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Cardiology Flashcards

1
Q

What does Atherosclerosis mean?

A

Athero – soft or porridge-like. Sclerosis – hardening. Atherosclerosis is a combination of atheromas (fatty deposits in the artery walls) and sclerosis (the process of hardening or stiffening of the blood vessel walls).

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2
Q

Which arteries does Atherosclerosis affect?

A

Atherosclerosis affects the 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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3
Q

What affects does atherosclerosis cause on the arteries

A

These plaques cause:

  • Stiffening of the artery walls leading to hypertension (raised blood pressure) and strain on the heart trying to pump blood against resistance
  • Stenosis leading to reduced blood flow (e.g. in angina)
  • Plaque rupture giving off a thrombus that blocks a distal vessel leading to ischaemia, for example in acute coronary syndrome)
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4
Q

Atherosclerosis Risk Factors can be classed as modifiable and non-modifiable

Name them

A

Non-Modifiable Risk Factors

  • Older age
  • Family history
  • Male

Modifiable Risk Factors

  • Smoking
  • Alcohol consumption
  • Poor diet (high sugar and trans-fat and reduced fruit and vegetables and omega 3 consumption)
  • Low exercise
  • Obesity
  • Poor sleep
  • Stress
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5
Q

Medical co-morbidities increase the risk of atherosclerosis and should be carefully managed to minimise the risk:

A
  • Diabetes
  • Hypertension
  • Chronic kidney disease
  • Inflammatory conditions, such as rheumatoid arthritis
  • Atypical antipsychotic medications

TOM TIP: Think about risk factors when taking a history from someone with suspected atherosclerotic disease (such as someone presenting with chest pain) and ask about their exercise, diet, past medical history, family history, occupation, smoking, alcohol intake and medications. This will help you score highly in exams and when presenting to seniors.

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6
Q

What are the End Results of Atherosclerosis

A
  • Angina
  • Myocardial Infarction
  • Transient Ischaemic Attacks
  • Stroke
  • Peripheral Vascular Disease
  • Mesenteric Ischaemia
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7
Q

What is QRISK 3 score?

A

This will calculate the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.

If they have more than a 10% risk of having a stroke or heart attack over the next 10 years (i.e. their QRISK 3 score is above 10%)

then you should offer a statin (current NICE guidelines are for atorvastatin 20mg at night).

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8
Q

All patients with _____ _______ _______ or _______ __ ______ for more than 10 years should be offered atorvastatin 20mg.

A

All patients with chronic kidney disease (CKD) or type 1 diabetes for more than 10 years should be offered atorvastatin 20mg.

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9
Q

For Primary Prevention of Cardiovascular Disease

What do you check in 3 months times?

A

NICE recommend checking lipids at 3 months and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol. Always check adherence before increasing the dose.

NICE also recommend checking LFTs within 3 months of starting a statin and again at 12 months. They don’t need to be checked after that if they are normal. Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use and they often don’t need stopping if the rise is less than 3 times the upper limit of normal.

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10
Q

What is the Secondary Prevention of Cardiovascular Disease

A

A – Aspirin (plus a second antiplatelet such as clopidogrel for 12 months)

A – Atorvastatin 80mg

A – Atenolol (or other beta-blocker – commonly bisoprolol) titrated to maximum tolerated dose

A – ACE inhibitor (commonly ramipril) titrated to maximum tolerated dose

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11
Q

What are some Notable Side Effects of Statins

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

Usually, the benefits of statins far outweigh the risks and newer statins (such as atorvastatin) are mostly very well tolerated.

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12
Q

What is Angina?

Radiation?

A

A narrowing of the coronary arteries reduces blood flow to the myocardium (heart muscle)

. During times of high demand such as exercise there is insufficient supply of blood to meet demand. This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms.

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13
Q

Angina is “_____” when symptoms are always relieved by rest or _____ _________.

A

Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN).

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14
Q

What is unstable angina

A

It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome.

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15
Q

Investigations of Angina

A

CT Coronary Angiography

All patients should have the following baseline investigations:

  • Physical Examination (heart sounds, signs of heart failure, BMI)
  • ECG
  • FBC (check for anaemia)
  • U&Es (prior to ACEi and other meds)
  • LFTs (prior to statins)
  • Lipid profile
  • Thyroid function tests (check for hypo / hyper thyroid)
  • HbA1C and fasting glucose (for diabetes)
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16
Q

What is CT Coronary Angiography

A

This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing.

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17
Q

WHat is Medical Management of Angina

There are three aims to medical management:

  • Immediate Symptomatic Relief
  • Long Term Symptomatic Relief
  • Secondary prevention of cardiovascular disease

Explain Immediate Symptomatic Relief

A
  • Their GTN spray is used required. It causes vasodilation and helps relieves the symptoms.
  • Take GTN, then repeat after 5 minutes. If there is still pain 5 minutes after the repeat dose – call an ambulance.
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18
Q

WHat is Medical Management of Angina

There are three aims to medical management:

  • Immediate Symptomatic Relief
  • Long Term Symptomatic Relief
  • Secondary prevention of cardiovascular disease

Explain Long Term Symptomatic Relief ?

A

is with either (or used in combination if symptoms are not controlled on one):

  • Beta blocker (e.g. bisoprolol 5mg once daily) or;
  • Calcium channel blocker (e.g. amlodipine 5mg once daily)

Other options (not first line):

  • Long acting nitrates (e.g. isosorbide mononitrate)
  • Ivabradine
  • Nicorandil
  • Ranolazine
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19
Q

WHat is Medical Management of Angina

  • There are three aims to medical management:
  • Immediate Symptomatic Relief
  • Long Term Symptomatic Relief
  • Secondary prevention of cardiovascular disease

Explain Secondary Prevention of cardiovascular disease ?

A
  • Aspirin (i.e. 75mg once daily)
  • Atorvastatin 80mg once daily
  • ACE inhibitor
  • Already on a beta-blocker for symptomatic relief.
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20
Q

Procedural / Surgical Interventions for Angina

A

Percutaneous Coronary Intervention (PCI) with coronary angioplasty

Coronary Artery Bypass Graft (CABG)

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21
Q

Explain the Percutaneous Coronary Intervention (PCI) with coronary angioplasty procedure

A

(dilating the blood vessel with a balloon and/or inserting a stent) is offered to patients with “proximal or extensive disease” on CT coronary angiography.

This involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent.

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22
Q

Explain Coronary Artery Bypass Graft (CABG) procedure

A

surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. The recovery is slower and the complication rate is higher than PCI.

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23
Q

TOM TIP: When examining a patient that you think may have coronary artery disease what should you check for?

A

heck for a midline sternotomy scar (previous CABG), scars around the brachial and femoral arteries (previous PCI) and along the inner calves (saphenous vein harvesting scar) to see what procedures they may have had done and to impress your examiners.

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24
Q
A
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25
Q

What is the Patho of ACS

A

Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast flowing artery it is made up mostly of platelets. This is why anti-platelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.

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26
Q

The Left Coronary Artery becomes the _______ and ____ ______ ________.

A

The Left Coronary Artery becomes the Circumflex and Left Anterior Descending (LAD).

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27
Q

Right Coronary Artery (RCA) curves around the right side and under the heart and supplies the:

A
  • Right atrium
  • Right ventricle
  • Inferior aspect of left ventricle
  • Posterior septal area
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28
Q

Circumflex Artery curves around the top, left and back of the heart and supplies the:

A
  • Left atrium
  • Posterior aspect of left ventricle
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29
Q

Left Anterior Descending (LAD) travels down the middle of the heart and supplies the:

A
  • Anterior aspect of left ventricle
  • Anterior aspect of septum
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30
Q

Three types of Acute Coronary Syndrome are

A
  • Unstable Angina
  • ST Elevation Myocardial Infarction (STEMI)
  • Non-ST Elevation Myocardial Infarction (NSTEMI)
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31
Q

How to make a diagnosis for ACS

A

When a patient presents with possible ACS symptoms (i.e. chest pain) perform an ECG:

If there is ST elevation or new left bundle branch block the diagnosis is STEMI.

If there is no ST elevation then perform troponin blood tests:

  • If there are raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
  • If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain
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32
Q

Symptoms ACS

A

Central, constricting chest pain associated with:

  • Nausea and vomiting
  • Sweating and clamminess
  • Feeling of impending doom
  • Shortness of breath
  • Palpitations
  • Pain radiating to jaw or arms
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33
Q

Symptoms for ACS should continue at rest for more than 20 minutes. If they settle with rest consider angina. Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a ______

A

Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina. Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”

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34
Q

ECG Changes of STEMI

A
  • ST segment elevation in leads consistent with an area of ischaemia
  • New Left Bundle Branch Block also diagnoses a “STEMI”
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35
Q

ECG Changes in NSTEMI:

A
  • ST segment depression in a region
  • Deep T Wave Inversion
  • Pathological Q Waves (suggesting a deep infarct – a late sign)
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36
Q

Which arteries supply which areas of the heart + ECG leads

A

Left Coronary Artery - Anterolateral - I, aVL, V3-6

LAD - Anterior - V1-4

Circumflex - Lateral - I, aVL, V5-6

Right Coronary Artery - Inferior - II, III, aVF

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37
Q

What are troponins

A

troponins are proteins found in cardiac muscle. The specific type of troponin, the normal range and diagnostic criteria vary based on different laboratories (so check your policy). Diagnosis of ACS typically requires serial troponins (e.g. at baseline and 6 or 12 hours after onset of symptoms). A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle. They are non-specific, meaning that a raised troponin does not automatically mean ACS.

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38
Q

There are alternative causes of raised troponins which are?

A
  • Chronic renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
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39
Q

Other Investigations for ACS

+ Imaging

A

Perform all the investigations you would normally arrange for stable angina:

  • Physical Examination (heart sounds, signs of heart failure, BMI)
  • ECG
  • FBC (check for anaemia)
  • U&Es (prior to ACEi and other meds)
  • LFTs (prior to statins)
  • Lipid profile
  • Thyroid function tests (check for hypo / hyper thyroid)
  • HbA1C and fasting glucose (for diabetes)

Plus:

  • Chest xray to investigate for other causes of chest pain and pulmonary oedema
  • Echocardiogram after the event to assess the functional damage
  • CT coronary angiogram to assess for coronary artery disease
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40
Q

Acute STEMI Treatment (always check local protocol)

A

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:

  • Primary PCI (if available within 2 hours of presentation)
  • Thrombolysis (if PCI not available within 2 hours)
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41
Q

What is Thrombolysis

Examples

A

Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.

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42
Q

Acute NSTEMI treatment: BATMAN

A

B – Beta-blockers unless contraindicated

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)

M – Morphine titrated to control pain

A – Anticoagulant: Fondaparinux (unless high bleeding risk)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

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

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43
Q

What is GRACE Score

And explain it

A

GRACE Score to assess for PCI in NSTEMI:

This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:

  • <5% Low Risk
  • 5-10% Medium Risk
  • >10% High Risk

If they are 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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44
Q

Complications of MI (Heart Failure DREAD)

A

D – Death

R – Rupture of the heart septum or papillary muscles

E – “Edema” (Heart Failure)

A – Arrhythmia and Aneurysm

D – Dressler’s Syndrome

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45
Q

What is Dressler’s Syndrome

A

This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart). It is less common as the management of ACS becomes more advanced.

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46
Q

How does Dressler’s syndrome present as?

A

It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function

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47
Q

A diagnosis of Dressler’s can be made with an ECG (____________________ __________________), echocardiogram (_____ _____) and raised inflammatory markers (_____ ____ _____).

A

A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

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48
Q

Management for Dressler’s Syndrome

A

Management is with NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone).

They may need pericardiocentesis to remove fluid from around the heart.

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49
Q

Secondary Prevention Medical Management (6 As) for Dressler’s Syndrome

A
  • Aspirin 75mg once daily
  • Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
  • Atorvastatin 80mg once daily
  • ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
  • Atenolol (or other beta blocker titrated as high as tolerated)
  • Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.

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50
Q

Secondary Prevention Lifestyle: ACS

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. diabetes and hypertension)
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51
Q

What are the Types of MI

A

This is slightly unnecessary knowledge for everyday practice but worth being aware of. It is worth avoiding as it could confuse people unless they are a medical registrar or cardiologist.

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

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52
Q

WHat is Acute Left Ventricular Failure (LVF)

A

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

This causes a backlog of blood (like too many buses waiting to pick up people at a bus stop) that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid and are unable to reabsorb fluid from the surrounding tissues.

This causes pulmonary oedema, which is where the lung tissues and alveoli become full of interstitial fluid. This interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms.

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53
Q

Acute Left Ventricular Failure (LVF)

Triggers

A
  • Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function)
  • Sepsis
  • Myocardial Infarction
  • Arrhythmias
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54
Q

Acute Left Ventricular Failure (LVF)

How does it typical presents

A

Acute LVF typical presents as a rapid onset breathlessness. This is exacerbated by lying flat and improves on sitting up. Acute LVF causes a type 1 respiratory failure (low oxygen without an increase in carbon dioxide in the blood).

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55
Q

Acute Left Ventricular Failure (LVF)

Symptoms

A
  • Shortness of breath
  • Looking and feeling unwell
  • Cough (frothy white/pink sputum)
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56
Q

Acute Left Ventricular Failure (LVF)

On Examination?

A
  • Increase respiratory rate
  • Reduced oxygen saturations
  • Tachycardia
  • 3rd Heart Sound
  • Bilateral basal crackles (sounding “wet”) on auscultation
  • Hypotension in severe cases (cardiogenic shock)
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57
Q

Acute Left Ventricular Failure (LVF)

There may also be signs and symptoms related to underlying cause, for example:

A

Chest pain in ACS

Fever in sepsis

Palpitations in arrhythmias

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58
Q

If they also have right sided heart failure you could find on examination

A
  • Raised Jugular Venous Pressure (JVP) (a backlog on the right side of the heart leading to an engorged jugular vein in the neck)
  • Peripheral oedema (ankles, legs, sacrum)
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59
Q

When you are on the wards and a nurse asks you to review a patient that has just started desaturating ask yourself how much fluid that patient has been given and whether they might not be able to process that much.

For example, an 85 year old lady with chronic kidney disease and aortic stenosis is prescribed 2 litres of fluid over 4 hours and then starts to drop her oxygen saturations. This is a common scenario and a dose of ___ ________ can often work like magic to clear some fluid and ease their breathing

A

IV furosemide

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60
Q

Acute Left Ventricular Failure (LVF)

Initial Ix

A
  • History
  • Clinical Examination
  • ECG (to look for ischaemia and arrhythmias)
  • Arterial Blood Gas (ABG)
  • Chest Xray
  • Bloods (routine bloods for infection, kidney function, BNP and consider troponin if suspecting MI)
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61
Q

More Ix for Acute Left Ventricular Failure (LVF)

A

B-type Natriuretic Peptide (BNP) Blood Test

Echocardiography (echo)

Chest Xray Findings

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62
Q

What is B-type Natriuretic Peptide (BNP)

Action?

A

is a hormone that is released from the heart ventricles when the cardiac muscle (myocardium) is stretched beyond the normal range. Finding a high result indicates the heart is overloaded (with blood) beyond its normal capacity to pump effectively.

The action of BNP is to relax the smooth muscle in blood vessels. This reduces the systemic vascular resistance making it easier for the heart to pump blood through the system. BNP also acts on the kidneys as a diuretic to promote the excretion of more water in the urine. This reduces the circulating volume helping to improve the function of the heart.

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63
Q

Other causes of a raised BNP include:

A
  • Tachycardia
  • Sepsis
  • Pulmonary embolism
  • Renal impairment
  • COPD
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64
Q

Chest Xray Findings of Acute Left Ventricular Failure (LVF)

A
  • Cardiomegaly
  • Upper lobe venous diversion
  • Bilateral pleural effusions
  • Fluid in interlobar fissures
  • Fluid in the septal lines (Kerley lines)
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65
Q

Management of Acute Left Ventricular Failure (LVF) and Pulmonary Oedema

A

Use the simple mnemonic Pour SOD for acute LVF:

  • Pour away (stop) their IV fluids
  • Sit up
  • Oxygen
  • Diuretics

Sit the patient upright. When lying flat the fluid in the lungs spreads to a larger area. When upright gravity takes it to the bases leaving the upper lungs clear for better gas exchange.

Oxygen if their oxygen saturations are falling (<95%). As always be cautious in patients with COPD.

Diuretics (e.g. IV furosemide 40mg stat). This reduces the circulating volume and means the heart is less overloaded allowing it to pump more effectively. This is like taking your backpack off when on a hike – it allows you to walk more easily.

Monitor fluid balance. Measuring fluid intake, urine output, U&E bloods and daily body weight is essential to balance their fluid input and output.

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66
Q

Other options to consider in severe acute pulmonary oedema or cardiogenic shock (not routinely used) include:

A

Intravenous opiates (opiates such as morphine act as vasodilators but are not routinely recommended).

Non-Invasive Ventilation (NIV). Continuous Positive Airway Pressure (CPAP) involves using a tight fitting mask to forcefully blow air into their lungs. This helps to open the airways and alveoli to improve gas exchange. If NIV does not work they may need full intubation and ventilation.

“Inotropes”, for example an infusion of noradrenalin. Inotropes strengthen the force of heart contractions and improve heart failure, however they need close titration and monitoring, so by this point you would need to send the patient to the local coronary care unit / high dependency unit / intensive care unit.

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67
Q

What is Chronic Heart Failure

A

Chronic heart failure is essentially the chronic version of acute heart failure. It is caused by either impaired left ventricular contraction (“systolic heart failure”) or left ventricular relaxation (“diastolic heart failure”). This impaired left ventricular function results in a chronic back-pressure of blood trying to flow into and through the left side of the heart.

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68
Q

Presentation of Chronic Heart Failure

A

There are some key features that patients with chronic heart failure present with:

  • Breathlessness worsened by exertion
  • Cough. They may produce frothy white/pink sputum.
  • Orthopnoea (the sensation of shortness of breathing when lying flat, relieves by sitting or standing). Ask them how many pillows they use at night.
  • Paroxysmal Nocturnal Dyspnoea (see below)
  • Peripheral oedema (swollen ankles)
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69
Q

What is Paroxysmal Nocturnal Dyspnoea (PND)

Presentation

A

Paroxysmal nocturnal dyspnoea is a term used to describe the experience that patients have of suddenly waking at night with a severe attack of shortness of breath and cough.

Patients will describe waking up and feeling acutely short of breath, with a cough and wheeze. They have to sit on the side of the bed or walk around the room and gasp for breath. They feel like they are suffocating and may want to open a window in an attempt to get air. Symptoms improve over several minutes.

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70
Q

PND is caused by a few proposed mechanisms:

A

Firstly, fluid settling across a large surface area of their lungs as they sleep lying flat. As they stand up the fluid sinks to the lung bases and their upper lungs clear and can be used more effectively.

Secondly, during sleep the respiratory centre in the brain becomes less responsive so their respiratory rate and effort does not increase in response to reduced oxygen saturation like it normally would when awake. This allows the person to develop more significant pulmonary congestion and hypoxia before waking up and feeling very unwell.

Thirdly, there is less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed and this worsens reduces the cardiac output.

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71
Q

Diagnosis of Chronic Heart Failure

A
  • Clinical presentation
  • BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
  • Echocardiogram
  • ECG
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72
Q

Chronic Heart Failure

Causes

A
  • Ischaemic Heart Disease
  • Valvular Heart Disease (commonly aortic stenosis)
  • Hypertension
  • Arrhythmias (commonly atrial fibrillation)
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73
Q

Management

First Line Medical Treatment (ABAL)

Chronic heart failure

A
  • ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily)
  • Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily)
  • Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone)
  • Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)
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74
Q

General Management of Chronic Heart Failure

A

This is based on NICE guidelines 2018. See the full guidelines before implementing treatment.

  • Refer to specialist (NT-proBNP > 2,000 ng/litre warrants urgent referral)
  • Careful discussion and explanation of the condition
  • Medical management (see below)
  • Surgical treatment in severe aortic stenosis or mitral regurgitation
  • Heart failure specialist nurse input for advice and support

Additional management:

  • Yearly flu and pneumococcal vaccine
  • Stop smoking
  • Optimise treatment of co-morbidities
  • Exercise at tolerated
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75
Q

WHat is Cor pulmonale

A

Cor pulmonale is right sided heart failure caused by respiratory disease. The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries. This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.

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76
Q

Respiratory Causes of Cor Pulmonale

A

COPD is the most common cause

Pulmonary Embolism

Interstitial Lung Disease

Cystic Fibrosis

Primary Pulmonary Hypertension

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77
Q

Symptoms of Cor Pulmonale

A

Often patients with early cor pulmonale are asymptomatic. The main presenting complaint is shortness of breath. Unfortunately shortness of breath is also caused by the the chronic lung diseases that lead to cor pulmonale. Patients may also present with peripheral oedema, increased breathlessness of exertion, syncope (dizziness and fainting) or chest pain

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78
Q

Examine the patient for the signs of cor pulmonale:

Examples

A
  • Hypoxia
  • Cyanosis
  • Raised JVP (due to a back-log of blood in the jugular veins)
  • Peripheral oedema
  • Third heart sound
  • Murmurs (e.g. pan-systolic in tricuspid regurgitation)
  • Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
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79
Q

Management for Cor Pulmonale

A

Management involves treating the symptoms and the underlying cause. Long term oxygen therapy is often used. The prognosis is poor unless there is a reversible underlying cause.

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80
Q

diagnosis of hypertension with a blood pressure above______ in clinic or ______ with ambulatory or home readings.

A

diagnosis of hypertension with a blood pressure above 140/90 in clinic or 135/85 with ambulatory or home readings.

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81
Q

essential hypertension is also known as

A

primary hypertension

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82
Q

There are secondary causes of hypertension that you can remember with the mnemonic ROPE:

A

R – Renal disease. This is the most common cause of secondary hypertension. If the blood pressure is very high or does not respond to treatment consider renal artery stenosis.

O – Obesity

P – Pregnancy induced hypertension / pre-eclampsia

E – Endocrine. Most endocrine conditions can cause hypertension but primarily consider hyperaldosteronism (“Conns syndrome”) as this may represent 2.5% of new hypertension. A simple test for this is a renin:aldosterone ratio blood test.

83
Q

Complications HTN

A
  • Ischaemic heart disease
  • Cerebrovascular accident (i.e. stroke or haemorrhage)
  • Hypertensive retinopathy
  • Hypertensive nephropathy
  • Heart failure
84
Q

Diagnosis HTN

A

NICE recommend measuring blood pressure every 5 years to screen for hypertension. It should be measured more often in patients that are on the borderline for diagnosis (140/90) and every year in patients with type 2 diabetes.

Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24 hour ambulatory blood pressure or home readings to confirm the diagnosis.

85
Q

Having your blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect is defined as more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.

A

“white coat syndrome”.

The white coat effect is defined as more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.

86
Q

Explain stages of HTN

A
87
Q

End Organ Damage

NICE recommend all patients with a new diagnosis of HTN should have:

A
  • Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
  • Bloods for HbA1c, renal function and lipids
  • Fundus examination for hypertensive retinopathy
  • ECG for cardiac abnormalities
88
Q

Medications used for HTN and examples with doses

A

A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)

B – Beta blocker (e.g. bisoprolol 5mg up to 20mg once daily)

C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)

D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)

ARB – Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily)

Angiotensin receptor blockers are used in place of an ACE inhibitor if the person does not tolerate ACE inhibitors (commonly due to a dry cough) or the patient is black of African or African-Caribbean descent. ACE inhibitors and ARBs are not used together.

89
Q

HTN Medical management is offered to: a

A

All patients with stage 2 hypertension

All patients under 80 years old with stage 1 hypertension that also have a Q-risk score of 10% or more, diabetes, renal disease, cardiovascular disease or end organ damage.

90
Q

Hypertension Management Guidelines depending on age

A
91
Q

Spironolactone is a ______ ____ ______ that works by blocking the action of _______ in the kidneys, resulting in sodium excretion and potassium reabsorption. This can be helpful when thiazide diuretics are causing _________

A

Spironolactone is a “potassium-sparing diuretic” that works by blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption. This can be helpful when thiazide diuretics are causing hypokalaemia.

92
Q

Using ___________ increases the risk of hyperkalaemia.____ _______ can also cause hyperkalaemia.

Thiazide like____ can cause also _______ disturbances. For this reason it is important to monitor U+Es regularly when using ACE inhibitors and all diuretics

A

Using spironolactone increases the risk of hyperkalaemia. ACE inhibitors can also cause hyperkalaemia. Thiazide like diuretics can cause also electrolyte disturbances. For this reason it is important to monitor U+Es regularly when using ACE inhibitors and all diuretics

93
Q

Treatment Targets for HTN depending on age

A
94
Q

S1 and S2 stands for

A

S1-closing of the atrioventricular valves

S2-closing of the semilunar valves

95
Q

What is A third heart sound (S3)

A

A third heart sound (S3) is heard roughly 0.1 seconds after the second heart sound. I think of it as rapid ventricular filling causing the chordae tendineae to pull to their full length and twang like a guitar string. This can be normal in young (15-40 years) healthy people because the heart functions so well that the ventricles easily allow rapid filling. In older patients it can indicated heart failure, as the ventricles and chordae are stiff and weak so they reach their limit much faster than normal. Picture this like tight hamstrings in an old de-conditioned patient sharply tightening as they start to bend over.

96
Q

WHat is 4th Heart Sound (S4)

A

A fourth heart sound (S4) is heard directly before S1. This is always abnormal and relatively rare to hear. It indicates a stiff or hypertrophic ventricle and is caused by turbulent flow from an atria contracting against a non-compliant ventricle

97
Q

Where is the Erb’s point

A

This is in the third intercostal space on the left sternal border and is the best area for listening to heart sounds (S1 and S2).

98
Q

Special manoeuvres can be used to emphasise certain murmurs:

What are they and what are they emphasisign

A
  • Patient on their left hand side (mitral stenosis)
  • Patient sat up, learning forward and holding exhalation (aortic regurgitation)
99
Q

Murmur Grade

Explain murmur grade

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

Grading a murmur is quite subjective but is helpful is assessing the severity of the defect and will make you sound clever. If in doubt it is probably grade 2 or 3

100
Q

How do you describe a Murmur?

A

his patient has a harsh / soft / 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 / crescendo-decrescendo shape.

This is suggestive of a diagnosis of mitral stenosis / aortic stenosis”

101
Q

Valvular heart disease can cause_________ (thickening both outwards and into the chamber) or __________ (thinning and expanding – think of blowing up a balloon) of the __________ in different heart areas.

A

Valvular heart disease can cause hypertrophy (thickening both outwards and into the chamber) or dilatation (thinning and expanding – think of blowing up a balloon) of the myocardium in different heart areas.

102
Q

When pushing against a stenotic valve the muscle has to try harder resulting in hypertrophy:

Mitral stenosis causes

Aortic stenosis causes

A

When pushing against a stenotic valve the muscle has to try harder resulting in hypertrophy:

Mitral stenosis causes left atrial hypertrophy.

Aortic stenosis causes left ventricular hypertrophy.

103
Q

When a leaky valve allows blood to flow back into a chamber it stretches the muscle resulting in dilatation:

Which valvular disease causes left artial dilation and which causes left ventricular

A

Mitral regurgitation causes left atrial dilatation.

Aortic regurgitation causes left ventricular dilatation.

104
Q

Mitral Stenosis is caused by

A

Rheumatic Heart Disease

Infective Endocarditis

105
Q

Mitral Stenosis is associated with

A

Malar flush. This is due to back-pressure of blood into the pulmonary system causing a rise in CO2 and vasodilation.

Atrial fibrillation. This is caused by the left atrium struggling to push blood through the stenotic valve causing strain, electrical disruption and resulting fibrillation.

106
Q
A
107
Q

It causes a mid-diastolic, low pitched “rumbling” murmur due to a low velocity of blood flow.

Which murmur is this

A

Mitral Stenosis

108
Q

Mitral Regurgitation can result in

A

congestive cardiac failure 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.

109
Q

It causes a pan-systolic, high pitched “whistling” murmur due to high velocity blood flow through the leaky valve. The murmur radiates to left axilla. You may hear a third heart sound.

Which valvular disease is this?

A

Mitral Regurgitation

110
Q

Mitral Regurgitation Causes

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

This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole. Flow during systole is slowest at the very start and end and fastest in the middle.

What type of murmur is this

A

Aortic Stenosis

112
Q

Is Aortic stenosis high pitched or low pitched

A

high

113
Q

Other signs: Aortic Stenosis

A
  • The murmur radiates to the carotids as the turbulence continues up into the neck
  • Slow rising pulse and narrow pulse pressure
  • Patients may complain of exertional syncope (light headedness and fainting when exercising) due to difficulty maintaining good flow of blood to the brain
114
Q

Causes: Aortic Stenosis

A

Idiopathic age related calcification

Rheumatic Heart Disease

115
Q

Aortic Regurgitation is what type of murmur

A

early diastolic, soft murmur

116
Q

Aortic Regurg is associated with what type of pulse

A

Corrigan’s pulse

117
Q

WHat is a Corrigan’s pulse

A

A Corrigan’s pulse is also called a collapsing pulse and is a rapidly appearing and disappearing pulse at carotid as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve back into the ventricles.

118
Q

Aortic Regurgitation can result in

A

ortic regurgitation results in heart failure due to a back pressure of blood waiting to get through the left side of the heart.

It can also cause an “Austin-Flint” murmur. This is heard at the apex and is an early diastolic “rumbling” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate.

119
Q

Aortic Regurgitation

Causes

A
  • Idiopathic age related weakness
  • Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
120
Q

Pathophysiology of Atrial Fib

A

Normal the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria of the heart. Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregularly. This due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node. An ECG will show an absence of p waves. This reflects the lack of coordinated atrial electrical activity. This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles.

121
Q

Atrial FIbrillation results in

A
  • Irregularly irregular ventricular contractions
  • Tachycardia
  • Heart failure due to poor filling of the ventricles during diastole
  • Risk of stroke

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

122
Q

Presentation of Atrial Fibrilliation

A

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

Presenting symptoms can be:

  • Palpitations
  • Shortness of breath
  • Syncope (dizziness or fainting)
  • Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
123
Q

There are two differential diagnoses for an irregularly irregular pulse:

What are they

A

Atrial fibrillation

Ventricular ectopics

124
Q

AF on an ECG

shows

A
  • Absent P waves
  • Narrow QRS Complex Tachycardia
  • Irregularly irregular ventricular rhythm
125
Q

Valvular Versus Non-Valvular AF

A

Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology itself has lead to the atrial fibrillation. AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis is classed as non-valvular AF.

126
Q

Most common causes of AF (remember that AF affects mrs SMITH)

A
  • Sepsis
  • Mitral Valve Pathology (stenosis or regurgitation)
  • Ischemic Heart Disease
  • Thyrotoxicosis
  • Hypertension
127
Q

There are two principles to treating atrial fibrillation:

Which are

A
  • Rate or rhythm control
  • Anticoagulation to prevent stroke
128
Q

NICE guidelines (2014) suggest all patients with AF should have rate control as first line unless:

A
  • There is reversible cause 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
129
Q

AF

Options for Rate Control:

A

Beta blocker is first line (e.g. atenolol 50-100mg once daily)

Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)

Digoxin (only in sedentary people, needs monitoring and risk of toxicity)

130
Q

AF

Rhythm Control

Rhythm control can be offered to patients where:

A
  • There is a reversible cause for their AF
  • Their AF is of new onset (<48 hours)
  • Their AF is causing heart failure
  • They remain symptomatic despite being effectively rate controlled

The aim of rhythm control is to return the patient to normal sinus rhythm. This can be achieved through a single “cardioversion” event that puts the patient back in to sinus rhythm or long term medical rhythm control that sustains a normal rhythm.

131
Q

What is the difference between Immediate and delayed cardioversion

A
  • Immediate cardioversion if the AF has been present for less than 48 hours or they are severely haemodynamically unstable.
  • Delayed cardioversion if the AF has been present for more than 48 hours and they are stable.
132
Q

There are two options for cardioversion

A

Pharmacological cardioversion

Electrical cardioversion

133
Q

AF

Pharmacological Cardioversion:

A

NICE guidelines (2014) say for pharmacological cardioversion first line is:

Flecanide

Amiodarone (the drug of choice in patients with structural heart disease)

134
Q

Electrical Cardioversion:

What is it

A

The aim of electrical cardioversion 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.

135
Q

Long Term Medical Rhythm Control for AF

A

Beta blockers are first line for rhythm control

Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion

Amiodarone is useful in patients with heart failure or left ventricular dysfunction

136
Q

What is Paroxysmal Atrial Fibrillation

A

Paroxysmal AF is when the AF comes and goes in episodes, usually not lasting more than 48 hours. Patients should still be anti coagulated based on CHADSVASc score. They may be appropriate for a “pill in the pocket” approach. This is where they take a pill to terminate their atrial fibrillation only when they feel the symptoms of AF starting. To be appropriate for a pill in the pocket approach they need to have infrequent episodes without any underlying structural heart disease. They also need to be able to identify when they are in AF and understand when the treatment is appropriate.

137
Q

What medication is used in Paroxysmal Atrial Fibrillation

A

Flecanide is the usual treatment for a “pill in the pocket” approach.

138
Q

What do you avoid in atrial flutter and why

A

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

139
Q

Why does AF patients need to be started on anticoagulation

A

The uncontrolled and unorganised movement of the atria leads to blood stagnating in the left atrium, particularly in the atrial appendage. Eventually this stagnated blood leads to a thrombus (clot). This clot then mobilises (becomes an embolus) and travels with the blood. It travels from the atria, to the ventricle, to the aorta then up in the carotid arteries to the brain. It can then lodge in the cerebral arteries and cause an ischaemic stroke.

140
Q

Wafarin prolongs what?

A

Prothrombine time

141
Q

What do we measure to assess how anticoagulated the patient is by warfarin

A

INR

international normalised ratio)

142
Q

if you start a patient on warfarin you need to closely monnitor

A

INR

143
Q

Warfarin is affected by the_____ ____ system in the liver.

A

Warfarin is affected by the cytochrome P450 system in the liver.

144
Q

Apixaban and dabigatran are taken ____ daily, rivaroxaban is taken ____ daily

A

Apixaban and dabigatran are taken twice daily, rivaroxaban is taken once daily

145
Q

When there is uncontrolled or life-threatening bleeding, the anticoagulant effects can be reversed using:

A

Andexanet alfa (apixaban and rivaroxaban)

Idarucizumab (a monoclonal antibody against dabigatran)

146
Q

DOACS have a number of advantages compared with warfarin

What are they?

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

147
Q

WHat is the CHA2DS2-VASc

A

This is a tool for assessing whether a patient with atrial fibrillation should be started on anticoagulation. It is essentially a list of risk factors, and if you have one or more of these risk factors then anticoagulation should be considered or started. The higher the score the higher the risk of developing a stroke or TIA and the greater the benefit from anticoagulation.

148
Q

CHA2DS2-VASc Mnemonic

And scoring system

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)

0: no anticoagulation
1: consider anticoagulation

>1: offer anticoagulation

149
Q

What tool do we use for Bleeding Risk

A

ORBIT Tool

he easiest way to calculate the ORBIT score is using an online calculator. It is scored based on:

  • Low haemoglobin or haematocrit
  • Age (75 or above)
  • Previous bleeding (gastrointestinal or intracranial)
  • Renal function (GFR less than 60)
  • Antiplatelet medications
150
Q

HAS-BLED is an alternative assessment tool that was commonly used for bleeding risk

WHat does it stand for

A

H – Hypertension

A – Abnormal renal and liver function

S – Stroke

B – Bleeding

L – Labile INRs (whilst on warfarin)

E – Elderly

D – Drugs or alcohol

151
Q

Arrhythmias

What are shockable and non-shockable rhythms

A

Shockable rhythms:

  • Ventricular tachycardia
  • Ventricular fibrillation

Non-shockable rhythms:

  • Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
  • Asystole (no significant electrical activity)
152
Q

What are Pacemakers

A

Pacemakers 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 in the left anterior chest wall or axilla) and the wires are implanted into the relevant chambers of the heart.

153
Q

It is worth noting that it is essential that pacemakers are removed prior to _______ in ________ patients

A

It is worth noting that it is essential that pacemakers are removed prior to cremation in deceased patients

154
Q

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)
155
Q

Whar is a single chamber pacemaker

A

Single-chamber pacemakers have leads in a single chamber, either in the right atrium or the right ventricle. They are placed in the right atrium if the AV conduction in the patient is normal and the issue is with the SA node. This way they stimulate depolarisation in the right atrium and this electrical activity then passes to the left atrium 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 patient is abnormal and they stimulate the ventricles directly

156
Q

What is a Dual-chamber Pacemaker

A

Dual-chamber pacemakers have leads in both the right atrium and right ventricle. This allows the pacemaker to synchronise the contractions of both atria and ventricles.

157
Q

Biventricular (triple-chamber) Pacemaker

What is this?

WHo are they usually seen in?

A

Biventricular pacemakers have leads in right atrium, right ventricle and left ventricle.

These are usually in patients with heart failure. The objective is to synchronise the contractions in these chambers to try to optimise the heart function. They are also called cardiac resynchronisation therapy (CRT) pacemakers.

158
Q

What are Implantable Cardioverter Defibrillators (ICDs)

A

Implantable Cardioverter Defibrillators continually monitor the heart and apply a defibrillator shock to cardiovert the patient back in to sinus rhythm if they identify a shockable arrhythmia.

159
Q

Patients that have had a valve replacement will have a scar. Usually this will be a

A

midline sternotomy scar

160
Q

a midline sternotomy scar

Describe it

Indications

A

straight down the middle of the sternum indicating a mitral or aortic valve replacement or CABG).

161
Q

Less commonly a right sided mini-thoracotomy incision can be used for minimally invasive_____ ____ replacement surgery.

A

Less commonly a right sided mini-thoracotomy incision can be used for minimally invasive mitral valve replacement surgery.

162
Q

Mechanical Heart Valves

Major Complications

A

Thrombus formation (blood stagnates and clots)

Infective endocarditis (infection in prosthesis)

Haemolysis causing anaemia (blood gets churned up in the valve)

163
Q

Mechanical valves cause a click

A click replaces S1 for metallic ______ ____

A click replaces S2 for metallic ______ ____

A

Mechanical valves cause a click

A click replaces S1 for metallic mitral valve

A click replaces S2 for metallic aortic valve

164
Q

A complication of surgical valve replacement is infection endocarditis

This is usually caused by one of three gram positive cocci organisms:

A
  1. Staphylococcus
  2. Streptococcus
  3. Enterococcus
165
Q

These are the four possible rhythms that you will see in a pulseless unresponsive patient. They can be categorised into shockable (meaning defibrillation may be effective) and non-shockable (meaning defibrillation will not be effective and should not be used).

Name some shockable rhythms

A

Ventricular tachycardia

Ventricular fibrillation

166
Q

These are the four possible rhythms that you will see in a pulseless unresponsive patient. They can be categorised into shockable (meaning defibrillation may be effective) and non-shockable (meaning defibrillation will not be effective and should not be used).

Name some Non-shockable rhythms

A
  • Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
  • Asystole (no significant electrical activity)
167
Q

Tachycardia Treatment Summary

Unstable patient:

A

Consider up to 3 synchronised shocks

Consider an amiodarone infusion

168
Q

Tachycardia Treatment Summary

In a stable patient:

A

Narrow complex (QRS < 0.12s)

  • Atrial fibrillation – rate control with a beta blocker or diltiazem (calcium channel blocker)
  • Atrial flutter – control rate with a beta 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 AF variation – seek expert help
169
Q

Atrial Flutter

What is it

What does it look like on ECG

A

Normally the electrical signal passes through the atria once, simulating a contraction then disappears through the AV node into the ventricles. Atrial flutter is caused by a “re-entrant rhythm” in either atrium. This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway. 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 to the AV node, causing 150 bpm ventricular contraction. It gives a “sawtooth appearance” on ECG with P wave after P wave.

170
Q

Associated Conditions:

for Atrial FLutter

A
  • Hypertension
  • Ischaemic heart disease
  • Cardiomyopathy
  • Thyrotoxicosis
171
Q

Treatment to atrial flutter is similar to atrial fibrillation:

Explain it

A
  • Rate/rhythm control with beta blockers or cardioversion
  • Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
  • Radiofrequency ablation of the re-entrant rhythm
  • Anticoagulation based on CHA2DS2VASc score
172
Q

Supraventricular Tachycardias (SVT) is caused by?

A

Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles. Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction.

173
Q

What SVT ECG changes

A

results in 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.

174
Q

WHat is Paroxysmal SVT

A

describes a situation where SVT reoccurs and remits in the same patient over time.

175
Q

There are three main types of SVT based on the source of the electrical signal:

WHat are they?

A
  • “Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.
  • “Atrioventricular 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. This ectopic electrical activity causes an atrial rate of >100bpm.
176
Q

Acute Management of Stable patients 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 monitoring.

  • Valsalva manoeuvre. Ask the patient 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 (calcium channel blocker)
  • Direct current cardioversion may be required if the above treatment fails
177
Q

How does adenosine work?

A

Adenosine works by slowing cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor, however it is quickly metabolised and sinus rhythm should return.

178
Q

A few key points on administering adenosine:

A
  • Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
  • Warn patient about the scary feeling of dying / 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
179
Q

Long Term Management of patients with paroxysmal SVT

A

When patients develops recurrent episodes of SVT then measures can be taken to prevent these episodes. The options are:

  • Medication (beta blockers, calcium channel blockers or amiodarone)
  • Radiofrequency ablation
180
Q

What is Wolff-Parkinson White Syndrome

A

Wolff-Parkinson White Syndrome is caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.

181
Q

The definitive treatment for Wolff-Parkinson White syndrome is ________ ______ of the accessory pathway.

A

The definitive treatment for Wolff-Parkinson White syndrome is radiofrequency ablation of the accessory pathway.

182
Q

Wolff-Parkinson White Syndrome

ECG Changes

A
  • Short PR interval (< 0.12 seconds)
  • Wide QRS complex (> 0.12 seconds)
  • “Delta wave” which is a slurred upstroke on the QRS complex
183
Q

WHat is Radiofrequency Ablation (RFA)

A

Catheter ablation is performed in a electrophysiology laboratory, often called a “cath lab”. It involves local or general anaesthetic, inserting a catheter in to 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. This way the operator can hopefully find the location of any abnormal electrical pathways. The operator may try to induce the arrhythmia to make the abnormal pathways 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. The aim is to remove the source of the arrhythmia.

184
Q

Radiofrequency Ablation (RFA) can be curative for certain cases of arrhythmia caused by abnormal electrical pathways, including:

A
  • Atrial Fibrillation
  • Atrial Flutter
  • Supraventricular Tachycardias
  • Wolff-Parkinson-White Syndrome
185
Q

What is Torsades de pointes

A

Torsades de pointes 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 progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.

186
Q

ECG FIndings for Torsades de pointes

A

A prolonged QT interval is the ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction

187
Q

When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress in to ________ ________. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest.

A

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

188
Q

Causes of Prolonged QT

A
  • Long QT Syndrome (inherited)
  • Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
  • Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
189
Q

Acute Management of Torsades de pointes

A
  • Correct the cause (electrolyte disturbances or medications)
  • Magnesium infusion (even if they have a normal serum magnesium)
  • Defibrillation if VT occurs
190
Q

Long Term Management of Prolonged QT Syndrome

A
  • Avoid medications that prolong the QT interval
  • Correct electrolyte disturbances
  • Beta blockers (not sotalol)
  • Pacemaker or implantable defibrillator
    *
191
Q

WHat are Ventricular Ectopics

A

Ventricular ectopics are premature ventricular beats caused by random electrical discharges from outside the atria. Patients often present complaining of random, brief palpitations (“an abnormal beat”). They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure).

192
Q

How are ventricular ectopics diagnosed

A

They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.

193
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.

194
Q

Management for Ventricular Ectopics

A
  • Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
  • Reassurance and no treatment in otherwise healthy people
  • Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)
195
Q

Explain First degree heart block

A

First-degree heart block occurs where 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 0.20 seconds (5 small or 1 big square).

196
Q

Explain Second Degree Heart Block

A

Second-degree heart block is where 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 several patterns of second-degree heart block described below

197
Q

Explain Wenckebach’s phenomenon (Mobitz Type 1)

A

This is where the atrial imputes becomes gradually weaker until it does not 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 show up as an increasing PR interval until the P wave no longer conducts to ventricles. This culminates in 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 repeats itself.

198
Q

Explain Mobitz Type 2

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.

199
Q

Explain Third Degree Heart Block

A

This is referred to as complete heart block. This is no observable relationship between P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.

200
Q

Treatment for Bradycardias / AV Node Blocks

Stable:

A

Observe

201
Q

Treatment for Bradycardias / AV Node Blocks

Unstable or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):

A

First 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)

In patients with high risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):

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

202
Q

Atropine is an _________ medication and works by inhibiting the __________ nervous system. This leads to side effects of ______ ________, urinary _______, dry eyes and constipation.

A

Atropine is an antimuscarinic medication and works by inhibiting the parasympathetic nervous system. This leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation.

203
Q
A

Diseases (40 decks)

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