Phase 2 - Cardio Flashcards

Question

Which heart defects cause right-left shunt

Answer 1

Tetralogy of Fallot Tricuspid atresia (abnormal narrowing)

Answer 2

- Complete transposition of great vessels - **Coarctation** of aorta - Pulmonary **stenosis** - Aortic stenosis - Coronary artery origin from pulmonary artery - Ebstein malformation (tricuspid is lower + malformed) - Endocardial fibroelastosis (connective tissue growth around myocardium -> restricting contractive ability)

Answer 3

Unstable angina NSTEMI STEMI (can be q-wave or non q-wave infarcts)

Answer 4

Cardiac chest **pain at rest** Cardiac chest pain with **crescendo pattern** Usually new onset or abrupt deterioration in previously stable angina Uncommon: - marked sweating - epigastric pain (more common in older patients, women, and patients with diabetes, chronic kidney disease, or dementia) - dyspnoea (laboured breathing) - syncope - nausea + vom (esp in women)

Answer 5

History (i.e. clinical symptoms, past history/family history, smoker) ECG done within 10 mins (not usually much change, maybe st depression or t wave flattening or elevation) Troponin (there is no significant rise in unstable angina) Confirmed with further diagnostic imaging like invasive coronary angiography or functional (stress) testing

Answer 6

Sublingual NITRATES to treat vasospasms CALCIUM CHANNAL BLOCKERS e.g. AMLODIPINE BETA BLOCKERS e.g. propanolol ((Clopidogrel (prodrug - can be unreliable as it can be rapidly inactivated by various metabolic processes) Prasugrel (more reliable pro-drug - less susceptible to genetic variations in metabolism) - typically use TICAGRELOR as alternative to clopidogrel Possibly low dose aspirin Basically antiplatelet and anticoagulent therapy done with cardiological advice))

Answer 7

Main difference lies in the fact STEMI can be diagnosed ob ECG at presentation; NSTEMI looks more normal on ECG (some ST depression or T wave abnormalities which looks same as unstable angina) so

Answer 8

Diabetes mellitus Hyperlipidaemia Hypertension Metabolic syndrome (diabetes, obesity + HTN) Renal impairment Peripheral arterial disease History of ischaemic heart disease and any previous treatment Family history (immediate relative getting coronary artery disease/ under 60 y/o) Obesity Advanced age Smoking Cocaine Physical inactivity

Answer 9

STEMI diagnosed via ST elevation on ECG (specifically ST elevation with RECIPROCAL DEPRESSION) NSTEMI typically diagnosed retrospectively from troponin (will be high) and other test results Can also be defined as Q-wave or non Q-wave retrospectively depending on whether new pathological Q waves develop on ECG because of it

Answer 10

STEMI or MIs in general associated with LBBB are associated with larger infarcts unless effectively treated (more likely to lead to pathalogical Q wave formation, heart failure or death)

Answer 11

Non-Q wave has poor R wave progression, ST elevation and Biphasic T wave Q wave MI has complete loss of R wave

Answer 12

* Cardiac chest pain * **unremitting** * usually severe but may be mild or absent * occurs **at rest** * associated with sweating, breathlessness, nausea and/or vomiting *one third occur in bed at night

Answer 13

* Early mortality - 30% outside hospital - 15% in hospital * Late mortality - 5-10% first year - 2-5% annually thereafter Higher risk associated with higher age, diabetes, renal failure, left ventricular systolic dysfunction (elevated NT-proBNP level) and other risk factors

Answer 14

*Get in to hospital quickly – 999 call *Paramedics – if ST elevation, contact primary PCI (percutaneous coronary intervention - ie coronary angioplasty) centre for transfer - Need to be able to get to PCI unit within 2hr, otherwise give fibrinolysis *Take aspirin 300mg immediately *Pain relief

Answer 15

*Make diagnosis *Bed rest *Oxygen therapy if hypoxic *Pain relief – opiates/ nitrates *Aspirin +/- platelet P2Y12 inhibitor *Consider beta-blocker *Consider other antianginal therapy *Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy

Answer 16

Usually from rupture of atherosclerotic plaque and subsequent arterial thrombosis Uncommon: - stress-induced (Tako-Tsubo) cardiomyopathy - coronary vasospasm without plaque rupture - drug abuse (ampethamines, cocaine) - dissection of coronary artery related to deffects of vessel connective tissue - thoracic aortic dissection

Answer 17

Protein complex which regulate actin-myosin contraction Highly sensitive marker for cardiac muscle injury - not specific for acute coronary syndrome Also positive in: * gram negative sepsis * pulmonary embolism * myocarditis * heart failure * arrhythmias * cytotoxic drugs * .....................and more (like exercising a lot!) - doesn't necessarily indicate permanent muscle damage but does indicate higher risk in people with suspected acute coronary syndrome

Answer 18

Causes irreversible inactivation of cyclo-oxygenase 1 (COX1) - COX1 is needed for synthesis of Thromboxane A2 which stimulates platelt aggregation and vasoconstriction - blocking this inhibits platelet aggregation

Answer 19

thrombin itself increases platelet activation so when thrombin generation by platelets is a prcoagulent produced by the platelets that acts in a positive feedback loop and increases risk/speed of arterial thrombosis

Answer 20

Clopidogrel (easily inactivated by metabolic processes) Prasugrel Ticagrelor (oral, reversibly-binding P2Y12 antagonist - used as alternative to clopidogrel)

Answer 21

P2Y12 amplifies platelet activation P2Y12 inhibitors are platelet inhibitors They are used in combination with aspirin for ACS as 'DUAL ANTIPLATELET THERAPY'

Answer 22

Abciximab Tirofiban Eptifibatide

Answer 23

GPIIb/IIIa stimulates aggregation and amplifies platelet activation GPIIb/IIIa antagonists are antiplatelets Used in combination with aspirin and oral P2Y12 inhibitors in management of patients UNDERGOING PCI (angioplasty with stent) Used selectively as increased RISK OF MAJOR BLEEDING but still useful in STEMI patients undergoing PCI to cover DELAYED ABSORPTION OF ORAL P2Y12 inhibitors (as opiates delay gastric emptying) as GPIIb/IIIa is the ONLY IV DRUG FOR ACS

Answer 24

Used in addition to antiplatelets Targets formation/activity of thrombin Inhibits fibrin formation AND platelet activation Typically used prior to angiography, for PCI or CABG (before surgery basically)

Answer 25

FONDAPARINUX - safer than heparins as it is a lower level of anticoagulation

Answer 26

Full-dose anticoagulents: - HEPARIN (usually unfractioned but sometimes given as ENOXAPARIN, a low-molecular-weight heparin) or - BIVALIRUDIN (direct thrombin inhibitor - EXPENSIVE, not used in Sheffield)

Answer 27

For an acute STEMI if primary PCI is not available

Answer 28

STREPTOKINASE alteplase, reteplase, and tenecteplase (not sure if relevant) ONLY GIVEN IF PRIMARY PCI NOT AVAILABLE (in acute STEMI)

Answer 29

STATINS ACE inhibitors Beta blockers Aldosterone antagonist (SPIRONOLACTONE, EPLERONONE)

Answer 30

Dose * Age * Weight * Disease states such as diabetes mellitus * Drug-drug interactions e.g. omeprazole and strong CYP3A inhibitors * Genetic variants: CYP2C19 loss-of-function alleles

Answer 31

*Bleeding e.g. epistaxis, GI bleeds, haematuria *Rash *GI disturbance

Answer 32

DYSPNOEA (laboured breathing) - usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel VENTRICULAR PAUSES - usually sinoatrial pauses, may resolve with continued treatment

Answer 33

Has shown better evidence for longterm mortality reduction but causes more adverse effect

Answer 34

P2Y12 inhibitor may be continued for LONGER THAN 1 YEAR after ACS IF there is a HIGH RISK of further ischaemic events in aspirin-treated patients who DO NOT HAVE EXCESSIVE RISK of life-threatening BLEEDING In patients WITHOUT HIGH LONGTERM RISK - can drop aspirin after a few months

Answer 35

treatment of choice for STEMI do angiogram to check for blockage - predilatation of occluded artery -position stent - deploy stent repeat angiogram 3 months later to check stent is staying in place

Answer 36

Coronary angiography usually done for patients with RAISED TROPONIN or UNSTABLE ANGINA REFRACTORY TO MEDICAL THERAPY NOT AMENABLE if patients have SEVERE DIFFUSE CORONARY ARTERY DISEASE

Answer 37

PCI - most common CABG (coronary artery bypass graft) - used in ~10% of patients with NSTE ACS

Answer 38

- If their actual diagnosis is not ACS - If a plaque ruptured without significant stenosis and the obstructive thrombus resolved by the time of angiography - If the cardiomyopathy was stress-induced (Tako-Tsubo)

Answer 39

DIagnosis: history, ECG (if ST elevation go straight to cath lab for PCI if possible), troponin +/- coronary angiography; consider other diagnoses if uncertain Pain relief as necessary: opiates (but can delay absorption of P2Y12 inhibitor); nitrates for unstable angina/coronary vasospasm (may be ineffective for MI) Check no active or recent life-threatening bleeding/severe anaemia (to check if anticoagulants can be given) If STEMI go straight for primary PCI (need anticoagulation - heparin beforehand) if possible; otherwise give fibrinolytics (unusual) Initial cardiac monitoring for arrhythmia Initial antithrombotic therapy: dual antiplatelet therapy (DAPT) + anticoagulant; - may use GPIIb/IIIa antagonist for PPCI (primary PCI) Revascularisation if MI or refractory/high risk unstable angina and if feasible Secondary prevention: - DAPT duration individualised - highdose statin (e.g. atorvastatin, 40-80mg daily) - high cholesterol is often inherited - BP control: * beta blocker if LV dysfunction, heart failure or ongoing ischaemia * aldosterone antagonist is heart failure and hypokalaemia

Answer 40

Angina is caused by a mismatch of oxygen demand and supply The commonest cause is ischaemic heart disease

Answer 41

Non-modifiable: AGE Family history MALE sex (1.5:1 ratio) Modifiable: - CIGARETTE SMOKING - DIABETES MELLITUS - HYPERLIPIDAEMIA (tho this could be genetic to a degree) - STRESS - Kidney disease - Hypertension (lower risk) - Obesity (lower risk) - Physical inactivity

Answer 42

Broadly related to either lack of supply or increased demand. Supply related: - ANAEMIA - HYPOXAEMIA - polychythemia (increased RBC conc - thicker blood, less able to travel through vessels) - Hypothermia -Hypovolaemia - Hypervolaemia Demand related: - HYPERTENSION - TACHYARRYTHMIA - VALVULAR HEART DISEASE - Hyperthyroidism - Hypertrophic cardiomyopathy

Answer 43

Exercise Cold weather Heavy meals (blood diverted to stomach) Emotional stress

Answer 44

Myocardial ischemia occurs when there is an imbalance between the heart's oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply: - Impairment of blood flow by proximal arterial stenosis, atherosclerotic plaques or thrombi narrowing arteries - Increased distal resistance e.g. as in left ventricular hypertrophy - Reduced oxygen-carrying capacity of blood

Answer 45

Poiseuille's law: Change in pressure = 8 x viscosity x length x flow / pi x radius to the power of 4 Bascially means coronary flow changes to the 4th power of the radius: nothing much happens until the diameter stenosis reacher 70% - then rapid decline ALSO! Ohm's law: V=IR ie. CHANGE in P = FLOW x RESISTANCE

Answer 46

Uses the Coronary flow reserve (CFR) - how much coronary arteries can increase under stress Body adapts to increasing pressure by lowering microvascular resistance In CHD fixed stenosis prevents adaptation of coronary arteries so high resistance and high pressure

Answer 47

Cresendo angina - getting progressively worse over a period of time Prinzmetal's angina - RARE coronary SPASM Microvsacular angina ('ANOCA') - angina with apparently normal main coronary arteries - caused by microvessels being unable to adapt -> increased resistance - mainly affects WOMEN - Cause unknown

Answer 48

Incidence Men 35/100,000/y (especially in older people) Women 20/100,000/y Prevalence Men 5% (5000/100,000) Women 4% (4000/100,000) Main takeaway is that prevalence is much higher than incidence indicating that many people are diagnosed and survive - i.e. good prognosis (1.7% died and 7% had non-fatal CV evens)

Answer 49

CHEST PAIN (typically described as tightness/weight/discomfort) - typically shows up after exertion or eating - mainly in chest radiating to neck, jaw, teeth, arms, back BREATHLESSNESS NO fluid retention (unlike heart failure) NOT USUALLY palpitations RARELY syncope or pre-syncope Can sometimes get pale and sweaty tho this typically indicates a more severe case

Answer 50

MYOCARDIAL ISCHAEMIA (what typically causes angina) - Pericarditis/myocarditis - AORTIC DISSECTION (severe tearing pain, front to back - typically will have many of risk factors esp hypertension - dangerous!) - Pulmonary embolism/pleurisy - Chest infection/pleurisy - Gastro-oesophagal (reflux, spasm, ulceration) - Musculo-skeletal problems - Psychological causes Typically if they say it is a severe pain it is probably not angina

Answer 51

- Reassure that it has good prognosis - Lifestyle changes (1st LINE) * Always try to get them to stop smoking first if they smoke * Reduce weight * Exercise * Improve diet - Give advice in cases of emergency - MEDS: * GTN SPRAY (sublingual glycerltrinitrate) * maybe aspirin * maybe beta-blockers * statins - Revascularisation if required/feasible

Answer 52

- Take history - Examination for exacerbating causes - INVESTIGATIONS: * routine bloods, LIPIDS, ECG (abnormal during periods of pain - st-t segement (esp ST DEPRESSION) changes associated with CAD (worse prognosis)) - DIAGNOSTIC TESTS: * CT cor angiogram (1st line test) * Other non-invasive if they have known CHD and uncertain history e.g. EXERCISE TESTING, MRI perfusion, myoview scan, stress ecocardiogram etc * Cor Angiogram - IF non-invasive INCONCLUSIVE or VERY HIGH RISK patient

Answer 53

- Non-invasive -Good RULE-OUT TEST and for spotting severe disease - Poor resolution - not good at seeing moderate disease well - Anatomical, not functional

Answer 54

Basically get patient to walk on treadmill while hooked to ECG - Good functional test - Relies on ability to exercise (not useful in elderly, obese, arthritic etc.)

Answer 55

Uses pharmacological stressor (regadenoson) to Increase HR and CO (to check for ischaemia) Fuzzy pictures: imperfect sensitivity and specificity

Answer 56

Uses pharmacological stressor and seeks regional wall abnormality Highly skilled operative required so not often used

Answer 57

BEST non invasive test - good sensitivity and specificity Not available everywhere

Answer 58

- Good sensitivity - Gold standard treatment for more serious CAD - Invasive - ANatomical, not functional

Answer 59

NITRATE (GTN or longacting oral nitrates) - dilates coronary arteries and reduces resistance - arterial vesodilation reduces afterload - also causes venous dilation so reduces venous pressure and ventricular preload/venous return Beta-blocker - reduces heart rate so lowers oxygen demand - reduces LV contractility - reduced cardiac output so less oxygen demand Statins - HMG-CoA reductase inhibitor (inhibits rate limiting step of cholesterol synthesis) - lower cholesterol as most people with angina have CAD and need to lower ldl ACE inhibitors: - block RAAS to reduce blood volume and hypertension - redcues production of Angiotensin 2 which is also a vasocontrictor so less vesoconstriction (reduced peripheral resistance) Calcium channel blocker (2nd line) - blocks entry of calcium thus reduces contraction (negative chronotropic and ionotropic effects) - heart has to do less work so lower oxygen demand - reduced arterial contraction/constriction reduces peripheral resistance and afterload Potentially potassium channal opener or Ivabradine (lowers heart rate)

Answer 60

Bradycardia Cold peripherals Erectile dysfunction Tiredness Nightmares DO NOT USE IN SEVERE ASTHMA

Answer 61

The vasodilation can cause HEADACHES (usually for around 3 days) until body adjusts

Answer 62

Flushing (from vasodilation) Postural hypotension Swollen ankles (blood can collect in legs and feet so odoema)

Answer 63

CYCLO-OXYGENASE 1 INHIBITOR - REDUCES PROSTAGLANDIN SYNTHESIS including THROMBOXANE 2 - Reduces platelet aggregation (also antipyretic, ANTI-INFLAMMATORY, ANALGESIC) Side effects: GASTRIC ULCERATION (it is an NSAID in higher conc.s) Typically given after one MI or if they have stent - not typically used for stable angina

Answer 64

Hypertension and DM treatment - esp if they also have IHD

Answer 65

internal mammary artery (typically for LAD bypass) saphenous vein (typically for right CA) or radial artery potentially

Answer 66

Pros: Less invasive than CABG Convenient Repeatable Acceptable Cons: Risk stent thrombosis Risk restenosis Can’t deal with complex disease Dual antiplatelet therapy required

Answer 67

Pros: Prognosis better Deals with complex disease Cons: Invasive (very) Risk of stroke, bleeding Can’t do if frail, comorbid One time treatment Length of stay (intensive care for 5 days normally) Time for recovery (~ 3 months)

Answer 68

STEMI: PCI commonly used and CABG not used NSETMI: PCI commonly used, CABG sometimes used Stable angina: both can be used depending on need and availability

Answer 69

Mechanically restrains filling volume of heart - initially stretch but becomes stiff at high tension ~50ml of serous fluid - small reserve volume If this volume is exceeded pressure is translated ro cardiac chambers Small amount of volume added to space has dramatic effects on filling but so does removal of a small amount – Tamponade physiology

Answer 70

Chronic, slow accumulation of serous fluid allows adaptation of parietal pericardium and heart This compliance reduces effect on diastolic filling of chambers - slow accumulation effusions rarely cause tamponade

Answer 71

An inflammatory pericardial syndrome with or without effusion (quick onset) Usually benign and self-limiting

Answer 72

If they have 2 of the following can diagnose as acute pericarditis - CHEST PAIN - ECG CHANGES (1% of cases with ST elevation have pericarditis) - Friction rub - more COMMON in SUBACUTE (more progressed than acute) - Pericardial effusion - usually mild

Answer 73

Difficult to quantify 1% in autopsy series 5% of A&E attendances with chest pain 1% of cases with ST elevation 80-90% of all pericarditis IDIOPATHIC - Seasonal with VIRAL TRENDS (management isn't affected by which virus) - HIGHER IN YOUNG, previously healthy patients

Answer 74

CHEST PAIN - severe - sharp and pleuritic (no constricting, crushing character of ischaemic pain) - RAPID ONSET - LEFT ANTERIOR CHEST OR EPIGASTRIUM - radiate to trapezius ridge of arm (from co-inervation by phrenic) - RELIEVED by SITTING FORWARD - EXACERBATED by LYING DOWN DYSPNOEA Cough Hiccups (phrenic irritation) Systemic disturbance - Viral prodrome, Antecedent fever - Skin rash, joint pain, eye Sx, weight loss Past medical history of: - Cancer - Rheumatological Dx - Pneumonia - Cardiac procedure (PCI, ablation) - MI

Answer 75

VIRAL (common): - Enteroviruses (coxsackieviruses, echoviruses), - herpesviruses (EBV, CMV, HHV-6), - adenoviruses, - parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis Bacterial (uncommon in uk): - mycobacterium TB (other bacteria rare) - TB effusion pericarditis - Purulent bacterial pericarditis and effusion (rare <1%) * staph, step and pneumococci (high mortality)

Answer 76

AUTOIMMUNE (common): - Sjögren syndrome, - rheumatoid arthritis, - scleroderma - systemic vasculitides NEOPLASTIC (most common non-infectious reason): - secondary metastatic tumours esp from lung, breast cancer and lymphoma Metabolic: - uraemia (usually from end-stage kidney disease) - myxoedema TRAUMATIC/IATROGENIC - Rare early onset of: * Direct injury (penetrating thoracic injury, oesophageal perforation) * Indirect injury (non-penetrating thoracic injury, radiation injury) - COMMON delayed onset of: * PERICARDIAL INJURY SYNDROMES (e.g. post-MI - damage to myocardium irritates pericardium) * IATROGENIC TRAUMA (e.g. PCI, pacemaker, radiofrequency ablation) Other: - amyloidosis - aortic dissection - pulmonary arterial hypertension - chronic heart failure

Answer 77

- MI/MYOCARDIAL ISCHAEMIA -AORTIC DISSECTION - Pneumonia - Pleurisy - Pulmonary Embolus - Pneumothorax - Costochondritis (inflammation at rib-sternum joint) - Gastro-oesophageal reflux - peritonitis - Pancreatitis - Herpes zoster (shingles)

Answer 78

Clinical examination: - Pericardial rub - pathognomonic - sinus tachycardia - fever - signs of effusion ECG Bloods CXR (chest x-ray) Echocardiogram

Answer 79

like crunching snow or scratching at left sternal edge - can just sound like more common murmurs

Answer 80

Pulsus paradoxus - can hear pulse but can't feel it peripherally upon inspiration - pressure in heart lowering output kussmaul sign - increased right atrial pressure -> increased jugular venous pressure on inspiration

Answer 81

Diffuse ST elevation Concave ST segment (sort of saddle shaped) - may resemble STEMI pattern NO RECIPROCAL ST DEPRESSION (unlike STEMI) PR depression - Mechanism: epicardial inflammation as adjacent to pericardium - parietal is inert

Answer 82

FBC: - shows modest increase in WCC, mild lymphocytosis ESR (erythrocyte sedimentation rate - reveals inflammatory activity) & CRP (C-reactive protein - also checks inflammation) - high ESR may suggest aetiology ANA (antineuclear antibody) in young females (to check for SLE: systemic lupus erythematosus - more common in females) TROPONIN - elevations suggest myopericarditis

Answer 83

- often normal in idiopathic - pneumonia common if bacterial - enlargement of cardiac silhouette can suggest effusion (only detectable at >300ml)

Answer 84

cardiac tamponade

Answer 85

Rapid filling of pericardial space with blood or other fluid - puts pressure on heart -> decreased diastolic filling -> reduced CO -> drop in blood pressure - can go into shock, cardiovascular collapse or MI - life threatening

Answer 86

haemorrhage slower growing effusions which eventually develop into tamponade: - TB, myocarditis - autoimmune - neoplasms - uremia - side effect of pericarditis

Answer 87

Beck's triad (signs of cardiac tamponade) - hypotension (weak pulse/narrow pulse pressure) - Raised jugular venous pressure/distension (related to sometimes getting Kussmaul sign) - muffled heart sounds - pulsus paradoxus - With large effusion, irregular ecg as the heart is bobbing about

Answer 88

may be absent in ASD (atrial septal defect), elevated diastolic pressures, pulmonary hypertension, aortic regurgiation

Answer 89

Not a lot of evidence mainly consensus opinion Sedentary activity until resolution of symptoms and ECG/CRP (-Probably only applies to athletes - 3 months) NSAID (Ibuprofen 600mg TDS PO 2/52) or Aspirin (750-1000mg BD PO 2/52) - very high doses Colchicine (0.5mg BD PO 3/12) limited by nausea and diarrhoea, reduces recurrence

Answer 90

- mostly good long term prognosis - cardiac tamponade rarely occurs in acute idiopathic pericarditis - Constrictive pericarditis may occur in 1% with acute idiopathic - reason for giving COLCHICINE 15-30% with acute will get recirrence

Answer 91

Low (1%): - for idiopathic and presumed viral Intermediate (2-5%) - autoimmune - immune mediated - neoplastic high (20-30%) - bacterial (esp TB and purulent)

Answer 92

Pericardectomy (~50% 5 year survival)

Answer 93

Dressler's syndrome (can cause pericarditis) - shows up ~1-2 weeks post MI

Answer 94

The build up of plaque (consisting particularly of cholesterol) in/on artery walls Starts gruel-like substance - becomes hard Causes stenosis and narrowing of arteries - major cause of death (especially from plaque rupture -> thrombus formation -> arterial blockage -> MI)

Answer 95

Age FAMILY HISTORY HIGH SERUM CHOLESTEROL TOBACCO SMOKING HYPERTENSION DIABETES Obesity

Answer 96

Found within peripheral and coronary arteries Focal distribution but can occur along the length of the artery Can be affected by haemodynamic factors e.g. May be more likely to form: - at areas of turbulence/changed flow e.g. bifurcations * turbulence causes altered endothelial function and cange in wall thickness leading to NEOINTIMA - there is a link to altered gene expression in key cells

Answer 97

The formation of new/thickened arterial intima by the migration and proliferation of cells from the media - typically around prosthesis or in atherosclerosis, esp in areas of turbulent flow

Answer 98

Lipid NECROTIC CORE Connective tissue FIBROUS CAP

Answer 99

Injury to endothelial cells initiates endothelial dysfunction Signals sent to circulating leukocytes -> they accumulate and migrate into vessel wall Inflammation occurs

Answer 100

LDL - can pass in and out of arterial wall and in excess can ACCUMULATE in arterial wall * Undergoes OXIDATION and GLYCATION (bonding of sugar to protein or lipid - without enzymatic regulation) ENDOTHELIAL DYSFUNCTION - response to injury

Answer 101

Chemoattractants (chemokines) released by the endothelial cells at the site of an injury which send signals to leukocytes. They produce a concentration gradient causing leukocytes movement towards injured site and then extravasation (chemotaxis). Integrins also help adhere leukocytes to endothelium before extravasation occurs.

Answer 102

IL-1 (canakinumab - IL-1 antibody drug) IL-6 (tocilizumab - IL-6 receptor inhibitor) IL-8 (works esp on neutrophils) IFN-gamma TGF-beta (transforming growth factor) MCP-1 (monocyte chemoattractant protein-1) (C reactive protein - produced by liver; increases during inflammation)

Answer 103

Fatty streaks Intermediate lesions Fibrous plaques OR Advanced lesions Plaque rupture OR Plaque erosion

Answer 104

Aggregations of LIPID-LADEN MACROPHAGES (foam cells) and T LYMPHOCYTES within INTIMA appear at early age (<10 years)

Answer 105

Lipid-laden macrophages (FOAM CELLS) T LYMPHOCYTES VASCULAR SMOOTH MUSCLE CELLS Adhesion/aggregation of PLATELETS to wall Isolated pools of extracellular lipid

Answer 106

Contains: - FOAM CELLS - T LYMPHOCYTES - SMOOTH MUSCLE CELLS - MACROPHAGES Forms the LIPID CORE and NECROTIC DEBRIS Covered by FIBROUS CAP - may be calcified Impedes blood flow and prone to rupture

Answer 107

Endoplasmic reticulum membrane proteins: - COLLAGEN - ELASTIN laid down by smooth muscle cells

Answer 108

Normally fibrous caps are RESORBED and REDIPOSITED as plaques grow and recede If balance shifts to more inflammatory conditions (increased enzyme activity) - weakens cap and plaque ruptures Basement membrane, collagen and necrotic tissue are exposed and the vessels in the plaque haemorrhage. -> Tissue factor triggers THROMBUS FORMATION and VESSEL OCCLUSION

Answer 109

Typically caused by small 'early lesions' Thickened fibrous cap may lead to collagen triggering thrombosis rather than tissue factor (as in plaque rupture)

Answer 110

Plaque rupture: - large lipid core with abundant inflammatory cells - red thrombus Plaque erosion: - small lipid core - more fibrous tissue - larger lumen - white thrombus - discontinued endothelium

Answer 111

red = rbcs and fibrin white = platelets and fibrinogen - also reffered to as platelet-rich clot

Answer 112

Extruded DNA and enzymes which cause cell activation and cytokine release

Answer 113

Plaque rupture: - Dyslipidaemia - Hypertension - Diabetes mellitus - Chronic kidney disease - Multi-vessel disease (- 6-6 weekday work hours; - more likely in winter?) - stent implantation - no-reflow after PCI - distal embolisation (partial/complete occlusion of epicardial coronary artery/branch due to down stream movement of thrombus/atheroma/fractured tip of guidewire/undeployed stent/air) - higher no. of major adverse cardiovascular events Plaque erosion: - Smoking - Women - <50 y/o - nearby bifurcation - anterior ischaemia (- summer) - anti-thrombotic - less microvascular damage after PCI - better myocardial perfusion

Answer 114

PCI - percutaneous coronary intervention Used to get restenosis but now uncommon due to drug eluting stents - made of steel and some titanium alloy with drug

Answer 115

They are monoclonal antibodies that inhibit PCSK9 protein in liver which leads to IMPROVED CLEARANCE OF CHOLESTEROL from blood Used for people who don't tolerate statins

Answer 116

Stage 1/Suspected hypertension: - clinical BP = 140/90 - offered ambulatory BP monitoring device to check * will show BP aroun 135/85 Stage 2: - clinical BP = 160/100 - ABPM = around 150/95 Severe: - SBP 180 - OR DBP 110

Answer 117

In stage 1 and under 80y/o if they have one or more of the following: - target organ damage - Established CVD - Renal disease - Diabetes - A 10-year CVD risk of 20% or more Anyone with stage 2 is offered antihypertensives

Answer 118

If under 80 y/o: Clinical BP <140/90; ABPM <135/85 If over 80 y/o: Clinical BP <150/90: ABPM <145/85

Answer 119

Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc) feels like flu-like infection with showers of infectious material around blood/body or causing damage to heart valves and heart failure

Answer 120

Left sided native IE (mitral or aortic) Left sided prosthetic IE Right sided IE (native or prosthetic but rarely prosthetic as rare to have PV or TV replaced) Device related IE (pacemakers, defibrillators, with or without valve IE) If it is a Prosthetic; can be Early (within year) or Late (after a year) post op - each type can have diff presentations, pathogens and outcomes

Answer 121

Common in: - the elderly - young iv drug abusers (affects tricuspid esp as injecting via veins) - young with congenital heart disease - anyone with prosthetic heart valves

Answer 122

- having abnormal valve (regurgitant/prosthetic more likely to get infected) - introduce infectious material into blood (e.g. iv drugs, tattoos), or onto heart during surgery - Having had IE before

Answer 123

Could get almost any type of sign/symptom depending on what organism it is and where the infection is Often get flu-like signs of systemic infection (fever, sweats etc) Emboli: stroke, pulmonary embolism, bone infections (ie pain - back pain common with staph aureus), kidney dysfunction, MI, peripheral stigmata Valve dysfunction (murmurs, weakness, palpitations), heart failure (e.g. fluid overload), arrythmia

Answer 124

Petechiae (little bruises) 10 to 15%, Splinter hemorrhages Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules - usually found on the pulp of the digits) Janeway lesions: erythematous, macular, non-tender lesions on the fingers, palm, or sole Roth spots on fundoscopy (with opthalmascope in eye)

Answer 125

- Do blood cultures - Do an echocardiogram this is usually enough to confirm BUT: - sometimes cultures remain negative due to prior antimicrobial therapy, type of cell media/microbiological methods used, or the organism has a long incubation period - echos aren't always very clear Can also check: - predisposing factors - fever - vascular phenomena - Immune phenomena (if they have all of the above alt options and an uncertain blood culture, it's probably IE) Can also check ECG for heart changes IE almost always shows raised CRP - INR may also rise WBC is rarely helpful

Answer 126

Transthoracic echocardiogram (~60% sensitivity so more likely to miss things) - safe - non-invasive, no discomfort Transoesophageal echocardiogram (~96% sensitivity) - more invasive, uncomfortable - generally safe - risk of perforation/aspiration

Answer 127

IV antimicrobials depending on culture sensitivities Treat complications (e.g. stroke rehab, absecess drainage, remove emboli etc.) Surgery

Answer 128

If infection does not resolve with antibiotics Complications (e.g. aortic root absecess, severe valve damage) To remove infected devices To replace valve AFTER infection cured To remove large vegetations before they embolise

Answer 129

To give prophylaxis (i.e. antibiotics) in high risk patients or those undergoing dental surgery

Answer 130

When the area of the aortic valve is reduced significantly (symptoms only occur when valve area a 1/4 of normal) Can be: - Supravalvular - Subvalvular - Valvular (most common)

Answer 131

Congenital: - congenital AS - conhenital bicuspid aortic valve Acquired - Degenerative calcification (usually with age - most common) - (higher risk in CAD?) - Rheumatic heart disease - Rare disease (Paget disease, postradiation (11-16 years after), SLE)

Answer 132

pressure gradient develops between the left ventricle and aorta. (causes increased afterload) LV function initially maintained by compensatory pressure hypertrophy When compensatory mechanisms exhausted, LV function declines.

Answer 133

Dyspnoea on exertion from heart failure (most common) Angina (from compensatory hypertrophy) Exertional syncope Sudden death

Answer 134

Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus) Heart sounds- soft or absent second heart sound, S4 gallop due to LVH. Ejection systolic murmur- crescendo-decrescendo character. (best heard in aorta but radiates to carotid) “Loudness” does NOT tell you anything about severity

Answer 135

38% go from mild AS to severe AS in 25 years (untreated) Onset of symptoms is indication of POOR PROGNOSIS if untreated - means compensatory mechanisms are failing

Answer 136

Angina + AS: 50% survive for 5 years. Syncope + AS: 50% survive for 3 years, HF + AS mean survival is <2 years. Risk of sudden cardiac death in asymptomatic or minimally symptomatic patients is rare (<2%) With valve replacement - lifespan is close to normal

Answer 137

Echocardiography Check: - LV size and function (LVH, Dilation, ejection fraction) - Doppler derived gradient and valve area (AVA)

Answer 138

Mild: >1.5 cm2 Moderate: 1 - 1.5 cm2 Severe: <1 cm^2 (mean gradient >40 mmHg)

Answer 139

General: - good dental hygiene - consider IE prophylaxis Medical - limited as AS is mechanical problem - VASODILATORS CONTRAINDICATED (makes BP fall more) Valve replacement: - surgery - Transcatheter Aortic Valve Implantation (TAVI)

Answer 140

- if patient has ANY SYMPTOMS with severe AS - decreasing EF - undergoing CABG with moderate/severe AS - consider intervention if asymptomatic with severee AS shows ADVERSE FEATURES in exercise testing

Answer 141

Backflow of blood from the LV to the LA during systole (Mild (physiological) MR is seen in 80% of normal individuals.)

Answer 142

Myxomatous degeneration (causes MV prolapse) Ischaemic MR Rheumatic heart disease IE

Answer 143

soft tumour made of gelatinous connective tissue

Answer 144

- from Prolapse - ruptured chordae tendoni - typically from MI - annulus dilation (gap forms between cusps) - typically from Heart failure

Answer 145

PURE VOLUME OVERLOAD Compensatory mechanisms: - LA enlargement, LVH, increased contractility -> pulmonary hypertension as blood backs up - progressive LV volume overload -> dilation -> HF

Answer 146

Auscultation: PANSYSTOLIC MURMUR (apex - radiates to axilla) - S3 as LV fills (dilated from HF/LA is overloaded) - if CHRONIC murmur intensity CORRELATES with SEVERITY - hyperdynamic apex beat displaced from LV hypertrophy/dilation Exertion Dyspnoea (PRINCIPLE EARLY manifestation) HF - can coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

Answer 147

Compensatory phase: 10-15 years EF <60% or symptomatic -> increased mortality from progressive dyspnoea and HF

Answer 148

ECG: LA enlargement, AF and LVH if severe CXR: LA enlargement, pulmonary artery enlargement ECHO esp TOE (gold standard): estimation of LA/LV size/function - valve structure assessment for treatment

Answer 149

Meds! - RATE CONTROL for AF (b-blockers, CCB, digoxin) - anticoagulant for AF/flutter - if ACUTE - NITRATE/DIURETICS - if chronic with congestive HF - chronic HF meds DON'T give prophylactic vasodilators (ACE-I, ARB, hydralazine) SURGERY if severe SERIAL ECHOCARDIOGRAPHY: - Mild: 2-3 years - Moderate: 1-2 years - Severe: 6-12 months IE prophylaxis maybe if high risk

Answer 150

ANY Symptoms at rest or exercise (repair if feasible) Asymptomatic: - If EF <60%, LVESD >40mm - If new onset atrial fibrillation/raised PAP >50 mmHg

Answer 151

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

Answer 152

Bicuspid valve Rheumatic heart disease IE

Answer 153

Combined pressure AND volume overload Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

Answer 154

Wide pulse pressure (e.g. 180/60mmHg) - most sensitive Hyperdynamic and displaced apical beat Auscultation: - DIASTOLIC BLOWING MURMUR at left strenal border * decrescendo murmur as some blood falls back in - SYSTOLIC EJECTION murmur (increased flow across aortic valve) - Austin flint murmur (apex) - regurgitant jet hits wall?? causes vibration

Answer 155

Asymptomatic until 4th or 5th decade Rate of Progression: 4-6% per year Progressive Symptoms include: - DYSPNOEA (most common): exertional, orthopnea (breathless whenlying down), and paroxsymal nocturnal dyspnea Palpitations: due to increased force of contraction and ectopics

Answer 156

CXR: enlarged silhouette, aortic root enlargement ECHO (gold standard): evaluate AV and aortic root with LV dimensions/function

Answer 157

Serial Echocardiograms - monitor progression IF congestive HF or hypertension - vasodilators (ACE-I improve SV) maybe IE prophylaxis Surgical - DEFINITIVE Tx (TAVI only if unsuitable for SAVR)

Answer 158

ANY Symptoms at rest or exercise Asymptomatic treatment if: - EF drops below 50% or LV dilated > 50mm at end systole indentifying symptoms can be complicated by co-morbidities like lung disease

Answer 159

Obstruction of LV inflow that prevents proper filling during diastole Transmitral gradients and symptoms from area < 2cm^2

Answer 160

Rheumatic heart disease: 77-99% of all cases Infective endocarditis: 3.3% Mitral annular calcification: 2.7% Decreasing incidence and prevelance due to less rhematic heart disease

Answer 161

LA dilation -> pulmonary congestion (PROGRESSIVE DYSPNOEA) -> Pulmonary venous HTN -> Right heart failure AND ruptures broncial vessels -> hemoptysis Increased transmitral pressure -> LA enlargement; AF

Answer 162

Disease of plateaus: Mild MS: 10 years after initial RHD insult Moderate: 10 years later Severe: 10 years later Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism High risk of stroke if AF + MS

Answer 163

PROMINANT A WAVE in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy Signs of right-sided heart failure: in advanced disease Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks Auscultation - DIASTOLIC MURMUR: - LOW-PITCHED rumble - APEX (due to slow, reduced filling) - best heard when LYING on LEFT side in HELD EXPIRATION - intensity DOESN'T CORRELATE

Answer 164

ECG - may show AF; LA enlargement CXR: LA enlargement, pulmonary congestion - maybe calcified MV ECHO (gold standard): Asses Mitral valve mobility, gradient, valve area, calcification

Answer 165

Serial echocardiography: Mild: 3-5 years Moderate:1-2 years Severe: yearly Medications: Mechanical issue so not disease affecting - β-blockers, CCBs, Digoxin control heart rate and prolong diastole for improved diastolic filling - Duiretics for fluid overload (from right heart failure) Percutaneous mitral balloon valvotomy (PMBV) or surgery maybe IE prophylaxis

Answer 166

pass balloon through mitral valve, blow it up -> should split the valve along commisures can't do if unfavourable anatomy or calcified

Answer 167

ANY SYMPTOMATIC patient where daily life affected or has issues at rest Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV

Answer 168

An inability of the heart to deliver blood (and O2) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures Typically EF <= 40% (can also indicate cardiomyopathy) (EF 41-49% is borderline - not necessarily HF, could be damage from MI etc.) (low cardiac filling pressures would just be like shock)

Answer 169

Class I: No limitation (Asymptomatic) Class II: Slight limitation (mild HF) - at moderate activity Class III: Marked limitation (Symptomatically moderate HF) - at moderate activity Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF) - symps even at rest

Answer 170

Site dependant: - Left-sided HF (most common) * weak left side - build up in pulmonary veins (pulmonary HTN) * usually from CAD or chronic high BP - Right-sided HF * weak RV - build up in veins (increased pressure) * usually from advanced left HF; sometimes from pulmonary HTN, pulm. embolism or lung disease like COPD * *cor pulmonale* (right side enlargement from lung issue) - biventricular HF: * both weak - symptoms of both Pumping ability: - HFrEF - reduced EF as heart muscle weak (systolic HF) * what we usually mean by HF - HFpEF - preserved EF from strong pumping but poor filling (diastolic HF) * becoming more common Can be acute (after MI/fibrillation - ISCHAEMIC HF) or chronic (from conditions like chronic HTN - more common - MYOPATHIC/HYPERTENISVE HF)

Answer 171

~ 50-70% for men ~ 55-75% for women (can vary some)

Answer 172

Myocardial dysfunction (most common) - usually from **IHD** - HTN - LVH -> greater oxygen demand + CA squeezed by muscle so poorer perfusion - Valvular (-> hypertrophy) - Endocardial - Pericardial (typically infections) - Cardiomyopathy - Dilated -> thinner/weaker wall -> systolic HF - Restrictive - stiff wall/less compliant - Alcohol excess (if very high) Risk factors: - MI - DM - myslipidaemia - old age - male - obesity - renal insufficiency - sleep apnoea - family history - cocaine abuse

Answer 173

When the cardiac myocytes themselves are diseased - needs to be inherent, not caused by something else Most myocardial damage is caused by other factors like IHD, HTN, alcohol etc.

Answer 174

mainly affects middle-aged/older men and older (>85) women (pre-menopausal women have some hormonal protection) Alcoholics

Answer 175

Symptoms: left HF: - breathlessness!! - coughing right HF: - swelling (esp legs) - increased weight (from fluid overload) - nausea - anorexia (because of ascites/fluid overload) - cold peripheries - Fatigue - reduced exercise tolerence/exertional dyspnoea - paroxsysmal nocturnal dyspnoea/coughing - ORTHOPNOEA (SOB when lying down) Signs: LH: - **tachycardia** - Pulm oedema - **rales/crepitations in lung bases (bubbling/rattling lung sound)** - pleural effusion on scan - Added heart sound + murmurs (S3 gallop + S4) - Displaced apax beat (cardiomegaly) - reduced BP if HFrEF RH: - raised JVP (neck vein distension) * hepatojugular reflux - peripheral/sacral pitting oedema - Hepatomegaly (esp if pulsatile and tender) - Ascites (fluid in abdomen) - weight gain from fluid overload

Answer 176

Acute MI Uncorrected BP Obesity Superimp. infection AF & arrhythmias -ve inotropes (Ca/beta) Excess alcohol Endocrine (DM/T4..) NSAIDS Treatment and Na+ noncompliance. Lack of information given to patient about diet, medications, etc

Answer 177

presence of risk factors presence of signs/symptoms (esp dyspnoea, tiredness, peripheral oedema, reduced exercise tolerence, high JVP, cardiomegaly) ECG (CAD, LVH, atrial enlargement, conduction abnormalities, MI signs if acute) Echo: - systolic: depressed/dilated left (/right) vent with low EF - diastolic: LVEF normal, LVH and abnormal diastolic filling CXR: - pulm congestion/oedema, cardiomegaly (tho not necessarily) elevated NT-proBNP (chronic), acute = moderate DECREASED SODIUM (usually <135 mmol/L), altered potassium Blood LIPIDS DECREASED in END-STAGE HF (troponin/CRP high in ACUTE)

Answer 178

ACE-I and B blockers(low dose, slow uptitration - only works if in SR) (1st line) - if ACE-I intolorent (e.g. afro-caribbean) * ARNI (ARB + Nep-I - Sacubatril-Valsartan) or SGLT2 inhib (Dapagliflozin) * Hydralazine/nitrates additionally if ARB ineffective * try Digoxin or Ivabradine(only works if in sinus rhythm) for lowering HR if nowt works MRA additionally to ACE if ineffective ICD coil - defib to stop sudden death from arrhythmias CRT - pacemaker Revascularisation for ischaemic HFrEF - doesn’t really work in asymptomatic ppl with CAD and HF Diuretics are given first in HFpEF but don't improve disease only reduce symptoms Treat underlying cause

Answer 179

Atrioventricular reentrant tachycardia i.e. most common Wolff-Parkinson-White syndrome arrhytmia Type of supraventricular tachy cardia that occurs due to an accessory conductive pathway (bundle of Kent) that lets impulse reenter atria and restart contraction before sa node has sent next signal - bundle can be antegrade(broad complex) or retrograde(more common - narrow complex) Notably seen by delta wave (slurring QRS causing sloped R wave) (and retrograde p wave after QRS?) - short PR interval - on ECG

Answer 180

Atrioventricular nodalreentrant tachycardia (most common SVT) Type of supraventricular tachycardia that occurs due to alt conductive pathway (beta pathway with fast conduction but longer refractory period; alpha pathway - slow conduction, fast ref period) very close to/inside AV node (still bypasses typical sa node timing) - both intially cancel each other out but when next impulse from sa comes, activates alpha - beta still in ref period, but comes out before prev impulse finished -> extra beat Usually missing p wave (inside QRS) or appears as pseudo r inversion at terminal portion

Answer 181

palpitations, syncope/pre-syncope, angina, dyspnoea - avnrt can have polyuria

Answer 182

Vagal maneuvers (stimulate vagus to slow heart) - 1st line - cold water on face/neck - carotid massage IV adenosine (for paroxysmal) IV verapamil (caution if have HFrEF) IV procainamide or beta blockers(IV metoprolol) (last line meds) NODE BLOCK AGENTS SHOULD BE AVOIDED IN ANTIDROMIC (antegrade bundle - impulse goes down bundle and up His/av) Cardioversion - RF catheter ablation can be curative

Answer 183

AVRT can cause sudden death from pre-excitation Catheter ablation can cause: (rare) - av block MI pericarditis cardiac tamponade pneumothorax femoral artery pseudoaneurysm

Answer 184

having an accessory pathway that alllows bypassing of av node so ventricles contract too quickly

Answer 185

when coronary artery goes into spasm and suddenly narrows precipitated by: - exercise, cold, alpha-agonists (vasoconstriction) * drugs like cocaine * tobacco smoking inflammatory states and insulin resistance have also been associated

Answer 186

type of aneurysm where intima of aorta splits and blood flows into cahnnel composed of inner/outer layer of media. Can occur in ascening or arch (URGENT - type A), or in descending aorta (type B) Usually occurs with discrete intimal tear but can occur without one Acute if <14 days

Answer 187

Typically: abrupt onset SEVERE/TEARING chest, back, abdominal pain - more likely to be in patient with high risk (e.g. MArfan's; Ehlers-Danlos), family history, or male in 50s Also: -syncope -heart/renal failure - mesenteric/limb ischaemia

Answer 188

Signs/symptoms: - acute severe chest pain -interscapular/lower pain - left/right BP differential - pulse deficit ECG to rule out MI - maybe ST depression (rarely ST elevation) CXR (do for all patients if possible - limited value in diagnosis) - maybe widened midiastinum - maybe pleural effusion in acute - maybe prominent aortic knob in chronic dissection CT (chest, abdo, pelvis) - 1st LINE! - intimal flap (acute and chronic) * may be thickenind if chronic - maybe calcification, fewer periaortic reactive changes TTE/TOE - intimal flap; 2 lumens may be seen Bloods - high creatinine/urea if renal failure - troponin to check if MI - anaemia if haemorrhage

Answer 189

initially if haemodynamically unstable: - advanced life support; haemodynamic support - opiod analgesia Confirmed acute: - beta blocker (1st LINE) - opioids - consider vasodilator - endovascular repair or open surgery if complicated (only need to consider if uncomplicated, may be able to treat with just meds) Confirmed chronic: - beta blocker (1st LINE) - maybe more hypertensives - life style advice - risk factor management - maybe endovasc repair/open surgery

Answer 190

Permanent pathological dilation of aorta (diameter >1.5x expected anteroposterior diamete of segment given sex/body type). Usually diameter = 3cm or more >90% originate below renal arteries

Answer 191

Usually asymptomatic - detected incidentally/through targeted screening Abdominal, back, groin pain most typical symptom. Uncommon: - palpable pulsatile abdominal mass (diagnostic factor if present) - hypotension - loss of consiousness - pallor - abdominal distension - fever

Answer 192

- cigarette smoking (elastin degradation) - family history of aortic disease - increased age male (increased prevalence) - female (increased risk of rupture) - congenital/connective tissue disorder weak: - hyperlipidaemia - atherosclerosis - central obesity - Hypertension - COPD (related to smoking) (- increased height, non-diabetic) -European

Answer 193

- presence of risk factors - Examination -palpating above umbilicus on either side of aorta 1st LINE: Aortic ultrasound elevated erythrocyte sedimentation rate/CRP - inflammatory AAA leukocytosis, anaemia on FBC if haemorrhage or infectious AAA - also +ve blood culture - maybe PET-CT GOLD STANDARD: computed tomography angiography (CTA) - useful if close to renal arteries * MRI as alt

Answer 194

Acute AAA (symptomatic aneurys OR RUPTURED): - 1st LINE: **urgent surgical repair if >5.5cm** [- IF RUPTURED - RESUSCITATION MEASURES] - Perioperative antibiotics - Analgesia - VTE prophylaxis ie standard surgery stuff Asymptomatic AAA <5.5cm (but not >4.0cm and rapidly growing) - 1st LINE: surveillance (via ultrasound) * annualy if <= 4.4 cm * every 3 months if >4.4 cm - aggressive cardiovasc risk management Asymptomatic but >= 5.5cm (or >4cm and rapidly growing ie >1 in 1 year) - 1st LINE: elective surgical repair - pre-op cardiovasc risk reduction - peri-op antibiotics - analgesia - VTE prophylaxis

Answer 195

- Aneurysm size/morphology (severity/risk of condition) - Age, life expectancy, fitness for surgery, comorbidities (including FBC/electrolytes, renal function, ECG, history + examination) - risk of rupture if not repaired (risk of complications in natural history) - short/long term benefits/risk (hosp stay, op risk, recovery, need for other procedures, need for survaillance)

Answer 196

Active CVD (ACS, decomp HF, significant arrhythmia etc.) Poor functional capacity (e.g. unable to walk up a hill, do heavy house work like scrubbing floor) Significant clinical risk factors (e.g. COPD, severe renal impairment (eGFR <30), past stroke etc.)

Answer 197

Rupture and Haemorrhage

Answer 198

BP >= 140/90 mmHg

Answer 199

Usually idiopathic (essential HTN) OBESITY (esp abdominal) Inactive (aerobic exercise <3 times/week) Moderate - high ALCOHOL intake Metabolic syndrome (insulin resistance /hyperinsulinaemia) DM High sodium intake (>1.5 g/day) (low fruit/veg) Black ancestry >60 y/o Family history (HTN or CAD) Sleep apnoea (dyslipidaemia) (stress) DRUGS: - NASIDS SNRIs (venlafaxine) Corticosteroids Oestrogen containing oral contraceptives Stimulants (e.g. methylphenidate for adhd) Antianxiety (gabapentine) Anti-TNFs (anti inflammatory)

Answer 200

MAINLY DIAGNOSED ON: - presence of risk factors - high BP IF RETINOPATHY (retinal haemorrhage) - MALIGNANT HYPERTENSION - Also: * papilloedema * acute kidney injury * stroke * acute coronary syndrome * aortic dissection IF ATYPICAL AND SUSPECTING 2nd-ary CAUSE: ECG to check for IHD/CAD Bloods: - fasting metabolic panel with GFR to check renal inisufficiency, hyperglycaemia, hypokalaemia (indikative of hyperaldosteronism is unprovoked), hyperuricaemia, pypercalcaemia - lipid panel (sheck for metabolic syndrome) - urinalysis - proteinuria/increased albumin - end organ damage - Hb - anaemia = renal failure; polycythemia = phaeochromocytoma (maybe) TSH other tests like renin, aldosterone, 24 urine free cortisol etc to check for secondary causes

Answer 201

Lifestyle changes: 1st LINE - Losing weight - reduce alcohol - lowering salt consumption - exercise - destress Drugs: - ACE-I/ARB - BB (not in asthma) - CCB - Diuretics (typically only alongside HF) Idividualised therapy if resistant to optimised triple therapy (without HF) (CONTRAINDICATED IF GOING UNDER ANAESTHESIA) Required LIFELONG Every 6 month follow-up

Answer 202

STROKE (haemorrhagic esp) IHD - angina, MI etc. Peripheral vascular disease Heart failure CKD Dementia (unsure whether it causes it but definitely linked) Aortic dissection

Answer 203

The development of a blood clot in a major deep artery - usually in the LEG, thigh, pelvis or abdomen (can also be in arm, portal, mesenterical, ovarian or retinal veins) DVT can cause impaired venous flow but is not usuallly life threatening itself. It can cause fatal pulmonary embolisms

Answer 204

- RECENTLY IMMOBILISED (>=3 days bed rest/surgery in past 12 weeks/hopitalisation >=4 days in past 2mth/recent fracture) - CO-MORBIDITIES (stroke, HF, resp failure, ACUTE INFLAMMATION/infalm conditions/infection) - ACTIVE CANCER (increased risk if metastatic) * Thalidomide, Erythropoetin - HISTORY OF VTE - INCREASED AGE - PREGNANCY/POSTNATAL PERIOD + Contraceptives/HrT * Oestrogen - THROMBOPHILIC CONDITIONS (FACTOR V LEIDEN) - some drugs (NSAIDs)

Answer 205

- could ACTIVATE COAG SYSTEM - COMPRESS/BLOCK flow - some chemo/bio agents e.g. EPO, Thalidomide - vasc acess devices increase risk

Answer 206

can be asymp - LEG SWELLING/PAIN (usually unilateral) - DILATION/DISTENSION of superficial veins - RED?DISCOLOURED SKIN (potentially cyanosis)

Answer 207

Assess pre-test ptobability of DVT with WELL'S SCORE - 2/more points = DVT likely 1ST LINE: VENOUS US (or CT) D-dimer - protein fragment released by clot break-up FBC, Urea/cratinine, LFTs, clotting screen (underlying)

Answer 208

ANTI-COAGs: - LMWH - unfractioned hep or fondaparinux - DOACs (Dabigatran, Apixiban etc) - Warferin For 3 months - CONTINUE AS PROPHYLAXIS if HIGH RISK - PHYSICAL EXERCISE - COMPRESSION STOCKING IVC FILTER if recurrent even with anti-coag Rarely: thrombolysis

Answer 209

PE if CHRONIC: - POST-THROMBOTIC SYNDROME * Chronic pain, swelling, discolouration, venous ulcers, valve incompetence

Answer 210

DYSPNOEA Pleuritic chest PAIN HYPOXAEMIA potential DVT symp High RISK: - HYPOTENSION - SYNCOPE - TACHYCARDIA - signs of R HF

Answer 211

NT-proBNP (b-type naturetic peptide)

Answer 212

Accumulation of lipids, macrophages and smooth muscle cells in intima of large + medium sized arteries

Answer 213

120 - 200 ms (3-5 mm)

Answer 214

110 - 120 ms (less than 3 mm)

Answer 215

Leads I and II

Answer 216

- NEGATIVE S wave dominant in V1, GROWS till at least V3 (linked to RV beat) - Disappears by V6 - POSITIVE R wave Grows from V1 - V4 (linked to LV beat) - everyhting slightly smaller in V6

Answer 217

Should always start ISOELECTRIC (may be very slightly elevated in V1/2 but typically ST elevation is PATHOLOGICAL)

Answer 218

I, II, V2-6 (because atrial depolarisation is goin in direction of those leads)

Answer 219

I, II, V2-V6

Answer 220

- BROAD QRS - Ventricular CONUDCTION DELAY/BUNDLE BRANCH BLOCK - Pre-excitation (has accessory pathway) - Small QRS complexes - OBESITY (has to pass through fat) - PERICARDIAL EFFUSION - Infiltrative cardiac disease - Tall QRS complexes - LV HYPERTROPHY (S/R waves >35mm) - THIN

Answer 221

- Narrow QRS: - SUPRAVENTRICULAR - conducted through His-Purkinje system - Broad QRS: - VENTRICULAR (conducted monocyt->monocyte = slower) - more dangerous, His-Purkinje not being used - Can also be Supraventricular with BUNDLE BRANCH BLOCK/PRE-EXCITATION

Answer 222

Can occur at any level - Sinus node disease - AV node/distal conduction problems (HEART BLOCK) - 1st degree, 2nd degree (type 1+2), 3rd degree

Answer 223

- PAIN - PALLOR - Poikilothermia (unable to maintain temp in affected area)/Perishable cold - Pulselessness - Paresthesia (numb) - Paralysis (weak movements) Also linked to COMPARTMENT syndrome PAD is type of arterial thrombosis

Answer 224

- Conduction tissue fibrosis - Ischaemia - Inflam/infiltrative disease - Drugs

Answer 225

WiLLiaM - Looks like a W in v1, M in v6 - High R, slurred S wave = W shape in V1 - Prominent R wave with dip in it - M shape in V6 Characteristic ecg shape due to LV depolarising later than RV Caused by: - IHD - Valvular disease Heart sound 2 - reversed splitting

Answer 226

MaRRoW - M in v1, W in v6 - RSR complex = M shape QRS complex in V1 - Wide slurred S wave = W shape in V6 Due to RV activation later than LV Caused by: - Pulm emboli - IHD - VSD Wide physiological S2 splitting

Answer 227

- Tall tented T waves - Flattened P waves - Broadening QRS - prolonged PR eventual sine wave pattern

Answer 228

- Flattening/SMALL INVERTED T wave - ST depression - Narrow QRS - PR prolongation - PROMINANT U waves - QT prolongation (less significant signs)

Answer 229

QT shortening

Answer 230

QT prolongation

Answer 231

ST elevation only occurs in the immediate aftermath after a while the ST elevation will go down but *prominant Q waves* will still be visible

Answer 232

Inferior leads (II, III, avF) = RCA Anterior leads (maybe v1, v2-v4) = LAD Lateral leads (I, aVL, V5, V6) = circumflex

Answer 233

Condition caused by long QT syndrome Rhythm may self-terminate or devolve into VF Characterised by gradual change in amplitude, RAPID IRREGULAR QRS + twisitng of QRS complex around isoelectric point (being more prominent in leds it should not be baso)

Answer 234

- Oft from DRUGS - antiarhythmics - antipsychotics - antiemetics - antifungals - antimicrobials - anything that slows metabolism/excretion of the above - Congenital (esp associated with congenital deafness) Risk factors (similar to AFib): - AGE - FEMALE - HYPOELECTROLYTES (K+, Ca2+, Mg) - heart disease - Bradycardia - DIURETIC use

Answer 235

- Treatunderlying - Magnesium - Heart rate increasing meds if still getting torsades?? - Defibrillation

Answer 236

- Pos inferior leads - Pos lead I - neg aVR - Biphasic V1 - <120 ms wide - <0.3mV (3 small squares) tall

Answer 237

* LOW amplitude – Atrial FIBROSIS, OBESITY, HYPERKALAEMIA * High amplitude ‘Tall’ – Right atrial enlargement * Broad NOTCHED ‘Bifid’ – LEFT atrial ENLARGEMENT * Alternative pacemaker foci – Focal atrial tacycardias – ‘wandering pacemaker’

Answer 238

- PROLONGED: - disorders of AV node/specialised conducting tissue - SHORTER: - Younger patients - PRE-EXCITATION (wolf-parkinson-white)

Answer 239

380-450 ms

Answer 240

STEMI, pericarditis (SADDLE-SHAPED) myocarditis

Answer 241

– Ischaemia/infarction – Myocardial strain (hypertrophy) – Myocardial disease (cardiomyopathy) are non-specific tho

Answer 242

Pulmonary Embolism Need to do CT angiogram to confirm

Answer 243

Pulmonary HTN

Answer 244

Mostly normal at rest - ST depression - T wave inversion

Answer 245

- SAW TOOTH pattern - P and T merge to make F waves - 2:1 ratio (2 f waves for every QRS)

Answer 246

Ischaemic disease of peripheral arteries

Answer 247

- SMOKING - HTN - CKD - Aging - Obesity - T2DM

Answer 248

- INTERMITTENT LIMB CLAUDICATION (least severe) - atherosclerosis -> partial lumen occlusions -> ischaemia + pain on exertion - CRITICAL LIMB ISCHAEMIA (most severe) - occlusion v big so blood supply barely able to meet metabolic demand -> pain at rest + risk of gangrene/infection When blood vessel is occluded: - **Irreversible** NERVE DAMAGE (**within 6hr**) - **irreversible** MUSCLE damage (**6-10hr**) - **skin signs last to appear** -> likely GANGRENOUS

Answer 249

- potential lack of lower limb pulse (ankle, dorsalis pedis) - ABPI <0.9 - SKIN signs: **COOLER, ULCERATIONS/PALE COLOUR** - BRUITS (pulsatile regions due to turbulent flow) - Buerger test +ve - any of 6Ps - **pallor, pain, pulseless, perishingly cold, paresthesia, paralysis**

Answer 250

1. Asymp 2. INTERMITTENT CLAUDICATION - 2a = >200m of pain free walking - 2b = <200m of walking before pain starts 3. CHRONIC limb ischaemia (pain at rest) 4. ISCHAEMIC ULCERS -> GANGRENE

Answer 251

- Buerger test (elevate leg at 45 degrees for 1 min) - +ve result - PALLOR then REACTIVE HYPERAEMIA - 1st LINE: **Ankle Brachial Pressure Index** - compare blood pressure in post+ant tibial artery to pressure in brachial artery w/ DOPPLER ULTRASOUND - 0.9 - 1.3 = normal - 0.5 - 0.9 = Intermittent claudication - <0.5 = critical chronic limb ischaemia - if absent or v low - risk of ACUTE LIMB TREATENING ISCHAEMIA - ECG, U+E, FBC - Colour duplex ultrasound - assess degree of stenosis CT angiography if surgery considered - GOLD but invasive so less used

Answer 252

- For intermittent claudication - **manage risk factors** (smoking ceassation, diet/exercise, lower BMI, ACE-I for BP control, statins, antiplatelets, T2DM drugs) - Chronic limb ischaemia - REVASCULARISATION surgery (PCI if small; BYPASS if larger) - aputation if severe - Acute limb threatening ischaemia - surgical emergancy - **REVASCULERISATION WITHIN 4-6 HOURS** - if not HIGH AMPUTATION RISK

Answer 253

- ACUTE LIMB THREATENING ISCHAEMIA - total occlusion due to embolic/**thrombotic** at site - 6Ps - the more you have, the more limb treatening (all 6 = deadly) - EMERGENCY - AMPUTATION - Permenant weakness - RHABDOMYOLYSIS - **Raised Ca2+ and K+ released into blood -> AKI + arrhythmias** Increased risk of cerebrovasc/CVD accidents

Answer 254

Ventricular tachyarrhythmia typically caused by congenital channelopathies where mutation affects cardiac ions channels and heart conduction. **A QT INTERVAL >480ms**

Answer 255

- Romano Ward Syndrome (Autosomal dominant) - Jervell and Lange-Nielsen Syndrome (autosomal recessive) - Hypokalaemia - Hypocalcaemia - Drugs: AMIODARONE, MAGNESIUM

Answer 256

- TORSADES DE POINTES - Spontaneous/development into VENTRICULAR FIBRILLATION - shapeless rapid oscillations on ECG - PULSELESS + -> CARDIAC ARREST (as no effective cardiac output) TREAT WITH ELECTRICAL DEFIBRILLATION (non synchronised as patient is pulseless)

Answer 257

- HYPERTROPHIC - RESTRICTIVE - DILATED These are muscular/conduction defects of the myocardium

Answer 258

MAIN CAUSE OF DEATH IN YOUNG PEOPLE Caused by an inherited AUTOSOMAL DOMINANT mutation of SARCOMERE PROTEINS (troponin T, myosin B) - can also become hypertrophic due to exercise, aortic stenosis etc

Answer 259

Thick non-compliant heart -> iMPAIRED DIASTOLIC FILLING -> REDUCED CARDIAC OUTPUT

Answer 260

- potentially SUDDEN DEATH (esp at younger age) - Chest pain - Palps - SOB - Syncope

Answer 261

- ECG (1st LINE) - ECHO (DEFINITIVE) - genetic testing

Answer 262

**Anti-arrhythmics** - B blocker - CCB - Amiodarone

Answer 263

MAIN CAUSE OF CARDIOMYOPATHY GENERALLY Caused by AUTOSOMAL DOM FAMILIAL (cytoskeleton gene mutation) + IHD, alcohol

Answer 264

Thin cardiac walls poorly contract -> reduced cardiac output

Answer 265

- SOB - HF (filling up + backing up) - AFib - Thromboemboli (not effectively pussing blood -> stasis)

Answer 266

- ECG - ECHO

Answer 267

Treat underlying + complications e.g. AF, HF

Answer 268

RARE Caused due to a rigid myocardium which fills poorly + contracts poorly (reduced CO) - granulomatous disease (sarcoidosis, amyloidosis) - idiopathic - PAST-MI (creates fibrotic tissue)

Answer 269

If severe: - Dyspnoea - S2 + S4 SOUNDS - Oedema + congestive HF - Narrow pulse pressure (normally 12/80; in this ~ 105/95 showing blood stasis as there is a reduced gradient)

Answer 270

- ECG - ECHO - **Cardiac catheterisation** (definitive)

Answer 271

NONE - consider transplant Patients typically die within 1 year (of presenting?)

Answer 272

Markedly raised Diastolic pressure - **>120mmHg (DIASTOLIC)** - typically 180/120 Px = **BLACK MALES 30-40**

Answer 273

- HF (LVH) - **Blurred vision** (PAPILLOEDEMA, Retinal haemorrhage) - Haematuria + renal failure (glomerulonephritis) - **Headache** (RISK OF CEREBRAL HAEMORRHAGE)

Answer 274

Normally raised preload -> rasied afterload -> raised CO (as according to Frank Sterling law) In HF Frank Sterling law is dysfunctional -> reduced CO - Compensatory mechanism is activated: RAAS (aldosterone + ADH) + Symp Nervous system (Adr/NAd) - temporarily till BP raised - Compensation soon fails so heart undergoes CARDIAC REMODELLING (reduced CO) in response to compensation - heart less well adapted to function -> raised RAAS + SNS will exacerbate fluid overload Heart failure affecting both R+L circuits = CONGESTIVE HEART FAILURE

Answer 275

- acute or chronic (time classified) - Ejection fraction classified - Normal EF - 50-70% - **>50% = Preserved ejection fraction** - DIASTOLIC FAILURE - filling issues - eg. cardiomyopathy, LVH (aortic stenosis) - **Ejection fraction reduced <40%** - SYSTOLIC FAILURE -> reduced CO - e.g. IHD

Answer 276

SOBASFat - SOB - Ankle Swelling - Fatigue

Answer 277

LABAS - Loop diuretic (Furosemide) - in acute, just for symptom relief - ACE-I + - B-blockers for all patients - Aldosterone antagonist (spironolactone) - SGLT2 inhibitors can also help + consider cardiac resync therapy (improves A-V co-ord)

Answer 278

Right heart enlargement due to lung disease Pulm arterioles constrict 🡪 increase pulmonary BP 🡪 harder for RV to pump against 🡪 hypertrophy and failure

Answer 279

Cyanotic congenital heart defect. Caused by a VSD flap moving up and into the direction of the pulm artery. This causes pulm artery stenosis and the VSD also causes the aort to move so the opening lays over the VSD. Because of the pulm stenosis and high pressure LH circulation, you get RVH. This then results in oxygen poor blood being shunted systemically due to the position of the aorta above the VSD. Hence -> cyanosis.

Answer 280

- CXR - **BOOT SHAPED HEART** - ECHO Infants oft seen in **knee to chest squatting position** as this increased preload + afterload -> improving cyanosis (should put patients in squat position in clinic to relieve symps)

Answer 281

Full surgical repair within 2 years of life (-> good prognosis)

Answer 282

Aorta narrowed at/just distal to DUCTUS ARTERIOSUS -> blood DIVERTED MASSIVELY THROUGH AORTIC ARCH BRANCHES -> Increased perfusion to upper body vs. lower body -> Upper body/collateral HTN

Answer 283

- Physical exam: - SCAPULAR BRUITS (HTN in collaterals) - Upper body HTN - CXR - NOTCHED RIBS appearance due tot DIALATED INTERCOSTAL VESSELS - CT Angiogram of aorta Treat with surgical repair/stenting

Answer 284

- Shunt usually L->R so NOT CYANOTIC - may overload RH circulation -> RVH -> EISENMENGER SYNDROME - better prognosis in younger as hearts more compliant Found on ECHO Foramen ovale oft spontaneously closes - otherwise -> SURGERY

Answer 285

- L->R so NON CYANOTIC - risk of RVH + EISENMENGER'S later on Small VSD = ASYMP Large VSD: - exercise intolerence - failure to thrive - harsh pansystolic murmer Diagnosed on ECHO may spontaneously close or may need SURGICAL closing

Answer 286

Hole in middle of heart - large opening between atria and ventricle and the area where the atria open is a VSD - big L->R shunt - **associated with DOWN'S** - Dyspnoea - Exercise intolerence - **Eventual Eisenmenger's** Hard to treat

Answer 287

Aorta -> pulm trunk shunt - risk of pulm overload + EISENMENGER'S - Dyspnoea - Failure to thrive - Machine-like murmur CXR, ECG + ECHO Treat with a PROSTAGLANDIN INHIB i.e. an NSAID (e.g. indomethacin) - may induce closure - if it doesn't work -> consider SURGERY

Answer 288

Systemic response to prior infection - typically Strep A (pyogenes) - Typically from PHARYNGITIS

Answer 289

Almost exclusively in developing countries - esp in young people

Answer 290

- M protein from s pyogenes similar to valve tissue of heart (*molecular mimicry*) - Ab against M protein cross-link -> Ab mediated destruction +/or INFLAMMATION Mostly affects MITRAL VALVE (70%, 25% = mitral + aortic) -> typically thickens leaflets -> MITRAL STENOSIS

Answer 291

- new murmur (esp MITRAL STENOSIS - low-pitched, rumbling, mid-diastolic murmur) - may have associated Sydenham Chorea - esp in kids (neuro effect of s pyogenes) - Arthritis - Erythema nodosum - PYREXIA - evidence of strep A infection

Answer 292

Bloods: - raised ESR/CRP - CXR - cardiomegaly/HF (M stenosis signs) - ECHO - details extent of valvular damage Histology: ASCHOFF BODIES (result from granulomatous inflammation of myocardium) - can be found on affected VALVES

Answer 293

JONES CRITERIA Major factors: - New murmur - Arthritis - Erythema nodosum - sydenham chorea Minor factors: - Pyrexia - raised CRP/ESR - arthralgia Diagnosed if: - **Recent S pyogenes infection + 2 major factors** OR - **1 major + 2 minor factors**

Answer 294

- Abx: - **IV BENZYLPENICILLIN STAT, then PHENOXYPENICILLIN for 10 days** For sydenham chorea - HALOPERIDOL

Answer 295

When PULMONARY HTN causes **reversal of a L-> R blood shunt** - leads to R->L shunt and oxygen poor blood being pumped systemically -> CYANOSIS

Answer 296

If presenting within 48hrs and haemodynamically stable -> IV HEPARIN + IMMEDIATE CARDIOVERSION If presenting after 48hrs or haemodynamically unstable - clot might have already formed so can't immediatly give cardioversion as it may cause embolism - treat with b blockers, heparin/DOACs for 4 weeks, then give cardioversion

Answer 297

- Hypovolemic - Rapid blood loss - Fluid loss e.g. dehydration - Cardiogenic - Heart pump failure e.g. HF, **MI**, cardiac tamponade, PE - Distributive - Anaphylactic, Septic - Obstructive - Pulm HTN, Pneumothorax, Acute pericardial tomponade, outflow obstructions e.g. valve stenosis

Answer 298

Life threatening hypoperfusion due to acute circulation failure -> tissue hypoxia + risk of organ dysfunction

Answer 299

- OFt presents with confusion _ reduced GCS - pulse weak + rapid - Skin= pale, cold, sweaty - vasoconstriction - RAISED CAPILLARY REFILL TIME (earliest, most accurate indicator) - after pressing down on hand for 5 s, takes 3 or more s to return to pinkcolour - Reduced urine output If hypotension is prolonged can cause life threatening organ failure after acute emergency recovery

Answer 300

Due to BLOOD LOSS (trauma, GI bleed), or FLUID LOSS (Dehydration) Presents with clammy, pale skin, confusion, HYPOTENSION + TACHYCARDIA Manage with ABCDE - airways, breathing (give O2), circulation (IV fluids)

Answer 301

Caused by uncontrolled bacterial infections Presents with pyrexia, warm peripheries + tachycardic, BOUDING PULSE Manage with ABCDE - give broad spec ABx

Answer 302

Caused by failure of heart pump: MI, tamponade, pulm emboli Presents with signs of HF, RAISED JVP, S4 is present Manage with ABCDE + treat underlying cause

Answer 303

Caused by IgE mediated Type 1 hypersensitivity reaction against an allergen -> caused excess vasoDILATION + bronchoCONSTRICTION 0> REDDUCED MEAN ARTERIAL PRESSURE + HYPOXIC Presents with HYPOTENSION + TACHYCARDIA - has URTICARIA, PUFFY FACE, flushing cheeks Manage with ABCDE + IM ADRENALINE (typically supposed to be 500 micrograms) - activates SNS + stress response (vascoconc + increased HR + breathing rate) - **it is usually a 1:100 solution ie 1 mg in 1 mL** - if in hospital can give IV or IM

Answer 304

Caused by spinal cord trauma e.g. from Road traffic accident -> DISRUPTED SNS but INTACT PSNS Presents with Hypotension + BRADYCARDIA, confusion, Hypothermia Manage with ABCDE + IV ATROPINE (blocks vagal tone -> more PSNS inhibition + more chance for SNS to work)

Answer 305

Kidney, Lung, Heart, Brain

Answer 306

BUFALO - Blood cultures - Urine sample - Fluids - Abx - Lactate - Oxygen Baso infection detection + control + haemodynamic stabilization

Phase 2 - Cardio Flashcards

(335 cards)