up to **10mg** OD, **candesartan** titrated up to **32mg** OD - ****_B_**eta Blocker** (bisoprolol/atenolol); titrated as tolerated up to **10mg** OD - ****_A_**ldosterone Antagonist** (spironolactone/eplerenone); added if symptoms persist or if there is reduced ejection fraction - ****_L_**oop Diuretics** (furosemide); **40mg** OD "
93
What monitoring is required for patients in chronic heart failure who are taking diuretics, ACE inhibitors or aldosterone antagonists
**_Repeat U&Es_** - Potential for electrolyte disturbances - Nephrotoxic drugs - Avoid AKI/CKD
94
What is cor pulmonale?
Cor pulmonale is another name for **right sided heart failure** that is **caused by respiratory disease**
95
What happens as a result of cor pulmonale?
- Pulmonary arterial hypertension - Right ventricular hypertrophy - Peripheral oedema
96
What are the most common causes of cor pulmonale?
- COPD; by far the most common - PE - Interstitial lung disease - Cystic fibrosis - Primary PAH; genetics
97
How do patients with cor pulmonale often present?
- Often asymptomatic - SOB; may be masked as a symptom of the underlying respiratory disease superimposed over the right sided heart failure - Periperhal oedema - Increased breathlessness on exertion - Syncope - Chest pain
98
What signs should be looked out for when examining a patient suspected of suffering for cor pulmonale
- Hypoxia - Cyanosis - Raised JVP - Peripheral oedema - 3rd heart sound (S3) - Murmurs; ESM --\> aortic stenosis, PSM --\> mitral regurgitation - Hepatomegaly; due to back pressure in hepatic vein
99
How can cor pulmonale be managed?
- Treating underlying caused (i.e. the respiratory disease) - Long-term oxygen therapy - Poor prognosis
100
What is the NICE definition of clinical and ambulatory hypertension?
- Clinic blood pressure \>140/90mmHg - Ambulatory blood pressure \>135/85mmHg
101
What is the primary cause of hypertension
Primary hypertension is the most common form (95%) and is also known as essential hypertension; this has **no known cause**
102
Outline the secondary causes of hypertension
"**_ROPE;_** - ****_R_**enal** disease; renal **artery stenosis** - ****_O_**besity** - ****_P_**regnancy induced** (pre-eclampsia if alongside proteinuria) - ****_E_**ndocrine**; hyperaldosteronism (**Conn's syndrome**), neuroendocrine (**phaechromatocytoma**) "
103
What are the major complications of hypertension?
- IHD - Cerebrovascular accident; stroke or haemorrhage - Hypertensive retinopathy - Hypertensive nephropathy - Heart failure
104
Outline how the diagnosis of hypertension is reached?
- Patients with clinic blood pressure \>140/90mmHg offered ambulatory blood pressure monitoring (ABPM) - If these patients are found to have an ABPM that is \>135/85mmHg then the diagnosis can be made
105
What are the stages of hypertension?
**_Stage 1;_** - CBP \>**140/90**mmHg - ABPM \>**135/85**mmHg * *_Stage 2;_** - CBP \>**160/100**mmHg - ABPM \>**150/95**mmHg * *_Stage 3;_** - CBP \>**180/120**mmHg
106
All patients with newly diagnosed hypertension should undergo investigation for end-organ damage, what does this involve?
- Urine **albumin:creatinine ratio**; looking for proteinuria and kidney damage - Urine **dipstick**; looking for haematuria and kidney damage - Ophthalmoscopy (**fundus examination**); looking for hypertensive retinopathy - **ECG**; looking for cardiac abnormailities
107
What dose of ramipril should a patient be on if being treated for hypertension?
Ramipril; 1.25mg - 10mg OD
108
What dose of bisoprolol should a patient be on if being treated for hypertension?
Bisoprolol; 5mg - 20mg OD
109
What dose of amlodipide should a patient be on if being treated for hypertension?
Amlodipine; 5mg - 10mg OD
110
What dose of indapamide should a patient be on if being treated for hypertension?
Indapamide; 2.5mg OD
111
What dose of candesartan should a patient be on if being treated for hypertension?
Candesartan; 8mg - 32mg OD
112
Outline the initial management for a patient with suspected hypertension?
- Establish a diagnosis; essential or secondary - Investiage possible end-organ damage - Advise on lifestyle
113
What is the treatment targets in terms of blood pressure when treating a patient for hypertension that is below the age of 80?
SBP \< 140mmHg DBP \< 90mmHg
114
What is the treatment targets in terms of blood pressure when treating a patient for hypertension that is above the age of 80?
SBP \< 150mmHg DBP \< 90mmHg
115
What is atrial fibrillation?
Atrial fibrillation - where the contraction of the atria is uncoordinated, rapid and **irregularly irregular**
116
What causes atrial fibrillation?
Atrial fibrillation arises due to disorganised electrical activity that overrides the normal, organised activity of the sinoatrial node
117
What changes may be seen on the ECG of a patient with atrial fibrillation?
**Absent P Waves**
118
What is the effect of atrial fibrillation on the contraction of the ventricles?
AF leads to irregular conduction of electrical impulses to the ventricles, causing irregularly irregular ventricular contractions
119
What conditions can occr as a result of atrial fibrillation?
- Tachycardia - Heart failure; due to poor filling of the ventricles during diastole - Risk of stroke; due to thrombosis
120
Why can atrial fibrillation result in ischaemic stroke?
Atrial fibrillation increases the tendency for blood to collect in the atria and form blood clots. These may embolise to the cerebral arteries and cause an ischaemic stroke
121
How to patients with atrial fibrillation often present?
- Palpitations - SOB - Syncope; either dizziness or fainting - Symptoms of associated; stroke, sepsis or thyrotoxicosis
122
What are the two differential diagnoses for an irregularly irregular pulse?
- Atrial fibrillation - Ventricular ectopics
123
How can atrial fibrillation and ventricular ectopics be distinguished on ECG?
- Ventricular ectopics disappear when the heart rate increases above a certain threshold; hence measurement after exercise may be useful - Ventricular beats will also have widended QRS complex (\>120ms)
124
Outline the ECG features of atrial fibrillation?
- Absent P waves - Narrow QRS Complex Tachycardia - Irregularly irregular ventricular rhythm
125
What is meant by valvular atrial fibrillation, how does this differ from non-valvular AF?
- Valvular atrial fibrillation is defined as **patients with AF** who **also have** moderate or servere **mitral stenosis** and/or mechanical heart valves - It is thought that valvular pathology itself leads to the atrial fibrillation - Non-valvular AF can be used to refer to AF in the absence of vavle pathology or with alternative valve pathology (mitral regurgitation/aortic stenosis)
126
Outline the most common causes of atrial fibrillation?
"**_MRS_ SMITH;** - ****_S_**epsis** - ****_M_**itral valve pathology**; either stenosis or regurgitation - ****_I_**schaemic heart disease** - ****_T_**yrotoxicosis** - ****_H_**ypertension** "
127
What are the two principles used in the treatment of atrial fibrillation?
- **Rate** _OR_ **Rhythm** Control - **Anticoagulation**; to minimise risk of stroke
128
What are the indications for rhythm control as first line over rate control in patients with atrial fibrillation?
- Reversible cause for the AF - AF is of new onset; within the last 48hrs - AF is causing heart failure - Patient remains symptomatic despite effective rate control
129
What is most often used as the first line treatment in patients with atrial fibrillation?
Rate control is most often the first line therapy apart from in a few exceptions
130
What are the pharmacological options for rate control in atrial fibrillation?
**- β-blockers** (atenolol); 50-100mg OD **- Calcium Channel Blockers** (diltiazem); not preferable in heart failure **- Digoxin**; only used in sedentary people, requires monitoring as carries risk of toxicity
131
What is the aim of rhythm control in the treatment of atrial fibrillation?
Return the patient to normal sinus rhythm
132
What are the two options for rhythm control in the treatment of atrial fibrillation?
- Single **cardioversion** event; pharmacological or electrical - Long-term **medical** rhythm control; pharmacological
133
What are the two different types of cardioversion and when are they used?
"**_Immediate Cardioversion;_** used if the AF has been present **\<48hrs** or the patient is severely **haemodynamically unstable** **_Delayed Cardioversion;_** used if the AF has been present for **\>48hrs** and the patient is **stable** "
134
When is delayed cardioversion given and what caveats are there to its used?
- Delayed cardioversion is given following anticoagulant therapy - Given after three weeks anticoagulant therapy - In the meantime, the patient must be given rate control
135
What are the two options for pharmacological cardioversion?
"**- Flecainide** (use-dependant Na+ channel blocker) ``` **- Amiodarone** (class III antidysrhythmic) " ```
136
Outline the process of electrical cardioversion in the treatment of atrial fibrillation?
- Sedation of patient - Administration of general anaesthetic - Delivery of rapid electrical shock using a cardiac defibrillator
137
What pharmacological options are available for the long-term medical rhythm control of atrial fibrillation?
**- β-blockers** (atenolol/bisoprolol); first-line **- Dronedarone** (class III antidysrhythmic); second-line, in patients post-cardioversion **- Amiodarone** (class III antidysrhythmic); used in patients with heart failure or left ventricular dysfunction
138
What is paroxysmal atrial fibrillation and how is it managed?
- AF that **transiently** comes and goes - Treated with **pill-in-the-pocket** approach - **Flecanide** is often the drug of choice
139
What are the conditions required for a pill-in-the-pocket approach with paroxysmal AF?
- Infrequent episodes - No underlying structural heart disease
140
When should flecanide not be used in the treatment of paroxysmal atrial fibrillation?
Contraindicated in atrial flutter as it can cause 1:1 AV conduction and susequent tachycardia
141
What is the aim of anticoagulant therapy in the treatment of atrial fibrillation?
To prevent thrombus formation
142
Without anticoagulation, what is the risk of stroke per year in a patient with atrial fibrillation?
5%
143
With anticoagulation, what is the risk of stroke per year in a patient with atrial fibrillation?
1-2%
144
By what degree does anticoagulation reduce that chances of stroke in patients with atrial fibrillation?
2/3rds
145
What scoring system is used to determine whether to commence anticoagulant therapy in a patient with atrial fibrillation?
"**_CHA2DS2VASc Score;_** - ****_C_**ongestive heart failure** = 1 - ****_H_**ypertension** = 1 - ****_A_**ge \>75** = 2 - ****_D_**iabetes** = 1 - ****_S_**troke** or TIA previously = 2 - ****_V_**ascular disease** = 1 - ****_A_**ge 65-74** = 1 - ****_S_**ex **_c_**ategory** (female) = 1 "
146
How can the CHA2DS2VASc score be used to inform whether to commence anticoagulant therapy in atrial fibrillation?
- CHA2DS2VASc **Score = 0**; **no anticoagulation** - CHA2DS2VASc **Score = 1**; **consider anticoagulation** - CHA2DS2VASc **Score = \>1; offer anticoagulation**
147
What is the risk of patients on anticoagulants for AF developing a signifcant bleed?
3% per year
148
What scoring system can be used to assess the risk of serious bleeds in patients who are anticoagulated for the treatment of atrial fibrillation?
"**_HAS-BLED Score;_** - ****_H_**ypertension** = 1 - ****_A_**bnormal** renal and/or liver function = 1 for each - ****_S_**troke** previously = 1 - ****_B_**leed** previously = 1 - ****_L_**abile INRs** (whilst on warfarin) = 1 - ****_E_**lderly** = 1 - ****_D_**rugs** or **alcohol =** 1 for each "
149
How can the HAS-BLED Score be used to assess the risk of serious bleeds in patients who are anticoagulated for the treatment of atrial fibrillation?
HAS-BLED **Score \< 3; low risk** HAS-BLED **Score 3 - 6; high risk** HAS-BLED **Score \> 6; very high risk**
150
What is meant by the INR, how does this relate to the coagulation properties of a patients' blood sample?
- INR = international normalised ratio - Comparison of the prothrombin time (PT) between test patient and a normal healthy adult - Prothrombin time indicates the time taken for the patients' blood to clot - An INR of 2 indicates that the patient has a prothrombin time twice that of a healthy adult
151
What is the target INR for patients treated with warfarin for atrial fibrillation?
An INR of between 2 - 3 is ideal for the treatment of atrial fibrillation
152
Which anticoagulants are now being used in the treatment of atrial fibrillation to prevent stroke?
**_DOACs;_** - Rivaroxaban; half-life of 7-15hrs - Apixaban; half-life of 12hrs - Endoxaban; half-life of 7-15hrs - Dabigatran; direct thrombin inhibitor
153
What are the benefits of using DOACs in the prevention of stroke in patients with AF?
- Shorter half-lives compared to warfarin; hence only needed to be taken once daily - No monitoring required - No major drug or food interactions - Equal or slightly better than warfarin in preventing stroke in AF - Equal or slightly less risk of bleeding that warfarin
154
What is the cause of the first heart sound (S1)
Closure of the atrioventricular valves (mitral and triscuspid) at the start of ventricular systole
155
What is the cause of the second heart sound (S1)
Closure of the semilunar valves (aortic and pulmonary) at the end of ventricular systole just prior to ventricular relaxation (diastole)
156
What is the root cause of a third heart sound (S3)
- Rapid ventricular filling - Sound itself is generated by 'plucking' of the chordae tendinae
157
When can an S3 heart sound be heard, what is it indicative of?
- Heard 0.1s after S2 - Normal in young healthy patients \<40y/o - Pathological in elderly patients; heart failure
158
When can a fourth heart sound (S4) be heard and what does it indicate?
- S4 is heard immediately before S1 - Always patholgoical - Indicates a stiff/hypertrophic ventricle - Sound itself results from turbulent flow between atria and non-compliant ventricle
159
What manoeuvre can be used to enhance the auscultation of a pansystolic mumur?
- PSM = Mitral regurgitation - Roll patient onto left hand side
160
What manoeuvre can be used to enhance the auscultation of aortic regurgitation?
- Sit patient up and lean them forward forward - Inhale, deeply exhale and hold
161
What aspects of a murmur should be assessed
"**_SCRIPT;_** - **_Site_**; location - ****_C_**haracter**; soft, blowing, crescendo, decrescendo - ****_R_**adiation**; carotids (aortic stenosis), left axilla (mitral regurgitation) - ****_P_**itch**; high, low, indicates velocity - ****_T_**iming;** systiolic or diastolic "
162
How can murmurs be classified depending on grade?
- Grade 1; difficult to hear - Grade 2; quiet - Grade 3; loud - Grade 4; loud with palpable thrill - Grade 5; as above + with stethoscope just off chest - Grade 6; as above + with stethoscope away from chest
163
What kind of valve defect causes hypertrophy?
- Stenosis
164
What kind of valve defect causes dilatation?
- Regurgitation
165
What kind of valve defect causes left atrial hypertrophy?
- Mitral stenosis
166
What kind of valve defect causes left ventricular hypertrophy?
- Aortic stenosis
167
What kind of valve defect causes left atrial dilatation?
- Mitral regurgitation
168
What kind of valve defect causes left ventricular dilatation?
- Aortic regurgitation
169
What are the causes of mitral stenosis?
- Rheumatic heart disease - Infective endocarditis
170
What symptoms/signs is mitral stenosis associated with?
- Malar flush; due to back-pressure of blood into pulmonary system, resulting in CO2 retention and subsequent vasodilatation - Atrial fibrillation; caused by the left atrium struggling to push blood through the stenotic valve
171
What condition can mitral regurgitation lead to?
Congestive cardiac failure (CCF); due to reduced ejection fraction as a result of backlog of blood
172
What are the causes of mitral regurgitation?
- Idiopathic weakening; increases with age - Ischaemic heart disease - Infective endocarditis - Rheumatic heart disease - Connective tissue disorders; *Ehlers Danlos Syndrome* (EDS) or *Marfan Syndrome*
173
What is the nature of the murmur heard in mitral regurgitation?
- Pan-systolic murmur - High pitched - Radiates to the left axilla - Heard alongside S3
174
What is the nature of the murmur heard in aortic stenosis?
- Ejection systolic murmur - Crescendo-decrescendo - Radiates to the carotid arterties
175
Other than an ejection systolic murmur, what other signs may be seen in a patieint with aortic stenosis?
- Slow rising pulse - Narrow pulse pressure - Exertional syncope
176
What are the causes of aortic stenosis?
- Idiopathic age-related **calcification** - Rheumatic heart disease - Bicuspid aortic valve
177
What is the nature of the heart murmur caused by aortic regurgitation?
- Early diastolic murmur - Soft in character
178
What is meant by Corrigan's pulse sign?
Collapsing pulse, rapidly appearing and disappearing
179
What condition can arise as a result of aortic regurgitation?
Heart failure
180
What is meant by an Austin-Flint murmur?
Austin-Flint Murmur; early diastolic murmur heard at the apex of the heart that resembles a rumble that is caused by the backflow of blood through the aortic valve and over the leaflets of the mitral valve causing a vibration
181
What are the causes of aortic regurgitation?
- Idiopathic age-related weakness - Connective tissue disease; Ehlers Danlos Syndrome or Marfan Syndrome
182
What kind of heart murmur can be heard here? [sound:1.0.m4a]
Aortic Regurtation
183
What kind of heart murmur can be heard here? [sound:2.0.m4a]
Aortic Stenosis
184
What kind of heart murmur can be heard here? [sound:3.0.m4a]
Mitral Regurgitation
185
What kind of heart murmur can be heard here? [sound:4.0.m4a]
Mitral Stenosis
186
Which kinds of scars may be seen in patients that have undergone valve replacement procedures?
**Midline sternotomy;** most often, could also indicate previous CABG **Right-sided mini-thoracotomy;** minimally invasive mitral valve replacements
187
What are the two types of prosthetic valves?
**Bioprosthetic valves;** porcine valves **Mechanical valves;** Starr-Edwards, Tilting-disc or St Jude
188
How do the lifespan of bioprosthetic and mechanical valves differ?
- Bioprosthetic valves; last up to 10 years - Mechanical valves; last over 20 years
189
What is the caveat to using mechanical valves?
- Patients require lifelong anticoagulation with warfarin - Target INR; 2.5 - 3.5
190
What is the target INR for a patient with a prosthetic mechanical valve who is anticoagulated with warfarin?
Target INR; 2.5 - 3.5
191
What are the major complications associated with mechanical valves?
- **Thrombus;** formation, blood stagnates and clots - **Infective endocarditis;** infection in prosthesis - **Haemolysis;** blood gets churned up in the valve causing anaemia
192
Which heart sound is replaced by a mechanical click as a result of a prosthetic mitral valve?
S1
193
Which heart sound is replaced by a mechanical click as a result of a prosthetic aortic valve?
S2
194
When can a transcatheter aortic valve implantation be used?
- Treatment for severe aortic stenosis - Patients high risk for open valve replacement
195
Outline the steps involved in transcatheter aortic valve replacement (TAVI)?
- Local or general anaesthetic - Catheter inserted into femoral artery - Fed wire up under X-Ray guidance - Balloon inflated to stretch the stenosed valve - Biprosthetic valve implanted into the located of the aortic valve
196
What kind of valve is used in a TAVI?
Bioprosthetic valve
197
What is the first-line valve replacement procedure offered in younger and/or healthy patients?
Open valve replacement
198
What is the long-term benefit of TAVI procedures?
Patients do not require life-long anticoagulation as the valve is bioprosthetic
199
What percentage of patients who have undergone open valve replacement go on to develop infective endocarditis?
2.5%
200
What percentage of patients who have undergone TAVI valve replacement go on to develop infective endocarditis?
1.5%
201
What is the mortality in patients who have developed infective endocarditis secondary to valve replacement?
15%
202
What are the most common organisms responsible for infective endocarditis in patients who have undergone valve replacement?
"**_Gram Positive Cocci;_** - ***Staphylococcus*** - ***Streptococcus*** - ***Enterococcus*** "
203
Where are pacemakers most commonly implanted?
- Left anterior chest wall - Left axilla
204
How long do the batteries in modern pacemakers last for?
Around 5 years
205
What electrical interventions are contraindicated in patients that have had pacemakers fitted?
- TENS machines - Diathermy in sugery
206
What are the main indications for the insertion of a pacemaker?
- **Symptomatic bradycardias** - **Mobitz type 2 (AV) heart block** - **3rd degree heart block** - **Severe heart failure;** for biventricular pacemakers - **Hypertrophic obstructive cardiomyopathy**; implantable cardioverter defibrillator (ICD)
207
What are the different types of pacemaker?
- Single chamber pacemakers - Dual chamber pacemakers - Biventricular (triple-chamber) pacemakers
208
Where in the heart can a single-chamber pacemaker be fitted?
Right atrium or right ventricle
209
When are single chamber pacemakers placed in the right atrium?
If AV conduction is normal and there is a problem with the SAN
210
When are single chamber pacemakers placed in the right ventricle?
Where there is a problem with AV conduction, and the ventricles need to be stimulated directly
211
Where are the leads in dual chamber pacemakers implanted?
Right atrium and right ventricle
212
Where are the leads in a biventricular (triple-chamber) pacemakers implanted?
Right atrium, right ventricle and left ventricle
213
When are biventricular (triple chamber) pacemakers used?
- In patients with heart failure - Used to synchronise the contractions to maximise heart function
214
What is the other term for biventricular (triple-chamber) pacemakers?
Cardiac resynchronisation therapy (CRT) pacemakers
215
Other than pacing-related pacemakers, what other type of pacemaker is there?
Implantable cardioverter defibrillator (ICD)
216
What is an implantable cardioverter defibrillator?
Implantable pacemakers that continually monitor the heart and apply a defibrillator shock to cardiovert the patient back to sinus rhythm if they identify a shockable arrhythmia
217
What ECG changes will be seen if a patient has been fitted with a single chamber pacemaker?
- In right atrium; vertical line either before the P wave - In right ventricle; vertical line before the QRS complex
218
What ECG changes will be seen if a patient has been fitted with a dual chamber pacemaker?
A vertical line before both the P wave and the QRS complex
219
What are the four cardiac arrest rhythms?
- Ventricular tachycardia (VT) - Ventricular fibrillation (VF) - Pulseless electrical activity (PEA) - Asystole
220
What are the two shockable cardiac arrest rhythms?
- Ventricular fibrillation (VF) - Ventricular tachycardia (VT)
221
What are the two non-shockable cardiac arrest rhythms?
- Pulseless electrical activity (PEA); all electrical activity except VT/VF where there is not a pulse - Asystole; no significant electrical activity
222
Pulseless electrical activity (PEA) can include normal sinus rhythm, T or F?
T - patients can be in a normal sinus rhythm without any palpable pulse, this is still a non-shockable rhythm
223
How is tachycardia treated in unstable patients?
- Consider **up to 3 synchronised shocks** - Consider **amiodarone** infusion
224
What are the three types of narrow complex tachycardia?
- Atrial fibrillation - Atrial flutter - Supraventricular tachycardia (SVT)
225
What are the three types of broad complex tachycardia?
- Ventricular tachycardia - Supraventricular tachycardia (SVT) with bundle branch block - Irregular AF variant
226
What is meant by a narrow complex tachycardia?
- Tachycardia with narrow QRS complex - Indicates non-ventricular rhythm - QRS \< 120ms (3x small squares)
227
What is meant by broad complex tachycardia?
- Tachycardia with widened QRS complex - Indicates a ventricular rhythm - QRS \> 120ms (3x small squares)
228
Outline the treatment of atrial fibrillation in a stable patient?
Rate control with β-blocker (**atenolo**l) or calcium channel blocker (**diltiazem**)
229
Outline the treatment for atrial flutter in a stable patient?
Rate control with β-blocker (atenolol/bisoprolol)
230
Outline the treatment for supraventricular tachycardia in a stable patient?
- Vagal manoeuvres; carotid massage - Adenosine bolus
231
Outline the treatment for ventricular tachycardia in a stable patient?
Amiodarone infusion
232
Outline the treatment for unclear broad complex tachycardias in a stable patient?
Amiodarone infusion
233
Outline the treatment for SVT with bundle branch block in a stable patient?
- Vagal manoeuvres; carotid massage - Adenosine bolus
234
What sort of rhythm causes atrial flutter?
- Atrial flutter is caused by **re-entrant** electrical activity in the atria - Creates a **self-perpetuating loop** of electrical activity - Due to an **extra** electrical **pathway**
235
What are the ECG features that are consistent with atrial flutter?
- **Atrial contraction at 300bpm**; indicated by P waves spaces by one large box (0.2s) - Ventricular contraction at 150bpm; QRS complexes separated by two large boxes (0.4s) - **Saw-tooth** appearance; due to sucessive P waves
236
What do the atria and ventricles fire at different rates in atrial flutter?
- Re-entrant electrical activity leads to self-perpetuating loop in the atria (300bpm) - Signal makes it through to the ventricles every second lap - Due to the long refractory period of the AV node (150bpm)
237
What conditions are associated with atrial flutter?
- Hypertension - Ischaemic heart disease - Cardiomyopathy - Thyrotoxicosis
238
Outline the treatment options in atrial flutter?
Similar to that of atrial fibrillation; - **Rate/rhythm control**; β-blockers or cardioversion - **Treat underlying condition**; HTN, IHD, cardiomyopathy - **Radiofrequency ablation**; long-term prevention - **Anticoagulation**; based on the CHA2DS2VASc core
239
What physical intervention/procedure can be used to ablate the abnormal rhythm in atrial fibrillation?
Radiofrequency ablation
240
What electrical activity causes a supraventricular tachycardia (SVT)?
- This occurs when electrical activity re-enters the atria from the ventricles - This electrical activity then passes back through the AVN into the ventricles
241
What kind of arrhythmia is caused by supraventricular tachycardia (SVT)?
Narrow complex tachycardia
242
How does SVT look on an ECG?
- Self-perpetuating loop - QRS --\> T --\> QRS --\> T.... - Narrow QRS (\<0.12s) - No P waves
243
What is meant by paroxysmal SVT?
- Transient periods of SVT - SVT reoccurs and remits in the same patient
244
What are the three types of SVT?
- **Atrioventricular nodal re-entrant tachycardia;** re-entry occurs through the AV node directly - **Atrioventricular re-entrany tachycardia;** re-entry occurs through an accessory pathway - **Atrial tachycardia;** signal originates in the atria elsewhere from the SAN, not re-entry but abnormal electrical activity (atrial rate \>100bpm)
245
What condition causes an atrioventricular re-entrant tachycardia?
**- Wolff-Parkinson-White** syndrome - Accessory pathway between the ventricles and the atria (**Bundle of Kent**) - Electrical acitivity conducted back from the ventricles to the atria
246
Outline the acute management of SVT in a stable patient?
**- Valsalva manoeuvre** **- Carotid sinus massage** **- Adenosine** or **verapamil** **- Direct current cardioversion**
247
What is the mechanism of action of adenosine in patients with SVT?
- Slows cardiac conduction through the AVN - Interrupts AVN directly or the accessory pathway
248
How is adenosine given in patients with SVT?
- Rapid bolus - Ensure reaches the heart with enough impact to interrupt the pathway - Will often cause brief period of asystole or bradycardia (counsel the patient on this)
249
What considerations need to be taken into account when deciding whether to give adenosine in the treatment of SVT?
**- Contraindications**; asthma, COPD, heart failure, heart block, severe hypotension **- Counsel the patient**; regarding the scary period of bradycardia or asystole - **Fast IV bolus into large proximal cannula**; grey cannula in ACF
250
What dose of adenosine can be given to treat SVT?
- Initially **6mg rapid bolus** into large cannula in ACF - If not sucessful in restoring sinus rhythm repeat with **12mg rapid bolus** **-** If not sucessful in restoring sinus rhythm repeat again with another **12mg rapid bolus** - If unsuccessful consider alternate
251
Outline the long-term management for patients with paroxysmal SVT?
- Medication; β-blockers, CCBs or amiodarone - Radiofrequency abblation
252
What ECG changes can be seen in a patient with Wolff-Parkinson-White syndrome?
"- **Shortened PR interval**; PR \< 0.12s (3 small boxes) **- Wide QRS complex**; QRS \> 0.12s (3 small boxes) **- Delta waves;** slurred upstroke of Q wave ![]() "
253
When are antiarrhythmic medications such as β-blockers, CCBs and adenosine, contraindicated in Wolff-Parkinson-White syndrome?
- If the patient has also developed atrial flutter or atrial fibrillation on the background of Wolff-Parkinson-White - Risk of choatic electrical activity through the accessory pathway - May result in polymorphic wide-complex tachycardia
254
Outline the steps involved in the radiofrequency ablation of arrhythmias
- Catheter ablation performed in a cath lab - Local or general anaesthetic - Catheter inserted into the **femoral veins** - Guided through venous system under X-ray - Electrical signals tested in different parts to identify location of accessory pathway - Radiofrequence ablation (heat) applied to the area - Scar tissue forms which can no longer conduct the electrical activity
255
Which arrhythmias can radiofrequency ablation (RFA) be used to cure?
- Atrial fibrillation - Atrial flutter - Supraventricular tachycardias - Wolff-Parkison-White Syndrome
256
What is Torsades de pointes
- A type of polymorphic ventricular tachycardia - Twisting tips - Looks like normal VT - QRS is twisting around the baseline
257
What ECG changes are seen in patients with Torsades de pointes?
"- Ventricular tachycardia - QRS twisting around baseline - QRS complex height gradually decreases and then increases again - Prolonged QT interval ![]() "
258
What causes the prolonged QT interval in torsades de pointes?
Prolonged repolarisation after a contraction
259
Outline what happens in Torsades de pointes?
- Prolonged repolarisation - Afterderpolarisations; random spontaneous depolarisations prior to proper repolarisation - Ventricular contraction before proper repolarisation - Recurrent ventricular contractions
260
What can Torsades de pointed lead to?
- Usually self-limiting - However, can progress to VT - Cardiac arrest
261
What are the causes of a prolonged QT interval?
**- LongQT syndrome**; inherited mutations in cardiac ion channels **- Medications**; antipsychotics, citalopram, flecanide, sotalol, amiodarone, macrolide antibiotics **- Eletrolyte disturbances**; hypokalaemia, hypocalcaemia, hypomagnesaemia
262
Outline the acute management options of Torsades de pointes?
**- Correct the underlying cause;** electrolyte disturbances or medications **- Magnesium infusion**; even if serum magnesium is normal **- Defibrillation;** if it progresses to VT
263
Outline the long-term management options in Torsades de pointes?
- Avoid QT-prolonging medications - Correct electrolyte disturbances - β-blockers; however NOT sotalol - Pacemaker or ICD
264
What are ventricular ectopic beats?
Premature ventricular beats caused by **electrical activity generated from outside the atria**
265
How can patients with ventricular ectopic beats often present?
Brief palpitations
266
What conditions predispose a patient to ventricular ectopics?
- IHD - Heart disease - Heart failure
267
How can ventricular ectopics be diagnosed on ECG?
- Individual, random QRS complexes - Background normal sinus rhythm - Broadened QRS complex (\>0.12s)
268
What is bigeminy?
Type of ventricular ectopic beat where these **ventricular ectopics occur after every sinus beat**
269
Outline the management options for patients with ventricular ectopics?
**- Bloods;** anaemia, electrolyte disturbances, thyroid function **- Reassurance;** no treatment in otherwide **healthy patients** **- Expert help;** in patients with a background of heart disease or concering clinical findings
270
What is meant by first degree heart block?
PR Interval \> 0.2s (5 small squares, 1 big square)
271
What are the three types of second degree heart block?
**- Mobitz Type 1;** increasing PR interval, cycle of skipped QRS **- Mobitz Type 2;** constant PR interval, no pattern of skipped QRS **- Fixed Ratio Blocks** (2:1, 3:1 etc.); contant PR interval, clear pattern of skipped QRS
272
What is meant by second degree heart block?
Where not all of the electrical impulses generated in the SAN make it through the AV node into the ventricles
273
What is meant by Wenckebach's phenomenon?
- This is Mobitz Type 1 second degree heart block - Gradually increasing PR interval until one P wave fails to elicit a QRS complex - After the dropped ventricular contraction (QRS) the PR interval is restored and generates a QRS again - This cycle repeats
274
What is Mobitz Type 2 second degree heart block?
- Intermittent non-conductive P waves - No change in PR interval - No pattern in skipped QRS complexes
275
What is the major risk of Mobitz Type 2 second degree heart block?
Asystole
276
What is 2:1 heart block?
- 2 P waves for every QRS complex
277
What is 3rd degree heart block?
- Complete heart block - No relationship between P waves and QRS complexes
278
What is the major risk in 3rd degree heart block?
Asystole
279
Outline the management options in stable patients with bradycardias and/or heart block?
- Observation - No treatment may be sufficient
280
Outline the management options in unstable patients with bradycardias and/or heart block and/or who have a risk of asystole?
**- Atropine 500μg IV** - If no improvement **repeat upto 6 doses** - Other **inotropes**; noradrenaline - Transcutaneous cardiac pacing; using a **defibrillator**
281
Outline the management options in unstable patients with bradycardias/heart block and have a severe risk of asystole?
**- Temporary transvenous cardiac paceing;** electrode inserted through the venous system into the RA or RV to stimulate contraction directly - **Permanent implantable pacemaker**; when available
282
Outline the management steps for NSTEM/unstable angina?
"**_DEFG;_** - ****_D_**APT**; aspirin (300mg) + ticagrelor/clopidogrel - ****_E_**nzymes**; troponins (TnT) - ****_F_**ondaparinux** (Xa inhibitor) - ****_G_**RACE** Scoring; to predict mortalility and/or need for PCI "
283
Outline all the secondary prevention strategies post-MI to prevent further cardiovascular disease?
"**_ABCD;_** - **_A_'s**; medical management with the 6 A's - **_β_-blocker**; if not atenolol as part of 6 A's - ****_C_**ardiac rehabilitation** and ****_c_**essation** of smoking - ****_D_**riving, **_d_**iet** and alcohol "
284
What kind of rhythm are patients who have had inferior myocardial infarctions particularly at risk of developing?
- Total (3rd degree) heart block - As a result of ischaemia of the AVN as a result of RCA occlusion
285
Outline the different types of aetiology that lead to the development of atrial fibrillation
**_Cardiac Causes;_** - HTN - IHD - Valvular disease - Cardiomyopathy **_Non-Cardiac Causes;_** - Alcohol and drugs - Infection - Hyperthyroidism - Electrolyte disturbances
286
How does the treatment of atrial fibrillation differ depending on when the arrhythmia developed?
- AF developed **_definitively_ within the last 48hrs**; consider cardioversion - AF **likely** to have been **present** for **longer than 48hrs**; anticoagulate for minimum of 3 weeks (to alleviate blood pooling) and/or perform a trans-oesophageal echo (TOE) prior to cardioversion
287
What are the indications for valve replacement in severe aortic stenosis?
"- Syncope - Chest pain - Dyspnoea - LVEF \>50% ![]() "