Phase 2 - Cardio

Question 1

What is atrial fibrillation

Answer 1

An irregular heartbeat (often faster than usual) that occurs when the electrical signal in the atria are uncoordinated. - it is the most common arrhythmia.It causes the atria to seem as though they are twitching. On an ecg instead of regular p waves, the atrial contraction looks like the baseline is a small scribble.It isn’t usually life-threatening

Question 2

What are the symptoms of atrial fibrillation

Answer 2

People may experience one or more of the following:- IRREGULAR heartbeat- Heart PALPITATIONS (rapid, fluttering, or pounding)- Chest PAIN- Extreme/General FATIGUE (blood delivered less effectively so less energy)- SOB- LIGHTHEADED/dizziness- WeaknessSome people experience no symptoms

Question 3

What are the risk factors for AFib

Answer 3

• HIGH BP (also increases with age - accounts for ~1 in 5 cases of AFib) - other heart conditions like coronery heart disease or vavlvular disease which create an inflammatory state- DIABETES- Left ventricular hypertrophy- HF- Ischemic heart disease- HYPERTHYROID- CKD- Advancing AGE- OBESITY- EUROPEAN ancestry - genetic component- Moderate to heavy alcohol use- Smoking

Question 4

Complications of AFib

Answer 4

Associated with an increased risk of ischaemic stroke- As the blood isn’t effectively pumped from the atria it can stagnate and form clots

Question 5

Pathophysiology of AFib

Answer 5

Not well understood but it is believed that the risk factors (particularly things like hypertension that can stretch and wear out the myocytes) cause stress to the cells which can lead to tissue heterogeneity: the cells take on different electrical properties causing atrial conduction to become uncoordinated so various different parts of the atria are contracting at different times. Multiple wavelet theory:Forms multiple wavelets as opposed to a single wave front.Automatic focus theory:specific area initiates alternate electrical impulses and overrides sa node. Thought to originate in cells around pulmonary vein entry point.

Question 6

Progression/Types of atrial fibrillation

Answer 6

Starts with paroxysmal AF - come and goes (<1 week)Repeated paroxysmal events cause further stress (potentially through calcium overload) - get progressive fibrosis of cells.Leads to Persistent AF - lasts >1 week without self-terminating (weeks to months)When it has lasted for >12 months - Long-standing persistent AFIf the patient and clinician decide not to definitively treat the dysrhythmia - Permanent AF

Question 7

Diagnosis/tests for AF

Answer 7

Persistent AF - _ECG_Paroxysmal AF - may use holter monitor- portable device that monitors rhythm over longer time period and records potential episodes of AF to check later

Question 8

Treatments for AF

Answer 8

Medication to control heart rate and anticoagulents (wouldn’t give they have very high hypertension as there at more risk of dissections etc)- Beta-blockers- CCB (VERAPAMIL)- Digoxin- Warfarin- direct-acting oral ANTICOAGs (DOACs) * Dabigatran, Apixaban, Rivaroxaban, Edoxaban ** lower risk of brain haemorrhage ** need less frequent blood monitering (don’t need regular INR) ** fewer interactions ** don’t need to adjust dose frequently depending on blood resultsCan get a RADIOFREQUENCY CATHETER ABLATION - some tissue is destroyed so the irregular electrical impulses aren’t conducted anymore- Might do a MAZE PROCEDURE so the impulses are forced through a maze like direction to better control and coordinate impulses and contraction- May put in an implantable PACEMAKER - contantly paces atrium- May get AV NODE ABLATION so separates ventricular contraction from atrial contraction ** Needs a ventricular pacemaker!

Question 9

What is a CHA2DS2-VASc score

Answer 9

It is a score that estimates the risk of stroke in people with non-rheumatic atrial fibrillation.Used to determine if treatment with anticoagulants/anti-platelets is requiredStands for:Congestive heart failure (left ventricular systolic dysfunction) (1 point)Hypertension (1 point)Age2 >= 75 (2 points)DIabetes Mellitus (1 point)S2 = prior stroke or TIA (transient ischaemic attack - mini self terminating stroke) or thromboembolism (2 points)Vascular disease (1 point)Age 65-74 years (1 point)Sex (1 point) - femaleIf positive for 1 point (moderate risk) - oral anticoagulent should be considered2 or more points (high risk) - oral anticoagulent recommended

Question 10

What is an ORBIT score

Answer 10

estimates risk of major bleeding for patients on anticoagulents for AFOlder age: 75 or over (1 point)Reduced Haemoglobin/Haemocrit/Anaemia (2 points)Bleeding history (2 point)Insufficient renal function (1 point)Treatment with anti-platelet agents (1 point)0-2 - low bleed risk3 - medium bleed risk4-7 - high bleed riskthink HARP B (Haematocrit, Age, Renal function, anti-Platlets, Bleeding history)

Question 11

Differential diagnosis of palpitations

Answer 11

• ISCHAEMIC heart disease- HF- Cardiomyopathy- VALVE disease- Wolff-Parkinson-White syndrome (AVRT)DrugsLifestyle factors:- alcohol misuse- caffine, nicotine, heroin, amphetamines, ecstasy, cannabis

Question 12

Atrial flutter vs Atrial fibrillation

Answer 12

In atrial flutter the rhythm in the atria is more organisedECG:In atrial flutter there is a more organised saw-tooth pattern of p-wavesIn AF the baseline is more scribbley and the ventricular rate is more irregularTreatment:Catheter ablation is the gold standard treatment for atrial flutterMedicine is the first line treatment for AF

Question 13

ECG variations for heart/AV block

Answer 13

1st degree is just elongated PR intervals (over 200ms - 5mm)2nd degree:- Mobitz type 1: complexes get closer together till a beat is missed then restarts pattern- Mobitz type 2: complexes seem regularly spaced by one is missed ocassionally3rd degree - p waves and qrs complex have different rhythms (individually they follow a rhythm but they don’t match each other)

Question 14

What do the waves on ecg correlate to

Answer 14

p waves - atrial depolarizationqrs complex - ventricular depolarisationt wave - ventricular repolarisation(sometimes get a u wave - end of ventricular repolarisation - seen in hypokalaemia)

Question 15

Normal conduction pathway of heart

Answer 15

• Starts at SA nodepropagates through both atria- Depolarization spreads to AV node- Passes through bundle of His- left and right bundle branches - Left = anterior and posterior fascicles- Purkinje fibres

Question 16

What is an ECG

Answer 16

A summation of electrical activity/events in the cardiac cycle

Question 17

Pacemakers of the heart

Answer 17

SA node - dominant - intrinsic rate: 60-100 beats/minAV node - back-up - intrinsic rate: 40-60 bpmVentricular cells - back-up - intrinsic rate: 20-45 bpm

Question 18

Standard calibration of ECG

Answer 18

25 mm/s-0.1 mV/mm1mm = 40ms5mm = 200ms (max length of normal PR interval)In this setting work out heart rate:300/no. of big sqares

Question 19

What chemicals is mycocardial hypertrophy triggered by? When is this an adaptive response

Answer 19

Hyperthrophic response triggered by:- angiotensin 2 (vasoconstrict)- IGF-1 (insulin-like growth factor 1 - e.g. acromegaly)- endothelin-1 (vasoconstrict)- TGF beta (transforming growth factor - a cytokine - inflam)They activate mitogen-activated protein kinase (growth)Adaptive in athletes and temporarily during pregnancy

Question 20

What occurs in fetal embryogenesis (in relation to heart formation)

Answer 20

Heart comprises of a SINGLE CHAMBER till 5TH WEEK of gestationDevided by intra-ventricular and intra-atrial SEPTA from ENDOCARDIAL CUSHIONS (Lateral cushions form rest of atrio-ventricular septa and valves)Muscular intra-ventricular septum grows upwards from apex producing 4 chambers and allowing valve development to occur

Question 21

Types of congenital heart disease

Answer 21

Overall may only complicate up to 1% of all live births- VENTRICULAR SEPTAL DEFECT (25-30%)- ATRIAL SEPTAL DEFECT (10-15%)- PATENT DUCTUS ARTERIOSUS (10-20%)- FALLOTS * (combination of VSD, right ventricular HYPERTROPHY, PULMONARY valve STENOSIS, shifting of AORTA so it LIES OVER the VSD and gets oxygen-rich and -poor blood) (4-10%)(less important)- Pulmonic stenosis (5-7%)- Coarctation of aorta (narrower part) (5-7%)- Aortic stenosis (4-6%)- Transposition of great arteries (2 main arteries are reversed) (4-10%)- Truncus arteriosus (2%)- Tricuspid atresia (tricuspid doesn’t form) (1%)Many die between 20-40 y/o

Question 22

Risk factors for congenital heart disease

Answer 22

It has multifactorial inheritance- particularly associated with HOMEOBOX GENES (DNA sequence that regulates large-scale anatomical features in early embryonic development)Trisomy 21 (Downs)Turners (X0)di-George Syndrome (22q11 deletion)Previous child with defect increases probability of second child with another defect- INFECTIONS like rubella- DRUGS: - tahlidomide - alcohol - phenytoin - amphetamines - lithium - oestrogenic steroids- DIABETES

Question 23

How are congenital heart defects classified

Answer 23

CyanosisIs it present or absent? - Cyanotic - tetralogy of Fallot, - TGA (transposition of great arteries) - truncus arteriosus (trunc of aorta/pulmon artery don’t seperate properly; mixed blood) - tricuspid abnormalities, - tapvr (total anomalous pulmonary venous return - oxygen rich blood from pulm vein goes into right heart instead of left; mixing with oxygen poor blood)- acyanotic - Ventral septal defectIf present, does it occur from birth or develop later?

Question 24

Which heart defects cause left right shunt

Answer 24

• VSD, - ASD, - PDA, - truncus arteriosus, - Total anomalous pulmonary venous drainage (pulmonary veins rejoins a vein so it drains into right side)- hypoplastic left heart syndrome

Question 25

Which heart defects cause right-left shunt

Answer 25

Tetralogy of FallotTricuspid atresia (abnormal narrowing)

Question 26

Which heart defects have no shunt

Answer 26

• 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)

Question 27

Which are acute coronary syndromes

Answer 27

Unstable anginaNSTEMISTEMI(can be q-wave or non q-wave infarcts)

Question 28

Clinical classification/presentation of unstable angina

Answer 28

Cardiac chest pain at restCardiac chest pain with crescendo patternUsually new onset or abrupt deterioration in previously stable anginaUncommon:- 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)

Question 29

Diagnosis of unstable angina

Answer 29

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

Question 30

Treatments for unstable angina

Answer 30

Sublingual NITRATES to treat vasospasms CALCIUM CHANNAL BLOCKERS e.g. AMLODIPINEBETA 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 clopidogrelPossibly low dose aspirinBasically antiplatelet and anticoagulent therapy done with cardiological advice))

Question 31

STEMI vs NSTEMI

Answer 31

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

Question 32

Risk factors for unstable angina (and cvd in general)

Answer 32

Diabetes mellitusHyperlipidaemiaHypertensionMetabolic syndrome (diabetes, obesity + HTN)Renal impairmentPeripheral arterial diseaseHistory of ischaemic heart disease and any previous treatmentFamily history (immediate relative getting coronary artery disease/ under 60 y/o)ObesityAdvanced ageSmokingCocainePhysical inactivity

Question 33

Diagnosis of myocardial infarction

Answer 33

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 resultsCan also be defined as Q-wave or non Q-wave retrospectively depending on whether new pathological Q waves develop on ECG because of it

Question 34

What is the importance of Left bundle branch block

Answer 34

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)

Question 35

Q wave vs non Q wave MI on ecg

Answer 35

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

Question 36

Clinical presentation of MI

Answer 36

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

Question 37

Risk of mortality associated with MI

Answer 37

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

Question 38

Immediate management of MIs

Answer 38

Get in to hospital quickly – 999 callParamedics – 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 fibrinolysisTake aspirin 300mg immediatelyPain relief

Question 39

Hospital management of MI

Answer 39

Make diagnosisBed restOxygen therapy if hypoxicPain relief – opiates/ nitratesAspirin +/- platelet P2Y12 inhibitorConsider beta-blockerConsider other antianginal therapyConsider urgent coronary angiography e.g. iftroponin elevated or unstable angina refractoryto medical therapy

Question 40

Causes of acute coronary syndromes

Answer 40

Usually from rupture of atherosclerotic plaque and subsequent arterial thrombosisUncommon:- 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

Question 41

What is troponin? When is it positive

Answer 41

Protein complex which regulate actin-myosin contractionHighly sensitive marker for cardiac muscle injury- not specific for acute coronary syndromeAlso 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

Question 42

What is the physiological effect of aspirin

Answer 42

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

Question 43

How does thrombin generation play a role in arterial thrombosis

Answer 43

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

Question 44

Name some P2Y12 antagonists

Answer 44

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

Question 45

What is the role of P2Y12 inhibitors

Answer 45

P2Y12 amplifies platelet activationP2Y12 inhibitors are platelet inhibitorsThey are used in combination with aspirin for ACS as ‘DUAL ANTIPLATELET THERAPY’

Question 46

Name 3 GPIIb/IIIa antagonists

Answer 46

AbciximabTirofibanEptifibatide

Question 47

What is the role of GPIIb/IIIa antagonists

Answer 47

GPIIb/IIIa stimulates aggregation and amplifies platelet activationGPIIb/IIIa antagonists are antiplateletsUsed 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

Question 48

What is the role of anticoagulants for ACS management

Answer 48

Used in addition to antiplateletsTargets formation/activity of thrombinInhibits fibrin formation AND platelet activationTypically used prior to angiography, for PCI or CABG (before surgery basically)

Question 49

Which drug is used in NSTEMI before doing a coronary angiography

Answer 49

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

Question 50

What drug is used during PCI for ACS treatment

Answer 50

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)

Question 51

When may fibrinolytic therapy be used in ACS

Answer 51

For an acute STEMI if primary PCI is not available

Question 52

Which fibrinolytic drugs may be used for STEMI

Answer 52

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

Question 53

Which drugs are used in secondary prevention of ACS

Answer 53

STATINSACE inhibitorsBeta blockersAldosterone antagonist (SPIRONOLACTONE, EPLERONONE)

Question 54

which factors affect response to clopidogrel

Answer 54

Dose* Age* Weight* Disease states such as diabetes mellitus* Drug-drug interactions e.g. omeprazole and strong CYP3Ainhibitors* Genetic variants: CYP2C19 loss-of-function alleles

Question 55

What are the adverse effects of P2Y12 inhibitors

Answer 55

Bleeding e.g. epistaxis, GI bleeds, haematuriaRash*GI disturbance

Question 56

What are the adverse effects of ticagrelor specifically

Answer 56

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

Question 57

What is the significence of ticagrelor as opposed to other P2Y12 inhibitors

Answer 57

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

Question 58

How long would you continue antiplatelet therapy after an MI

Answer 58

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 BLEEDINGIn patients WITHOUT HIGH LONGTERM RISK- can drop aspirin after a few months

Question 59

What is primary PCI

Answer 59

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

Question 60

When is revascularisation done for NSTE ACS

Answer 60

Coronary angiography usually done for patients with RAISED TROPONIN or UNSTABLE ANGINA REFRACTORY TO MEDICAL THERAPYNOT AMENABLE if patients have SEVERE DIFFUSE CORONARY ARTERY DISEASE

Question 61

What are the types of revascularisation procedures

Answer 61

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

Question 62

When may patients have ACS without obstructive coronary artery disease

Answer 62

• 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)

Question 63

General ACS management overview

Answer 63

DIagnosis: history, ECG (if ST elevation go straight to cath lab for PCI if possible), troponin +/- coronary angiography; consider other diagnoses if uncertainPain 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 arrhythmiaInitial 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 feasibleSecondary 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

Question 64

In general terms what causes angina? What is the most common specific cause?

Answer 64

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

Question 65

What are risk factors for ischaemic heart disease (IHD) and subsequently angina of ischaemic origin

Answer 65

Non-modifiable:AGEFamily historyMALE 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

Question 66

What are the intrinsic exacerbating factors of angina/IHD?

Answer 66

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- HypervolaemiaDemand related:- HYPERTENSION- TACHYARRYTHMIA- VALVULAR HEART DISEASE- Hyperthyroidism- Hypertrophic cardiomyopathy

Question 67

What are environmental exacerbating factors for angina

Answer 67

ExerciseCold weatherHeavy meals (blood diverted to stomach)Emotional stress

Question 68

Pathophysiology of angina/myocardial ischaemia

Answer 68

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

Question 69

What physics equations relate to blood vessel function

Answer 69

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

Question 70

How does the body normally adapt to increased exertion

Answer 70

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

Question 71

Aside from stable and unstable angina, what are other types of angina

Answer 71

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

Question 72

What is the relevance of the epidemiology of stable angina

Answer 72

IncidenceMen 35/100,000/y (especially in older people)Women 20/100,000/yPrevalenceMen 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)

Question 73

Symptoms of angina

Answer 73

CHEST PAIN (typically described as tightness/weight/discomfort)- typically shows up after exertion or eating- mainly in chest radiating to neck, jaw, teeth, arms, backBREATHLESSNESSNO fluid retention (unlike heart failure)NOT USUALLY palpitationsRARELY syncope or pre-syncopeCan sometimes get pale and sweaty tho this typically indicates a more severe case

Question 74

Differential diagnoses of chest pain

Answer 74

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 causesTypically if they say it is a severe pain it is probably not angina

Question 75

Treatment of angina

Answer 75

• 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

Question 76

How do you diagnose angina

Answer 76

• 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

Question 77

Pros and cons of CT coronary angiography

Answer 77

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

Question 78

Pros and cons of exercise testing (for heart issues)

Answer 78

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.)

Question 79

What is a myoview scan

Answer 79

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

Question 80

What is a stress echo test for heart problems

Answer 80

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

Question 81

Pros and cons of perfusion MRI for heart issues

Answer 81

BEST non invasive test- good sensitivity and specificityNot available everywhere

Question 82

Pros and cons of cor angiography

Answer 82

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

Question 83

Drug treatment for angina (types of drugs and how they work)

Answer 83

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 returnBeta-blocker- reduces heart rate so lowers oxygen demand- reduces LV contractility- reduced cardiac output so less oxygen demandStatins- HMG-CoA reductase inhibitor (inhibits rate limiting step of cholesterol synthesis)- lower cholesterol as most people with angina have CAD and need to lower ldlACE 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 afterloadPotentially potassium channal opener or Ivabradine (lowers heart rate)

Question 84

Side effects and contraindications of beta blockers

Answer 84

BradycardiaCold peripheralsErectile dysfunctionTirednessNightmaresDO NOT USE IN SEVERE ASTHMA

Question 85

Side effect of nitrates

Answer 85

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

Question 86

Side effects of calcium channal blockers

Answer 86

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

Question 87

Aspirin - function, side effects, when is it used

Answer 87

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

Question 88

What are ACE inhibitors usually used for

Answer 88

Hypertension and DM treatment- esp if they also have IHD

Question 89

Which blood vessels are used for CABG

Answer 89

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

Question 90

pros and cons of PCI

Answer 90

Pros:Less invasive than CABGConvenientRepeatableAcceptableCons:Risk stent thrombosisRisk restenosisCan’t deal with complex diseaseDual antiplatelet therapy required

Question 91

Pros and cons of CABG (coronary artery bypass graft)

Answer 91

Pros:Prognosis betterDeals with complex diseaseCons:Invasive (very)Risk of stroke, bleedingCan’t do if frail, comorbidOne time treatmentLength of stay (intensive care for 5 days normally)Time for recovery (~ 3 months)

Question 92

PCI vs CABG use for acute and chronic coronary syndromes

Answer 92

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

Question 93

Physiology of the pericardium in relation to pathology

Answer 93

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

Question 94

How does a chronic pericardial effsuion occur

Answer 94

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

Question 95

What is acute pericarditis

Answer 95

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

Question 96

How is acute pericarditis clinically diagnosed

Answer 96

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

Question 97

Epidemiology of pericarditis

Answer 97

Difficult to quantify1% in autopsy series5% of A&E attendances with chest pain1% of cases with ST elevation80-90% of all pericarditis IDIOPATHIC- Seasonal with VIRAL TRENDS (management isn’t affected by which virus)- HIGHER IN YOUNG, previously healthy patients

Question 98

Clinical presentation of pericarditis

Answer 98

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 DOWNDYSPNOEACoughHiccups (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

Question 99

Aetiology of pericarditis (causes) - infectious reasons

Answer 99

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

Question 100

Non-infectious aetiology of pericarditis

Answer 100

AUTOIMMUNE (common):- Sjögren syndrome, - rheumatoid arthritis, - scleroderma- systemic vasculitidesNEOPLASTIC (most common non-infectious reason): - secondary metastatic tumours esp from lung, breast cancer and lymphomaMetabolic:- uraemia (usually from end-stage kidney disease)- myxoedemaTRAUMATIC/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

Question 101

Differential diagnosis for pericarditis

Answer 101

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

Question 102

Investigations/examination for pericarditis

Answer 102

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

Question 103

What does pericardial rub sound like

Answer 103

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

Question 104

What are the clinical signs of pericardial effusion

Answer 104

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

Question 105

What does the ECG look like in pericarditis

Answer 105

Diffuse ST elevationConcave ST segment (sort of saddle shaped)- may resemble STEMI patternNO RECIPROCAL ST DEPRESSION (unlike STEMI)PR depression- Mechanism: epicardial inflammation as adjacent to pericardium - parietal is inert

Question 106

Blood tests done for pericarditis

Answer 106

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

Question 107

What does CXR look like in pericarditis

Answer 107

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

Question 108

What is a complication of pericardial effusion

Answer 108

cardiac tamponade

Question 109

What is cardiac tamponade

Answer 109

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

Question 110

What can cause cardiac tamponade

Answer 110

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

Question 111

Signs of tamponade

Answer 111

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

Question 112

Why may pulsus paradoxus not be present in pericardial effusion

Answer 112

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

Question 113

Management of pericarditis

Answer 113

Not a lot of evidence mainly consensus opinionSedentary 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 dosesColchicine (0.5mg BD PO 3/12) limited by nausea and diarrhoea, reduces recurrence

Question 114

Prognosis of pericarditis

Answer 114

• 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 COLCHICINE15-30% with acute will get recirrence

Question 115

How much does colchicine reduce recurrence rate

Answer 115

50%

Question 116

How can risk of developing constriction in pericarditis be classified

Answer 116

Low (1%):- for idiopathic and presumed viralIntermediate (2-5%)- autoimmune- immune mediated- neoplastichigh (20-30%)- bacterial (esp TB and purulent)

Question 117

What is a treatment given for Tuberculous effusion TB pericarditis

Answer 117

Pericardectomy (~50% 5 year survival)

Question 118

What is the name of post cardiac injury syndromes

Answer 118

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

Question 119

What is atherosclerosis?

Answer 119

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

Question 120

Risk factors for atherosclerosis

Answer 120

AgeFAMILY HISTORYHIGH SERUM CHOLESTEROLTOBACCO SMOKINGHYPERTENSIONDIABETES Obesity

Question 121

Distribution of atherosclerotic plaques within body

Answer 121

Found within peripheral and coronary arteriesFocal distribution but can occur along the length of the arteryCan 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

Question 122

What is neointima

Answer 122

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

Question 123

What does the structure of an atherosclerotic plaque consist of

Answer 123

LipidNECROTIC COREConnective tissueFIBROUS CAP

Question 124

What is the response to injury hypothesis of atherosclerosis

Answer 124

Injury to endothelial cells initiates endothelial dysfunctionSignals sent to circulating leukocytes -> they accumulate and migrate into vessel wallInflammation occurs

Question 125

What 2 things primarily cause inflammation of arterial wall in atherosclerosis

Answer 125

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

Question 126

What stimulates the movement/adhesion of leukocytes at sites of inflammation

Answer 126

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.

Question 127

Which inflammatory cytokines are found in plaques

Answer 127

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

Question 128

What are the stages of atherosclerosis

Answer 128

Fatty streaksIntermediate lesionsFibrous plaques OR Advanced lesionsPlaque rupture OR Plaque erosion

Question 129

What do fatty streaks consist of and when do they appear

Answer 129

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

Question 130

What are intermediate atherosclerotic lesions composed of

Answer 130

Lipid-laden macrophages (FOAM CELLS)T LYMPHOCYTESVASCULAR SMOOTH MUSCLE CELLSAdhesion/aggregation of PLATELETS to wallIsolated pools of extracellular lipid

Question 131

What is the make-up of fibrous plaques/advanced lesions

Answer 131

Contains:- FOAM CELLS- T LYMPHOCYTES- SMOOTH MUSCLE CELLS- MACROPHAGESForms the LIPID CORE and NECROTIC DEBRISCovered by FIBROUS CAP- may be calcifiedImpedes blood flow and prone to rupture

Question 132

What is the fibrous cap of an atherosclerotic plaque made of

Answer 132

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

Question 133

What occurs in plaque rupture

Answer 133

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

Question 134

When does plaque erosion occur

Answer 134

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

Question 135

Plaque rupture vs plaque erosion

Answer 135

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

Question 136

Red thrombus vs white thrombus

Answer 136

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

Question 137

What are neutrophil extracellular traps (NET)?

Answer 137

Extruded DNA and enzymes which cause cell activation and cytokine release

Question 138

What are the differences in clinical characteristics between people who have plaque rupture vs plaque erosion

Answer 138

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 eventsPlaque erosion:- Smoking- Women- <50 y/o- nearby bifurcation- anterior ischaemia(- summer)- anti-thrombotic- less microvascular damage after PCI- better myocardial perfusion

Question 139

Main treatment of CAD

Answer 139

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

Question 140

example of drug on stents

Answer 140

Sirolimus

Question 141

What doe PCSK9 inhibitors do

Answer 141

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

Question 142

Stages of hypertension severity diagnosing criteria

Answer 142

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

Question 143

When are antihypertensive drugs offered to patients

Answer 143

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 moreAnyone with stage 2 is offered antihypertensives

Question 144

What are BP targets for patients with hypertension

Answer 144

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

Question 145

What is infective endocarditis

Answer 145

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

Question 146

Types of infective endocarditis

Answer 146

Left sided native IE (mitral or aortic)Left sided prosthetic IERight 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

Question 147

Epidemiology of IE

Answer 147

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

Question 148

Risk factors for IE

Answer 148

• 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

Question 149

Clinical presentation of IE

Answer 149

Could get almost any type of sign/symptom depending on what organism it is and where the infection isOften 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 stigmataValve dysfunction (murmurs, weakness, palpitations), heart failure (e.g. fluid overload), arrythmia

Question 150

What types of peripheral stigmata can you get with IE

Answer 150

Petechiae (little bruises) 10 to 15%,Splinter hemorrhagesOsler’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 soleRoth spots on fundoscopy (with opthalmascope in eye)

Question 151

Diagnosis of IE

Answer 151

• Do blood cultures- Do an echocardiogramthis 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 clearCan 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 changesIE almost always shows raised CRP- INR may also riseWBC is rarely helpful

Question 152

What are the 2 types of echo

Answer 152

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

Question 153

Treatment of IE

Answer 153

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

Question 154

When is surgery required for IE

Answer 154

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

Question 155

What is sometimes recommended to prevent IE

Answer 155

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

Question 156

What is Aortic Stenosis

Answer 156

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)

Question 157

What is the normal area of the aortic valve

Answer 157

3-4 cm^2

Question 158

Aetiology/causes of AS

Answer 158

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

Question 159

Pathophysiology of AS

Answer 159

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

Question 160

Clinical presentation of AS

Answer 160

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

Question 161

Physical signs of AS

Answer 161

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

Question 162

Natural history of AS

Answer 162

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

Question 163

Prognosis of AS

Answer 163

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

Question 164

Investigation of AS

Answer 164

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

Question 165

Grading of AS (using AVA)

Answer 165

Mild: >1.5 cm2Moderate: 1 - 1.5 cm2Severe: <1 cm^2(mean gradient >40 mmHg)

Question 166

Management/treatment of AS

Answer 166

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

Question 167

When are interventions for AS indicated

Answer 167

• 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

Question 168

Define mitral regurgitation

Answer 168

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

Question 169

Aetiology of Chronic MR

Answer 169

Myxomatous degeneration (causes MV prolapse)Ischaemic MRRheumatic heart diseaseIE

Question 170

What does myxomatous mean

Answer 170

soft tumour made of gelatinous connective tissue

Question 171

Types of MR

Answer 171

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

Question 172

Pathophysiology of MR

Answer 172

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

Question 173

Signs and symptoms of MR

Answer 173

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/dilationExertion Dyspnoea (PRINCIPLE EARLY manifestation)HF - can coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

Question 174

Natural history of MR

Answer 174

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

Question 175

Investigations for MR

Answer 175

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

Question 176

Management/treatment of MR

Answer 176

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

Question 177

When is surgery indicated in severe MR

Answer 177

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

Question 178

Define aortic regurgitation

Answer 178

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

Question 179

Etiology of chronic AR

Answer 179

Bicuspid valveRheumatic heart diseaseIE

Question 180

Pathophysiology of AR

Answer 180

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

Question 181

Physical signs of AR

Answer 181

Wide pulse pressure (e.g. 180/60mmHg) - most sensitiveHyperdynamic and displaced apical beatAuscultation:- 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

Question 182

Natural history of AR

Answer 182

Asymptomatic until 4th or 5th decadeRate of Progression: 4-6% per yearProgressive Symptoms include:- DYSPNOEA (most common): exertional, orthopnea (breathless whenlying down), and paroxsymal nocturnal dyspneaPalpitations: due to increased force of contraction and ectopics

Question 183

DIagnostic investigation of AR

Answer 183

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

Question 184

Management of AR

Answer 184

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

Question 185

When is surgery indicated for AR

Answer 185

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

Question 186

Define mitral stenosis

Answer 186

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

Question 187

Normal mitral valve area

Answer 187

4-6 cm^2

Question 188

Etiology of Mitral Stenosis

Answer 188

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

Question 189

Pathophysiology of Mitral S

Answer 189

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

Question 190

Natural history of MS

Answer 190

Disease of plateaus: Mild MS: 10 years after initial RHD insultModerate: 10 years laterSevere: 10 years laterMortality: Due to progressive pulmonary congestion, infection, and thromboembolismHigh risk of stroke if AF + MS

Question 191

Signs of MS

Answer 191

PROMINANT A WAVE in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy Signs of right-sided heart failure: in advanced diseaseMitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeksAuscultation - 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

Question 192

DIagnostic investigation of Mitral S

Answer 192

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

Question 193

Management of mitral s

Answer 193

Serial echocardiography: Mild: 3-5 yearsModerate:1-2 yearsSevere: yearlyMedications: 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 surgerymaybe IE prophylaxis

Question 194

How does PMBV work and when can’t it be used

Answer 194

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

Question 195

Indications for Mitral valve replacement

Answer 195

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

Question 196

What is Heart failure

Answer 196

An inability of the heart to deliver blood(and O2) at a rate commensurate with therequirements of the metabolising tissues,despite normal or increased cardiac fillingpressuresTypically 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)

Question 197

NYHA class grading of HF

Answer 197

Class I: No limitation (Asymptomatic)Class II: Slight limitation (mild HF) - at moderate activityClass III: Marked limitation (Symptomaticallymoderate HF) - at moderate activityClass IV: Inability to carry out any physicalactivity without discomfort (symptomaticallysevere HF) - symps even at rest

Question 198

What are the different types of HF

Answer 198

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 bothPumping 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 commonCan be acute (after MI/fibrillation - ISCHAEMIC HF) or chronic (from conditions like chronic HTN - more common - MYOPATHIC/HYPERTENISVE HF)

Question 199

Normal EF for male and female

Answer 199

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

Question 200

Aetiology/risk factors of HF

Answer 200

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

Question 201

What does cardiomyopathy mean in particular

Answer 201

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

Question 202

Basic epidemiology of HF

Answer 202

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

Question 203

Signs and symptoms of HF

Answer 203

Symptoms:left HF:- breathlessness!!- coughingright 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 HFrEFRH:- 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

Question 204

Causes of acute decompensation of chronicheart failure

Answer 204

Acute MIUncorrected ­BPObesitySuperimp. infectionAF & arrhythmias-ve inotropes (Ca/beta)Excess alcoholEndocrine (DM/T4..)NSAIDSTreatment and Na+ noncompliance.Lack of information given to patient about diet, medications, etc

Question 205

Diagnosis of HF

Answer 205

presence of risk factorspresence 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 fillingCXR:- pulm congestion/oedema, cardiomegaly (tho not necessarily)elevated NT-proBNP (chronic), acute = moderateDECREASED SODIUM (usually <135 mmol/L), altered potassiumBlood LIPIDS DECREASED in END-STAGE HF(troponin/CRP high in ACUTE)

Question 206

Treatment for HF

Answer 206

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 worksMRA additionally to ACE if ineffectiveICD coil - defib to stop sudden death from arrhythmiasCRT - pacemakerRevascularisation for ischaemic HFrEF - doesn’t really work in asymptomatic ppl with CAD and HFDiuretics are given first in HFpEF but don’t improve disease only reduce symptomsTreat underlying cause

Question 207

What is AVRT

Answer 207

Atrioventricular reentrant tachycardia i.e. most common Wolff-Parkinson-White syndrome arrhytmiaType 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

Question 208

What is AVNRT

Answer 208

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 beatUsually missing p wave (inside QRS) or appears as pseudo r inversion at terminal portion

Question 209

symptoms of avrt/avnrt

Answer 209

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

Question 210

Treatment of avrt/avnrt

Answer 210

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

Question 211

Complications of AVRT/AVNRT

Answer 211

AVRT can cause sudden death from pre-excitationCatheter ablation can cause: (rare)- av blockMIpericarditiscardiac tamponadepneumothoraxfemoral artery pseudoaneurysm

Question 212

What is pre-excitation

Answer 212

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

Question 213

What is prinzmetal angina

Answer 213

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

Question 214

What is aortic dissection

Answer 214

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 oneAcute if <14 days

Question 215

Presentation of aortic dissection

Answer 215

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 50sAlso:-syncope-heart/renal failure- mesenteric/limb ischaemia

Question 216

Diagnosis of Aortic dissection

Answer 216

Signs/symptoms:- acute severe chest pain-interscapular/lower pain- left/right BP differential- pulse deficitECG 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 dissectionCT (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 seenBloods- high creatinine/urea if renal failure- troponin to check if MI- anaemia if haemorrhage

Question 217

Treatment of aortic dissection

Answer 217

initially if haemodynamically unstable:- advanced life support; haemodynamic support- opiod analgesiaConfirmed 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

Question 218

Define Abdominal aortic aneurysm

Answer 218

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

Question 219

Presentation/symptoms of AAA

Answer 219

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

Question 220

Risk factors for AAA

Answer 220

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

Question 221

Diagnosis of AAA

Answer 221

• presence of risk factors- Examination -palpating above umbilicus on either side of aorta1st LINE: Aortic ultrasoundelevated erythrocyte sedimentation rate/CRP - inflammatory AAAleukocytosis, anaemia on FBC if haemorrhage or infectious AAA- also +ve blood culture- maybe PET-CTGOLD STANDARD:computed tomography angiography (CTA)- useful if close to renal arteries* MRI as alt

Question 222

Treatment for AAA

Answer 222

Acute AAA (symptomatic aneurys OR RUPTURED):- 1st LINE: urgent surgical repair if >5.5cm[- IF RUPTURED - RESUSCITATION MEASURES]- Perioperative antibiotics- Analgesia- VTE prophylaxisie standard surgery stuffAsymptomatic 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 managementAsymptomatic 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

Question 223

What factors need to be taken into account when debating between surgery/not surgery

Answer 223

• 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)

Question 224

What might make you unfit for surgery

Answer 224

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.)

Question 225

Complications for aortic aneurysm

Answer 225

Rupture and Haemorrhage

Question 226

Define Hypertension

Answer 226

BP >= 140/90 mmHg

Question 227

Aetiology/risk factors for HTN

Answer 227

Usually idiopathic (essential HTN)OBESITY (esp abdominal)Inactive (aerobic exercise <3 times/week)Moderate - high ALCOHOL intakeMetabolic syndrome (insulin resistance /hyperinsulinaemia)DMHigh sodium intake (>1.5 g/day)(low fruit/veg)Black ancestry>60 y/oFamily history (HTN or CAD)Sleep apnoea(dyslipidaemia)(stress)DRUGS:- NASIDSSNRIs (venlafaxine)CorticosteroidsOestrogen containing oral contraceptivesStimulants (e.g. methylphenidate for adhd)Antianxiety (gabapentine)Anti-TNFs (anti inflammatory)

Question 228

Diagnostic investigations for HTN

Answer 228

MAINLY DIAGNOSED ON:- presence of risk factors- high BPIF RETINOPATHY (retinal haemorrhage) - MALIGNANT HYPERTENSION- Also: * papilloedema * acute kidney injury * stroke * acute coronary syndrome * aortic dissectionIF ATYPICAL AND SUSPECTING 2nd-ary CAUSE:ECG to check for IHD/CADBloods:- 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

Question 229

Treatment for HTN

Answer 229

Lifestyle changes: 1st LINE- Losing weight- reduce alcohol- lowering salt consumption- exercise- destressDrugs:- 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 LIFELONGEvery 6 month follow-up

Question 230

Complications of high BP

Answer 230

STROKE (haemorrhagic esp)IHD - angina, MI etc.Peripheral vascular diseaseHeart failureCKDDementia (unsure whether it causes it but definitely linked)Aortic dissection

Question 231

Define Deep vein thrombosis

Answer 231

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

Question 232

RIsk factors for DVT

Answer 232

• 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)

Question 233

How can could cancer cause DVT

Answer 233

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

Question 234

SIgns/symptoms of DVT

Answer 234

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

Question 235

Diagnosis of DVT

Answer 235

Assess pre-test ptobability of DVT with WELL’S SCORE- 2/more points = DVT likely1ST LINE: VENOUS US (or CT)D-dimer - protein fragment released by clot break-upFBC, Urea/cratinine, LFTs, clotting screen (underlying)

Question 236

Treatment of DVT

Answer 236

ANTI-COAGs:- LMWH- unfractioned hep or fondaparinux- DOACs (Dabigatran, Apixiban etc)- WarferinFor 3 months - CONTINUE AS PROPHYLAXIS if HIGH RISK- PHYSICAL EXERCISE- COMPRESSION STOCKINGIVC FILTER if recurrent even with anti-coagRarely: thrombolysis

Question 237

Complications of DVT

Answer 237

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

Question 238

Symptoms of PE

Answer 238

DYSPNOEAPleuritic chest PAINHYPOXAEMIApotential DVT sympHigh RISK:- HYPOTENSION- SYNCOPE- TACHYCARDIA- signs of R HF

Question 239

What is the first line test for HF

Answer 239

NT-proBNP(b-type naturetic peptide)

Question 240

Define atherosclerosis

Answer 240

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

Question 241

How long should a normal PR interval be

Answer 241

120 - 200 ms (3-5 mm)

Question 242

Normal width of QRS complex

Answer 242

110 - 120 ms (less than 3 mm)

Question 243

Which leads should the QRS complex be dominantly upright in normally

Answer 243

Leads I and II

Question 244

In which lead should all waves be negative

Answer 244

aVR

Question 245

Pattern of QRS complex from V1 to V6

Answer 245

• 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

Question 246

Normal state of ST segment

Answer 246

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

Question 247

Which leads should P waves and T waves be upright in

Answer 247

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

Question 248

In which leads should Q waves not really be visible

Answer 248

I, II, V2-V6

Question 249

Types of QRS abnormalities

Answer 249

• 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

Question 250

Types of Tachycardias

Answer 250

• 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

Question 251

Types of Bradycardias

Answer 251

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

Question 252

What are the 6 P’s of Arterial thrombosis/Peripheral arterial disease

Answer 252

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

Question 253

Causes of bradycardia

Answer 253

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

Question 254

Left bundle branch block

Answer 254

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 V6Characteristic ecg shape due to LV depolarising later than RVCaused by:- IHD- Valvular diseaseHeart sound 2 - reversed splitting

Question 255

Right bundle branch block

Answer 255

MaRRoW - M in v1, W in v6- RSR complex = M shape QRS complex in V1- Wide slurred S wave = W shape in V6Due to RV activation later than LVCaused by:- Pulm emboli- IHD- VSDWide physiological S2 splitting

Question 256

ECG of Hyperkalaemia

Answer 256

• Tall tented T waves- Flattened P waves- Broadening QRS- prolonged PReventual sine wave pattern

Question 257

Hypokalaemia ECG

Answer 257

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

Question 258

Hyper calcaemia ECG

Answer 258

QT shortening

Question 259

Hypocalcaemia ECG

Answer 259

QT prolongation

Question 260

What is a sign of an old STEMI

Answer 260

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

Question 261

In which leads would you typically see which types of MI

Answer 261

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

Question 262

What is Torsades de pointes

Answer 262

Condition caused by long QT syndromeRhythm may self-terminate or devolve into VFCharacterised 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)

Question 263

Causes/risk factors of torsades de pointes

Answer 263

• 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

Question 264

Treatment for torsades

Answer 264

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

Question 265

Normal P wave

Answer 265

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

Question 266

Abnormalities of P waves

Answer 266

• 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’

Question 267

PR interval abnormalities

Answer 267

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

Question 268

Normal QT interval when corrected for heart rate

Answer 268

380-450 ms

Question 269

What conditions can cause ST elevation

Answer 269

STEMI, pericarditis (SADDLE-SHAPED)myocarditis

Question 270

T wave abnormalities can indicate which main conditions

Answer 270

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

Question 271

What is the S1Q3T3 sign indicative of

Answer 271

Pulmonary EmbolismNeed to do CT angiogram to confirm

Question 272

What does Tall R waves on right leads and Tall S waves on left indicate

Answer 272

Pulmonary HTN

Question 273

Stable angina ECG

Answer 273

Mostly normal at rest- ST depression- T wave inversion

Question 274

Atrial flutter ECG

Answer 274

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

Question 275

Define peripheral vascular disease

Answer 275

Ischaemic disease of peripheral arteries

Question 276

Risk factors of PVD

Answer 276

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

Question 277

Pathophys of PVD

Answer 277

• 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/infectionWhen blood vessel is occluded:- Irreversible NERVE DAMAGE (within 6hr)- irreversible MUSCLE damage (6-10hr)- skin signs last to appear -> likely GANGRENOUS

Question 278

Symptoms of PVD

Answer 278

• 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

Question 279

Fontaine classification

Answer 279

1. Asymp2. INTERMITTENT CLAUDICATION - 2a = >200m of pain free walking - 2b = <200m of walking before pain starts3. CHRONIC limb ischaemia (pain at rest)4. ISCHAEMIC ULCERS -> GANGRENE

Question 280

Diagnosis of PVD

Answer 280

• 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 stenosisCT angiography if surgery considered - GOLD but invasive so less used

Question 281

Treatment of PVD

Answer 281

• 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

Question 282

Complications of PVD

Answer 282

• 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 + arrhythmiasIncreased risk of cerebrovasc/CVD accidents

Question 283

Define Long QT syndrome

Answer 283

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

Question 284

Causes of long QT syndrome

Answer 284

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

Question 285

Complication of Long QT

Answer 285

• 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)

Question 286

Types of cardiomyopathy

Answer 286

• HYPERTROPHIC- RESTRICTIVE- DILATEDThese are muscular/conduction defects of the myocardium

Question 287

Hypertrophic Cardiomyopathy aetiology

Answer 287

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

Question 288

Pathophys of hypertrophic cardiomyopathy

Answer 288

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

Question 289

resentation of Hypertrophic cardiomyopathy

Answer 289

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

Question 290

Diagnosis of Hypertrophic cardiomyopathy

Answer 290

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

Question 291

Treatment of hypertrophic cardiomyopathy

Answer 291

Anti-arrhythmics- B blocker- CCB- Amiodarone

Question 292

Dilated cardiomyopathy aetiology

Answer 292

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

Question 293

Pathophys of dilated cardiomyopathy

Answer 293

Thin cardiac walls poorly contract -> reduced cardiac output

Question 294

Sx of dilated cardiomyopathy

Answer 294

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

Question 295

diagnosis of dilated cardiomyopathy

Answer 295

• ECG- ECHO

Question 296

Tx of dilated cardiomyopathy

Answer 296

Treat underlying + complications e.g. AF, HF

Question 297

Restrictive cardiomyopathy pathophys + aetiology

Answer 297

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

Question 298

Sx of restrictive cardiomyopathy

Answer 298

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)

Question 299

Dx of restrictive cardiomyopathy

Answer 299

• ECG- ECHO- Cardiac catheterisation (definitive)

Question 300

Treatment of restrictive cardiomyopathy

Answer 300

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

Question 301

Define Malignant HTN + common patient

Answer 301

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

Question 302

Sx of malignant HTN

Answer 302

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

Question 303

Pathophysiology of HF

Answer 303

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 overloadHeart failure affecting both R+L circuits = CONGESTIVE HEART FAILURE

Question 304

Classification of HF

Answer 304

• 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

Question 305

Cardinal non-specific signs of HF

Answer 305

SOBASFat- SOB- Ankle Swelling- Fatigue

Question 306

Standard Pharm treatment for HF

Answer 306

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)

Question 307

Define cor pulmonale

Answer 307

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

Question 308

Tetralogy of Fallot pathophys

Answer 308

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.

Question 309

Investigations Tetralogy of Fallot

Answer 309

• CXR - BOOT SHAPED HEART- ECHOInfants 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)

Question 310

Treatment of ToF

Answer 310

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

Question 311

Coarctation of Aorta pathophys

Answer 311

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

Question 312

Investigations/treatment for Coarctation

Answer 312

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

Question 313

Atrial septal defect

Answer 313

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

Question 314

VSD

Answer 314

• L->R so NON CYANOTIC- risk of RVH + EISENMENGER’S later onSmall VSD = ASYMPLarge VSD:- exercise intolerence- failure to thrive- harsh pansystolic murmerDiagnosed on ECHOmay spontaneously close or may need SURGICAL closing

Question 315

Atrioventricular septal defect

Answer 315

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’sHard to treat

Question 316

Patent ductus arteriosus

Answer 316

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

Question 317

Define Rheumatic fever

Answer 317

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

Question 318

Epidemiology of Rheumatic fever

Answer 318

Almost exclusively in developing countries- esp in young people

Question 319

Pathophys of Rheumatic fever

Answer 319

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

Question 320

Sx of Rheumatic fever

Answer 320

• 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

Question 321

Dx of Rheumatic fever

Answer 321

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

Question 322

Criteria for Dx of Rheumatic fever

Answer 322

JONES CRITERIAMajor factors:- New murmur- Arthritis- Erythema nodosum- sydenham choreaMinor factors:- Pyrexia- raised CRP/ESR- arthralgiaDiagnosed if:- Recent S pyogenes infection + 2 major factors OR- 1 major + 2 minor factors

Question 323

Treatment of Rheumatic fever

Answer 323

• Abx: - IV BENZYLPENICILLIN STAT, then PHENOXYPENICILLIN for 10 daysFor sydenham chorea - HALOPERIDOL

Question 324

Define Eisenmenger’s syndrome

Answer 324

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

Question 325

Management of 1st onset AFib

Answer 325

If presenting within 48hrs and haemodynamically stable -> IV HEPARIN + IMMEDIATE CARDIOVERSIONIf 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

Question 326

4 categories of shock + examples of each

Answer 326

• 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

Question 327

Define shock

Answer 327

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

Question 328

Recognising shock

Answer 328

• 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 outputIf hypotension is prolonged can cause life threatening organ failure after acute emergency recovery

Question 329

Hypovolemic shock

Answer 329

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

Question 330

Septic shock

Answer 330

Caused by uncontrolled bacterial infectionsPresents with pyrexia, warm peripheries + tachycardic, BOUDING PULSEManage with ABCDE - give broad spec ABx

Question 331

Cardiogenic shock

Answer 331

Caused by failure of heart pump: MI, tamponade, pulm emboliPresents with signs of HF, RAISED JVP, S4 is presentManage with ABCDE + treat underlying cause

Question 332

Anaphylactic shock

Answer 332

Caused by IgE mediated Type 1 hypersensitivity reaction against an allergen-> caused excess vasoDILATION + bronchoCONSTRICTION 0> REDDUCED MEAN ARTERIAL PRESSURE + HYPOXICPresents with HYPOTENSION + TACHYCARDIA- has URTICARIA, PUFFY FACE, flushing cheeksManage 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

Question 333

Neurogenic shock

Answer 333

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

Question 334

Which key organs are particularly at risk from shock

Answer 334

Kidney, Lung, Heart, Brain

Question 335

Investigations/management algorithm for sepsis

Answer 335

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