Cardiology Flashcards

Question

STEMI: what treatment would be provided if the patient is unsuitable for PCI?

Answer 1

1) Thrombolysis e.g. alteplase or tenecteplase - Offered if symptom onset is greater than 12h OR PCI not available within 120 mins - IV administration of a thrombolytic or ‘clot-busting’ agent 2) Anticoagulation - Unfractionated heparin 3) ECG: if the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI

Answer 2

Immediate management: 1) Oxygen: if SpO2 is <94%, and aim for 94-98%, unless the patient has COPD (88 - 92%) 2) Analgesia: morphine and sublingual glyceryl trinitrate 3) Dual antiplatelets: Aspirin 300mg AND - Clopidogrel if not undergoing PCI OR - Fondaparinux: offer to all patients unless undergoing immediate coronary angiography - Unfractionated heparin: alternative to fondaparinux if renal impairment. Remember ‘MONAC’ (Morphine, Oxygen (if sPO2 <94%), Nitrates, Aspirin, Clopidogrel)

Answer 3

6As - 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) - Atenolol (or other beta blocker) - Aldosterone antagonist for those with clinical heart failure

Answer 4

- 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 5

Because when a thrombus forms in a fast flowing artery it is made up mostly of platelets.

Answer 6

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

Answer 7

The inability of the heart to deliver blood and thus oxygen at a rate that matches the requirements of the body

Answer 8

Chronic heart failure = chronic acute heart failure. Caused by: - Impaired left ventricular contraction (“systolic HF”) - aka HFrEF - Impaired left ventricular relaxation (“diastolic heart failure”) - aka HFpEF

Answer 9

- HF can result from structural/functional defects that impair the heart's function - When the heart fails, the following systems compensate to maintain CO and perfusion. However, these compensatory mechanisms eventually lead to cardiac remodelling, which further exacerbates heart failure. - Sympathetic system activation - BP falls → detected by baroreceptors → sympathetic activation → positively inotropic/chronotropic → CO increases - Increased catecholamine release - RAAS system activation

Answer 10

- Ischemic heart disease - main cause - Cardiomyopathy - Valvular heart disease (aortic stenosis/mitral regurgitation) - Hypertension - Alcohol excess - Cor pulmonale - Anaemia - Arrhythmias - Hyperthyroidism

Answer 11

Congestive HF = both-sided HF Congestive refers to sodium and water retention

Answer 12

Right-sided heart failure caused by respiratory disease Disease of lung/pulmonary vessels → pulmonary hypertension → RV hypertrophy → RHF with venous overload, peripheral oedema, hepatic congestion

Answer 13

LV weakened/stiffened > cannot pump oxygen-rich blood from lung to body properly, causing backflow into the pulmonary circulation Causes: increased LV afterload (e.g. HTN) or increased LV preload (e.g. aortic regurgitation)

Answer 14

RV weakened/stiffened > inability to pump blood to and from the lungs > backflow into systemic veins Causes: increased RV afterload (e.g. pulmonary HTN) or increased RV preload (e.g. tricuspid regurgitation)

Answer 15

- Acute/chronic HF can be further classified as follows: - HF with reduced ejection fraction where LVEF <40% (HFrEF) - traditionally known as systolic HF - HF with mildly reduced ejection fraction (HFmrEF) - LVEF 41% to 49% - HF with preserved ejection fraction (normal or near-normal left ventricular function) (HFpEF) where LVEF > 50% - traditionally known as diastolic HF - Left-sided heart failure - Right-sided heart failure

Answer 16

-Previous CVD - Older age - Prior HF - Family history of IHD or cardiomyopathies - Hypertension - Diabetes - Smoking - Excess alcohol intake

Answer 17

- Myocardial infarction (MI) - Hypertension - Diabetes mellitus - Dyslipidaemia

Answer 18

3 non-specific cardinal signs: Shortness of breath Ankle swelling (peripheral oedema) Fatigue

Answer 19

Symptoms: - Shortness of breath - Fatigue and weakness - Cough (frothy white/pink sputum) Signs: - Peripheral or central cyanosis - Displaced apex beat - Tachycardia + tachypnoea - 3rd Heart Sound - Bilateral basal crackles (sounding “wet”) on auscultation - Hypotension in severe cases (cardiogenic shock)

Answer 20

Symptoms: - Swelling of legs - Abdominal distention - Fatigue and weakness Signs - 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) + pitting - Hepatosplenomegaly - Ascites

Answer 21

Symptoms of both LV and RV failure

Answer 22

- SOB worsened by exercise - Orthopnea (SOB when lying down) - Cough - with pink/white sputum - Paroxysmal Nocturnal Dyspnoea (waking up at night with severe attack of SOB, cough and wheezing) - Peripheral oedema (swollen ankles)

Answer 23

1) FBC: anaemia as possible cause of HF 2) U&Es: renal failure as possible cause of HF 3) Arterial blood gas: type 1 respiratory failure. 4) B-type natriuretic peptides (BNP) levels raised 5) ECG: assess for abnormalities such as arrhythmias and myocardial infarction 6) Chest x-ray: A - Alveolar oedema (batwing opacities) B - Kerley B lines (lines seen at lung periphery C - Cardiomegaly D - Dilated upper lobe vessels E - Pleural Effusion

Answer 24

1) Transthoracic echocardiogram 2) ECG - abnormal, broad QRS complexes with evidence of LV hypertrophy 3) CXR: - A - Alveolar oedema (batwing opacities) - B - Kerley B lines - C - Cardiomegaly - D - Dilated upper lobe vessels - E - Pleural Effusion 4) B-type natriuretic peptide (BNP) test - raised BNP levels

Answer 25

OMFFG oxygen, morphine, furosemide, fluid restriction (<1.5L a day), GTN spray (not routine) Surgery: - If acute HF is due to aortic stenosis, then surgical aortic valve replacement - Mechanical assist device

Answer 26

Conservative management- lifestyle changes - stop smoking! -eat less salt, optimise weight and nutrition - avoid NSAIDs/verapamil Medical management: AABCDD 1st line: ACE-I + B-blocker 2nd line: ARB + nitrate 3rd line: cardiac resynchronization or digoxin diuretics: furosemide (symptom relief)

Answer 27

Right-sided heart failure caused by respiratory disease

Answer 28

Disease of lung/pulmonary vessels → pulmonary hypertension → RV cannot pump blood out effectively > RV hypertrophy to compensate → RHF with venous overload, peripheral oedema, hepatic congestion

Answer 29

- Most common: COPD - Pulmonary Embolism - Interstitial Lung Disease - Cystic Fibrosis - Primary Pulmonary Hypertension

Answer 30

Symptoms: - Early cor pulmonale - asymptomatic - Main symptom is SOB, but non-specific as SOB can be caused by the chronic lung disease that leads to cor pulmonale - Peripheral oedema - Breathlessness on exertion - Syncope - Chest pain

Answer 31

Examine the patient for signs of cor pulmonale: - 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

Answer 32

- Treat symptoms - Treat underlying cause - Long-term oxygen therapy Prognosis is poor unless there is a reversible cause

Answer 33

- Dilation of the abdominal aorta, with a diameter of more than 3cm. - > 90% originate below the renal arteries - The mortality of a ruptured AAA is around 80%

Answer 34

- Histologically - degradation of collagen and elastin and loss of smooth muscle cells in 3 layers - tunica intima, media and adventitia > vessel dilatation - Infiltration of lymphocytes and macrophages and neovascularisation

Answer 35

- A true aneurysm involves all 3 layers of the arterial wall - False aneurysm (or pseudoaneurysm) is formed by only a single layer of fibrous tissue - 1% of AAA

Answer 36

- Men are affected significantly more often and at a younger age than women - Increased age - Family history - Smoking - Hypertension - Existing cardiovascular disease

Answer 37

AAAs are classified by size as it corresponds to severity: Normal: less than 3cm Small aneurysm: 3 – 4.4cm Medium aneurysm: 4.5 – 5.4cm Large aneurysm: above 5.5cm

Answer 38

Most patients are asymptomatic, detected incidentally during routine screening. Other ways it can present include: - Non-specific abdominal pain - Pulsatile and expansile mass in the abdomen when palpated with both hands - As an incidental finding on an abdominal x-ray, ultrasound or CT scan Or they can present when the aneurysm ruptures.

Answer 39

Acute appendicitis - pain often periumbilical and is localised to the lower right quadrant

Answer 40

- Severe abdominal pain that may radiate to the back or groin - Haemodynamic instability (hypotension and tachycardia) - RED FLAG! - Grey-Turner’s sign - flank bruising secondary to retroperitoneal haemorrhage - Pulsatile and expansile mass in the abdomen - Collapse - Loss of consciousness AAA = surgical emergency - do not delay treatment!

Answer 41

1st line investigation: aortic ultrasound

Answer 42

Conservative management by managing risk factors for aneurysm < 5.5cm in diameter - Stop smoking - Healthy diet and exercise - Optimising the management of hypertension, diabetes and hyperlipidaemia

Answer 43

- Yearly for patients with aneurysms 3-4.4cm - 3 monthly for patients with aneurysms 4.5-5.4cm

Answer 44

- Patients with symptomatic aneurysm - If aneurysm diameter is >4cm and growing more than 1cm per year - If aneurysm diameter above 5.5cm

Answer 45

Surgical repair involves inserting an artificial “graft” into the section of the aorta affected by the aneurysm. Two methods to insert the graft: - Open repair via a laparotomy - Endovascular aneurysm repair (EVAR) using a stent inserted via the femoral arteries

Answer 46

1) Urgent surgical repair: for a symptomatic AAA - Management is same as elective surgery but performed urgently! 2) Urgent surgical repair: for a ruptured AAA - NICE 2020 guidelines: EVAR is preferred for women, and men > 70 for an infrarenal AAA. Otherwise, open repair is preferred.

Answer 47

- A condition where a blood clot (thrombus) forms in the pulmonary arteries. - Usually due to deep vein thrombosis (DVT) that developed in the legs > embolise to venous system> right side of the heart > pulmonary arteries in the lungs. - Embolism block blood flow in pulmonary arteries > blood unable to reach the lungs > extra strain on the right side of heart

Answer 48

A deep vein thrombosis (DVT) is the formation of a blood clot in the deep veins of the leg or pelvis.

Answer 49

Venous thromboembolism (VTE).

Answer 50

The risk factors for DVT and PE are dependent on Virchow’s triad An abnormality in any one of the three components can result in thrombus formation. 1) Hypercoagulability: - Pregnancy - Hormone therapy with oestrogen - Malignancy - Polycythaemia (high RBCs) - Systemic lupus erythematosus - Thrombophilia (blood more likely to clot) 2) Venous stasis e.g. immobility, long-haul flights 3) Endothelial damage e.g. smoking, recent surgery or trauma

Answer 51

Signs and symptoms can be subtle. - Shortness of breath - Cough with or without blood (haemoptysis) - Pleuritic chest pain (inflammation of the tissue between the lungs and ribcage) - Hypoxia - Tachycardia - Raised respiratory rate - Low-grade fever - Haemodynamic instability > hypotension Might be S+S of DVT: unilateral leg swelling and tenderness

Answer 52

1) Unilateral calf pain, redness and swelling 2) Oedema 3) Tender and redness over affected area, particularly over deep veins) 4) Distention of superficial veins

Answer 53

D-dimer is a sensitive (95%), but not specific, blood test for VTE: - Raised in DVT - However also raised in conditions such as pneumonia, malignancy, heart failure, surgery or pregnancy. So further investigations needed: Wells score ≥ 2 (DVT likely): - Doppler ultrasound of the leg is required to diagnose deep vein thrombosis. - Repeat USS if negative - 6 - 8 days after if positive D-dimer and wells score ≥ 2 Wells score ≤ 1 (DVT unlikely): - D-Dimer with 4-hour result - If D-Dimer is raised: duplex ultrasound within 4 hours - If D-Dimer is normal: a DVT is unlikely, consider alternative diagnosis

Answer 54

Perform a Wells score and proceed based on the outcome: - Likely: perform a CT pulmonary angiogram - Unlikely: perform a d-dimer and if positive perform a CTPA Tests for definitive diagnosis: - Gold standard is CT pulmonary angiogram - chest CT scan with IV contrast to highlight the pulmonary arteries Alternative cause assessment: Hx, examination, CXR ECG change: normal sinus rhythm/ sinus tachycardia, new right bundle branch block, S1Q3T3 pattern (deep S wave in lead 1, pathologic wave in lead 3, inverted T wave in lead 3

Answer 55

It is used to predict the risk of a patient presenting with symptoms of DVT or PE actually having the disease. It takes into account risk factors and clinical findings e.g., tachycardia and haemoptysis. Score ≤ 4 = PE unlikely Score > 4 = PE likely Signs and symptoms of a DVT - 3.0 PE is the number 1 diagnosis or equally likely - 3.0 Tachycardia (>100 BPM) - 1.5 Immobilisation for more than three days or surgery in the previous four weeks - 1.5 Previous, objectively diagnosed PE or DVT - 1.5 Haemoptysis - 1.0 Malignancy with treatment within the last 6 months, or palliative - 1.0

Answer 56

- Apixaban or rivaroxaban (anticoagulation) - LMWH as alternative if renal impairment

Answer 57

Long term anticoagulation - Warfarin - NOACs/DOACs (direct-acting oral anticoagulants) such as apixaban (okay for cancer paitents) - LMWH as an alternative if renal impairment Continue anticoagulation for: - 3 months if there is a reversible cause (then review) - Beyond 3 months if the cause is unclear, there is recurrent VTE, or there is an irreversible underlying cause such as thrombophilia - 3-6 months in active cancer (then review)

Answer 58

Thrombolysis - injecting a fibrinolytic medication (clot buster by breaking down fibrin!) Massive risk of bleeding = dangerous Only use in patients with massive PE where benefits > risks Thrombolytic agents e.g., alteplase

Answer 59

Aortic dissection is when a break or tear forms in the aortic wall intima, causing blood flow into a new false lumen formed between the intima and media. Three layers - intima, media and adventitia

Answer 60

Ascending aorta and aortic arch - as under the most stress from blood exiting the heart

Answer 61

- Most common - chronic hypertension! - Increasing age - male sex - smoking - poor diet (high in saturated fat and sugars) - Reduced physical activity - Raised cholesterol

Answer 62

- Atherosclerotic aneurysmal disease - Bicuspid aortic valve - Ehlers-Danlos Syndrome - Marfan’s Syndrome

Answer 63

A classification system for aortic dissection: -Type A – affects the ascending aorta before the brachiocephalic artery (~first 10cm of aorta) - Type B – affects the descending aorta after the left subclavian artery

Answer 64

A classification system for aortic dissection: - Type I – begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta - Type II – isolated to the ascending aorta - Type IIIa – begins in the descending aorta and involves only the section above the diaphragm - Type IIIb – begins in the descending aorta and involves the aorta below the diaphragm.

Answer 65

- Acute severe chest pain (tearing or ripping pain) - Interscapular (between shoulders) and lower pain - Differences in blood pressure between the arms (more than a 20mmHg difference is significant) - Radial pulse deficit (the radial pulse in one arm is decreased or absent and does not match the apex beat)

Answer 66

- CT (chest, abdomen, and pelvis) = initial investigation to confirm the diagnosis - intimal flap - ECG + chest x-ray to rule out other causes e.g., STEMI - Echocardiography - intimal flap

Answer 67

- Myocardial infarction - Acute coronary symdrome - Aortic aneurysm

Answer 68

- ABCDE, O2 therapy (aim SpO2 94%, 88% - 92% COPD), IV resuscitation - Surgical emergency! The type of surgery depends on the type of aortic dissection - Analgesia (e.g., morphine) - Beta-blockers to control BP and HR to reduce stress on aortic walls.

Answer 69

Open surgery (midline sternotomy) to remove the affected section of the aorta and replace it with a synthetic graft. The aortic valve might need to be replaced too.

Answer 70

Thoracic endovascular aortic repair (TEVAR). A stent graft is inserted into the affected section of the aorta via a catheter in the femoral artery

Answer 71

- Cardiac tamponade - Myocardial infarction - Aortic valve regurgitation - Stroke - Paraplegia (motor or sensory impairment in the legs) - Death

Answer 72

The narrowing of the arteries supplying the limbs and periphery, which reduces the blood supply to these areas. It usually refers to the lower limbs, resulting in symptoms of claudication.

Answer 73

The main cause is atherosclerosis

Answer 74

1) Non-modifiable risk factors: - Older age - Family history - Male 2) Modifiable risk factors: - Smoking - Alcohol consumption - Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s) - Low exercise / sedentary lifestyle - Obesity - Poor sleep Stress

Answer 75

Atherosclerotic plaques in the arterial walls are caused by chronic inflammation and activation of the immune system in the artery wall. This can lead to the following: - Stiffening > hypertension > strain on heart - Stenosis > reduced blood flow - Plaque rupture > thrombus > ischaemia in distal limb

Answer 76

- Most patients are asymptomatic, so look out for the presence of risk factors - Intermittent claudication - due to limb ischaemia - Thigh or buttock pain with walking that is relieved with rest

Answer 77

This is known as critical limb ischaemia- caused by inadequate supply of blood to a limb to allow normal function at rest 6 Ps Pain Pallor Pulseless Paralysis Paraesthesia (abnormal sensation or “pins and needles”) Perishing cold

Answer 78

Acute limb ischaemia - sudden onset of ischaemia in a limb. Typically due to a thrombus blocking arterial supply to a distal limb.

Answer 79

Ankle-brachial pressure index (ABPI) Duplex ultrasound – ultrasound that shows the speed and volume of blood flow Angiography (CT or MRI) – using contrast to highlight the arterial circulation

Answer 80

The ratio between the systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm. Taken using a Doppler probe For example: ankle SBP of 80 vs. arm SBP of 100 gives a ratio of 0.8 (80/100).

Answer 81

Normal - no presence of PAD

Answer 82

Mild peripheral arterial disease

Answer 83

Moderate to severe peripheral arterial disease

Answer 84

Severe PAD to critical ischaemic.

Answer 85

- Lifestyle changes - Exercise training - walking to near maximal claudication, then rest and repeat - Optimise management of co-morbidities (such as hypertension and diabetes) Medical treatments: - Atorvastatin 80mg - Clopidogrel 75mg once daily (or aspirin) - Naftidrofuryl oxalate (peripheral vasodilator)

Answer 86

Revasculation surgery: - Endovascular angioplasty and stenting - Endarterectomy (removal of fatty deposits) - Bypass surgery (new path around affected artery) - Amputation of the limb if it is not possible to restore the blood supply

Answer 87

- Endovascular thrombolysis – catheter inserted through the arterial system to apply thrombolysis directly into the clot - Endovascular thrombectomy – catheter inserted through the arterial system, and thrombus is removed by aspiration or mechanical devices - Surgical thrombectomy – cutting open the vessel and removing the thrombus - Amputation of the limb if it is not possible to restore the blood supply

Answer 88

Pericardial effusion is where excess fluid (more than 50ml) collects within the pericardial cavity. Pericardial effusion can be acute or chronic.

Answer 89

The pericardium consists of visceral (inner) and parietal (outer) layers. Between them is the pericardial cavity, which has potential space Pericardial effusion = pericardial cavity filled with fluid > inward pressure on the heart which makes it difficult for it to expand during diastole.

Answer 90

- Pericarditis can causes inflammation > pericardial effusion - Pericarditis can result from: - Infection (e.g., tuberculosis, HIV, EBV) - Autoimmune and inflammatory conditions (e.g., SLE and RA) - Injury to the pericardium Conditions which cause increased venous pressure, reducing drainage from the pericardial cavity: - Congestive heart failure - Pulmonary hypertension

Answer 91

Cardiac tamponade - pericardial effusion large enough to raise intra-pericardial pressure > heart cannot fill properly during diastole > decreased CO > medical emergency!

Answer 92

It depends on how quickly the effusion develops: - Rapid onset - cardiac tamponade can cause haemodynamic compromise and collapse - Slowly developing, chronic effusions may initially be asymptomatic. As pressure rises, symptoms can include: - Chest pain - Shortness of breath - A feeling of fullness in the chest - Orthopnoea (shortness of breath on lying flat)

Answer 93

- Tachycardia - Hypotension - Distant heart sounds - Elevated jugular venous pressure - Pulsus paradoxus (decrease in systolic arterial pressure) >10 mmHg.

Answer 94

The investigation of choice is echocardiogram as it can: - Diagnose pericardial effusion - Assess the size of the effusion - Assess the effect on the heart function (haemodynamic effect) Fluid analysis is performed on the pericardial fluid to diagnose the underlying cause

Answer 95

- ECG - electrical alternans i.e., varying amplitude of QRS complexes - Transthoracic echocardiogram - large pericardial effusion - CXR - enlarged heart - FBC - raised WBC count and inflammatory markers might indicate pericarditis

Answer 96

Treatment of the underlying cause with aspirin, NSAIDs, colchicine or steroids (e.g., infection) Drainage of larger effusion: - Needle pericardiocentesis (echocardiogram guided) - Surgical drainage

Answer 97

Urgent pericardiocentesis!

Answer 98

A combination of four pathologies affecting the heart: - Pulmonary valve stenosis - Right ventricular hypertrophy - Ventricular septal defect (VSD) - Overriding aorta

Answer 99

1. Pulmonary valve stenosis - narrowing of the pulmonary valve makes it difficult for deoxygenated blood to leave the right ventricle into the pulmonary circulation 2. Right ventricular hypertrophy - RV compensates for increased resistance by undergoing hypertrophy (boot-shaped heart) 3. Ventricular septal defect (VSD) - gap between the RV and LV, which allows shunting of blood between them. Due to RV hypertrophy, pressure in the RV > LV and deoxygenated blood is shunted from RV to LV 4. Overriding aorta - aorta entrance sits above the septal defect, meaning that a greater proportion of deoxygenated blood enters the aorta and systemic circulation from RV

Answer 100

- Rubella infection - Increased age of the mother (over 40 years) - Alcohol consumption in pregnancy - Diabetic mother

Answer 101

Investigation of choice: echocardiogram Echo produces coloured pictures of the heart - doppler flow studies to assess the severity, gives you audio and visuals of blood flow through heart. Chest x-ray - boot-shaped heart due to RV hypertrophy

Answer 102

Most TOF cases are picked up at antenatal scans before the baby is born - Ejection systolic murmur due to pulmonary stenosis - newborn baby check - HF in severe cases present < 1 years old - Milder cases will present in older children as signs and symptoms of HF develop: - Cyanosis (blue discolouration of the skin due to low oxygen saturation) - Clubbing - Poor feeding - Poor weight gain - Ejection systolic murmur heard loudest in the pulmonary area (second intercostal space, left sternal border) - “Tet spells”

Answer 103

Intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode.

Answer 104

- Children might squat or put their knees to their chest as this increases peripheral vascular resistance by bending the femoral arteries which encourage blood to enter the pulmonary arteries.

Answer 105

Definitive treatment choice - total surgical repair by open heart surgery Neonates - given prostaglandin infusion to keep ductus arteriosus open to allow LV > RV shunt Prognosis - 90% will live to adulthood if surgery successful

Answer 106

- Coarctation of the aorta is a congenital condition with narrowing of the aortic arch, usually around the ductus arteriosus (70% cases infant, 30% adults) - Severity of the coarctation (or narrowing) can vary from mild to severe. - Often associated with an underlying genetic condition, particularly Turners syndrome (one X chromosome in females)

Answer 107

Narrowing of the aorta reduces the pressure of blood flowing to the arteries that are distal to the narrowing. It increases the pressure in areas proximal to the narrowing, such as the heart and the first three branches of the aorta.

Answer 108

- Ductus arteriosus remains patent (open), allowing RV to LV shunt - Pressure in aorta after coarctation is lower than in pulmonary arteries > deoxygenated blood from RV goes to LV via ductus arteriosus into the lower extremities Results in lower limb cyanosis in infants

Answer 109

- Ductus arteriosus is closed and forms the ligamentum arteriosum - No mixing of deoxygenated and oxygenated blood - Pressure higher in areas proximal to narrowing, pressure lower in areas distal to narrowing - Upstream - increased flow into aortic branches > increased pressure in upper limbs and head > increased risk of berry aneurysm and aortic dissection - Downstream - lower pressure so inadequate blood flow to lower limbs = weak pulses - Results in claudication - Kidneys respond to low blood flow by activating RAAS > hypertension

Answer 110

- Neonates = weak femoral pulses often only symptom - Perform four limb blood pressure check: - High BP in limbs supplied by arteries before the coarctation - Low BP in limbs supplied by arteries that come after the coarctation - Systolic murmur below left clavicle and scapula Signs might include: - Tachypnoea and increased work of breathing - Poor feeding - Grey and floppy baby

Answer 111

- ECG - may show normal heart, but may show RVH or LVH - CxR - may be normal, but may show cardiomegaly and/or posterior rib notching in adults due to vessel enlargement - Echocardiogram - narrowing in the thoracic aorta; pressure gradient across narrowing - colour doppler will clearly show high velocity turbulent flow after the narrowing

Answer 112

- If mild, patients can live symptom-free until adulthood but might need surgery as an adult - Severe case - emergency surgery shortly after birth - Prostaglandin E infusion - keeps ductus arteriosus open before surgery - allowing blood flow through the ductus arteriosus into the systemic circulation distal to the coarctation. - Surgery is then performed to correct the coarctation and to ligate the ductus arteriosus.

Answer 113

Shock is a life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to cells and oxygen utilisation by the cells. Causes: - Decreased blood perfusion of tissues - Inadequate blood oxygen saturation - Increased oxygen demand from the tissues

Answer 114

Shock resulting from the loss of intravascular volume

Answer 115

Shock resulting from pump dysfunction where tissue hypoperfusion resulting from loss of cardiac output induces tissue (cellular) inflammation.

Answer 116

Haemorrhagic causes: gastrointestinal bleeding and trauma. Non-haemorrhagic causes include burns, dehydration, third-space losses and diabetic ketoacidosis.

Answer 117

Most commonly occurs after MI, but infections such as sepsis can cause it too.

Answer 118

Clammy, pale skin, confusion, hypotension and tachycardia

Answer 119

ABCDE (airways, breathing, circulation, disability and exposure) - GIve O2 for airways + breathing - Give IV fluids

Answer 120

Heart failure signs such as oedema, increased JVP and S4 heart sound.

Answer 121

- ABCDE - fluid resuscitation + O2 therapy etc. - Treat underlying cause

Answer 122

Shock resulting from the failure of vasoregulation, which results in a fall in systemic vascular resistance with vasodilation and warm peripheries. Causes include sepsis, anaphylaxis, and brainstem or spinal injury (neurogenic).

Answer 123

It is usually a result of a combination of shock: - Distributive: (failure of vasoregulation): results in a fall in systemic vascular resistance with vasodilation and, classically, warm peripheries. - Cardiogenic: pump dysfunction As a result of uncontrolled septicemia (bacterial infection in the bloodstream)

Answer 124

Pyrexia, warm peripheries, bounding (strong) pulse

Answer 125

- ABCDE - O2 therapy and IV fluids - Broad spectrum Abx

Answer 126

Shock caused by spinal cord injury, e.g., in a road traffic accident. This leads to disrupted SNS but intact PNS.

Answer 127

Hypotension, confusion, bradycardia, hypothermia.

Answer 128

ABCDE - IV fluids, O2 therapy IV atropine - block vagal, allows more PNS inhibition and gives a chance for SNS to work

Answer 129

Anaphylaxis is a life-threatening medical emergency, caused by a severe type 1 hypersensitivity reaction. This causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise.

Answer 130

Immunoglobulin E (IgE) mediate type 1 hypersensitivity reactions. IgE stimulates mast cells to release histamine and other pro-inflammatory chemicals rapidly. This is called mast cell degranulation.

Answer 131

Immunoglobulin E (IgE) mediate type 1 hypersensitivity reactions. Two phases: - Sensitisation - The IgE antibodies are formed in response to an antigen (or allergen); some people have genetic deposition IgE binds to high-affinity receptors on mast cell surface > primed to react on the second exposure - Subsequent exposure to allergen: IgE stimulates mast cells to release histamine and other pro-inflammatory chemicals rapidly. This is called mast cell degranulation. This causes rapid onset of symptoms with airway, breathing and/or circulation compromise

Answer 132

Patients present with a history of exposure to an allergen (although it can be idiopathic). There will be a rapid onset of allergic symptoms: - Urticaria (hives) - Itching - Angio-oedema, with swelling around lips and eyes - Abdominal pain Additional symptoms that indicate anaphylaxis are: - Shortness of breath - Wheeze - Swelling of the larynx, causing stridor (noisy breathing) - Tachycardia - Lightheadedness - Collapse

Answer 133

1. Rapid assessment:  ABCDE 2. Call for help (resus team or ambulance) 3. IM adrenaline (dose based on age) 4. If no response after 5 mins - a second IM adrenaline injection + IV bolus (0.9% NaCl solution) 5. If no improvement: - Confirm resuscitation team or ambulance has been called - Follow refractory anaphylaxis algorithm

Answer 134

- Adult and child >12 years: 500 micrograms IM (0.5 mL) - Child 6–12 years: 300 micrograms IM (0.3 mL) - Child 6 months to 6 years: 150 micrograms IM (0.15 mL) - Child <6 months: 100–150 micrograms IM (0.1–0.15 mL)

Answer 135

Second anaphylactic reaction after successful treatment of the first. All patients should be assessed and observed for in hospital a period of time after the anaphylactic reaction - 6 - 12 hrs

Answer 136

Measuring the serum mast cell tryptase, a mast-cell-specific protease. Elevated serum tryptase levels = massive mast-cell degranulation, 6 hours in blood then disappears. NICE recommendations: - As soon as possible after emergency treatment for anaphylaxis - 1-2 hours after onset of first symptoms of anaphylaxis (and no later than 4 hours) - Another sample after 24 hours to establish baseline.

Answer 137

The proportion of a population found to have the disease at a point in time.

Answer 138

The rate at which new cases occur in a population in a certain time period.

Answer 139

- Food-induced anaphylaxis = highest in young children - In < 30 years old = food and exercise - Atopy (genetic disposition to allergic conditions) /Asthma - History of anaphylaxis - Exposure to common sensitizer (e.g. latex in healthcare professionals

Answer 140

A type of supraventricular tachycardia (SVT), characterised by a chaotic irregular atrial arrhythmia.

Answer 141

Mnemonic: PIRATES - Pulmonary: PE and COPD - Ischaemic heart disease - Rheumatic heart disease: any valvular abnormality - Anaemia, Alcohol, Advancing age - Thyroid disease: hyperthyroidism - Electrolyte disturbance: e.g hypo/hyperkalaemia and hypomagnesemia - Sepsis and Sleep apnoea

Answer 142

Normally, the SA node produces electrical activity that coordinates the contraction of the atria and heart. In AF, the contractions of the atria are uncoordinated and irregular because the uncoordinated electrical discharges produced in the atria override the regular impulses produced in the SA node

Answer 143

1) Increasing age: 5% of aged 70-75 years, and 10% aged 80-85 years 2) Diabetes mellitus 3) Hyperthyroidism 4) Hypertension 5) Congestive heart failure 6) Valvular heart disease 7) Coronary artery disease 8) Dietary and lifestyle factors: excessive caffeine intake, alcohol abuse, obesity, smoking, medication use (e.g. thyroxine or beta-agonists)

Answer 144

- First episode - Paroxysmal: recurrent episodes lasting < 7 days - Persistent: recurrent episodes lasting > 7 days - Permanent: continuous atrial fibrillation that is also refractory (does not respond) to treatment.

Answer 145

Normally, the SA node produces electrical activity that coordinates the contraction of the atria and heart. In AF, atrial contractions are uncoordinated and irregular because the uncoordinated electrical discharges produced in the atria override the regular impulses produced in the SA node.

Answer 146

Symptoms: - Red flag: chest pain - Red flag: syncope - Palpitations - Dyspnoea Signs: - Irregularly irregular pulse - Red flag: hypotension suggests haemodynamic instability - Red flag: evidence of heart failure e.g. such as pulmonary oedema

Answer 147

- ECG - irregularly irregular QRS complexes with absent P waves and chaotic baseline - 24-hour ambulatory ECG monitoring for paroxysmal AF - If new myocardial ischaemia = immediate DC cardioversion (restoration of normal sinus rhythm) - KardiaMobile: cardiac event recorder - NICE recommends it for detecting paroxysmal AF with palpitations - Serum electrolytes: electrolytes, magnesium, calcium and phosphate - TFTs: hyperthyroidism is a secondary cause of AF

Answer 148

- Absent P waves - Irregularly irregular QRS complexes - Choatic baseline

Answer 149

Rate-control - does not restore sinus rhythm but controls heart rate to reduce the long-term effects on function. OR Rhythm control - aims to restore sinus rhythm, known as "cardioversion", which can be electrical or pharmacological.

Answer 150

Onset > 48 hours or unknown

Answer 151

Younger age Onset < 48 hours No underlying heart disease Reversible cause of AF Failure of rate control Haemodynamic instability acutely

Answer 152

First line: Beta-blocker e.g. bisoprolol Or Rate-limiting CCB e.g. diltiazem (avoid if HF - use digoxin) Non-cardioselective beta-blockers (e.g propranolol) should be avoided in asthmatic patients due to the risk of bronchospasm

Answer 153

Flecainide or amiodarone: if no evidence of structural/ischaemic heart disease Amiodarone: if structural/ischaemic heart disease is present

Answer 154

Second line: combination therapy with any 2 below: - Beta‑blocker (e.g. bisoprolol) - Diltiazem - Digoxin

Answer 155

Electrical: synchronised DC (cardioversion) shock with general anaesthesia - Immediate cardioversion - AF onset < 48 hours or severely haemodynamically unstable. - Delayed cardioversion - AF onset > 48 hours, and they are stable - Amiodarone 4 weeks before and up to 12 months after delayed cardioversion to maintain sinus rhythm

Answer 156

Left atrial ablation if drug treatment fails or unsuitable: radiofrequency energy is delivered to pulmonary veins - they supply the area causing premature depolarization - ~75% success rate Permanent AF: pace and ablate - pacing and AV node ablation

Answer 157

AF increases the risk of stroke; anticoagulants lower this risk x2 -3 E.g. warfarin or Direct acting Oral Anticoagulants (DOACS) like apixaban

Answer 158

- 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 But a lot more expensive.

Answer 159

AF increases the risk of stroke; anticoagulants lower this risk x2 -3 E.g. warfarin or Direct acting Oral Anticoagulants (DOACS) like apixaban.

Answer 160

- If the patient is haemodynamically unstable (abnormal BP): - Shock: hypotension (systolic BP <90 mm Hg) - Syncope: transient loss of consciousness - Myocardial ischaemia: chest pain and/or evidence on ECG - Heart failure: pulmonary oedema and/or raised jugular venous pressure

Answer 161

Hypertension, IHD, angina, MI (or ACS), arrhythmias and heart failure

Answer 162

Beta-adrenoceptor blocking drugs (beta-blockers) block the beta-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, and liver. Thus, they block the effects of the hormone adrenaline, causing the heart to beat more slowly (negatively chronotropic) and with less force (negatively inotropic), which lowers blood pressure. Beta blockers also help widen veins and arteries to improve blood flow - useful in IHD

Answer 163

Abdominal discomfort; bradycardia; fatigue, cold peripherals, vivid dreams (fat-soluble), erectile dysfunction Water-soluble beta-blockers are less likely to enter the brain, unlike fat-soluble ones, so they are less likely to cause sleep disturbances and nightmares

Answer 164

Because beta-blockers are excreted by the kidneys and patients with renal impairment might not excrete the drug as effectively.

Answer 165

Hypertension, heart failure, prophylaxis after MI

Answer 166

ACE inhibitors block the action of angiotensin-converting enzyme, which prevents conversion of angiotensin I to angiotensin II - Angiotensin II has three main effects: - Constriction of blood vessels - so ACEis cause blood vessel dilation - Reabsorption of water by the kidneys - so ACEis lower BV - Release of the hormone aldosterone, which also causes water re-absorption by the kidneys - so ACEi lower BV Blood vessel dilation and decreased water reabsorption by the kidney lead to lowered blood pressure.

Answer 167

People of black African or Caribbean origin as they are usually less dependent on renin so the RAAS is less implicated in MI - give calcium-channel blockers instead.

Answer 168

- Hypotension - Persistent dry cough - Hyperkalaemia - Cause or worsen renal failure

Answer 169

- Chronic heart failure for symptomatic relief of fluid overload

Answer 170

Loop diuretics inhibit water reabsorption from the ascending limb of the loop of Henlé in the renal tubule by inhibiting Na+/K+/2Cl- co-transporters.

Answer 171

- Dehydration - Hypotension - Hyponatremia - Hypokalaemia

Answer 172

Shock resulting from the loss of intravascular volume

Answer 173

- A type of supraventricular tachycardia - Caused by reentry circuit in or around AV node. - Two separate pathways form the re-entrant circuit: - Alpha pathway - slow conduction, short refectory period - Beta pathway - fast conduction, long refectory period

Answer 174

Atrioventricular nodal re-entry tachycardia (AVNRT) is the most common type of SVT.

Answer 175

1. Sudden onset/offset palpitations. 2. Neck pulsation. 3. Chest pain. 4. Shortness of breath.

Answer 176

No - the P waves are within the QRS complex.

Answer 177

Acute treatment: vagal manoeuvre and adenosine. Chronic treatment (prevent further episodes): Amiodarone, Procainamide Definitive treatment: radiofrequency catheter ablation (RFA) of the slow alpha pathway

Answer 178

A type of heart arrhythmia caused by an accessory pathway, or an extra electrical conduction pathway, connecting the atria and ventricles The most common is Wolff-Parkinson-White syndrome.

Answer 179

"Bundle of kent" - congenital muscle strands connect the atria and ventricles - accessory pathway. This can result in pre-excitation of ventricles

Answer 180

- Shorter PR interval (<120ms) - Delta wave (slurred upstroke to QRS due to pre-excitation of ventricles) - Longer QRS complex (>110ms)

Answer 181

Radiofrequency ablation of the accessory pathway (bundle of kent)

Answer 182

Hypertension is defined as a blood pressure reading of ≥140/90 mmHg (ambulatory blood pressure monitoring ≥135/85 mmHg).

Answer 183

Primary (90 - 95%) and secondary.

Answer 184

Primary hypertension, otherwise known as essential hypertension, has no known underlying secondary cause and is responsible for 90-95% of cases of hypertension.

Answer 185

R – Renal disease. Most common O – Obesity P – Pregnancy-induced hypertension/pre-eclampsia E – Endocrine. Most endocrine conditions (for example, hyperthyroidism) can cause hypertension but primarily consider hyperaldosteronism (“Conns syndrome”)

Answer 186

1) Non-modifiable risk factors: increasing age, African heritage, family history 2) Modifiable risk factors: obesity, sedentary lifestyle, alcohol excess, smoking, high sodium intake (>1.5g/day), stress

Answer 187

Symptoms 1) Asymptomatic: most common presentation 2) Headaches: classically occipital and worse in the morning Signs 1) Malignant hypertension (≥180/120 mmHg): - Hypertensive retinopathy - Visual disturbance - Cardiac symptoms e.g. chest pain - Oliguria or polyuria 2) Secondary hypertension: signs of the underlying cause For example, hyperthyroidism causes weight loss, sweating and palpitations

Answer 188

1) Blood-pressure reading: both arms If the clinic blood pressure is ≥140/90mmHg, take a second reading. Record the lower of the 2 measurements as the clinic blood pressure. Arms pressure difference ≥ 15 mmHg, take higher reading 2) Ambulatory blood pressure monitoring (ABPM): If patient's BP between 140/90 mmHg and 180/120 mmHg to confirm the diagnosis Blood pressure is measured over a 24 hour period, with at least 2 measurements per hour during waking hours At least 14 measurements are required 3) Home blood pressure monitoring (HBPM): Offered if ABPM is not appropriate; HPBM involves the patient checking their blood pressure manually throughout the day - over 7 days.

Answer 189

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.

Answer 190

1) Stage 1 Hypertension Clinic Reading: >140/90 Ambulatory / Home Readings >135/85 2) Stage 2 Hypertension Clinic Reading: >160/100 Ambulatory / Home Readings >150/95 3) Stage 3 Hypertension Clinic Reading: >180/120 Ambulatory / Home Readings: >180/120

Answer 191

- Fundoscopy: assess for hypertensive retinopathy - 12-lead ECG: assess for ischaemic changes and evidence of left ventricular hypertrophy - Albumin:creatinine ratio (ACR) and urinalysis: assessing for renal dysfunction, as evidenced by elevated ACR and proteinuria or haematuria on urinalysis - Bloods: HbA1c, U&Es, total cholesterol and HDL cholesterol

Answer 192

1) Establish a diagnosis. 2) Investigate for possible causes and end organ damage. 3) Advise on lifestyle. This includes recommending a healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.

Answer 193

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) ARB is used if ACEi is not tolerated or the patient is of Afro-Caribbean or African descent.

Answer 194

There are slightly different guidelines for younger patients and those aged over 55 or black: Step 1: Aged less than 55 and non-black use A. Aged over 55 or black of African or African-Caribbean descent - use C. Step 2: A + C. Alternatively A + D or C + D. If black then use an ARB instead of A. Step 3: A + C + D Step 4: A + C + D + additional (see below) For step 4, if the serum potassium is ≤ 4.5 mmol/l then consider a potassium-sparing diuretic such as spironolactone. If the serum potassium is > 4.5 mmol/l, consider an alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol). Seek specialist advice if the blood pressure remains uncontrolled despite treatment at step 4.

Answer 195

< 80 years Systolic Target: < 140 Diastolic Target: < 90 > 80 years Systolic target: < 150 Diastolic target: < 90

Answer 196

1) Coronary artery disease: for every +20/10 mmHg in BP, there is a doubling of mortality related to IHD 2) Cerebrovascular accident 3) Congestive heart failure: hypertensive patients x3 more likely 4) Chronic kidney disease

Answer 197

Atrioventricular (AV) block is a cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles.

Answer 198

Delayed atrioventricular conduction through the AV node. Despite this, every atrial impulse makes it to a ventricular contraction, meaning every P wave results in a QRS complex.

Answer 199

ECG - PR interval > 0.20 seconds (200ms) (5 small or 1 big square).

Answer 200

Usually asymptomatic

Answer 201

- Usually no further treatment if asymptomatic, patients are monitored If symptomatic - Identify and correct electrolyte imbalance - Identify and stop AV-nodal blocking medications (e.g. beta-blockers, CCB, digoxin)

Answer 202

Some 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 different types: 1) Wenckebach’s phenomenon (Mobitz Type 1) 2) Mobitz Type 2 3) 2:1 Block

Answer 203

This is where the atrial impulse 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.

Answer 204

ECG - PR prolongation until a QRS complex is dropped, i.e. PR interval progressively elongates

Answer 205

This is where there is intermitted (random) 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 a 3:1 block. The PR interval remains normal. There is a risk of asystole (heart stopping) with Mobitz Type 2.

Answer 206

PR intervals are consistently prolonged (not consistently prolonging), with randomly dropped QRS complexes.

Answer 207

This is referred to as complete heart block. Electrical signal from atria to ventricle completely blocked. P waves and QRS complexes therefore occur independently. Ventricles: escape beats at ~30bpm

Answer 208

P waves and QRS complexes occurring independently of each other.

Answer 209

There are pacemaker cells in the ventricles that depolarise at a rate of about 20 - 40 bpm. Under normal conditions, these slower pacemakers are suppressed by the more rapid impulses from above (i.e. sinus rhythm). However, if the ventricles do not receive a signal from the atria, such as in 3rd-degree heart block, then the ventricular pacemaker cells will kick in, leading to escape beats of about 20 - 40 bpm.

Answer 210

First-degree: AV nodal blocking drugs: beta-blockers, CCB, digoxin, adenosine Second-degree Morbitz type 1: drugs (above), inferior wall MI Mobitz type II: drugs (above), inferior wall MI, rheumatic fever Third-degree: acute MI, hypertension, structural heart defects

Answer 211

Usually non but some people can experience light-headedness, dizziness and syncope

Answer 212

Fatigue, dyspnoea, syncope, chest pain

Answer 213

Syncope, confusion, dyspnoea, SEVERE CHEST PAIN There is a significant risk of asystole (DYING) with third-degree heart block

Answer 214

For all: identify and treat electrolyte imbalances + stop AV nodal blocking meds 1) Asymptomatic: - 1st line is the discontinuation of AV-nodal blocking drugs, identify and treat electrolyte imbalances. - 2nd line: permanent pacemaker (PPM) implantation for Morbitz type II 2) Symptomatic second or third-degree: 1st line is the discontinuation of AV-nodal blocking drugs, identifying and treating electrolyte imbalances and temp pacing (transcutaneous) 2nd: PPM for MT I and II second-degree and third-degree

Answer 215

The branch bundles describe the conduction fibres that run along the ventricular septum - divided into right and left bundle branches. They derive from the Bundle of His which conducts the electrical impulses from the AV node A Bundle Branch block is the blockage of the electrical signal in the LBB or RBB, preventing the electrical signal from travelling from the atria to the ventricles.

Answer 216

Either physiological or the result of damage to the right bundle branch: - underlying lung pathology (COPD, pulmonary emboli, cor pulmonale) - Congenital heart disease (e.g. atrial septal defect) - Ischaemic heart disease

Answer 217

1) The SA node acts as the initial pacemaker 2) Depolarisation reaches the atrioventricular node 3) Depolarisation through the bundle of His occurs only via the left bundle branch. The left branch still depolarises the septum as normal. 4) The left ventricular wall depolarises as normal. 5) The right ventricular walls are eventually depolarised by the left bundle branch. This occurs by a slower, less efficient pathway.

Answer 218

Always pathological! Left bundle branch block may be due to conduction system degeneration (e.g. fibrosis) or ischaemic heart disease, cardiomyopathy and valvular heart disease. LBBB may also occur after cardiac procedures which damage the left bundle branch or His bundle.

Answer 219

1) The sino-atrial node acts as the initial pacemaker 2) Depolarisation reaches the atrioventricular node 3) Depolarisation down the bundle of His occurs only via the right bundle branch. The septum is abnormally depolarised from right to left. 4) The right ventricular wall is depolarised as normal. 5) The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway.

Answer 220

Acute: heart attacks, ischaemia, myocarditis Chronic: hypertension, IHD, cardiomyopathies

Answer 221

WiLLiaM "W" shape in the QRS complex of lead V1 "M" shape in lead V6

Answer 222

MaRRoW "M" shape in lead V1 (RSR wave) "W" shape in lead V6 (Deep S wave)

Answer 223

If it has been present since birth and is asymptomatic, then no treatment is needed. If it is caused by another heart disease, for example, IHD, then optimise treatment for the underlying condition. If severe, cardiac resynchronization pacemaker implantation. This device has electrical leads going to both RV and LV. These leads can pace the ventricles at the same time, causing them both to contract at the same time, which helps improve cardiac function.

Answer 224

Infective endocarditis (IE) is an infection of the endocardium or other endothelial-lined structures such as heart valves. This usually involves two pathological variables: an abnormal endocardium and a bacterial source.

Answer 225

The mitral valve is most commonly affected Tricuspid valve most associated with IVDU 1) Acute - Develops over days to weeks - Most commonly associated with staph aureus - Rapid valvular destruction 2) Subacute - Develops over weeks to months - Most commonly associated with strep viridans 3) Non-bacterial thrombotic ‘marantic’ - Non-infective cause of endocarditis secondary to thrombus formation on the valvular surface - Associated with malignancy or SLE (Libman-Sacks endocarditis)

Answer 226

1) Rheumatic fever, valvular pathology, prosthetic valves, or congenital heart disease associated with an abnormal endocardium. 2) Any cause of an abnormal endocardium → turbulent blood flow and thrombus formation thrombus becomes infected due to a bacterial source, such as IV drug use or an infected cardiac device. Bacterial colonisation of the thrombus → formation of vegetations → valvular damage

Answer 227

1) Male gender: x2.5 times more likely 2) Previous infective endocarditis 3) Prosthetic heart valves 4) Congenital heart disease 5) Rheumatic heart disease 6) Intravenous drug use (IVDU)

Answer 228

1) Elderly. 2) IVDU. 3) Those with prosthetic valves. 4) Those with rheumatic fever

Answer 229

1) Staph aureus - most common (IVDU, prosthetic valves) 2) Staph epidermis (coagulase-negative staph) (prosthetic valves and indwelling lines) 3) Streptococcus bovis (colon cancer) 4) Strep viridans (alpha haemolytic) (native valves) 5) Strep mitis and sanguinis (viridans streptococci) (poor dental hygiene, infection post-dental procedure)

Answer 230

Vegetation - lumps of fibrin hanging off the heart valves.

Answer 231

1. Atrial surface of AV valves. 2. Ventricular surface of semilunar (aortic and pulmonary) valves.

Answer 232

1) Fever or chills 2) Headache 3) Shortness of breath 4) Night sweats, malaise, fatigue, weight loss 5) Joint pain: may be due to septic emboli

Answer 233

1) Heart murmur +/- evidence of heart failure 2) Janeway lesions: painless plaques on palms and soles due to septic microemboli 3) Osler’s nodes: painful nodules on fingers or toes due to immune complex deposition 4) Splinter haemorrhages: red-plum lines under the nails due to microemboli 5) Roth’s spots: white centred retinal haemorrhages 6) Mild splenomegaly

Answer 234

Diagnosed using modified Duke's criteria (see specific flashcard). Investigations: 1) Inflammatory markers: raised WCC (especially neutrophilia), raised CRP and ESR 2) Blood cultures - detects causative organism 3) Echocardiogram (echo): vegetation = confirms diagnosis - 1st line is transthoracic echo - TOE is gold standard 4) ECG (prolonged PR interval)

Answer 235

The Modified Duke Criteria requires 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria for a diagnosis of infective endocarditis. Major: 1) ≥ 2 positive blood cultures 2) Echo TOE shows vegetation Minor: 1) Immunological signs (e.g. Roth's spots, Olser's nodes) 2) 1 positive blood culture 3) Pyrexia ≥ 38c 4) IVDU 5) Predisposing heart condition 6) Septic emboli

Answer 236

First line: IV antibiotics: - 4 weeks - 6 weeks for patients with prosthetic valve Second line: Surgery: aim to remove infected tissue and repair or replace affected valves

Answer 237

1) Empirical: - Native - amoxicillin +/- gentamicin - Prosthetic - vancomycin + gentamicin and rifampicin 2) Staphylococci - Native - flucloxacillin - Prosthetic - flucloxacillin + rifampicin + gentamicin 3) Staphylococci (MRSA) - Native - vancomycin + rifampicin - Prosthetic - vancomycin + gentamicin and rifampicin 4) Streptococci - Native - benzylpenicillin +/- gentamicin

Answer 238

It restrains filling of the heart

Answer 239

The pericardium is formed of the parietal and visceral layers, innervated by the phrenic nerve. Pericarditis is the inflammation of the pericardium - pericardial effusion can develop, which can lead to cardiac tamponade

Answer 240

1) 80 - 90% are idiopathic 2) Viral (common) e.g. coxsackievirus - most common viral cause

Answer 241

- Male gender - 20-50 years of age - Previous myocardial infarction - Viral or bacterial infection - Systemic autoimmune disorders

Answer 242

- Chest pain! Described as severe, sharp and pleuritic. Rapid onset. Pain can radiate to the arm. Relieved by leaning forward. - Prodromal viral illness: e.g. upper respiratory tract infection - Fever and myalgia - Shortness of breath - Peripheral oedema - suggestive of RHF secondary to pericarditis

Answer 243

- Pericardial rub - squeaky sound heard at the left sternal edge as the patient leans forward - Tachycardia - Tachypnoea

Answer 244

1) ECG: widespread saddle-shaped ST-elevation and PR depression 2) Chest X-ray: pericardial effusion; “water-bottle heart” 3) Transthoracic echocardiogram: exclude a pericardial effusion or tamponade 4) ESR and CRP: raised indicates inflammation

Answer 245

Myocardial infarction, rule out ASAP!

Answer 246

1) Acute idiopathic or viral pericarditis: - 1st line: NSAIDs and colchicine - 2nd line: NSAIDs, colchicine and low-dose prednisolone 2) Bacterial pericarditis - IV antibiotics and pericardiocentesis with washout, culture and sensitivities 3) Cardiac tamponade: - Urgent therapeutic pericardiocentesis 4) Refractory pericarditis: - Pericardectomy

Answer 247

The parietal pericardium is able to adapt when effusions accumulate slowly and so tamponade is prevented.

Answer 248

Viral infection.

Answer 249

1) Hypertrophic (HCM) 2) Dilated (DCM) 3) Arrhythmogenic right/left ventricular (ARVC/ALVC).

Answer 250

Sarcomeric gene mutations e.g. beta myosin, troponin T mutations. About 1 in 500 people are affected.

Answer 251

- Autosomal dominant familial - cytoskeleton gene mutation - IHD - Alcohol - Haemochromatosis

Answer 252

- Granulomatous disease (sarcoidosis, amyloidosis) - Idiotipathic - Post-MI fibrosis

Answer 253

Autosomal dominant -Ventricular dilation and dysfunction = poor contractility. offspring have 50% chance of inheriting the disease

Answer 254

Systole is normal but diastole is affected; the heart is unable to relax properly due to thickening of the ventricular walls.

Answer 255

Ventricular dilation and dysfunction = poor contractility.

Answer 256

Ridgid fibrotic myocardium, which restricts filling during diastole and contracts poorly.

Answer 257

- Angina. - Dyspnoea. - Syncope. SUDDEN DEATH IS POSSIBLE!

Answer 258

DCM usually presents with symptoms similar to those seen in heart failure: - Breathlessness - Fatigue - Oedema

Answer 259

- Severe dyspnoea - Oedema - S3 and S4 heart sounds - Congestive heart failure - Narrow pulse pressure (105/95 mmHg)

Answer 260

- ECG - large QRS complexes, large inverted T waves. - Echo (definitive) - Genetic testing

Answer 261

ECG and echo (definitive)

Answer 262

ECG, echo, cardiac catheterisation (definitive)

Answer 263

1) Asymptomatic: - At risk of sudden death - implantable cardioverter-defibrillator - Not at risk of sudden death - observation 2) Symptomatic: - Negative inotropic and chronotropic agents

Answer 264

- Pacemaker –monitor and pace your heart rhythm by delivering electrical impulses if your heart misses a beat or is beating too slowly - Implantable cardioverter defibrillator (ICD) – to monitor your heart rhythm and deliver an electrical shock to restore your heart’s normal rhythm if your rhythm becomes dangerous

Answer 265

None, consider heart transplant Patients usually die within a year of diagnosis

Answer 266

The pathological narrowing of the aortic valve orifice results in obstruction of blood flow. - Progressive disease, with decades of preclinical period - Often preceded by aortic sclerose, the thickening + stiffening of the valve leaflets without narrowing of the orifice.

Answer 267

- Calcification and fibrosis of aortic valve - 80% - Congenital bicuspid valves - valve leaflets are subject to abnormal mechanical stress predisposing them to degeneration and calcification - Rheumatic fever - developing countries and rare

Answer 268

1) Advancing age: increase in calcification 2) Congenital bicuspid valve: presents 20+ years earlier than patients with trileaflet valves 3) Turner syndrome and coarctation of the aorta - higher incidences of bicuspid valves 4) Rheumatic fever 5) Chronic kidney disease: abnormal calcium homeostasis 6) Hypertension, smoking, high LDL cholesterol: increase risk of aortic sclerosis

Answer 269

- The aortic orifice is restricted e.g. by calcific deposits and so there is a pressure gradient between the LV and the aorta. - LV function is initially maintained due to compensatory hypertrophy. - Overtime this becomes exhausted = LV failure.

Answer 270

- Exertional syncope. - Angina. - Exertional dyspnoea. - Onset of symptoms is associated with poor prognosis.

Answer 271

- Slow rising carotid pulse and decreased pulse amplitude. - Soft or absent heart sounds. - Ejection systolic murmur over aortic area

Answer 272

1) ECG: features of left ventricular hypertrophy 2) Transthroacic echocardiography: abnormal - Aortic valve area: reduced - Mean aortic pressure gradient: increased - LVEF: this may be reduced if there is heart failure

Answer 273

- Ensure good dental hygiene. - Consider IE prophylaxis. - Aortic valve replacement or Transcatheter aortic valve implantation (TAVI)

Answer 274

1) Symptomatic patients with aortic stenosis. 2) Any patient with decreasing ejection fraction. 3) Any patient undergoing CABG with moderate/severe aortic stenosis.

Answer 275

The inability of the mitral valve to close properly, allowing backflow of blood from the LV to the LA during systole.

Answer 276

1) Myxomatous degeneration (prolapse of mitral valve). 2) Ischaemic mitral regurgitation. 3) Rheumatic heart disease. 4) IE.

Answer 277

- Dyspnoea on exertion. - Evidence of heart failure - peripheral oedema etc. - Pansystolic murmur (always there). - Soft 1st heart sound. - 3rd heart sound. - In chronic MR the intensity of the murmur correlates with disease severity.

Answer 278

- ECG. - Transthoracic echocardiogram: estimates LA/LV size and function

Answer 279

- Rate control for AF e.g. beta blockers. - Anticoagulation for AF. - Diuretics for fluid overload. - IE prophylaxis i.e. Abx - If symptomatic = surgery

Answer 280

A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.

Answer 281

- Bicuspid aortic valve. - Rheumatic fever - Infective endocarditis

Answer 282

Pressure and volume overload in the LV due to backflow of blood from aorta. LV dilatation and hypertrophy to compensate Progressive dilatation leads to HF eventually

Answer 283

Symptoms: - Dyspnoea on exertion. - Orthopnea. - Palpitations. - Paroxysmal nocturnal dyspnea (waking up at night with episods of breathlessness and wheezing) Signs: - Wide pulse pressure (difference between systolic and diastolic) - Diastolic blowing murmur. - Systolic ejection murmur.

Answer 284

- Echocardiogram - confirms the diagnosis and detects the origin of the regurgitant jet - CXR - cardiomegaly possible - ECG - ST-T waves changes, conduction abnormalities

Answer 285

Acute: - Inotropes - Urgent aortic valve replacement/repair - Vasodilators e.g. ACEi. Ongoing: - Surgery if symptomatic - aortic valve surgery - Regular echoes to monitor progression. - IE prophylaxis

Answer 286

Narrowing of the mitral valve that causes obstruction of blood flow from LA to LV, which prevents proper filling during diastole.

Answer 287

1) Rheumatic heart disease. 2) IE. 3) Calcification.

Answer 288

Narrowing of mitral valve orifice has two main pathological consequences: 1) LA pressure higher than LV -> pulmonary congestion (oedema) - Pulmonary venous hypertension causes RHF symptoms. 2) Limits filling of the left ventricle, so limiting cardiac output.

Answer 289

Symptoms: - Dyspnoea. - Haemoptysis. - RHF symptoms. Signs: - ‘a’ wave in jugular venous pulsations. - Signs of RHF (see RHF flashcard). - Pink patches on cheeks due to vasoconstriction. - Low pitched diastolic murmur. - Loud opening 1st heart sound snap.

Answer 290

1) ECG - AF, LA enlargement, RV hypertrophy 2) CXR - enlarged left atrium 3) transthoracic echocardiogram is the gold standard - hockey stick-shaped mitral deformity

Answer 291

- If AF rate control, then beta-blockers/CCB. - Anticoagulation if AF. - Balloon valvuloplasty or valve replacement. - IE prophylaxis.

Answer 292

The problem is mechanical and so medical therapy does not prevent progression.

Answer 293

- Aortic dissection - Pericarditis - Pulmonary embolism

Answer 294

- Stable angina - Non-ST elevation myocardial infarction - ST-elevation myocardial infarction

Answer 295

- STEMI - Unstable angina - Aortic dissection For STEMI, the DDx are the same (swap for non-STEMI)

Answer 296

- Pneumonia - Pulmonary embolism - Asthma

Answer 297

- Aging - COPD - Pneumonia

Answer 298

- Acute coronary syndrome - Infective endocarditis - Mitral stenosis

Answer 299

- Mitral regurgitation - Mitral stenosis - Aortic stenosis

Answer 300

- Aortic sclerosis (stiffening) - Ischaemic heart disease - Hypertrophic cardiomyopathy (HCM)

Answer 301

- Unexplained AF

Answer 302

- Athlete's heart - LVH due to hypertension

Answer 303

- Pulmonary valve stenosis - Ventricular septal defect

Answer 304

- Aortic stenosis

Answer 305

- Atrial flutter - Wolff-Parkinson-White syndrome

Answer 306

Atrial flutter with variable atrioventricular (AV) conduction

Answer 307

- Supraventricular tachycardia - AF

Answer 308

- Drug-induced hypertension - CKD

Answer 309

- Cellulitis - Calf muscle tear

Answer 310

- Unstable angina - Non-STEMI - STEMI

Answer 311

- Spinal stenosis - Arthritis

Answer 312

- Simple hypotension - Syncope or pre-syncope

Cardiology Flashcards

(336 cards)