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Take 2: Electric Boogaloo > Phase 2 - Cardio > Flashcards

Phase 2 - Cardio Flashcards

1
Q

What is atrial fibrillation

A

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

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2
Q

What are the symptoms of atrial fibrillation

A

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

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3
Q

What are the risk factors for AFib

A
  • 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
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4
Q

Complications of AFib

A

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

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5
Q

Pathophysiology of AFib

A

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.

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6
Q

Progression/Types of atrial fibrillation

A

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

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7
Q

Diagnosis/tests for AF

A

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

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8
Q

Treatments for AF

A

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!

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9
Q

What is a CHA2DS2-VASc score

A

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

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10
Q

What is an ORBIT score

A

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)

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11
Q

Differential diagnosis of palpitations

A
  • ISCHAEMIC heart disease- HF- Cardiomyopathy- VALVE disease- Wolff-Parkinson-White syndrome (AVRT)DrugsLifestyle factors:- alcohol misuse- caffine, nicotine, heroin, amphetamines, ecstasy, cannabis
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12
Q

Atrial flutter vs Atrial fibrillation

A

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

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13
Q

ECG variations for heart/AV block

A

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)

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14
Q

What do the waves on ecg correlate to

A

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

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15
Q

Normal conduction pathway of heart

A
  • 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
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16
Q

What is an ECG

A

A summation of electrical activity/events in the cardiac cycle

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17
Q

Pacemakers of the heart

A

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

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18
Q

Standard calibration of ECG

A

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

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19
Q

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

A

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

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20
Q

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

A

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

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21
Q

Types of congenital heart disease

A

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

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22
Q

Risk factors for congenital heart disease

A

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

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23
Q

How are congenital heart defects classified

A

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?

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24
Q

Which heart defects cause left right shunt

A
  • 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
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25
Q

Which heart defects cause right-left shunt

A

Tetralogy of FallotTricuspid atresia (abnormal narrowing)

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26
Q

Which heart defects have no shunt

A
  • 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)
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27
Q

Which are acute coronary syndromes

A

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

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28
Q

Clinical classification/presentation of unstable angina

A

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)

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29
Q

Diagnosis of unstable angina

A

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

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30
Q

Treatments for unstable angina

A

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))

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31
Q

STEMI vs NSTEMI

A

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

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32
Q

Risk factors for unstable angina (and cvd in general)

A

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

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33
Q

Diagnosis of myocardial infarction

A

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

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34
Q

What is the importance of Left bundle branch block

A

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)

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35
Q

Q wave vs non Q wave MI on ecg

A

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

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36
Q

Clinical presentation of MI

A
  • 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
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37
Q

Risk of mortality associated with MI

A
  • 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
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38
Q

Immediate management of MIs

A

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

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39
Q

Hospital management of MI

A

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

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40
Q

Causes of acute coronary syndromes

A

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

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41
Q

What is troponin? When is it positive

A

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

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42
Q

What is the physiological effect of aspirin

A

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

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43
Q

How does thrombin generation play a role in arterial thrombosis

A

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

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44
Q

Name some P2Y12 antagonists

A

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

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45
Q

What is the role of P2Y12 inhibitors

A

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

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46
Q

Name 3 GPIIb/IIIa antagonists

A

AbciximabTirofibanEptifibatide

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47
Q

What is the role of GPIIb/IIIa antagonists

A

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

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48
Q

What is the role of anticoagulants for ACS management

A

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)

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49
Q

Which drug is used in NSTEMI before doing a coronary angiography

A

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

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50
Q

What drug is used during PCI for ACS treatment

A

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)

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51
Q

When may fibrinolytic therapy be used in ACS

A

For an acute STEMI if primary PCI is not available

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52
Q

Which fibrinolytic drugs may be used for STEMI

A

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

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53
Q

Which drugs are used in secondary prevention of ACS

A

STATINSACE inhibitorsBeta blockersAldosterone antagonist (SPIRONOLACTONE, EPLERONONE)

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54
Q

which factors affect response to clopidogrel

A

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

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55
Q

What are the adverse effects of P2Y12 inhibitors

A

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

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56
Q

What are the adverse effects of ticagrelor specifically

A

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

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57
Q

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

A

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

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58
Q

How long would you continue antiplatelet therapy after an MI

A

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

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59
Q

What is primary PCI

A

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

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60
Q

When is revascularisation done for NSTE ACS

A

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

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61
Q

What are the types of revascularisation procedures

A

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

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62
Q

When may patients have ACS without obstructive coronary artery disease

A
  • 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)
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63
Q

General ACS management overview

A

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

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64
Q

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

A

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

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65
Q

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

A

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

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66
Q

What are the intrinsic exacerbating factors of angina/IHD?

A

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

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67
Q

What are environmental exacerbating factors for angina

A

ExerciseCold weatherHeavy meals (blood diverted to stomach)Emotional stress

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68
Q

Pathophysiology of angina/myocardial ischaemia

A

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

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69
Q

What physics equations relate to blood vessel function

A

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

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70
Q

How does the body normally adapt to increased exertion

A

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

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71
Q

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

A

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

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72
Q

What is the relevance of the epidemiology of stable angina

A

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)

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73
Q

Symptoms of angina

A

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

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74
Q

Differential diagnoses of chest pain

A

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

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75
Q

Treatment of angina

A
  • 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
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76
Q

How do you diagnose angina

A
  • 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
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77
Q

Pros and cons of CT coronary angiography

A
  • Non-invasive-Good RULE-OUT TEST and for spotting severe disease- Poor resolution - not good at seeing moderate disease well- Anatomical, not functional
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78
Q

Pros and cons of exercise testing (for heart issues)

A

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.)

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79
Q

What is a myoview scan

A

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

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80
Q

What is a stress echo test for heart problems

A

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

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81
Q

Pros and cons of perfusion MRI for heart issues

A

BEST non invasive test- good sensitivity and specificityNot available everywhere

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82
Q

Pros and cons of cor angiography

A
  • Good sensitivity- Gold standard treatment for more serious CAD- Invasive- ANatomical, not functional
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83
Q

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

A

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)

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84
Q

Side effects and contraindications of beta blockers

A

BradycardiaCold peripheralsErectile dysfunctionTirednessNightmaresDO NOT USE IN SEVERE ASTHMA

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85
Q

Side effect of nitrates

A

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

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86
Q

Side effects of calcium channal blockers

A

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

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87
Q

Aspirin - function, side effects, when is it used

A

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

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88
Q

What are ACE inhibitors usually used for

A

Hypertension and DM treatment- esp if they also have IHD

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89
Q

Which blood vessels are used for CABG

A

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

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90
Q

pros and cons of PCI

A

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

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91
Q

Pros and cons of CABG (coronary artery bypass graft)

A

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)

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92
Q

PCI vs CABG use for acute and chronic coronary syndromes

A

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

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93
Q

Physiology of the pericardium in relation to pathology

A

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

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94
Q

How does a chronic pericardial effsuion occur

A

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

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95
Q

What is acute pericarditis

A

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

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96
Q

How is acute pericarditis clinically diagnosed

A

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

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97
Q

Epidemiology of pericarditis

A

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

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98
Q

Clinical presentation of pericarditis

A

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

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99
Q

Aetiology of pericarditis (causes) - infectious reasons

A

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)

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100
Q

Non-infectious aetiology of pericarditis

A

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

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101
Q

Differential diagnosis for pericarditis

A
  • MI/MYOCARDIAL ISCHAEMIA-AORTIC DISSECTION- Pneumonia- Pleurisy- Pulmonary Embolus- Pneumothorax- Costochondritis (inflammation at rib-sternum joint)- Gastro-oesophageal reflux- peritonitis- Pancreatitis- Herpes zoster (shingles)
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102
Q

Investigations/examination for pericarditis

A

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

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103
Q

What does pericardial rub sound like

A

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

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104
Q

What are the clinical signs of pericardial effusion

A

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

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105
Q

What does the ECG look like in pericarditis

A

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

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106
Q

Blood tests done for pericarditis

A

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

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107
Q

What does CXR look like in pericarditis

A
  • often normal in idiopathic- pneumonia common if bacterial- enlargement of cardiac silhouette can suggest effusion (only detectable at >300ml)
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108
Q

What is a complication of pericardial effusion

A

cardiac tamponade

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109
Q

What is cardiac tamponade

A

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

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110
Q

What can cause cardiac tamponade

A

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

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111
Q

Signs of tamponade

A

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

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112
Q

Why may pulsus paradoxus not be present in pericardial effusion

A

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

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113
Q

Management of pericarditis

A

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

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114
Q

Prognosis of pericarditis

A
  • 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
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115
Q

How much does colchicine reduce recurrence rate

A

50%

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116
Q

How can risk of developing constriction in pericarditis be classified

A

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

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117
Q

What is a treatment given for Tuberculous effusion TB pericarditis

A

Pericardectomy (~50% 5 year survival)

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118
Q

What is the name of post cardiac injury syndromes

A

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

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119
Q

What is atherosclerosis?

A

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)

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120
Q

Risk factors for atherosclerosis

A

AgeFAMILY HISTORYHIGH SERUM CHOLESTEROLTOBACCO SMOKINGHYPERTENSIONDIABETES Obesity

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121
Q

Distribution of atherosclerotic plaques within body

A

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

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122
Q

What is neointima

A

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

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123
Q

What does the structure of an atherosclerotic plaque consist of

A

LipidNECROTIC COREConnective tissueFIBROUS CAP

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124
Q

What is the response to injury hypothesis of atherosclerosis

A

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

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125
Q

What 2 things primarily cause inflammation of arterial wall in atherosclerosis

A

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

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126
Q

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

A

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.

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127
Q

Which inflammatory cytokines are found in plaques

A

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)

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128
Q

What are the stages of atherosclerosis

A

Fatty streaksIntermediate lesionsFibrous plaques OR Advanced lesionsPlaque rupture OR Plaque erosion

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129
Q

What do fatty streaks consist of and when do they appear

A

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

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130
Q

What are intermediate atherosclerotic lesions composed of

A

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

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131
Q

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

A

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

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132
Q

What is the fibrous cap of an atherosclerotic plaque made of

A

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

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133
Q

What occurs in plaque rupture

A

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

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134
Q

When does plaque erosion occur

A

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

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135
Q

Plaque rupture vs plaque erosion

A

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

136
Q

Red thrombus vs white thrombus

A

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

137
Q

What are neutrophil extracellular traps (NET)?

A

Extruded DNA and enzymes which cause cell activation and cytokine release

138
Q

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

A

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

139
Q

Main treatment of CAD

A

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

140
Q

example of drug on stents

A

Sirolimus

141
Q

What doe PCSK9 inhibitors do

A

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

142
Q

Stages of hypertension severity diagnosing criteria

A

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

143
Q

When are antihypertensive drugs offered to patients

A

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

144
Q

What are BP targets for patients with hypertension

A

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

145
Q

What is infective endocarditis

A

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

146
Q

Types of infective endocarditis

A

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

147
Q

Epidemiology of IE

A

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

148
Q

Risk factors for IE

A
  • 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
149
Q

Clinical presentation of IE

A

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

150
Q

What types of peripheral stigmata can you get with IE

A

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)

151
Q

Diagnosis of IE

A
  • 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
152
Q

What are the 2 types of echo

A

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

153
Q

Treatment of IE

A

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

154
Q

When is surgery required for IE

A

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

155
Q

What is sometimes recommended to prevent IE

A

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

156
Q

What is Aortic Stenosis

A

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)

157
Q

What is the normal area of the aortic valve

A

3-4 cm^2

158
Q

Aetiology/causes of AS

A

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)

159
Q

Pathophysiology of AS

A

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.

160
Q

Clinical presentation of AS

A

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

161
Q

Physical signs of AS

A

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

162
Q

Natural history of AS

A

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

163
Q

Prognosis of AS

A

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

164
Q

Investigation of AS

A

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

165
Q

Grading of AS (using AVA)

A

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

166
Q

Management/treatment of AS

A

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)

167
Q

When are interventions for AS indicated

A
  • 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
168
Q

Define mitral regurgitation

A

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

169
Q

Aetiology of Chronic MR

A

Myxomatous degeneration (causes MV prolapse)Ischaemic MRRheumatic heart diseaseIE

170
Q

What does myxomatous mean

A

soft tumour made of gelatinous connective tissue

171
Q

Types of MR

A
  • from Prolapse- ruptured chordae tendoni - typically from MI- annulus dilation (gap forms between cusps) - typically from Heart failure
172
Q

Pathophysiology of MR

A

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

173
Q

Signs and symptoms of MR

A

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

174
Q

Natural history of MR

A

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

175
Q

Investigations for MR

A

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

176
Q

Management/treatment of MR

A

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

177
Q

When is surgery indicated in severe MR

A

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

178
Q

Define aortic regurgitation

A

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

179
Q

Etiology of chronic AR

A

Bicuspid valveRheumatic heart diseaseIE

180
Q

Pathophysiology of AR

A

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

181
Q

Physical signs of AR

A

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

182
Q

Natural history of AR

A

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

183
Q

DIagnostic investigation of AR

A

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

184
Q

Management of AR

A

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

185
Q

When is surgery indicated for AR

A

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

186
Q

Define mitral stenosis

A

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

187
Q

Normal mitral valve area

A

4-6 cm^2

188
Q

Etiology of Mitral Stenosis

A

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

189
Q

Pathophysiology of Mitral S

A

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

190
Q

Natural history of MS

A

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

191
Q

Signs of MS

A

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

192
Q

DIagnostic investigation of Mitral S

A

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

193
Q

Management of mitral s

A

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

194
Q

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

A

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

195
Q

Indications for Mitral valve replacement

A

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

196
Q

What is Heart failure

A

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)

197
Q

NYHA class grading of HF

A

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

198
Q

What are the different types of HF

A

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)

199
Q

Normal EF for male and female

A

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

200
Q

Aetiology/risk factors of HF

A

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

201
Q

What does cardiomyopathy mean in particular

A

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.

202
Q

Basic epidemiology of HF

A

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

203
Q

Signs and symptoms of HF

A

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

204
Q

Causes of acute decompensation of chronicheart failure

A

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

205
Q

Diagnosis of HF

A

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)

206
Q

Treatment for HF

A

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

207
Q

What is AVRT

A

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

208
Q

What is AVNRT

A

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

209
Q

symptoms of avrt/avnrt

A

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

210
Q

Treatment of avrt/avnrt

A

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

211
Q

Complications of AVRT/AVNRT

A

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

212
Q

What is pre-excitation

A

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

213
Q

What is prinzmetal angina

A

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

214
Q

What is aortic dissection

A

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

215
Q

Presentation of aortic dissection

A

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

216
Q

Diagnosis of Aortic dissection

A

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

217
Q

Treatment of aortic dissection

A

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

218
Q

Define Abdominal aortic aneurysm

A

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

219
Q

Presentation/symptoms of AAA

A

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

220
Q

Risk factors for AAA

A
  • 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
221
Q

Diagnosis of AAA

A
  • 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
222
Q

Treatment for AAA

A

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

223
Q

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

A
  • 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)
224
Q

What might make you unfit for surgery

A

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.)

225
Q

Complications for aortic aneurysm

A

Rupture and Haemorrhage

226
Q

Define Hypertension

A

BP >= 140/90 mmHg

227
Q

Aetiology/risk factors for HTN

A

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)

228
Q

Diagnostic investigations for HTN

A

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

229
Q

Treatment for HTN

A

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

230
Q

Complications of high BP

A

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

231
Q

Define Deep vein thrombosis

A

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

232
Q

RIsk factors for DVT

A
  • 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)
233
Q

How can could cancer cause DVT

A
  • could ACTIVATE COAG SYSTEM- COMPRESS/BLOCK flow- some chemo/bio agents e.g. EPO, Thalidomide- vasc acess devices increase risk
234
Q

SIgns/symptoms of DVT

A

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

235
Q

Diagnosis of DVT

A

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)

236
Q

Treatment of DVT

A

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

237
Q

Complications of DVT

A

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

238
Q

Symptoms of PE

A

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

239
Q

What is the first line test for HF

A

NT-proBNP(b-type naturetic peptide)

240
Q

Define atherosclerosis

A

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

241
Q

How long should a normal PR interval be

A

120 - 200 ms (3-5 mm)

242
Q

Normal width of QRS complex

A

110 - 120 ms (less than 3 mm)

243
Q

Which leads should the QRS complex be dominantly upright in normally

A

Leads I and II

244
Q

In which lead should all waves be negative

A

aVR

245
Q

Pattern of QRS complex from V1 to V6

A
  • 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
246
Q

Normal state of ST segment

A

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

247
Q

Which leads should P waves and T waves be upright in

A

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

248
Q

In which leads should Q waves not really be visible

A

I, II, V2-V6

249
Q

Types of QRS abnormalities

A
  • 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
250
Q

Types of Tachycardias

A
  • 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
251
Q

Types of Bradycardias

A

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

252
Q

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

A
  • 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
253
Q

Causes of bradycardia

A
  • Conduction tissue fibrosis- Ischaemia- Inflam/infiltrative disease- Drugs
254
Q

Left bundle branch block

A

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

255
Q

Right bundle branch block

A

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

256
Q

ECG of Hyperkalaemia

A
  • Tall tented T waves- Flattened P waves- Broadening QRS- prolonged PReventual sine wave pattern
257
Q

Hypokalaemia ECG

A
  • Flattening/SMALL INVERTED T wave- ST depression- Narrow QRS- PR prolongation- PROMINANT U waves- QT prolongation (less significant signs)
258
Q

Hyper calcaemia ECG

A

QT shortening

259
Q

Hypocalcaemia ECG

A

QT prolongation

260
Q

What is a sign of an old STEMI

A

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

261
Q

In which leads would you typically see which types of MI

A

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

262
Q

What is Torsades de pointes

A

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)

263
Q

Causes/risk factors of torsades de pointes

A
  • 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
264
Q

Treatment for torsades

A
  • Treatunderlying- Magnesium- Heart rate increasing meds if still getting torsades??- Defibrillation
265
Q

Normal P wave

A
  • Pos inferior leads- Pos lead I- neg aVR- Biphasic V1- <120 ms wide- <0.3mV (3 small squares) tall
266
Q

Abnormalities of P waves

A
  • 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’
267
Q

PR interval abnormalities

A
  • PROLONGED: - disorders of AV node/specialised conducting tissue- SHORTER: - Younger patients - PRE-EXCITATION (wolf-parkinson-white)
268
Q

Normal QT interval when corrected for heart rate

A

380-450 ms

269
Q

What conditions can cause ST elevation

A

STEMI, pericarditis (SADDLE-SHAPED)myocarditis

270
Q

T wave abnormalities can indicate which main conditions

A

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

271
Q

What is the S1Q3T3 sign indicative of

A

Pulmonary EmbolismNeed to do CT angiogram to confirm

272
Q

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

A

Pulmonary HTN

273
Q

Stable angina ECG

A

Mostly normal at rest- ST depression- T wave inversion

274
Q

Atrial flutter ECG

A
  • SAW TOOTH pattern - P and T merge to make F waves- 2:1 ratio (2 f waves for every QRS)
275
Q

Define peripheral vascular disease

A

Ischaemic disease of peripheral arteries

276
Q

Risk factors of PVD

A
  • SMOKING- HTN - CKD- Aging- Obesity- T2DM
277
Q

Pathophys of PVD

A
  • 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
278
Q

Symptoms of PVD

A
  • 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
279
Q

Fontaine classification

A
  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
280
Q

Diagnosis of PVD

A
  • 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
281
Q

Treatment of PVD

A
  • 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
282
Q

Complications of PVD

A
  • 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
283
Q

Define Long QT syndrome

A

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

284
Q

Causes of long QT syndrome

A
  • Romano Ward Syndrome (Autosomal dominant)- Jervell and Lange-Nielsen Syndrome (autosomal recessive)- Hypokalaemia- Hypocalcaemia- Drugs: AMIODARONE, MAGNESIUM
285
Q

Complication of Long QT

A
  • 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)
286
Q

Types of cardiomyopathy

A
  • HYPERTROPHIC- RESTRICTIVE- DILATEDThese are muscular/conduction defects of the myocardium
287
Q

Hypertrophic Cardiomyopathy aetiology

A

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

288
Q

Pathophys of hypertrophic cardiomyopathy

A

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

289
Q

resentation of Hypertrophic cardiomyopathy

A
  • potentially SUDDEN DEATH (esp at younger age)- Chest pain- Palps- SOB- Syncope
290
Q

Diagnosis of Hypertrophic cardiomyopathy

A
  • ECG (1st LINE)- ECHO (DEFINITIVE)- genetic testing
291
Q

Treatment of hypertrophic cardiomyopathy

A

Anti-arrhythmics- B blocker- CCB- Amiodarone

292
Q

Dilated cardiomyopathy aetiology

A

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

293
Q

Pathophys of dilated cardiomyopathy

A

Thin cardiac walls poorly contract -> reduced cardiac output

294
Q

Sx of dilated cardiomyopathy

A
  • SOB- HF (filling up + backing up)- AFib- Thromboemboli (not effectively pussing blood -> stasis)
295
Q

diagnosis of dilated cardiomyopathy

A
  • ECG- ECHO
296
Q

Tx of dilated cardiomyopathy

A

Treat underlying + complications e.g. AF, HF

297
Q

Restrictive cardiomyopathy pathophys + aetiology

A

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

298
Q

Sx of restrictive cardiomyopathy

A

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)

299
Q

Dx of restrictive cardiomyopathy

A
  • ECG- ECHO- Cardiac catheterisation (definitive)
300
Q

Treatment of restrictive cardiomyopathy

A

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

301
Q

Define Malignant HTN + common patient

A

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

302
Q

Sx of malignant HTN

A
  • HF (LVH)- Blurred vision (PAPILLOEDEMA, Retinal haemorrhage)- Haematuria + renal failure (glomerulonephritis)- Headache (RISK OF CEREBRAL HAEMORRHAGE)
303
Q

Pathophysiology of HF

A

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

304
Q

Classification of HF

A
  • 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
305
Q

Cardinal non-specific signs of HF

A

SOBASFat- SOB- Ankle Swelling- Fatigue

306
Q

Standard Pharm treatment for HF

A

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)

307
Q

Define cor pulmonale

A

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

308
Q

Tetralogy of Fallot pathophys

A

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.

309
Q

Investigations Tetralogy of Fallot

A
  • 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)
310
Q

Treatment of ToF

A

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

311
Q

Coarctation of Aorta pathophys

A

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

312
Q

Investigations/treatment for Coarctation

A
  • 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
313
Q

Atrial septal defect

A
  • 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
314
Q

VSD

A
  • 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
315
Q

Atrioventricular septal defect

A

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

316
Q

Patent ductus arteriosus

A

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

317
Q

Define Rheumatic fever

A

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

318
Q

Epidemiology of Rheumatic fever

A

Almost exclusively in developing countries- esp in young people

319
Q

Pathophys of Rheumatic fever

A
  • 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
320
Q

Sx of Rheumatic fever

A
  • 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
321
Q

Dx of Rheumatic fever

A

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

322
Q

Criteria for Dx of Rheumatic fever

A

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

323
Q

Treatment of Rheumatic fever

A
  • Abx: - IV BENZYLPENICILLIN STAT, then PHENOXYPENICILLIN for 10 daysFor sydenham chorea - HALOPERIDOL
324
Q

Define Eisenmenger’s syndrome

A

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

325
Q

Management of 1st onset AFib

A

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

326
Q

4 categories of shock + examples of each

A
  • 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
327
Q

Define shock

A

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

328
Q

Recognising shock

A
  • 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
329
Q

Hypovolemic shock

A

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)

330
Q

Septic shock

A

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

331
Q

Cardiogenic shock

A

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

332
Q

Anaphylactic shock

A

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

333
Q

Neurogenic shock

A

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)

334
Q

Which key organs are particularly at risk from shock

A

Kidney, Lung, Heart, Brain

335
Q

Investigations/management algorithm for sepsis

A

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

Take 2: Electric Boogaloo (20 decks)

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