Cardiology Flashcards

Question

What is the Patho of ACS

Answer 1

**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.

Answer 2

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

Answer 3

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

Answer 4

* Left atrium * Posterior aspect of left ventricle

Answer 5

* Anterior aspect of left ventricle * Anterior aspect of septum

Answer 6

* Unstable Angina * ST Elevation Myocardial Infarction (STEMI) * Non-ST Elevation Myocardial Infarction (NSTEMI)

Answer 7

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

Answer 8

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

Answer 9

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”**

Answer 10

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

Answer 11

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

Answer 12

**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

Answer 13

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.

Answer 14

* Chronic renal failure * Sepsis * Myocarditis * Aortic dissection * Pulmonary embolism

Answer 15

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

Answer 16

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)

Answer 17

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.**

Answer 18

**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%).

Answer 19

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.

Answer 20

**D** – Death **R** – Rupture of the heart septum or papillary muscles **E** – “Edema” (Heart Failure) **A** – Arrhythmia and Aneurysm **D** – Dressler’s Syndrome

Answer 21

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.

Answer 22

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

Answer 23

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**).

Answer 24

Management is with **NSAIDs (aspirin / ibuprofen)** and in more severe cases **steroids (prednisolone).** They may need **pericardiocentesis** to remove fluid from around the heart.

Answer 25

* 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 procedure**s depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.

Answer 26

* 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)

Answer 27

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

Answer 28

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.

Answer 29

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

Answer 30

**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).

Answer 31

* Shortness of breath * Looking and feeling unwell * Cough (frothy white/pink sputum)

Answer 32

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

Answer 33

Chest pain in ACS Fever in sepsis Palpitations in arrhythmias

Answer 34

* 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)

Answer 35

IV furosemide

Answer 36

* 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)

Answer 37

B-type Natriuretic Peptide (BNP) Blood Test Echocardiography (echo) Chest Xray Findings

Answer 38

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.

Answer 39

* Tachycardia * Sepsis * Pulmonary embolism * Renal impairment * COPD

Answer 40

* Cardiomegaly * Upper lobe venous diversion * Bilateral pleural effusions * Fluid in interlobar fissures * Fluid in the septal lines (Kerley lines)

Answer 41

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.

Answer 42

**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.**

Answer 43

Chronic heart failure is essentially the chronic version of acute heart failure. It is caused by either impaired left ventricular contraction **(“systolic heart failure”) o**r 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.

Answer 44

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)

Answer 45

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.

Answer 46

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.

Answer 47

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

Answer 48

* Ischaemic Heart Disease * Valvular Heart Disease (commonly aortic stenosis) * Hypertension * Arrhythmias (commonly atrial fibrillation)

Answer 49

* **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)

Answer 50

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

Answer 51

Cor pulmonale is r**ight 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.**

Answer 52

COPD is the most common cause Pulmonary Embolism Interstitial Lung Disease Cystic Fibrosis Primary Pulmonary Hypertension

Answer 53

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

Answer 54

* 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**)

Answer 55

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.

Answer 56

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

Answer 57

primary hypertension

Answer 58

**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.

Answer 59

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

Answer 60

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 pressur**e or home readings to confirm the diagnosis.

Answer 61

“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.

Answer 62

* 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

Answer 63

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.

Answer 64

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.

Answer 65

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.**

Answer 66

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

Answer 67

S1-closing of the atrioventricular valves S2-closing of the semilunar valves

Answer 68

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.

Answer 69

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

Answer 70

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).

Answer 71

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

Answer 72

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

Answer 73

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”

Answer 74

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.

Answer 75

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.**

Answer 76

**Mitral regurgitation** causes left atrial dilatation. **Aortic regurgitation** causes left ventricular dilatation.

Answer 77

Rheumatic Heart Disease Infective Endocarditis

Answer 78

**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.

Answer 79

Mitral Stenosis

Answer 80

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.

Answer 81

Mitral Regurgitation

Answer 82

* 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

Answer 83

Aortic Stenosis

Answer 84

* 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

Answer 85

Idiopathic age related calcification Rheumatic Heart Disease

Answer 86

early diastolic, soft murmur

Answer 87

Corrigan’s pulse

Answer 88

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.

Answer 89

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.

Answer 90

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

Answer 91

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.

Answer 92

* 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.

Answer 93

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)

Answer 94

Atrial fibrillation Ventricular ectopics

Answer 95

* Absent P waves * Narrow QRS Complex Tachycardia * Irregularly irregular ventricular rhythm

Answer 96

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.

Answer 97

* **S**epsis * **M**itral Valve Pathology (stenosis or regurgitation) * **I**schemic Heart Disease * **T**hyrotoxicosis * **H**ypertension

Answer 98

* Rate or rhythm control * Anticoagulation to prevent stroke

Answer 99

* 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

Answer 100

**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)

Answer 101

* 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.

Answer 102

* 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.

Answer 103

Pharmacological cardioversion Electrical cardioversion

Answer 104

NICE guidelines (2014) say for pharmacological cardioversion first line is: **Flecanide** **Amiodarone** (the drug of choice in patients with structural heart disease)

Answer 105

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.

Answer 106

**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

Answer 107

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.

Answer 108

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

Answer 109

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

Answer 110

The uncontrolled and unorganised movement of the atria leads to blood stagnating in the left atrium, particularly in th**e 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.**

Answer 111

Prothrombine time

Answer 112

INR international normalised ratio)

Answer 113

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

Answer 114

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

Answer 115

**Andexanet alfa (apixaban and rivaroxaban)** **Idarucizumab (a monoclonal antibody against dabigatran)**

Answer 116

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

Answer 117

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.

Answer 118

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

Answer 119

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

Answer 120

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

Answer 121

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)

Answer 122

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.

Answer 123

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

Answer 124

* Symptomatic bradycardias * Mobitz Type 2 AV block * Third degree heart block * Severe heart failure (biventricular pacemakers) * Hypertrophic obstructive cardiomyopathy (ICDs)

Answer 125

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

Answer 126

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.

Answer 127

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.

Answer 128

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.

Answer 129

midline sternotomy scar

Answer 130

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

Answer 131

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

Answer 132

Thrombus formation (blood stagnates and clots) Infective endocarditis (infection in prosthesis) Haemolysis causing anaemia (blood gets churned up in the valve)

Answer 133

Mechanical valves cause a click A click replaces S1 for metallic **mitral valve** A click replaces S2 for metallic **aortic valve**

Answer 134

1. Staphylococcus 2. Streptococcus 3. Enterococcus

Answer 135

Ventricular tachycardia Ventricular fibrillation

Answer 136

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

Answer 137

Consider up to 3 synchronised shocks Consider an amiodarone infusion

Answer 138

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 S**VT with bundle branch block** treat as normal SVT * If irregular may be AF variation – seek expert help

Answer 139

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.

Answer 140

* Hypertension * Ischaemic heart disease * Cardiomyopathy * Thyrotoxicosis

Answer 141

* **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

Answer 142

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.

Answer 143

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.

Answer 144

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

Answer 145

* **“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.

Answer 146

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 cardioversio**n may be required if the above treatment fails

Answer 147

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.

Answer 148

* 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

Answer 149

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**

Answer 150

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.

Answer 151

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

Answer 152

* Short PR interval (\< 0.12 seconds) * Wide QRS complex (\> 0.12 seconds) * “Delta wave” which is a slurred upstroke on the QRS complex

Answer 153

**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.

Answer 154

* Atrial Fibrillation * Atrial Flutter * Supraventricular Tachycardias * Wolff-Parkinson-White Syndrome

Answer 155

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.

Answer 156

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

Answer 157

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.

Answer 158

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

Answer 159

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

Answer 160

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

Answer 161

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).

Answer 162

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

Answer 163

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.

Answer 164

* 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)

Answer 165

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).

Answer 166

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

Answer 167

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.

Answer 168

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.

Answer 169

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.

Answer 170

**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

Answer 171

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.**

Cardiology Flashcards

(203 cards)