Cardiology COPY COPY Flashcards

Question

What is the plaque erosion stage of atherosclerosis?

Answer 1

- Small early lesions - Fibrous cap does not disrupt - Luminal surface underneath the clot may not have enough endothelium present but is smooth muscle rich - Prominent lipid core

Answer 2

1️⃣ Initiation of inflammation and endothelial cell dysfunction 2️⃣ Stimulus for adhesion of leukocytes - release of chemo-attractants 3️⃣ Dysfunctional endothelial cells allow the transmigration of LDLs into the tunica intima 4️⃣ Accumulation of LDLs tunica intima cause dysfuntional endothelial cells to release ROS and metalloproteases which function to oxidised the LDL → activated oxLDL 5️⃣ The activation of oxLDLs causes endothelial cells to express adhesion receptors for leukcocytes on their surface, leading to uptake of LDLs and monocytes 6️⃣ Surface of macrophages contain a scavenger receptor which facilitates the uptake of oxidised LDLs to form a foam cells 7️⃣ Foam cells have multiple pathophysiological functions: - Release chemokines to attract more macrophages - Release IGF-1 into tunica media to promote migration of SMCs (from media to intima) that increase collagen synthesis leading to the hardening of the atherosclerotic plaque 8️⃣ During this process, foam cells will die → releasing lipid content. This drives the growth of the plaque 9️⃣ Death of foam cells also causes release of contents which causes increased inflammation 🔟 T-cells also facilitate inflammation 🔟+ Excessive growth of the plaque causes it to rupture, leading to accumulation of the RBC, platelets and clotting factors → thrombosis

Answer 3

Cholesterol/ high LDLs in the blood damages the endothelial cells ROS from inflammation.

Answer 4

Selectins cause leukocyte rolling and firm adhesion to the blood vessel walls.

Answer 5

Release chemokines and attract further macrophages to the tunica intima Release IGF-1 into the tunica media to promote migration of Smooth muscle cells from the tunica media into the tunica intima which increases the collagen synthesis and leads to the hardening of the atherosclerotic plaque.

Answer 6

A macrophage that has been up take into the tunica intima that expresses scavenger receptors that will uptake oxidised LDLs This uptake forms a foam cell.

Answer 7

A macrophage that has been up take into the tunica intima that expresses scavenger receptors that will uptake oxidised LDLs This uptake forms a foam cell.

Answer 8

DNA material that attracts neutrophils Proinflammatory cytokines ROS These all lead to increased inflammation.

Answer 9

- IL1, 6 and 8. - IFN-γ - strong proinflammatory cytokine - TGF-β - involves in wound healing - Chemokines (e.g. Monocyte Chemoattractant Protein-1)

Answer 10

Percutaneous Coronary Intervention Drugs

Answer 11

Non-surgical procedure that uses a catheter to place a stent into a narrowed blood vessel

Answer 12

The recurrence of abnormal narrowing of an artery or valve after corrective therapy

Answer 13

Taxol and Sirolimus - work by reducing SMC proliferation after placement of stent. The stent is washed (eluted) with these drugs

Answer 14

Irreversible inhibitor of platelet cyclo-oxygenase to prevent Thromboxane A2 production and further platelet aggregation

Answer 15

Inhibitors of the stimulatory P2Y12 ADP receptor on platelets preventing platelet response amplification

Answer 16

Inhibit HMG CoA reductase - reduces cholesterol synthesis

Answer 17

PCSK9 inhibitors

Answer 18

1. Smoking. 2. High levels of LDL's. 3. Obesity. 4. Low exercise 5. Diabetes. 6. Hypertension. 7. Alcohol consumption

Answer 19

Tunica Media

Answer 20

Fatty streaks.

Answer 21

Chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release e.g. IL-1, IL-6 -> inflammation!

Answer 22

1. Capture. 2. Rolling. 3. Slow rolling. 4. Adhesion. 5. Trans-migration.

Answer 23

The development of an atherosclerotic plaque.

Answer 24

It is an inflammatory process!

Answer 25

Spectrum of acute cardiac conditions ranging from unstable angina to varying degrees of MI

Answer 26

Atherosclerotic rupture and consequential arterial thrombosis!

Answer 27

Anti-platelet medications: Aspirin Clopidogrel Ticagrelor Since a thrombus formed in a fast flowing artery are mostly made up of platelets.

Answer 28

Coronary vasospasm without plaque rupture Drug abuse (amphetamines, cocaine) Spontaneous Coronary Artery Dissection

Answer 29

Amphetamines Cocaine

Answer 30

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

Answer 31

tear in lining, lining comes away from the wall of the artery and blocks vessel.

Answer 32

Atherosclerosis -> plaque rupture -> platelet aggregation -> thrombosis formation -> ischaemia -> hypoxia of cells -> angina infarction -> necrosis of cells -> permanent heart muscle damage and ACS.(MI)

Answer 33

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 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 Another cause such as musculoskeletal chest pain

Answer 34

Protein complex functioning to regulate actin and myosin contraction

Answer 35

Consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle. However they are non specific so a raised troponin does not automatically mean ACS

Answer 36

Highly sensitive marker for cardiac muscle injury - increased levels is very indicative of myocardial cause

Answer 37

not specific for ACS → also increases in conditions that causes stress in myocardium (e.g. PE, gram negative sepsis, myocarditis)

Answer 38

Chronic renal failure Sepsis Myocarditis Aortic dissection Pulmonary Embolism

Answer 39

Angina is a type of Ischaemic Heart Disease (IHD) characterised by chest pain It is an imbalance of O2 supply/demand mismatch to the heart due to reduced blood flow from a blockage

Answer 40

Narrowing of the coronary arteries due to atherosclerosis.

Answer 41

Stable Unstable Decubitus Crescendo Angina Prinzmetals's Vasospastic Microvascular Angina

Answer 42

Unstable Angina

Answer 43

An acute coronary syndrome (ACS) that is defined by the absence of biochemical evidence of myocardial damage but characterised by chest pain at rest/minimal exertion

Answer 44

1. Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis. 2. Increased distal resistance = LV hypertrophy. 3. Reduced O2 carrying capacity e.g. anaemia. 4. Coronary artery spasm. 5. Thrombosis.

Answer 45

1. Smoking. 2. Diabetes. 3. High cholesterol (LDL). 4. Obesity/sedentary lifestyle. 5. Hypertension.

Answer 46

1. Increasing age. 2. Gender - Males 3. Family history/genetics.

Answer 47

Central, Crushing 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 48

On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.

Answer 49

On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina.

Answer 50

When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!

Answer 51

In CV disease: Epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can't drop anymore and flow can't increase to meet metabolic demand = angina!

Answer 52

70% occlusion of the artery. This still allows enough blood flow through the artery at rest.

Answer 53

Occlusion of an artery (70%) leading to ischaemia of the myocardial tissue resulting in chest pain. At rest enough blood can still flow through the artery to meet the demands of the tissue. Upon exercise or exertion, the tissue requires more oxygen and therefore a greater blood flow at which point the flow through the stenosed artery is not adequate enough and hence results in chest pain upon exertion.

Answer 54

Stable angina

Answer 55

Subendocardium. The coronary arteries struggle to perfuse the deeper layers of the myocardium either due to coronary artery stenosis or LV hypertrophy resulting in ischaemia to this portion of the tissue.

Answer 56

Central Crushing chest Pain on exertion/rest /emotion/cold/heavy meals. May radiate to one or both arms, neck, jaws or teeth. Worsens with time Other Symptoms: Dyspnoea, nausea, sweatiness, faintness

Answer 57

Stable angina occurs in periods of roughly 20 mins upon exertion or exercise. Unstable angina can be continuously painful at rest or even minimal exertion. Decubitus angina causes pain when lying down flat.

Answer 58

Both are commonly caused by atherosclerotic plaque causing obstruction of a coronary artery. In unstable angina, the plaque may rupture causing blood to leak out and a secondary thrombus to form which occludes the artery further creating an even narrower lumen for blood to flow through.

Answer 59

Angina results in pain due to myocardial ischaemia where the heart tissue is starved of oxygen but is still alive. MI is when the ischaemia has resulted in infarction that has led to the death of the heart tissue. Angina is therefore reversible and MI is not.

Answer 60

angina where patients may or may not have atherosclerosis of the coronary vessels. instead ischaemia occurs due to vasospasms of the coronary arteries where they constrict so much they can cause ischaemia. These can occur at any time not just on rest or on exertion.

Answer 61

Not clearly understood but likely due to vasoconstriction factors such as Thromboxane A2 release

Answer 62

Transmural Ischaemia All layers of the heart wall supplied by the coronary arteries are affected.

Answer 63

AT rest: Normal On exertion: ST segment depression due to subendocardium ischaemia.

Answer 64

ST segment elevation due to transmural ischaemia.

Answer 65

Relieved upon rest (after approx 5 mins) OR Symptoms relieved by GTN spray

Answer 66

Cardiac troponin (Troponin T and I): Released into the blood when cardiac muscle is damaged. Highly sensitive but not specific. Creatine Kinase - MB (CK-MB): Helpful to determine re-infarction as levels should drop back to normal 36-72 hours after.

Answer 67

Rise within 3-12 hours Peak at 24-48 hours Return to baseline by 5-14 days <14g/l normal = no MI, 14-30 ng/l = possible MI, >30ng/l = definite MI

Answer 68

Often they are normal since the ischaemia has not killed the cells and thus the troponin have not been released sometimes they may be elevated

Answer 69

1. Risk factor modification. 2. Low dose aspirin.

Answer 70

1. Risk factor modification. 2. Pharmacological therapies for symptom relief and to reduce the risk of CV events. 3. Interventional therapies e.g. PCI.

Answer 71

1. Beta blockers. 2. Nitrates e.g. GTN spray. 3. Calcium channel blockers.

Answer 72

Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. Myocardial work is reduced and so is myocardial demand = symptom relief.

Answer 73

1. Bradycardia. 2. Tiredness. 3. Erectile dysfunction. 4. Cold peripheries.

Answer 74

They might be contraindicated in someone with asthma or in someone who is bradycardic.

Answer 75

Nitrates e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.

Answer 76

Ca2+ blockers are arterodilators and negative Chronotropic/ionotropic agents: Reduced O2 demand -> reduced BP -> reduced afterload -> reduced myocardial demand.

Answer 77

1. Aspirin. 2. Statins.

Answer 78

Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced. Caution: Gastric ulcers!

Answer 79

They reduce the amount of LDL in the blood.

Answer 80

May be normal May have some ST depression/T wave inversion/depression

Answer 81

May be normal May have some ST depression/T wave inversion

Answer 82

Immediate Symptomatic Relief - GTN sublingual stray Long Term Symptomatic Relief - Beta Blocker (Atenolol) or Calcium Channel Blocker (Amlodipine) Secondary Prevention of CVD: Aspirin Atorvastatin ACE inhibitor Already on a beta blocker

Answer 83

Clinical Hx of pain / relief ECG : Rest - normal Exertion - ST depression/Flat T waves CT Angiography - Stenosed atherosclerotic artery

Answer 84

Referral for revascularisation Through PCI or CABG

Answer 85

Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.

Answer 86

1. PCI. 2. CABG.

Answer 87

1. Less invasive. 2. Convenient and acceptable. 3. High risk of restenosis.

Answer 88

1. Good prognosis after surgery. 2. Very invasive. 3. Long recovery time.

Answer 89

History ECG - may present as ST-segment depression, transient ST-segment elevation, or T-wave inversion No elevation in troponin - unstable angina not associated with damage to the heart

Answer 90

- Cardiac chest pain at rest or during minimal exertion - Severe and of new onset cardiac chest pain - Cardiac chest pain with crescendo pattern (distinctly more severe, prolonged, or frequent than before)

Answer 91

Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to COMPLETE occlusion of an artery by thrombus.

Answer 92

Non-ST Elevated Myocardial Infarction (NSTEMI) ST Elevated Myocardial Infarction (STEMI) Silent MI

Answer 93

ST elevation and tall T waves Will produce pathological Q waves some tome after an MI There may be a new LBBB in larger MIs (WiLLiaM) V1 – W shape V6 – M shape

Answer 94

ST depression T wave inversion Q waves may be present hours/days after infarct (often a retrospective diagnosis)

Answer 95

4th heart sound – due to forceful contraction of the atria to overcome a stiff or dysfunctional ventricle Pansystolic murmur – due to papillary muscle dysfunction or rupture

Answer 96

NSTEMI occurs after a partial occlusion of major Coronary artery STEMI occurs after complete occlusion of a major Coronary artery.

Answer 97

Risk Factor modification: Stop smoking Lose weight Healthy diet Exercise Anti-platelet therapy: - Aspirin (300mg initially then 75mg daily) - Dual therapy with P2Y12 receptor inhibitors - Clopidogrel (300 mg initially then 75mg for 12 months), ticagrelor (180 mg initially then 90 mg twice daily) or prasugrel Platelet glycoprotein IIb/IIIa receptor inhibitor for high risk patients (Abciximab) PCI (if risk assessment score (GRACE) is medium/high) and CABG Anti-coagulants: Heparin/LMWH e.g. enoxaparin has better efficacy than unfractionated heparin Fondaparinux Other Sx Control: Nitrates – GTN spray or IV infusion Beta blockers – bisoprolol Statins ACE inhibitors - Ramipril Calcium channel blockers (if beta blocker contraindicated) – amlodipine

Answer 98

DARTHVADER: Death Arrhythmias Ruptured septum Tamponade HF Valve disease Aneurysm of ventricle Dressler’s syndrome – pericarditis and pericardial effusion after 2-12 weeks Embolism Reoccurrence of ACS

Answer 99

MONAC: Morphine Oxygen (if Sats < 94%) Nitrates (GTN) Aspirin (300mg) Clopidogrel (dual antiplatelet)

Answer 100

GRACE score: low risk - monitor Med-High risk - angiogram / PCI

Answer 101

PCI May also have thrombolysis (IV alteplase) or CABG

Answer 102

6 As Aspirin (75g once daily) Another antiplatelet - Ticagrelor/Clopidogrel Atorvastatin (80mg once dail) ACE inhibitors (ramipril) Atenolol (or another bB) Aldosterone antagonist (spironolactone) in those with clinical heart failure

Answer 103

Post myocardial infarction syndrome Occurs around 2-6 weeks post MI Localised immune response causing pericarditis.

Answer 104

thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

Answer 105

DREAD: Death Rupture of the heart septum/papillary muscles Edema (causing heart failure) Arrythmia and Aneurysm Dressler's Syndrome

Answer 106

Ventricular Septum - Right HF LV wall - Cardiac tamponade Papillary Muscles - Mitral regurgitation/prolapse

Answer 107

Immediate: Ventricular Fibrillation (cardiac arrest) - most common cause of death post MI <24hrs: Cardiogenic shock Bradyarrythmias 3-5 days: Mitral regurgitation - papillary muscle rupture Ventricular septal rupture 2-6 weeks: Dressler syndrome

Answer 108

MI Stable/unstable angina Pericarditis Aortic aneurysm Endocarditis Pulmonary Embolism Pneumothorax

Answer 109

Left Coronary Artery: Heart area - Anterolateral ECG leads - I, aVL, V3-V6 LAD: Heart area - Anterior ECG leads - V1-4 Circumflex: Heart area - Lateral ECG leads - I aVL, V5-6 Right Coronary Artery: Heart area - Inferior ECG leads - II, III, aVF

Answer 110

600/100,000 for men. 200/100,000 for women

Answer 111

- Procoagulant activity; release of *thrombin* - Dense granule secretion; contributes to platelet activation - Alpha granule secretion; contributes to coagulation and inflammation - Platelet-fibrin clot; fibrin acts as glue that keeps the thrombus growing and allow it block of arteries to cause MI.

Answer 112

(1) Shear flow (2) Initial adhesion GPIb/VWF (3) Rolling GPIb/VWF/α2β1/collagen (4) Stable adhesion activation/aggregation GPVI, GPIIb/IIIa (5) Platelets are activated by ADP (vai P2Y12R), causing them to change shape, aggregate and seal off the endothelial breach

Answer 113

Aspirin, P2Y12 Inhibitors and GPIIb/IIIa antagonists

Answer 114

Clopidogrel Ticagrelor Prasugrel

Answer 115

Increases risk of bleeding! Serious bleeding must subside prior to administration and risk of thrombosis vs. risk of bleeding must be monitored throughout use.

Answer 116

Cover for delayed absorption of oral P2Y12 Inhibitors occuring due to opiates delaying gastric emptying

Answer 117

Targets formation and/or activity of thrombin; inhibiting both fibrin formation and platelet activation

Answer 118

Fondaparinux (a pentasaccharide) is used prior to coronary angiography

Answer 119

Full Dose: Heparin (unfractionated or LMWH) Bivalirudin

Answer 120

When a diabetic patient may not experience typical chest pain during an acute coronary syndrome

Answer 121

Ischaemic Heart Disease (IHD) Acute Coronary Syndrome (ACS)

Answer 122

Angina is stable if symptoms are always relieved by rest or GTN (glyceryl Trinitrate) spray.

Answer 123

CT Coronary Angiography

Answer 124

- Common: anaemia and hypoxaemia - Uncommon: polycythemia, hypothermia, hypovolaemia, hypervolaemia

Answer 125

- Common: hypertension, tachyarrhythmia, valvular heart disease - Uncommon: hyperthyroidism, hypertrophic cardiomyopathy

Answer 126

- Age - Smoking - Family history - Diabetes mellitus - Hyperlipidemia - Hypertension - Kidney disease - Obesity - Physical inactivity - Stress

Answer 127

- Impairment of blood flow by proximal arterial stenosis (e.g. atherosclerosis) - Increased distal resistance (e.g. left ventricular hypertrophy) - Reduced oxygen carrying capacity of blood (e.g. anaemia)

Answer 128

Flow = Change in pressure / Resistance

Answer 129

Relationship between flow, pressure and resistance; combination of Ohm's law and vessel resistance equation. Radius has to fall below 75% before symptoms

Answer 130

Cardiac – ACS, Aortic dissection, pericarditis, myocarditis Respiratory – PE, pneumonia, pleurisy, lung cancer MSK – rib fracture, chest trauma, costochondritis (inflammation of the cartilage between the ribs and sternum) GORD Oesophageal spasm Anxiety/panic attacks

Answer 131

SOCRATES: Site Onset Character Radiation Associated symptoms Time/Duration Exacerbating features Severity

Answer 132

- Heavy, tight pain - Located centrally - Provoked by cold weather, big meals, exertion - Relieved by rest, GTN spray - Associated SOB

Answer 133

Patient undertakes mild exercise on a treadmill and ECG is run simultaneously - any abnormailites, refer patient to catheterisation lab

Answer 134

IV radio-labelled agent travels to the coronary arteries - areas of darkness signify a blockage.

Answer 135

Factors influencing psychological responses (cognitive; behavioural; emotional) to the social environment and pathophysiological changes

Answer 136

Coronary prone behaviour is the collection of behaviours and attitudes associated with heart disorders especially coronary heart disease and cardiovascular disorders.

Answer 137

- Aggressiveness/Anger (biggest risk factor) - Ambition - Competitiveness - Hostility (biggest risk factor) - Impatience - Sense of time urgency - Need for achievement

Answer 138

Depression and Anxiety Low quantity and quality of social support High demanding jobs/low control of jobs

Answer 139

Outer Fibrous layer - Continuous with the central tendon of the Diaphragm Serous layer: Outer Parietal - lines the inner surface of the fibrous pericardium Inner Visceral - forms the outer layer of the heart (Epicardium)

Answer 140

Pericardial cavity: Contains 50ml of serous fluid to minimise the friction generated when the heart contracts

Answer 141

Roots of the great vessels: Aortal Pulmonary Artery Pulmonary Veins SVC IVC

Answer 142

- **Fixes the heart** in the mediastinum and limits its motion. - **Prevents overfilling** of the heart. The relatively inextensible fibrous layer of the pericardium limits the filling pressure and volume of the heart - **Lubrication**. A thin film of fluid between the two layers of the serous pericardium reduces the friction generated by the heart as it moves within the thoracic cavity - **Protection from infection**. The fibrous pericardium serves as a physical barrier between the muscular body of the heart and adjacent organs prone to infection, such as the lungs.

Answer 143

Volume of pericardial fluid changes based on the physiological state of the heart.

Answer 144

Reduction in cardiac output due to a raised intrapericardial pressure secondary to a pericardial effusion. As there is a greater pressure, the heart chambers cannot expand during diastole reducing SV and CO

Answer 145

Beck's Triad Pulsus Paradoxus Tachycardia and Hypotension Soft heart sounds

Answer 146

Slow accumulation of fluid allowing for adaptation of the parietal pericardium

Answer 147

Increased compliance reduces the effect on diastolic filling and therefore slow accumulating effusion does not often cause tamponade.

Answer 148

Accumulation of excess fluid in the pericardial cavity; the pericardial fluid contains blood components such as fibrin, RBCs and WBCs

Answer 149

Inflammation of the pericardium commonly due to viral infection.

Answer 150

Acute Chronic effusive Chronic Constrictive

Answer 151

Males - 20-50yrs

Answer 152

Infection - Coxsackie Virus Dressler's Syndrome Autoimmune Neoplastic Metabolic Traumatic Iatrogenic - PCI

Answer 153

HEAP: Herpes virus Enterovirus (Coxsackie) Adenovirus Parovirus

Answer 154

Sjogren's Syndrome SLE Rheumatoid Arthritis Scleroderma Systemic Vasculitides

Answer 155

persistent inflammation of acute pericarditis causes the heart to be encased with a rigid fibrotic calcified pericardial sac which prevents adequate diastolic filling of the ventricles

Answer 156

ECG: (diagnostic) - PeRicardiTiS (PR dep and ST elev) Concave Saddle Shaped ST elevation (in all leads) PR depression ECHO - exclude pericardial effusion/tamponade CXR - Bottle water silhouette FBC - increased WCC Chest Pain ESR/CRP - High ESR may suggest aetiology Pericardial Rub

Answer 157

Pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop If this fluid accumulation impacts the hearts function this is cardiac tamponade

Answer 158

Sharp severe pleuritic chest pain - radiate to left shoulder due to phrenic nerve Pain is relieved when sitting forward Pain is exacerbated when lying flat or on inspiration

Answer 159

Severe pleuritic chest pain Dyspnoea Cough/hiccups - phrenic involvement Systemic disturbance - weight loss, joint pain, fever

Answer 160

Extra heart sound heard upon auscultation One systolic - Two diastolic Sound resembles scratching.

Answer 161

Pulsus paradoxus Kussmaul's Sign - rise in JVP on inspiration Tachycardia and Hypotension soft heart sounds - effusion obscures beat and sounds

Answer 162

Three clinical signs associated with pericardial tamponade: - Falling BP - Hypotension (weak pulse or narrow pulse pressure) - Muffled heart sounds - Raised jugular venous pressure.

Answer 163

MI - has no pericardial rub/not related to lying down (ST elevation not saddle shaped) pneumonia Aortic Dissection PE

Answer 164

Period of sedentary activity until resolution of inflammation NSAIDS (2 weeks) + Gastric Protection (PPI) Colchicine (3 weeks) Consider Abx for bacterial aetiology

Answer 165

Inhibits migrations of neutrophils to site of inflammation to reduce risk of reoccurrence

Answer 166

Pericardial effusion - cardiac tamponade myocarditis constrictive pericarditis

Answer 167

Echocardiogram - Echo free space around heart CXR – large heart ECG – low voltage QRS complexes and sinus tachycardia

Answer 168

ECHO - diagnostic Beck's Triad ECG - varying QRS peaks CXR - big globular heart

Answer 169

Urgent pericardiocentesis

Answer 170

treat underlying cause NSAIDS Colchicine

Answer 171

Typically pericarditis RF are all factors related to pericarditis

Answer 172

Emotional stress Large meals Cold weather

Answer 173

Resistance = 8lu/pi r^4 l - length of vessel U - viscosity R - radius of vessel

Answer 174

patients present with angina over a period of months that gets progressively worse

Answer 175

Men - 5% (5000/100,000) Women - 4% (4000/100,000)

Answer 176

headache due to vasodilation

Answer 177

postural hypotension Swollen ankles Flushing

Answer 178

Balloon Stent Angioplasty with Stent

Answer 179

Viral infection

Answer 180

Idiopathic Infection: Viral (most common) – HIV, Coxsackie B, echovirus Bacterial – TB Fungal – Histoplasma spp. Malignancy MI Autoimmune (immune system attacking the pericardium): Sjogren’s RA SLE Dressler syndrome (inflammation of pericardium after MI damaging it)

Answer 181

An inspiratory decrease in systolic BP >10mmHg. (not a paradox but exaggeration of normal physiology) Caused by increased venous return to the right side of the heart during inspiration The increased RV volume therefore occupies more space within the rigid pericardium and impairs LV filling Paradox: On physical exam, beats are detected on cardiac auscultation during inspiration which cannot be palpated at the radial pulse. This is associated with increased JVP (kussmauls sign)

Answer 182

A disease of the heart muscle tissue where there is impaired ability to contract and/or there is electrical conduction dysfunction.

Answer 183

Generally they are inherited conditions but can be acquired

Answer 184

Family history Hypertension Obesity Diabetes Previous MI

Answer 185

Preload - the volume of blood entering the ventricles that causes a greater stretch on the ventricles. Afterload - The pressure that must be overcome in order to eject blood from the ventricles during systole. Contractility

Answer 186

Hypertrophic Cardiomyopathy (HCM) Dilated Cardiomyopathy (DCM) Arrhythmogenic Right/Left ventricular Cardiomyopathy (ARVC/ALVC) Restrictive Cardiomyopathy.

Answer 187

Dilated Cardiomyopathy

Answer 188

Occurs when genes encoding proteins involved in the Myocardial tissue are dysfunctional resulting in poor/altered function myocardial cells and further pathology.

Answer 189

Where the Myocardial cells structure and function becomes damaged through: Toxins inflammation infection systemic disorders

Answer 190

ECHO Some with MRI Troponins may be elevated.

Answer 191

Dilation/thinning of the ventricular walls (chamber enlargement) causing weakness of the ventricular myocardial cell contraction. Systolic function is impaired leading to poorly ejected blood Can result in biventricular congestive HF.

Answer 192

Can be Asymptomatic May present as congestive heart failure. Dyspnoea Weakness Fatigue Oedema Raised JVP Pulmonary congestion Cardiomegaly 3rd/4th Heart Sounds

Answer 193

Idiopathic - Gene mutations often in cytoskeletal genes. Infection Ischaemia Alcoholism Thyrotoxicosis

Answer 194

More common in males 35/100,000 Median age - 50

Answer 195

ECHO - Marked Dilatation CXR - Cardiomegaly, pulmonary oedema ECG - May have tachycardia/arrhythmias

Answer 196

Tx of underlying conditions - AF/ HF Bed rest Loop and Thiazide Diuretics for fluid overload ACEi Beta Blockers Heart transplant

Answer 197

Unexplained primary cardiac hypertrophy (often on LV wall and interventricular septum) leading to impaired diastolic filling and a reduced stroke volume. due to thick heart and reduced compliance

Answer 198

Diastole is main issue. Enlarged heart walls. ventricles are stiff LV does not relax properly and so diastolic filling is impaired.

Answer 199

Autosomal Dominant mutation in Sarcomeric genes: Beta-myosin heavy chain Troponin T alpha tropomyosin.

Answer 200

Most may be asymptomatic Variable dyspnoea Chest pain / palpitations Syncope Sudden death

Answer 201

Progressive Heart Failure Sudden Cardiac Death

Answer 202

Forceful Apex beat Late ejection systolic Murmur (crescendo-decrescendo similar to AS) S4 Heart sound - stiff ventricle so sound as blood hits non compliant wall. Jerky Carotid pulse Alpha wave in JVP.

Answer 203

1/500 Men and black people more likely

Answer 204

Hypertrophic Cardiomyopathy

Answer 205

ECG - LVH, ST segment changes, DEEP T wave inversion CXR - variable, left atrial enlargement ECHO - large LV walls

Answer 206

Amiodarone - reduce risk of arrythmias and sudden death Treat chest pain: Beta blockers and CCB - Verapamil Implantable cardioverter defibrillator

Answer 207

Digoxin Digoxin can increase inotropy which may exacerbate heart symptoms in patients with HCM that have preserved systolic function

Answer 208

Most common cause of sudden death in young and adults (especially athletes)

Answer 209

Sudden Death

Answer 210

Associated with Desmosome gene mutations Fibro-fatty replacement of the RV myocytes leading to impaired ability of RV muscle to contract due to muscle cell loss.

Answer 211

A autosomal recessive genetic condition associated with ARVC and diffuse palmoplantar keratoderma and woolly hair

Answer 212

Arrythmias - main feature Palpitations Presyncope/syncope RHF Death possible on first presentation

Answer 213

Atrial Fibrillation

Answer 214

Unknown but may be due to apoptosis, inflammation or genetics

Answer 215

1/2000 Mainly affects males 30-50% of cases have autosomal dominant genetic predisposition

Answer 216

ECHO - RV wall Dimensions and abnormalities RV angiography ECG - In leads V1, 2 and 3, Epsilon wave, T wave inversion MRI - fatty infiltration and fibrosis on RV wall.

Answer 217

Standard heart failure medication. Beta blockers in asymptomatic patients. Amiodarone - Tx for arrythmias Heart transplant

Answer 218

Dilated cardiomyopathy.

Answer 219

Rigid Fibrotic Myocardium Increased myocardial stiffness despite normal LV cavity size and function. Increased stiffness restricts diastolic filling as the ventricle is incompliant.

Answer 220

Granulomatous disease - Amyloidosis (Amyloid heart disease) / Sarcoidosis. infiltrative myocardial disease Loffler Endo(myo)carditis Haemochromatosis

Answer 221

between 1/1000 to 1/1500 5% of all cardiomyopathies Mainly affects the elderly, tropical Africa

Answer 222

Similar to constructive pericarditis Features of RV failure Dyspnoea Elevated JVP Hepatomegaly Ascites 3rd and 4th heart sounds

Answer 223

ECHO - thickened ventricular walls, valves and atrial septum. ECG - Low amplitude signals MRI - to distinguish between cardiomyopathies.

Answer 224

Tx underlying cause Heart Transplant

Answer 225

Heart failure sudden death Poor prognosis.

Answer 226

Arrhythmia

Answer 227

Developing arrythmia

Answer 228

Also known as ‘stress-induced cardiomyopathy’ or ‘broken-heart syndrome’. A stressful event can lead to characteristic apical ballooning with transient systolic dysfunction. Thought to be related to catecholamine-induced spasm of the small vessels in the microvasculature. The condition preferentially affects postmenopausal women.

Answer 229

Gene mutations in genes that are involved in ion channel proteins resulting in channelopathies.

Answer 230

Arrythmias

Answer 231

Long QT Short QT Brugada Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)

Answer 232

Ventricular Tachycardia

Answer 233

Recurrent Syncope

Answer 234

A channelopathy caused by a mutation in the cardiac sodium channel gene

Answer 235

Asymptomatic May have syncope Can cause sudden death

Answer 236

Ventricular fibrillation Polymorphic Ventricular Tachycardia

Answer 237

Characteristic ST elevation with partial RBBB pattern in V1 and V2

Answer 238

Inherited condition likely a cardiomyopathy or channelopathy

Answer 239

Marfans Vascular Ehler Danlos (EDS) Loeys-Dietz

Answer 240

The pressure required to fill the ventricle to the same diastolic volume

Answer 241

Stroke (ischaemic and haemorrhagic) Myocardial Infarction Heart failure Chronic renal disease Cognitive decline Premature death

Answer 242

- Define Stage 1 Hypertension. Clinical = 140/90 Ambulatory = 135/85 - Define Stage 2 Hypertension Clinical = 160/100 Ambulatory = 150/95 - Define severe Hypertension. Clinical = 180/110

Answer 243

Lifestyle modification Antihypertensive drug therapy

Answer 244

Individuals aged 80 or below and individuals who have one or more of the following: - Target organ damage - Established CVD - Renal disease - Diabetes - 10-year CVD risk of >20%

Answer 245

- Cardiac output and peripheral resistance - Interplay between the RAAS and sympathetic nervous system (NA) - Local vascular vasoconstrictor and vasodilator mediators

Answer 246

1. Kidneys sense low BP and renin is released from juxtaglomerular cells. 2. Renin converts angiotensinogen to angiotensin I 3. ACE from the lungs converts angiotensin I to angiotensin II 4. Angiotensin II (extremely potent vasoconstrictor) stimulates aldosterone release resulting in increased Na+ and thus water reabsorption which leads to increased blood volume and thus blood pressure

Answer 247

Drop in BP results in the release of noradrenaline, leading to vasoconstriction and increased contractility of the heart thus increasing peripheral resistance and cardiac output and thus BP. Also results in renin release which further augments RAAS

Answer 248

Prevent ACE converting angiotensin I to Angiotensin II and therefore inhibiting the CVS effects of Angiotensin II

Answer 249

- Ramipril - Enalapril - Perindopril - Trandolapril

Answer 250

- Hypertension - Heart Failure - Diabetic nephropathy

Answer 251

Related to reduced Angiotensin II: Hypotension Acute renal failure Hyperkalaemia Teratogenic effects in pregnancy Related to increased Kinin Production: Cough Rash Anaphylactoid reactions

Answer 252

ACE breaks down bradykinin. If ACE is inhibited then bradykinin levels increase This can cause a persistent dry cough

Answer 253

They block the receptors of angiotensin II preventing its binding and it inducing effects.

Answer 254

- Candesartan - Losartan - Valsartan - Telmisartan

Answer 255

- Hypertension (and when ACEi is contradicted due to cough) - Diabetic nephropathy - Heart failure (when ACEi contraindicated - acts on AT-1 receptor)

Answer 256

- Symptomatic hypotension (esp. in volume depleted patients) - Hyperkalaemia - Potential renal dysfunction - Rash - Angiooedema - Teratogenic in pregnancy

Answer 257

These block the calcium channels from allowing Ca entry into cardiomyocytes.

Answer 258

- Hypertension - IHD (angina) - Arrhythmias

Answer 259

- *Dihydropyridines (e.g.* amlodopine, nifedipine, felodipine) - *Phenylalkylamines* (e.g. verapamil) - *Benzothiozepines* (e.g. diltiazem)

Answer 260

Amlodipine: Preferentially affect Vascular smooth muscle and act as peripheral arterial vasodilators

Answer 261

Verapamil: Directly affects the heart - negatively chronotropic, negatively ionotropic

Answer 262

Diltiazem: Intermediate heart and peripheral vascular effects

Answer 263

Due to peripheral vasodilation (Dihydropyridines): - Flushing - Headache - Peripheral oedema - Palpitations Due to negative chrontropic effect (Phenylalkylamines and Benzothiozepines): - Bradycardia - Atrioventricular block - Postural hypotension Due to negative ionotropic effect (Benzothiozepines) - Worsening of HF Verapamil causes constipation

Answer 264

Beta adrenoceptor blockers that prevent the effects of adrenaline and noradrenaline in the sympathetic nervous system. They work on B1 and B2 receptors.

Answer 265

- Bisoprolol - Propranolol - Atenolol - Carvedilol

Answer 266

- IHD - angina - HF - Arrhythmia - Hypertension

Answer 267

Metoprolol Bisoprolol (Atenolol is mostly B1 but not entirely cardioselective)

Answer 268

Propranolol Nadolol Carvedilol

Answer 269

- Fatigue - Headache - Sleep disturbance - Bradycardia - Hypotension - Cold peripheries - Erectile dysfunction

Answer 270

Asthma PVD - Claudication or Raynauds Heart Failure - when given in standard doses or acutely

Answer 271

Increased excretion of water, salt and metabolites in urine

Answer 272

- Hypertension - Heart failure

Answer 273

Thiazide diuretics - act on distal tubule blocking Na/Cl exchanger Loop diuretics - act on ascending loop of henle, blocks Na/K/2Cl (NKCC2) transporter Potassium-sparing diuretics (Aldosterone antagonists) - Retain Potassium

Answer 274

- Thiazide diuretics: bendroflumethiazide, hydrochlorothiazide - Loop diuretics: furosemide, bumetanide - Potassium-sparing diuretics: spironolactone, eplerenone

Answer 275

- Hypovolaemia (mainly loop) - Hypotension (mainly loop) - Hypokalaemia - Hyponatraemia - Hypomagnesaemia - Hypocalcaemia - Hyperuricaemia (gout) - Erectile dysfunction (thiazides) - Impaired glucose tolerance (thiazides)

Answer 276

Act on the CNS: Moxonidine Methyldopa

Answer 277

During pregnancy for gestational hypertension

Answer 278

First line: ACEi or ARB Second Line: ACEi/ARB + CCB Third Line: ACEi/ARB + CCB + Thiazide Fourth line (Resistance HTN): Consider addition of Spironolactone, alpha blocker, beta blocker

Answer 279

First line: CCB Second Line: ACEi/ARB + CCB Third Line: ACEi/ARB + CCB + Thiazide Fourth line (Resistance HTN): Consider addition of Spironolactone, alpha blocker, beta blocker

Answer 280

Rapid rise in BP leading to vascular damage

Answer 281

Sx - Headache, Visual Disturbances Signs: Systolic BP >200 Diastolic BP > 130 Bilateral renal haemorrhage - exudates - papilloedema

Answer 282

Hypertensive Emergencies: AKI HF Encephalopathy

Answer 283

Sodium Nitroprusside

Answer 284

Complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired and cannot satisfy the needs of metabolising tissues

Answer 285

Systolic: Left Ventricular Systolic Dysfunction (Most common) - caused by contractility dysfunction Diastolic: Heart failure with preserved ejection fraction (HFPEF) - caused by dysfunction during diastole (filling) Acute/Chronic Heart Failure

Answer 286

Failure to contract Ejection fraction <40% (SV/EDV) Caused by: - IHD - MI - Hypertension - Cardiomyopathy

Answer 287

Inability to relax and fill There is reduced preload because there is abnormal filling of the LV Ejection fraction >50% Caused by: - Constrictive pericarditis - Cardiac tamponade - Hypertension

Answer 288

Annual incidence of 10% in patients over 65 50% of patients die within 5 years

Answer 289

Age – 65+ Obesity Gender – male People who have had a previous MI

Answer 290

Vasodilator therapy via neurohumoral blockade (RAAS-SNS)

Answer 291

Diuretics - often loop

Answer 292

A (first Line) - ACEi + BB therapy (low dose titrated up slowly) B: Aldosterone Antagonist (Spironolactone) C: ARNI (ARB + Neprilysin inhibitor) - Entresto ( combination of Valsartan + Sacubitril) D: SGLT2 inhibitor - Dapagliflozin E: ACEi intolerance - ARB F: ACEi and ARB intolerance - Hydralazine/nitrate combination G: consider Digoxin

Answer 293

Arterial and Venous dilators These reduce both preload (venous dilation) and afterload (arterial dilation) to lower the BP

Answer 294

IHD (Angina) Heart Failure

Answer 295

- Isosorbide mononitrate (tablet) - GTN spray - GTN infusion (acute/ severe angina)

Answer 296

- Headache - GTN spray syncope - Potential tolerance to the drug

Answer 297

Atrial Naturetic Peptide (ANP) - Atria Brain Naturetic Peptide (BNP) - Brain and Ventricles

Answer 298

Stretching of atrial and ventricular muscle cells, raised atrial or ventricular pressures and volume overload

Answer 299

Increases renal excretion of sodium (natriuresis) and water (diuresis)

Answer 300

Relax vascular smooth muscle (except efferent arteriole) of renal glomeruli to preserve filtration pressure in kidney whilst still removing Na+ and thus water thus no renal damage)

Answer 301

Increased vascular permeability

Answer 302

Reduces aldosterone, angiotensin II, endothelin (most potent vasoconstrictor) and ADH release

Answer 303

Counter-regulatory system to the renin-angiotensin system

Answer 304

NEP or Neprilysin

Answer 305

NEP inhibition increases levels of natriuretic peptides

Answer 306

Sacubitril - is a neprilysin inhibitor Entresto (ARNI) - is a combination of sacubitril and valsartan (ARB) - VERY EFFECTIVE IN HEART FAILURE

Answer 307

Sodium Channel Blockers: 1A: quinidine 1B: lidocaine 1C: flecainide

Answer 308

Beta-blockers: - non-selective (e.g.propranolol, nadolol, carvedilol) - beta-1 selective (e.g. bisoprolol, metoprolol)

Answer 309

It blocks both Beta adrenoceptors and can block sodium channels too

Answer 310

Prolongs action potential: Amiodarone blocks potassium channels during repolarisation to increase the AP. *Cause QT prolongation; potential for significant side effects in patient with QT prolongation*

Answer 311

Calcium channel blockers (only phenylalkylamines and benzothiozepines): Verapamil and Diltiazem Verapamil is more effective than amlodipine as it does not affect calcium channel at rest

Answer 312

Rhythm control (sympathetic drive, e.g. adrenaline worsens arrhythmias)

Answer 313

Rate control (sympathetic drive, e.g. adrenaline worsens arrhythmias)

Answer 314

- Bradycardia - Interstitial Lung Disease - Thyroid (hyper and hypo) - Corneal (ocular)/cutaneous (skin) - Hepatic dysfunction/hypotension when IV (due to solvents) - Photosensitivity - Drug interactions

Answer 315

Cardiac glycoside

Answer 316

Inhibits Na/K pump; Therefore Na/Ca exchanger is not active as Na conc increases in the cell Therefore Ca is not removed from the cell causes an increase in Ca2+ inside the cells of the heart Increases contraction of myocytes

Answer 317

- Bradycardia (increased vagal tone) - Slows AV conduction (increased vagal tone) - Increased ectopic activity - Increased force of contraction (direct +ve inotropic effect) by increasing intracellular calcium

Answer 318

- Atrial Fibrillation; reduces ventricular rate response - Severe heart failure; has a positive inotropic effect

Answer 319

- Narrow therapeutic range - Nausea - Vomiting - Diarrhoea - Gynaecomastia - Confusion

Answer 320

These are often Congenital defects that occur during pregnancy to the heart that are not necessarily inherited that cause heart problems. They can range from minor to life incompatible

Answer 321

Bicuspid Aortic Valve Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD) Coarctation of the Aorta Fallot's Tetralogy Patent Ductus Arteriosus Patent Foramen Ovale

Answer 322

Combination of four congenital abnormalities affecting the structure of the heart. This causes oxygen-deficient blood to flow out of the heart and to the rest of the body.

Answer 323

Ventricular Septal Defect (VSD) - hole between 2 ventricles Over-riding Aorta - Allows blood from both ventricles to entre the aorta RV Hypertrophy - thickening of RV muscle Pulmonary Stenosis - Narrowing of the exit from the RV to pulmonary circulation

Answer 324

There is a greater pressure in the RV than the LV and so blood is shunted into the LV → cyanosis as blood is not oxygenated

Answer 325

Severity dependent on degree of pulmonary stenosis Cyanosis Clubbing Poor Feeding / weight gain Tet spells Ejection Systolic Murmur (pulm stenosis) Increase Hb concentration

Answer 326

Unknown but likely genetic influence

Answer 327

Most common complex cardiac abnormality. 10% of congenital heart conditions

Answer 328

CXR - boot shaped heart ECHO CG (doppler)- anatomy and degree of stenosis/assess flow

Answer 329

Early surgical intervention within 2 years Mortality of 5%

Answer 330

An abnormal connection between the LV and RV causing a left to right shunt enabling more blood to enter the pulmonary circulation.

Answer 331

There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic.

Answer 332

Size Matters: Small - Asymptomatic Large: Very high pulmonary blood flow in infancy leads to pulmonary hypertension and eventual Eisenmenger’s complex Small, breathless baby, poor feeding, failure to thrive Increased respiratory rate Tachycardia Big heart on chest X ray Murmur varies in intensity

Answer 333

25% of congenital abnormalities 1-4/1000

Answer 334

May close on its own Surgical repair (may provide furosemide/ACEi if moderately sized lesion

Answer 335

High pressure pulmonary blood flow leads to damage in pulmonary vasculature → increased resistance to blood flow (pulmonary hypertension) → RV pressure increases → shunt direction reverses (RV to LV) → cyanosis

Answer 336

Causes de-oxygenated blood to skip the lungs and go back around the body Once pulmonary HTN is high enough to cause the reversal, only a transplant is curative Causes marked cyanosis, clubbing, heart failure, syncope, high RBC Very poor prognosis

Answer 337

- Stroke - Endocarditis - Risk of death

Answer 338

A common structural defect where there is a hole in the septum between the 2 atria

Answer 339

Ostium Primum - associated with AV valve abnormalities Ostium Secundum (85% of ASD) - Asymptomatic

Answer 340

Typically affects 40-60 years M>F

Answer 341

There is a higher pressure in the LA than the RA and so blood is shunted from the left to right; not cyanotic. This may be reverse if Eisenmenger's Syndrome develops

Answer 342

Pulmonary flow murmur - increased blood to pulm circulation Fixed split-second heart sound (delayed closure of pulmonary valve because more blood has to get out) Dyspnoea Exercise intolerance Atrial arrhythmias from RA dilation

Answer 343

CXR: Large heart Large pulmonary arteries ECG: Right bundle branch block (RBBB) due to RV dilatation ECHO: Hypertrophy and dilation of right side of heart and pulmonary arteries

Answer 344

Surgical Repair Percutaneous repair

Answer 345

A hole between the atria and the ventricles 2 per 10,000 Strong association with Downs

Answer 346

Complete defect: Breathlessness Poor feeding Poor weight gain Partial Defect: Can present in later adulthood. Similar to ASD/VSD Tachycardia Dyspnoea Exercise intolerance

Answer 347

- Enlargement of the heart - Heart failure - inability to adequately supply body oxygen - Eisenmenger's Syndrome - Exercise intolerance - Pulmonary hypertension - Pneumonia

Answer 348

Pulmonary artery banding if large defect in infancy – band reduces flow to lungs thereby reducing pulmonary hypertension and Eisenmenger’s syndrome Surgical repair – very challenging Partial defect may be left alone if there is no right heart dilatation

Answer 349

Ductus arteriosus fails to close after birth; allows abnormal transmission of blood from the aorta to the pulmonary artery. Pulmonary arterial and left atrial flow increase

Answer 350

Normally following birth the PDA closes. If patent then there is a left to right shunt Increases Pulmonary volume causing Pulm HTN and eisenmenger's syndrome.

Answer 351

- Pulmonary hypertension and RHF (due to Eisenmenger's reaction) - Breathlessness - Poor feeding, failure to thrive - Risk of endocarditis

Answer 352

Large: Develop big heart Torrential flow from the aorta to the pulmonary arteries in infancy Breathless, poor feeding, failure to thrive Continuous “MACHINERY” murmur Eisenmenger’s syndrome

Answer 353

Small: Little flow from the aorta to Pulmonary arteries Usually asymptomatic Murmur found incidentally Endocarditis risk

Answer 354

CXR – large shunt between aorta and pulmonary arterial system may be prominent ECG – may demonstrate LA abnormality and LV hypertrophy Echocardiogram – may show dilated LA and LV

Answer 355

Surgical or percutaneous closure Local anaesthetic Indomethacin - (prostaglandin inhibitor) can be given to stimulate duct closure.

Answer 356

Narrowing of the Aorta Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing of the aorta distal to the ductus arteriosus

Answer 357

Associated with Bicuspid aortic valves Turner’s syndrome Berry aneurysms Patent ductus arteriosus M>F

Answer 358

Right arm Hypertension (may have left arm hypotension) Lowe pressure in vessels distal to Coarctation Bruits (buzzes) over the scapulae and back Murmur

Answer 359

CXR – dilated aorta indented at site of coarctation ECG – LV hypertrophy CT – can accurately demonstrate coarctation and quantify flow

Answer 360

Surgical repair Percutaneous repair Balloon dilation (preferred for re-coarctation) and stenting RISK OF ANEURYSM FORMATION AT SITE OF REPAIR

Answer 361

Failure of the foramen ovale to close after birth

Answer 362

No symptoms If no other abnormalities then normal health

Answer 363

Aortic valve has 2 cusps rather than 3. Get turbulence generation instead of laminar flow in the aorta

Answer 364

Can work well at birth and go unoticed Exercise exacerbates complications Abnormal degradation of the aortic valve over time - requires valve replacement

Answer 365

1-2% of general Population. Most common congenital heart defect

Answer 366

Ix - ECHO Tx - Surgical valve replacement

Answer 367

VSD ASD PDA Left to right shunt But this can lead to Eisenmenger's Syndrome due to the increased pulmonary flow and subsequent Pulmonary HTN.

Answer 368

Tetralogy of Fallot Right to left shunt.

Answer 369

Blood is diverted massively through the aortic arch branches and therefore you have increased perfusion to the upper body and less to the lower body.

Answer 370

CXR - notched ribs CT angiogram

Answer 371

Bicuspid Aortic Valve

Answer 372

None Consider transplant

Answer 373

VSD, ASD, PDA

Answer 374

Aortic Aneurysm development

Answer 375

Narrowing of the outflow tracts of the right ventricles This results in increased resistance of the pulmonary circulation leading to RV hypertrophy 8-12% of Congenital Heart Defects

Answer 376

Normotensive Stage 1 Hypertension Stage 2 Hypertension Severe Hypertension (Stage 3)

Answer 377

90/60 - <120/ <80

Answer 378

- ABP 135/85 - Clinic 140/90

Answer 379

- ABP 150/95 - Clinic 160/100

Answer 380

Clinic 180/120

Answer 381

When it is Idiopathic (no known cause) 95% of cases

Answer 382

When the underlying cause is known 5% of cases

Answer 383

CHAPS: Cushings Syndrome/CKD Hyperaldosteronism (Conn's Syndrome) Aorta Coarctation Phaeochromocytoma Stenosis of Renal Arteries.

Answer 384

Increased Age Blacker ethnicity Overweight - biggest RF Decreased exercise/sedentary lifestyle smoking diabetes stress increased salt intake Family Hx

Answer 385

CKD as a result of diabetic nephropathy

Answer 386

Rapid rise in blood pressure which damages vasculature Pathological hallmark is fibrinoid necrosis Usually with severe hypertension + bilateral retinal haemorrhages and exudates

Answer 387

When there is sign of immediate damage: Papilloedema Acute kidney injury Acute stroke ACS Aortic dissection

Answer 388

All mechanisms where there is increased CO from Increased RAAS and SNS activity. Mechanisms where there is increased TPR will increase BP

Answer 389

BP = CO x TPR

Answer 390

CKD OSA Glomerulonephritis - increased renin Renal Artery stenosis - increase renin Coarctation of the Aorta

Answer 391

Phaeochromocytoma Cushings Conns (hyperaldosteronism) Acromegaly Thyroid Dysfunction

Answer 392

Lupus Scleroderma

Answer 393

Mostly Asymptomatic May have a pulsatile headache (but no more than general population) Found on screening

Answer 394

Early onset (<30yrs) with no risk factors Hypertension resistant to 3 drugs Malignant hypertension If patient has other specific symptoms indicative of secondary causes

Answer 395

Glucocorticoids Oral contraceptives SSRIs NSAIDs EPO Stimulants Anti-TNFs

Answer 396

Fasting glucose Cholesterol

Answer 397

Underlying secondary causes should be excluded: Age < 40 years Reduced eGFR (suggestive of renal disease) Proteinuria or haematuria (suggestive of renal disease) Hypokalaemia and hypernatraemia (suggestive of Conn’s syndrome) Hypertension that is sudden onset, variable or worsening.

Answer 398

In clinic: BP reading in hospital of 140/90 or higher Then ABPM for 24 hours to confirm diagnosis (BP 135/85 + throughout day twice per hour) Assess end organ damage Home BPM: 2 measurements taken daily for 4-7 days

Answer 399

Elevated BP in a clinical setting Px should have ABPM monitoing prior to diagnosis of HTN

Answer 400

ECG/ECHO - LV Hypertrophy Fundoscopy - papilloderma U&Es - hypokalaemia in Conns Urinalysis, Proteinuria and Haematouria Serum creatine GLucose Renal function

Answer 401

Stop Smoking Exercise - lose weight Control diet

Answer 402

CCBs ACEi/ARBs Diuretics B-blockers

Answer 403

Aged < 80 years with stage 1 hypertension and with one of the following; end organ damage, cardiovascular disease, renal disease, diabetes or 10-year cardiovascular risk ≥10%. of any age with stage 2 hypertension of any age with stage 3 hypertension (consider immediate treatment)

Answer 404

1st Line - ACEi/ ARB (if ACEi are Contraindicated) 2nd Line - ACEi/ ARB (if ACEi is CI) + CCB 3rd Line - ACEi/ ARB (if ACEi is CI) + CCB + Thiazide 4th Line (resistant HTN) - ACEi/ (ARB if ACEi is CI) + CCB + Thiazide + 4th drug: 4th drug if K+ > 4.5 = alpha/beta blocker 4th drug if K+ < 4.5 = Spironolactone

Answer 405

1st Line - CCB 2nd Line - ACEi/ ARB (if ACEi is CI) + CCB 3rd Line - ACEi/ ARB (if ACEi is CI) + CCB + Thiazide 4th Line (resistant HTN) - ACEi/ ARB (if ACEi is CI) + CCB + Thiazide + 4th drug: 4th drug if K+ > 4.5 = alpha/beta blocker 4th drug if K+ < 4.5 = Spironolactone

Answer 406

T2DM takes precedence and Therefore first line is ACEi

Answer 407

Chronic heart disease MI Stroke - Common complication Heart failure Peripheral arterial damage Aortic aneurysm Chronic kidney disease Vascular dementia

Answer 408

When patients are undergoing general anaethesia

Answer 409

Renal function impairement Otherwise, no monitoring as concordance with treatment an issue Evidence shows going off medication causes hypertension to return

Answer 410

Low risk patients - 160/100 (stage 2) High risk patients (diabetes, sign of end organ damage, risk of coronary events) - 140/90

Answer 411

Patients < 80 years: clinic BP < 140/90 mmHg / ABPM < 135/85 mmHg Patients ≥ 80 years: clinic BP < 150/90 mmHg / ABPM < 145/85 mmHg

Answer 412

Cardiac valves may become incompetent (regurgitant), stenotic (narrow) or both. Abnormal valves produce turbulent blood flow, which is heard as a murmur on auscultation, a few murmurs are also felt as a thrill on palpation.

Answer 413

Narrowing of the aortic valve

Answer 414

Stiff/thick valve leaflets Obstructs forward flow Increasing Afterload leads to systemic or pulmonary congestion Stenotic Valve on RHS = Systemic Venous Congestion Stenotic Valve on LHS = Pulmonary Venous Congestion

Answer 415

Mitral Aortic Pulmonary Tricuspid

Answer 416

Causes insufficiency and proximal chamber dilation. This is due to loss of structural chamber integrity and strength

Answer 417

Poorly sealed valve leaflets Defective and floppy backflow of the blood through the valve (incompetance) Valvular Regurgitation on RHS = Systemic Venous congestion Valvular Regurgitation on LHS = Pulmonary Venous congestion

Answer 418

Increased upstream pressure resulting in proximal chamber dilation and hypertrophy This leads to the heart becoming large and rigid and poorly compliant

Answer 419

Regurgitant - Defective and floppy Stenotic - Narrowed valve lumen

Answer 420

Aortic Regurgitant and stenosis Mitral Regurgitant and stenosis

Answer 421

RILE (Right = inspiration and Left = Expiration) Pulmonary/Tricuspid on RHS on insipration

Answer 422

RILE (Right = inspiration and Left = Expiration) Aortic/Mitral heard on LHS on Expiration

Answer 423

ARMS (Aortic regurgitance / Mitral Stenosis) on Diastolic ASMR (Aortic Stenosis / Mitral Regurgitance) on Systolic

Answer 424

Rheumatic Heart disease (Most common - post strep pyogenes infection)

Answer 425

Valve calcification Infective endocarditis

Answer 426

Thickening and immobility of valve leads to obstruction of blood flow from LA to LV 🡪 increased LA pressure, pulmonary hypertension and right heart dysfunction AF is common due to elevation of LA pressure and dilatation Thrombus may form in the dilated atrium and give rise to systemic emboli e.g. the brain causing a stroke Chronically elevated LA pressure leads to an increase in pulmonary pressure and pulmonary oedema

Answer 427

Progressive exertional dyspnoea Cough productive of blood-tinged sputum Haemoptysis – coughing up blood due to rupture of bronchial vessels due to elevated pulmonary pressure Right HF Fatigue Weakness Abdominal/lower leg swelling Palpitations – due to AF Chest pain

Answer 428

Malar Flushed Cheeks - due to low CO2 Pulmonary HTN - Dyspnoea A wave on JVP Loud S1 Snap - due to thickend valve cusps Low pitched MID-DIASTOLIC murmur - loudest at apex and expiration when Px lies on LHS

Answer 429

Low pitched - due to decreased pulse and decreased CO MID DIASTOLIC Murmur Loudest at APEX Best heard on EXPIRATION when Px is lying on LHS

Answer 430

CXR - LA enlarged ECG - Afib, M shaped P waves due to LA enlarged GS - ECHO - Assess valve area

Answer 431

Diuretics - Furosemide for HF Rate control - BB/digoxin Anticoagulants if AF (Warfarin) Surgical: Percutaneous balloon Valvotomy - Stent opening mitral valve Mitral valve replacement

Answer 432

Myxomatous degeneration - Mitral Valve prolapse Connective tissue disorders - Marfans, Ehlers Danlos Infective Endocarditis

Answer 433

Females Increased Age Low BMI Prior MI or Connective Tissue disorder

Answer 434

Exertional dyspnoea Fatigue and lethargy Palpitations Right sided HF and can lead to congestive heart failure

Answer 435

Mitral valve fails to prevent reflux of blood into LA Increased LA pressure increased pulmonary pressure Pulmonary Oedema

Answer 436

PAN SYSTOLIC BLOWING murmur RADIATES to AXILLA Loudest at APEX Soft S1 and Prominent S3 in heart failure (severe cases)

Answer 437

Gold standard = ECHO - LA size and LV function analysis ECG CXR

Answer 438

Mitral Valve Regurgitation

Answer 439

ACEi + beta blockers IE Prophylaxis Serial ECHO Monitoring If severe (Sx at rest) then Valve repair/replacement

Answer 440

1/4 of the lumen size

Answer 441

Aortic Stenosis

Answer 442

LV dilation and hypertrophy

Answer 443

Congenital Bicuspic valve <70yrs Calcification due to Age >70yrs Rheumatic Valvular Disease

Answer 444

Supravalvular SubValvular Valvular

Answer 445

Ageing leads to aortic valve thickening and clacifications obstructing the normal LV outflow. Increased afterload Leads to increased LV pressure and compensatory LV hypertrophy. May lead to relative ischaemia causing angina arrhythmia and LV failure

Answer 446

SAD: Syncope (exertional) Angina Dyspnoea - related to HF

Answer 447

Slow rising (pulsus tardus) and weak (pulsus parvus) carotid pulse Heart sounds: Soft or absent 2nd heart sound – may become soft or inaudible when the valve becomes immobile Prominent 4th heart sound – due to LV hypertrophy Ejection systolic murmur – crescendo – decrescendo character

Answer 448

Ejection Systolic Crescendo Decrescendo Radiates to CAROTIDS At Right sternal Boarder - 2nd IC space

Answer 449

ECHO - LV size and function, aortic valve area (doppler derived gradient) ECG - LVH - ST depression and T-wave inversion in aVL, V5 and V6 CXR

Answer 450

Surgical Tx if symptomatic: Healthy Px - Open repair/replacement More at risk (>75yrs) TAVI - Transcutaneous Aortic Valve Implant

Answer 451

Leakage of blood into LV during diastole due to ineffective coaptation of aortic cusps

Answer 452

Congenital Bicuspid Valve RHD Connective tissue disorders - Marfans, Ehlers Danlos

Answer 453

Leakage of blood back into the LV during diastole due to ineffective closure of the cusps LV dilation and hypertrophy to maintain CO Reduced diastolic BP Relative ischaemia Leads to LV failure

Answer 454

Exertional dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea Palpitations Angina Syncope

Answer 455

Quincke - nailbed Pulsates when pressed De Musset - Head nodding with heart beat Wide pulse pressure LV failure Early Diastolic Murmur Austin Flint Murmur (severe)

Answer 456

EARLY DIASTOLIC BLOWING murmur At RIGHT Sternal boarder - 2nd IC space Austin Flint murmur (severe)

Answer 457

ECHO - Evaluate Aortic valve root and dimensions ECG - Evidence of LVH CXR - Cardiomegaly

Answer 458

Consider Infective endocarditis prophylaxis - Also considered as a DDx Vasodilators (ACEi to improve SV and reduce regurgitance if Px is asymptomatic or HTN) Surgical Valve replacement if symptomatic

Answer 459

Infection of the heart valves or other endocardial lined structure within the heart (e.g. septal defects, pacemaker leads, surgical patches)

Answer 460

Used to be a disease of the young affected by rheumatic heart disease Now it is a disease of: - The elderly (in an ageing population) - Young IV drug abusers - Young congenital heart disease - Anyone with prosthetic heart valves or pacemakers - Poor dental hygiene More common in males

Answer 461

Left-sided Native (mitral or aortic) Left-sided Prosthetic (early - within a year, late - after a year) Right-sided IE (rarely prosthetic). Device related (e.g. pacemakers, defibrillators)

Answer 462

Left-sided; are more likely to cause thrombo-emboli systematically. Right-side more likely to spread to cause a pulmonary embolism

Answer 463

Bacteria: S.aureus (most common in IVDU, T2DM, surgery) S. Viridans - Dental problems P. aeruginosa S.bovis HACEK Organisms

Answer 464

Male, Elderly, Prosthetic Valves Young IV Drug user Young w/Congenital heart defect Rheumatic Heart Disease

Answer 465

Usually Mitral valve (LHS) In IVDU it will more commonly affect Tricuspid Valve (RHS) due to injecting into veins and travelling to RHS of heart

Answer 466

Abnormal/damaged endocardium leads to increased platelet deposition. Bacteria virulence factors can adhere to this Vegetation Propagation involves activation of clotting cascade Inhabiting MOs cause cardiac valve distortion and cardiac failure + sepsis Typically around the valves

Answer 467

Valvular Regurgitation Than can lead to Ventricular insufficiency and subsequent increased risk of HF

Answer 468

Fever + Non-specific Symptoms New valve regurgitation Sepsis Emboli of unknown origin General Sx: Headache Malaise Confusion Night sweats

Answer 469

FROM JANE: Fever Roth’s spots – retinal haemorrhages Osler’s nodes – painful spots on hand Murmur - arrhythmia Janeway lesion – painless spots Anaemia Nail-bed splinter haemorrhages (splinter) Emboli – MI, stroke, PVD

Answer 470

Made using DUKE CRITERIA - 2 major or 1 major + 2 minor: Major: - Positive blood culture with typical IE microorganism - Echocardiograph showing endocardial involvement (e.g. vegetation, abscess) or new valvular regurgitation. Minor: - Fever (>38) - Pre-disposing factor (e.g. predisposing heart condition, IV drug user) - Vascular phenomena (e.g. major arterial emboli, septic pulmonary infarcts, intracranial haemorrhage, Janeway lesions, conjunctival haemorrhage) - Immunological problems (e.g. glomerulonephritis, Osler's nodes, Roth's spots, rheumatoid factor) - Microbiological evidence (e.g. positive blood culture (non-IE typical microorganism) or serological evidence of infection with organism consistent with IE)

Answer 471

Transoesophageal Echo (TOE): DIAGNOSTIC Generally safe but risk of perforation or aspiration Easiest if ventilated (but never ventilate just for TOE) Transthoracic echo (TTE): Safe Non-invasive No discomfort Often poor images so lower sensitivity ECG - conduction abnormalities, low QRS voltage, ST elevation, heart block, ventricular tachycardia, and supraventricular tachycardia CXR – cardiomegaly Blood cultures - IE organisms

Answer 472

Atrial surface of AV valves Ventricular surface of SL valves.

Answer 473

S.aureus - Vancomycin + rifampicin ( +gentamycin if prosthetic valve) S.viridans - Benzypenicillin + gentamycin for 4-6 weeks Surgery - remove valve if incompetent and replace with prosthetic Tx complications

Answer 474

Heart failure Aortic root abscess Septic emboli Sepsis

Answer 475

Inability of the heart to deliver blood thus oxygen that is commensurate with the requirement of the metabolising tissues despite normal or increased cardiac filling

Answer 476

- Class I - no limitation (asymptomatic) - Class II - slight limitation (mild HF Sx with normal activity) - Class III - marked limitation (symptomatically moderate HF Sx at less than normal activity) - Class IV - inability to carry out any physical activity without discomfort (symptomatically severe HF Sx at rest)

Answer 477

80-years-old (men; 78, women; 82)

Answer 478

Measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction

Answer 479

Systolic Heart failure - blood cant be pumped out of the LV well enough Diastolic Heart Failure - Not enough blood fills the ventricles during diastole In both cases blood builds up in the lungs causing congestion and fluid build up.2

Answer 480

HF-Reduced Ejection Factor (Left Ventricular Ejection Factor <40%) HF-Preserved Ejection Factor (Left Ventricular Ejection Factor >50% with dilated LA(>34ml/m2 AND and LVH) HF-Pulmonary Hypertension (Pulmonary Artery Pressure >40mmHg) HF-Valve (stenosis or regurgitation)

Answer 481

Myocardial dysfunction resulting from IHD

Answer 482

Hypertension Ischaemic Heart Disease Alcohol excess Cardiomyopathy Valvular disease - Aortic Stenosis, Mitral Regurgitation Arrythmias - Atrial Fibrillation Endocarditis Pericarditis

Answer 483

Borderline - 40-50% Systolic HF - <40%

Answer 484

Decreased CO, fails to increase with exertion Could be due to: - Pump failure – systolic HF, may be due to decreased heart rate e.g. anti-arrhythmic drugs - Excessive pre-load - Mitral regurgitation, fluid overload - Chronic increased afterload – occurs in aortic stenosis, hypertension – difficult for the heart muscle to push against it

Answer 485

Normal cardiac function but unable to meet increased demands for perfusion. Anaemia Pregnancy Hyperthyroidism

Answer 486

Left heart failure would cause congestion in the pulmonary circulation. Right heart failure would cause congestion in the systemic circulation Both can affect each other - eg. RHS HF can cause LHS HF

Answer 487

Decreased Contractility: - Coronary Artery Disease - Volume Overload (Valvular disease, Neurohormonal) - Dilated Cardiomyopathy Increased Afterload: - Hypertension - Aortic Stenosis

Answer 488

Stiff non-compliant left ventricle: Chronic Hypertension, Aortic Stenosis, HOCM can also cause diastolic failure by increasing hypertrophy of LV wall. This then decreases volume of the ventricle leading to a reduced filling room and reduced preload. Restrictive cardiomyopathy, Pericardial Constriction, Myocardial Fibrosis - less compliant LV walls due to increased stiffness. therefore the walls cannot stretch when filling leading to reduced preload

Answer 489

Sympathetic Stimulation - increased preload and afterload RAAS activation - increased preload through increased fluid retention Cardiac changes - Ventricular dilation, myocyte hypertrophy Overtime these cause increased stress on heart and contribute to HF

Answer 490

Ischaemic heart disease - myocardial damage/infarction can lead to scarring which doesnt contract and so the EF is reduce

Answer 491

Activation of SNS improves ventricular function by increasing HR and myocardial contractility Constriction of venous capacitance vessels redistributes centrally, and increased preload further augments ventricular function (via Frank-Starling mechanism) Also increases afterload by causing arteriolar constriction which eventually reduces CO and worsens HF

Answer 492

Fall in CO and increased sympathetic tone lead to diminished renal perfusion 🡪 activation of RAAS 🡪 increased salt and water retention Further increases venous pressure and maintains stroke volume by Starling mechanism As salt and water retention increases, This causes fluid overload peripheral and pulmonary congestion causes oedema and contributes to dyspnoea Angiotensin II also causes arteriolar constriction which increases afterload increasing myocardial work an exacerbating HF

Answer 493

Dilated cardiomyopathy - chamber grows and there is increases preload leading to increased contraction strength temporarily. over time the muscle walls get thinner and will end up becoming inefficient and reduce contractility

Answer 494

Chronic hypertension - increased afterload causes LV hypertrophy. This increases the O2 demand, and squeezes coronary arteries decreasing O2 supply to the myocardium. Overtime the heart muscle fatigues and becomes inefficient at pumping blood.

Answer 495

SOB Fatigue Ankle Swelling - fluid retention

Answer 496

IHD Hypertension - As arterial pressure increases, harder for LV to pump blood out 🡪 LV hypertrophy 🡪 greater demand for oxygen - Coronaries squeezed by extra muscle 🡪 less blood delivered to tissue Cardiomyopathy: - Dilated – heart chamber dilates (grows in size) in order to fill ventricle with more blood (increased preload) - Over time, muscle wall gets thinner and weaker 🡪 systolic HF - Restrictive – heart wall becomes stuff 🡪 less compliant 🡪 can’t stretch Aortic stenosis – narrowing of aortic valve

Answer 497

Breathlessness (dyspnoea) Cough Orthopnoea - SOB on lying flat - relieved by standing (causes crackles on auscultation) Paroxysmal Nocturnal Dyspnoea Peripheral Oedema

Answer 498

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.

Answer 499

Cardiomegaly (displaced apex beat) Pulmonary Oedema Bi-basal Crackles 3rd and 4th heart sounds (S3 in Dilated Ventricle and S4 in a less compliant) Pleural effusion Crepitations in lung bases Tachycardia Reduced BP Cool peripheries Heart murmur

Answer 500

Left ventricular failure: (most common cause of RHF) - Fluid build-up 🡪 increased pressure in pulmonary artery 🡪 harder for right side to pump blood into Hypertension Pulmonary stenosis Lung disease (cor pulmonale) – harder to exchange oxygen - Pulmonary arterioles constrict 🡪 increase pulmonary BP 🡪 harder for RV to pump against 🡪 hypertrophy and failure Atrial/ventricular shunt – blood moves from L🡪R - Leads to increased volume on right side 🡪 RV hypertrophy - More prone to ischaemia (systolic dysfunction) and has a small filling volume (diastolic dysfunction)

Answer 501

SOB Peripheral oedema Ascites Nausea Anorexia

Answer 502

Raised JVP – JVP distension Hepatomegaly/Splenomegaly Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed Ascites Weight gain (fluid)

Answer 503

Clinical presentation BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP) ECG - ascertain underlying cause - ischaemia, LVH, HTN, Arrhythmia GS - Echocardiogram (TTE) - Done if BNP and ECG abnormal (Ascertain underlying cause) CXR - (ABCDE) Alveolar oedema, Kerley Blue lines, Cardiomegaly, Dilated Upper lobe vessels, Plural Effusions

Answer 504

- Tachycardia and hypotension - Shortness of Breath - Fatigue - Displaced apex beat - Raised JVP - common in RHF - Additional heart sounds/ murmurs, - Hepatomegaly (e.g. pulsatile/ tender) - RHF - Peripheral/ sacral oedema - Ascites

Answer 505

Anything that increases myocardial work: - Age over 65 years - Men (due to lack of oestrogen protection) - Obesity - African descent - Individuals who have had an MI - Alcohol excess - Hyperthyroidism - Anaemia - Pregnancy

Answer 506

Framingham Boston

Answer 507

- Avoid large meals - Education - Weight loss - Cardiac Rehab - Smoking cessation - Exercise - Vaccination

Answer 508

ABAL: ACEi Beta Blockers Aldosterone Antagonists (MRA) Loop Diuretics

Answer 509

Reduce Mortality: 1. ARNI (Entresto) / ACEi / ARB 2. SGLT2 inhibitor 3. Beta Blockers (Bisoprolol) 4. ACEi 5 Aldosterone Antagonists (spironolactone, Eplerenone) Reduce Sx: Diuretics - Loop/Thiazide Digoxin

Answer 510

50% mortality in 5 years

Answer 511

No therapy to reduce Mortality Tx underling cause of HFpEF Symptom Mx - ACEi, BB, Diuretics (loop, thiazide, AA) Digoxin

Answer 512

Right sided Heart failure caused by respiratory disease.

Answer 513

The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension >25mmHg) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries. Causes RV Hypertrophy and overtime this will become inefficient leading to HF. This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.

Answer 514

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

Answer 515

Early Cor pulmonale - Asymptomatic Later: SOB Peripheral Oedema Dyspnoea - on exertion Syncope Chest Pain

Answer 516

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 517

ECHO - Evidence of increased pressure Spirometry - Chronic lung disease Evidence GS - Right Heart Catheterisation - Measure Pulm Pressures

Answer 518

Treat symptoms and underlying cause. Long term oxygen therapy may be used.

Answer 519

Increased Age Family Hx Male

Answer 520

Angina Myocardial Infarction Transient Ischaemic Attacks Stroke Peripheral Vascular Disease Mesenteric Ischaemia

Answer 521

Angina Myocardial Infarction Transient Ischaemic Attacks Stroke Peripheral Vascular Disease Mesenteric Ischaemia

Answer 522

Primary Prevention – for patients that have never had cardiovascular disease in the past. Secondary Prevention – for patients that have had angina, myocardial infarction, TIA, stroke or peripheral vascular disease.

Answer 523

Advice on diet, exercise and weight loss Stop smoking Stop drinking alcohol Tightly treat co-morbidities (such as diabetes)

Answer 524

4 As: A – Aspirin (plus a second antiplatelet such as clopidogrel for 12 months) A – Atorvastatin 80mg A – Atenolol (or other beta-blocker – commonly bisoprolol) A – ACE inhibitor (commonly ramipril) titrated to maximum tolerated dose

Answer 525

Major circulatory disorder characterised by arterial obstruction, leading to reduced blood supply and ischaemia in the lower limbs. Most commonly caused by atherosclerosis

Answer 526

Acute limb ischaemia (also known as acute limb-threatening ischaemia) describes a sudden decrease in perfusion due to arterial occlusion, and can result in rapid ischaemia.

Answer 527

Critical limb ischaemia is defined as rest or night pain for greater than 2 weeks, with or without tissue loss such as ulceration.

Answer 528

Atherosclerosis causing a blockage of blood flow. Intermittent Claudication: Blockage causes nerve pain due to release of adenosine in response to ischaemia Critical Limb Ischaemia: Severe occlusion of arteries and blood supply is barely adequate to meet metabolic demand leading to pain at rest and increased risk of gangrene and infection.

Answer 529

Hip or buttocks pain – aorta or iliac arteries Thigh – common femoral artery Upper 2/3rd of calf – superior femoral artery Lower 1/3rd of calf – popliteal artery Foot – tibial or peroneal artery

Answer 530

Nerve pain caused by the release of adenosine in response to limb muscle ischaemia caused by atherosclerosis (PVD)

Answer 531

Varying symptoms: - Asymptomatic - ABPI (ankle brachial Pressure index) <0.9 - Bruits (pulsatile regions due to turbulent blood flow) - Aching / burning in the legs - Intermittent claudication (pain on exercise relieved by rest) Critical Limb Ischaemia: - Rest pain (critical limb ischaemia) - Skin ulceration and gangrene.

Answer 532

Signs: Absent femoral, popliteal or foot pulses. Cold white legs.

Answer 533

Complete occlusion of the vessel - due to embolic/thrombotic event. Foot pain at rest - relieved by hanging out the side of bed at night Causes 6 Ps

Answer 534

Pulselessness Pallor Pain Perishingly Cold Paralysis Paraesthesia

Answer 535

Stage 1. Asymptomatic Stage 2. Intermittent Claudication (pain on exertion) Stage 3. Critical Limb Ischaemia (pain at rest) Stage 4. Ischaemic ulcers - Gangrene

Answer 536

Ankle Brachial Pressure Index (ABPI): 0.5 - 0.9 = Intermitted Claudication <0.5 = Chronic Limb Ischaemia Colour Doppler (DUPLEX) ultrasound - confirm site and degree of stenosis. CT angiography if surgery considered.

Answer 537

Assessment of Arterial Sufficiency: - With the patient supine, elevate both legs to an angle of 45 degrees and hold for one to two minutes. Observe the colour of the feet. Pallor indicates ischaemia. It occurs when the peripheral arterial pressure is inadequate to overcome the effects of gravity. The poorer the arterial supply, the less the angle to which the legs have to be raised for them to become pale. - Then sit the patient up and ask them to hang their legs down over the side of the bed at an angle of 90 degrees. Gravity aids blood flow and colour returns in the ischaemic leg. The skin at first becomes blue, as blood is deoxygenated in its passage through the ischaemic tissue, and then red, due to reactive hyperaemia from post-hypoxic vasodilatation.

Answer 538

Compares Blood in post/ant. tibial artery to brachial artery. 0.9-1.3 = normal

Answer 539

Intermittent Claudication RF management: - Quit smoking - Treat hypertension - Lower cholesterol - Improve diabetes - Improve diet Medication - Clopidogrel Chronic Limb Ischaemia: - Revascularisation surgery (PCI/Bypass graft) - Local Thrombolysius with t-PA - In Ischaemic limb emergency - PCI within 4-6 hours otherwise amputation.

Answer 540

Smoking Hypertension Ageing Obesity CKD T2DM

Answer 541

Gout / cellulitis But deep duskiness of skin and sudden deterioration rules this out.

Answer 542

Amputation Critical Limb/acute limb ischaemia Permanent limb weakness Rhabdomyolysis Increased risk of CVD.

Answer 543

Permanent dilation of the aorta exceeding 50% where >3cm diameter. Often Infra-renal (below renal arteries)

Answer 544

- AAAs have a reported prevalence of 1.3-12.7% in the UK - M>F - Most common in the elderly: >60

Answer 545

Idiopathic, Smoking, obesity, HTN, Family Hx Connective tissue disorders - Marfans, Ehlers Danlos

Answer 546

Smooth muscle, elastic and structural degradation of the vascular wall in ALL 3 LAYERS of the vascular tunic. Due to MMPs being released from atherosclerotic inflammation Increased Leukocyte infiltration leads to increased vessel diameter to > 3cm +

Answer 547

AAA more than 5.5cm diameter

Answer 548

Medical Emergency requires immediate surgical repair 80% mortality prior to reaching hospital.

Answer 549

Usually asymptomatic

Answer 550

Sudden epigastric pain, Radiating to flank Pulsatile mass in abdomen Hypotensive and Tachycardic

Answer 551

- **Pulsatile abdominal mass** - **Tachycardia and hypotension:** red flags signifying ruptured AAA - **Grey-Turner’s sign:** flank bruising secondary to retroperitoneal haemorrhage - **Cullen’s sign:** pre-umbilical bruising

Answer 552

Acute pancreatitis - Does not tend to have a pulsatile feel. GI bleed Perforated GI ulcer Appendicitis Pyelonephritis

Answer 553

Abdominal Duplex Ultrasound High sensitivity and Specificity If ruptured then none - medical Emergency

Answer 554

Unruptured - manage RF and Surveillance ASx and <5.5cm - monitor Sx and>5.5 - surgery (endovascular repair or open surgery)

Answer 555

Stabilise ABCDE + fluids AAA Graft surgery repair.

Answer 556

25/100,000 incidence at 50yrs. Rises with age. Males

Answer 557

Tear in the intima resulting in blood dissecting through the tunica media causing separation of the layers of the aortic wall. Creates a false lumen in the diseased media and splits the wall.

Answer 558

Type A – involves ascending aorta (most common) Type B – doesn’t involve ascending aorta

Answer 559

Genetic link, Atherosclerosis, Inflammatory, Trauma: Mechanical stress causes a tear in the intima of the aortic lining. This causes blood to enter the aortic wall under pressure causing a haematoma and separates the layers.

Answer 560

Connective tissue disorders - Marfans, Ehlers Danlos Hypertension Cocaine Use Aortic Aneurysm Smoking Hypercholesterolaemia

Answer 561

Sinotubular junction - Aortic root near aortic valve Just distal to Left Subclavian Artery (descending thoracic aorta)

Answer 562

- **Sudden onset, severe ‘tearing’ or ‘ripping’ chest pain** that may radiate to the back and down the arms - **Syncope:** red flag symptom

Answer 563

Absent peripheral pulses Unequal BP in left and right arm Neurological signs due to involvement of branch arteries Aortic regurgitation, cardiac tamponade Compression of other arteries – renal, subclavian

Answer 564

Transoesophageal ECHO (if haemodynamically unstable) OR CT angiogram (if Px is haemodynamically stable) Shows intimal Flap and False lumen CXR - Shows widened mediastinum

Answer 565

Surgical: Open repair/Endovascular aortic repair Medication (to reduced HR and BP): Special Beta Blockers - Esmolol Vasodilator - Sodium Nitroprusside

Answer 566

Cardiac Tamponade Aortic Insufficiency Pre renal AKI Stroke - Ischaemic

Answer 567

**Arrhythmias** are abnormal heart rhythms. They result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle.

Answer 568

> 100 bpm.

Answer 569

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 570

1. Sudden death. 2. Syncope. 3. Dizziness. 4. Palpitations. 5. Can also be asymptomatic.

Answer 571

1. Supra-ventricular tachycardia's. 2. Ventricular tachycardia's.

Answer 572

They arise from the atria or atrio-ventricular junction.

Answer 573

Supraventricular tachycardias are often associated with narrow complexes.

Answer 574

1. Atrial fibrillation. 2. Atrial flutter. 3. AV node re-entry tachycardia (AVNRT) - Most common SVT 4. Accessory pathway - Wolfson Parkinson White 5. Focal atrial tachycardia. (sinus Tachycardia)

Answer 575

The ventricles.

Answer 576

Ventricular tachycardias are often associated with broad complexes.

Answer 577

Ventricular Tachycardia Ventricular Fibrillation

Answer 578

RBBB / LBBB 1, 2, 3 Heart Block Sinus Bradycardia

Answer 579

Irregularly irregular atrial firing Rhythm

Answer 580

Any condition that causes a raised atrial pressure Heart Failure CAD RHD HTN secondary to mitral valve stenosis Idiopathic

Answer 581

60+ T2DM HTN Valve defects Hx of MI

Answer 582

Rapid re-entrant ectopic foci (300-600 Bpm) Causes atrial spasm Causes atrial blood to pool and therefore reduces CO and increases risk of thromboembolic events.

Answer 583

1. Palpitations. 2. Shortness of breath. 3. Fatigue. 4. Chest pain. 5. Increased risk of thromboembolism and therefore stroke. 6. Syncope

Answer 584

Paroxysmal (episodic) Persistent (longer than 7 days) Permanent (sinus Rhythm unrestorable)

Answer 585

ECG is diagnostic Irregularly Irregular pulse w/ narrow QRSs <120ms No P waves (fibrillatory squiggles)

Answer 586

1. Rate control - beta blockers, CCB and digoxin. 2. Rhythm control - electrical cardioversion or pharmacological cardioversion using flecainide. 3. Flecainide can be taken on a PRN basis in people with infrequent symptomatic paroxysms of AF. 4. Long term - catheter ablation and a pacemaker. 5. Anticoagulation (warfarin)

Answer 587

CHADS2 VASc.

Answer 588

CHADS2 VASc: Congestive HF Hypertension Age > 75 Age 65-74 Diabetes Mellitus Stroke/TIA Vascular disease Sex - Female Used to calculate stroke risk. 0 = No 1 = consider oral anticoagulation / aspirin 2 = Oral Anticoagulation (warfarin/Rivaroxaban)

Answer 589

Beta blockers, CCB and digoxin.

Answer 590

Electrical cardioversion or pharmacological cardioversion using flecainide.

Answer 591

Catheter ablation - it targets the triggers of AF.

Answer 592

Heart failure Ischaemic stroke Mesenteric Ischaemia

Answer 593

Irregular organised atrial firing 250-350 bpm

Answer 594

Similar to aetiology of AF

Answer 595

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 596

Dyspnoea Palpitations Syncope

Answer 597

F wave - saw tooth pattern Often has a 2:1 block - 2 p waves for every 1 QRS

Answer 598

Acutely unstable - DC Synchronised Cardioversion Stable - Rhythm/Rate (amiodarone + BB) control w/ oral coagulation (prevent thromboemboli) Radiofrequency ablation - long term

Answer 599

An AV Reciprocating Tachycardia (AVRT) There is an accessory pathway that exists for impulse conduction called the bundle of Kent between atria and ventricles This is a Pre excitation syndrome (excites ventricles early causing a delta wave) This is not re-entry through the AVN. Often hereditary

Answer 600

Palpitations Dizziness Dyspnoea

Answer 601

Slurred DELTA WAVES Short PR interval (<0.12s) Wide QRS (>0.12s)

Answer 602

1. Valsalva Manoeuvre If Vagal manoeuvres are ineffective then: 2. IV adenosine (6mg, then 12mg then 12mg) to cease conduction. 3. Consider surgical radiofrequency ablation

Answer 603

Atrial Fibrillation Atrial Flutter Supraventricular Tachycardias Wolf parkinson White syndrome

Answer 604

A ventricular Tachyarrhythmia typically caused by a congenital channelopathy where mutations affect ion channels. This causes the QT interval to be 480ms +

Answer 605

Romano ward syndrome Hypokalaemia and Hypocalcaemia Drugs - Amiodarone/magnesium

Answer 606

Polymorphic ventricular tachycardia in patients with prolonged QT. Rapid irregular QRS complexes which twist around baseline. Can cease spontaneously or develop into ventricular fibrillation.

Answer 607

This involves very rapid irregular ventricular activation with no mechanical effect i.e. no cardiac output. Ventricular fibrillation (VF) occurs when the ventricular muscle fibres contract independently. Shapeless rapid osscillations on ECG patients becomes pulseless and goes into cardiac arrest - no effective cardiac output

Answer 608

Electrical defibrillation (DC Cardioversion)

Answer 609

Rapid cardiac rhythm > 100bpm, QRS complex <120ms: Supraventricular tachycardia Atrial fibrillation/flutter

Answer 610

Rapid cardiac rhythm >100bpm, QRS complex >120ms Ventricular tachycardia Supraventicular tachycardia with bundle branch block/pre-excitation

Answer 611

1. Ischaemia. 2. Fibrosis of the atrium. 3. Inflammation. 4. Drugs.

Answer 612

1. CAD. 2. Cardiomyopathy. 3. Fibrosis.

Answer 613

First degree prolonged PR interval Second degree - Mobitz type I and Type II Some atrial impulses fail to reach the ventricles Third degree Complete dissociation between atrial and ventricular activity

Answer 614

1:1 conduction - Every P wave has QRS followed Prolonged PR interval >200ms

Answer 615

No symptoms No treatment

Answer 616

LEV’s disease IHD – scar tissue from myocyte death blocks conduction pathway Myocarditis Hypokalaemia Drugs - block AVN conduction (BB/CCB/Digoxin)

Answer 617

When some P waves are conducted and others aren't 2:1 conduction - Every other P wave is followed by a QRS complex

Answer 618

Mobitz I Mobitz II

Answer 619

PR interval gradually increases until AV node fails and no QRS is seen. This then Repeats

Answer 620

PR interval is constant but every nth QRS complex is missing. There is a sudden unpredictable loss of AV conduction and so loss of QRS.

Answer 621

Type I: Patient often experiences light headedness, dizziness and syncope Type II: Patients often experience chest pain, SOB, syncope and postural hypotension

Answer 622

Type I - Caused by AV node block - Beta blockers, CCB, Digoxin, inferior MI Type II - Caused by Intra-nodal block - Inferior MI, Rheumatic Fever

Answer 623

Complete heart block Atrial activity fails to conduct to the ventricles. P waves and QRS complexes therefore occur independently.

Answer 624

Acute MI HTN Structural heart disease

Answer 625

IV Atropine Permanent Pace maker

Answer 626

Where electrical conduction down the left/right bundle branch in the bundle of HIS/septum is blocked/delayed often by fibrosis. This causes the impulse conduction to the ventricles to occur at different times creating a second R wave in the leads associated with the right/left ventricles on an ECG. In LBBB - LV contraction later than RV In RBBB - RV contraction later than LV

Answer 627

Acute Ischaemia and MI Myocarditis Chronic HTN Cardiomyopathies Left - IHD, valvular disease Right - PE, IHD, valvular disease

Answer 628

A 'W' shape would be seen in the QRS complex of lead V1 and a 'M' shape in V6. WiLLiaM.

Answer 629

A 'M' shape would be seen in the QRS complex of lead V1 and a 'W' shape in V6. MaRRoW.

Answer 630

T wave flattening and inversion ST segment depression first → progresses to ST elevation Q waves (old infarction)

Answer 631

Anterior leads: V2, V3, V4

Answer 632

Lateral: V5, V6

Answer 633

Inferior: II, III, aVF

Answer 634

1. Tall 'tented' T waves. 2. Flat P waves. 3. Broad QRS. 4. Short QT interval

Answer 635

1. Flat T waves. 2. Prolonged PR Interval 3. QT prolongation. 4. ST depression. 5. Prominent U waves.

Answer 636

1. QT prolongation. 2. T wave flattening. 3. Narrowed QRS. 4. Prominent U waves.

Answer 637

1. QT shortening. 2. Tall T waves. 3. No P waves.

Answer 638

When a thrombus forms in deep leg vein Below calf - less concerning and most common Above calf/thigh - life threatening

Answer 639

Virchow's triad Factors: Venous Stasis - Immobility, Hypercoagulability - OCP, HRT, Pregnancy, Polycythaemia Endothelial Injury - smoking, age, malignancy

Answer 640

- **Unilateral swelling** - **Oedema** - **Tender and erythematous** - **Distention of superficial veins** - **Phlegmasia cerulea dolens:** occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). This leads to ischaemia and a blue and painful leg

Answer 641

Unilateral calf pain, redness and swelling

Answer 642

Clinical history + WELLs Score >2 = high risk D-dimer raised and Duplex ultrasound (gold standard) (D dimer normal excludes DVT, but positive does not confirm) CT or MR venogram

Answer 643

Clinical Hx WELLs Score 2 or more = likely DVT --> Duplex Ultrasound (diagnostic) WELLs Score 1 or Less --> D-Dimer test --> If raised --> Duplex Ultrasound

Answer 644

1st Line DOAC anticoagulant therapy Rivaroxaban/Apixaban 2nd Line LMWH (if above CI in renal impairment) Warfarin

Answer 645

Cellulitis - S.aureus / S.pyogenes Leukocytosis

Answer 646

Compression stockings Early mobilization Leg elevation

Answer 647

PE Post-thrombotic Syndrome Recurrence of thrombosis

Answer 648

- Caused by diastolic filling of the ventricle - Considered normal if < 30 years old (may persist in women up to 50 years old) - Heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

Answer 649

- Caused by atrial contraction against a stiff ventricle - therefore coincides with the P wave on ECG - in HOCM a double apical impulse may be felt as a result of a palpable S4 - May be heard in aortic stenosis, HOCM, hypertension

Answer 650

- Closure of mitral and tricuspid valves - Soft if long PR or mitral regurgitation - Loud in mitral stenosis

Answer 651

- Closure of aortic and pulmonary valves - Soft in aortic stenosis splitting during inspiration is normal

Answer 652

Increased Turbulent blood flow: Increased Velocity of blood: - Through a stenosed valve/ narrow VSD/ASD - Increased contractile strength of myocardium - Decreased Diameters - through HOCM narrowing the exit of the ventricle to the Aorta Decreased Viscosity of blood - through anaemia Blood flow back across incompetent valves

Answer 653

All Physicians Earn Too Much: Aortic Valve - R. 2nd ICS - CoA, AS, AR Pulmonic Valve - L. 2nd ICS - PS, PR, ASD ERBS Point - L 3rd ICS - S1 +S2, HOCM Tricuspid Valve - L 4th ICS - TS, TR, VSD Mitral Valve - L 5th ICS, (MCL) - MR, MS

Answer 654

Best Heard - Right parasternal boarder, 2nd intercostal space Radiates to - Carotids as it flows up through the aortic arch vessels

Answer 655

Best Heard - Right Parasternal Boarder, 2nd intercostal space Radiates to - Left upper sternal boarder (2nd/3rd ICS) due to blood flowing back across the left side of the heart

Answer 656

Best Heard - Left 5th ICS, mid clavicular line Radiates to - Axilla as blood is flowing up into the left atria which is towards the axilla

Answer 657

Blowing Murmurs are usually regurgitation murmurs: Aortic Regurgitation Mitral Regurgitation

Answer 658

Valvular Stenosis: Aortic Stenosis Mitral Stenosis

Answer 659

Patent ductus Arteriosus

Answer 660

High pitch due to high pressure gradients as the blood flows from the LV to the RV through the VSD

Answer 661

Low pitch Due to low pressure gradient from the atria to the ventricles But high blood flow across the valve creates a low pitch

Answer 662

Harsh High pitch High pressure gradients High blood flow across the valve

Answer 663

Aortic/Pulmonic Stenosis: Valves are rigid and so upon LV contraction the valves bow (not open properly) causing an EJECTION CLICK sound as blood hits the underside of the valve. CRESCENDO DECRESCENDO murmur as the blood velocity increases during systole and then falls of as the blood is ejected HOCM: CRESCENDO DECRESCENDO murmur with NO ejection click Coarctation of the Aorta

Answer 664

Mitral/Tricuspid Regurgitation: Murmur occurs through entire systolic time period as blood is flowing back across the valve into the atria the entire time the ventricles contract VSD: As the LV contracts blood is flowing across the VSD into the RV causing turbulent flow in the RV.

Answer 665

Aortic/Pulmonic Regurgitation: During Early diastole (right at the start) the LV pressure decreases so blood can back flow across the Aortic valve hitting the LV wall causing turbulent flow Lots of blood flows in early diastole which falls off in late diastole. This causes a DECRESCENDO Murmur Mitral/Tricuspid Stenosis: OPENING SNAP (immediately at the start of diastole) followed by lots of blood entering the ventricles in early diastole which then reduces as diastole progresses causing a DECRESCENDO murmur

Answer 666

A Continuous "Machine" Murmur due to a constant shunt from the aorta to the pulmonary artery

Answer 667

Arterial circulation - High pressure (platelet rich) Venous Circulation - Low pressure (fibrin rich)

Answer 668

Coronary Cerebral Peripheral Other sites

Answer 669

Atherosclerosis Inflammatory Infection Trauma Tumours Unknown

Answer 670

Myocardial Infarction Cerebral Vascular Disease Peripheral Vascular Disease

Answer 671

Anti-platelets: Aspirin LMWH or Fondraparinux Thrombolytic therapy: Streptokinase OR TpA Reperfusion - PCI

Answer 672

Heparin has a high risk of bleeding

Answer 673

Peripheral - Ileofemoral, Femoro-popliteal Other sites - Cerebral, Visceral

Answer 674

Signs and Sx are very non-specific Blood tests - D-dimer - sensitive but not specific Imaging usually required

Answer 675

Virchows Triad

Answer 676

Anti-Coagulants: Heparin/LMWH Warfarin DOAC

Answer 677

Glycosaminoglycan Given by Infusion Binds to anti-thrombin and increases its activity. Indirect thrombin inhibitor

Answer 678

Smaller molecule of heparin that is excreted renally. Weight adjusted dose given via SC injection Used for Tx and Prophylaxis

Answer 679

Anticoagulant that prolongs the Prothrombin time Prevents synthesis of Active factors II, VII, IX, X Antagonist of Vitamin K

Answer 680

New oral anticoagulant drugs/ Direct oral anticoagulant drugs Directly act on Factor II or X

Answer 681

Mechanical/chemical thromboprophylaxis Early mobilisation and good hydration

Answer 682

4 hours Monitor with APTT (anti-prothrombin time)

Answer 683

12 hours and therefore can be given once daily and not necessarily needed to be monitored

Answer 684

Extended thromboprophylaxis and treatment of AF, DVT and PE Not used in pregnancy

Answer 685

Inhibits Cyclo-oxygenase irreversibly. Prevents thromboxane formation and therefore inhibits platelet aggregation

Answer 686

Give Vitamin K

Answer 687

Mechanical: Hydration Early mobilisation Compression stockings Chemical: LMWH

Answer 688

25,000 people die per year due to DVT/PE in the UK

Answer 689

DVT leads to increased compartment pressure resulting in venous hypertension. This can compress the arterioles reducing their blood suplly and resulting in ischaemia to the local tissues.

Answer 690

When an embolus (often from a thrombus/DVT) travels through the venous circulation and into the pulmonary circulation to get lodged in the pulmonary vasculature.

Answer 691

Signs: Tachycardia Tachypnoea Pleural rub SX: Breathlessness Pleuritic chest pain High RFs

Answer 692

DDx of chest pain and SOB

Answer 693

CXR - usually normal ECG - Sinus Tachy - S1Q3T3 D-Dimer and CTPA (GS - CT scan and Pulmonary angiogram) Blood gases - Type I resp failure (Decreased O2/CO2)

Answer 694

Supportive Tx and Tx underlying cause Apixaban DOAC LWMH (if CI for renal impairment)

Answer 695

Early mobilisation and hydration. Anticoagulation

Answer 696

Thrombolytics - Alteplase (clot buster)

Answer 697

True - weakening of arterial wall leading to dilation False Mycotic

Answer 698

Left ventricular failure (DCM) Constrictive pericarditis Mitral Regurgitation

Answer 699

Aortic stenosis HOCM Hypertension

Answer 700

An autoimmune condition triggered by streptococcus bacteria that causes an inflammatory reaction in cardiac and joint tissue.

Answer 701

Pharyngeal infection with Group A strep (S. pyogenes)

Answer 702

2-4 weeks post Strep infection: Body produces antibodies against S. pyogenes M protein toxin. Abs cross react with Px own tissues through molecular mimicry Abs attack Px Joint, heart, skin and NS tissues causing an inflammatory reaction.

Answer 703

Type 2 hypersensitivity reaction.

Answer 704

Recent sore throat (infection) Chest pain (pleuritic) SOB Joint pain - oligo/poly arthritis Non-pruritic rash Sydenham's Chorea

Answer 705

Heart: Heart Murmur - MR or AR Tachycardia/Bradycardia HF Joints - Tender joints Skin: Erythema marginatum rash Subcutaneous nodules

Answer 706

Irregular, uncontrolled rapid movements of the limbs

Answer 707

Jones Criteria: 2 Major OR 1 Major + 2 Minor Major (JONES): J – Joint arthritis O – Organ inflammation, such as carditis N – Nodules E – Erythema marginatum rash S – Sydenham chorea Minor: (FEAR) F - Fever E - ECG Changes (prolonged PR interval) without carditis A - Arthralgia without arthritis R - Raised inflammatory markers (CRP and ESR)

Answer 708

Throat swab for bacterial culture ASO (anti-strep Antibodies) titres ECHO/ECG/CXR for heart involvement

Answer 709

Conservative Mx: Bed rest, analgesia Antibiotics: IV Benzylpenicillin STAT followed by Penicillin V for 10 days Tx system involvement: NSAIDs - joint pain Aspirin/Steroids - Carditis Diazepam - Sydenham's Chorea

Answer 710

Rheumatic Heart Disease: (occurs in 30-50% of rheumatic fever cases) Valvular Heart Disease - Mitral stenosis (and aortic) Heart Failure Infective endocarditis Atrial fibrillation

Answer 711

Rheumatic Fever

Answer 712

Cardiac troponin (Troponin T and I) Released into the blood when cardiac muscle is damaged. Highly sensitive but not specific.

Answer 713

Cardiac – ACS, Aortic dissection, pericarditis, myocarditis Respiratory – PE, pneumonia, pleurisy, lung cancer MSK – rib fracture, chest trauma, costochondritis (inflammation of the cartilage between the ribs and sternum) GORD Oesophageal spasm Anxiety/panic attacks

Answer 714

Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion (meaning there is inadequate glucose and oxygen for aerobic cellular respiration), resulting in generalised hypoxia and/or inability of cells to utilise oxygen.

Answer 715

- Hypotension stimulates baroreceptors in aortic arch and carotid sinuses causing increased sympathetic nervous activity with “spill-over” of noradrenaline into the circulation - Later this is augmented by the release of adrenaline from the adrenal medulla which causes vasoconstriction - Vasoconstriction, together with increased myocardial contractility and HR help to restore BP and CO - Reduced perfusion of the renal cortex stimulates the juxtaglomerular apparatus to release renin - Renin converts angiotensinogen to angiotensin I which is then converted into angiotensin II (in the lungs by ACE) which stimulates the release of aldosterone from the zona glomerulosa causing water and sodium retention - This helps to restore the circulating volume

Answer 716

- Septic – infection with any organism 🡪 acute vasodilation from inflammatory cytokines - Anaphylactic – Type-I IgE-mediated hypersensitivity, release of histamine - Neurogenic – spinal cord injury, epidural or spinal anaesthesia - Hypovolaemic – loss of >20% of body’s blood or fluid supply, severe fluid loss makes it impossible for the heart to pump a sufficient amount of blood around the body

Answer 717

Hypovolaemic (reduced preload) – low blood volume Haemorrhagic: -Trauma -GI bleeding -Fractures -Ruptured aortic aneurysms Non-haemorrhagic (fluid loss): -Burns – heat increases permeability of capillaries so more plasma leaks -Severe diarrhoea and vomiting 🡪 dehydration -Intestinal obstruction (fluid accumulates in intestines) -Pancreatitis

Answer 718

Pump failure- Heart isn't Pumping - Acute MI - Myocarditis - Atrial and ventricular arrhythmias - Bradycardias - Rupture of valve cusp Obstructive: - Obstruction to outflow - Massive PE - Tension pneumothorax Restricted cardiac filling: - Cardiac tamponade - Constrictive pericarditis

Answer 719

Skin is pale, cold, sweaty and vasoconstricted Rapid, weak pulse Reduced pulse pressure – MAP may be maintained (note – arterial BP NOT a good indicator of shock since it will be maintained until a very large amount of blood loss Reduced urine output Confusion, weakness, collapse and coma Capillary refill time (CRT) – if it takes more than 3 seconds to turn pink after 5 seconds of compression, this is the earliest and most accurate sign of shock

Answer 720

- Airways – ensure patency - Breathing – give 100% O2 and correct immediately life-threatening problems e.g. congestive cardiac failure, bronchospasm, tension pneumothorax - Circulation IV access Give fluid and blood if acute blood loss Ensure haemostasis i.e. stop bleeding - Stabilise BP Fluid replacement Medications that increase heart contractility, vasoconstriction and retain fluid Vasoconstriction - adrenaline - Supplemental oxygen or airway intubation

Answer 721

Systemic Inflammatory Response syndrome (SIRS) defined as: Temperature of >38˚C or <36˚C Tachycardia >90 BPM Respiratory rate >/= 20 breaths per minute OR PaCO2 <4.3kPa WBC > 12 x 109/L or < 4 x 109/L

Answer 722

Current ore recent Infection + Pyrexia and rigors Nausea and vomiting Vasodilation with warm peripheries Bounding pulse

Answer 723

Airways Breathing Circulation Antibiotics - Community-acquired pneumonia – ceftriaxone - MRSA – vancomycin - Pseudomonas – cefepime + metronidazole Treat underlying cause: - Haemorrhage - Sepsis - Anaphylaxis

Answer 724

Type I Hypersensitivity - Massive release of mediators from mast cells and basophils induced by cross-linking of surface IgE with trigger antigen leads to an increase in vascular permeability, vasodilation and respiratory smooth muscle contraction

Answer 725

Onset of symptoms usually within 5-60 minutes of antigen exposure Swollen tongue, lips Laryngeal oedema Swollen epiglottis `Warm peripheries and hypotension due to profound vasodilation Urticaria Angio-oedema Wheezing and SOB due to bronchospasm Upper airway obstruction due to laryngeal oedema Low BP – due to vasodilation, increased vascular permeability and fluid loss from vascular space

Answer 726

Remove the precipitating cause e.g. stop administration of offending drug Oxygen – high flow Adrenaline – 0.5mL injected IM, IV if patient is in cardiac arrest, half doses for patients taking amitriptyline, imipramine or beta blockers Fluids – 500-1000mL 0.9% saline Chlorphenamine (antihistamine) Hydrocortisone Admit for observation due to risk of second late reaction Prevent further attacks

Answer 727

Inadequate tissue perfusion Skin – cold, pale, clammy, slate-grey Brain – drowsiness and confusion Increased sympathetic tone Tachycardia – narrow pulse pressure and weak pulse Sweating BP may be maintained initially but hypotension develops later Bradycardia

Answer 728

Signs of myocardial failure Characterised by - Chest pain - Respiratory distress - JV distension - Hypotension - Crackles in lung ECG – ST elevation V1-6 Gallop rhythm Pulmonary oedema