Cardiology - AS Flashcards

Question

2nd degree heart block - Wenckebach/Mobitz I?

Answer 1

- Progressive lengthening of PR interval - One non-conducted P wave - Next conducted beat has shorter PR interval

Answer 2

Constant PR Occasional non-conducted P wave - Often wide QRS - Block is usually in bundle branches of Purkinje fibres.

Answer 3

Two P waves per QRS | Normal consistent PR intervals.

Answer 4

P waves and QRS @ different rates - Dissociation Abnormally shaped QRS - Ventricular origin (40bpm)

Answer 5

MaRRoW Wide QRS RSR pattern in V1. qRs in V6.

Answer 6

``` Infarct - inferior MI Normal Variant Congenital - ASD, VSD, Fallot's Hypertrophy - RVH (PE, Cor Pulmonale). PE ```

Answer 7

WiLLiaM Wide QRS with Notched at top T wave inversion in Lateral leads.

Answer 8

Fibrosis LVH - AS, HTN Infarct - Inferior MI Coronary HD

Answer 9

RBBB + Left anterior fascicular block (RBBB + left anterior hemiblock)

Answer 10

RBBB + LAFB + 1st Degree AV block. (3rd not 1st I think)

Answer 11

SAN fails to depolarise Abnormal P wave Normal QRS 60-80bpm

Answer 12

Usually no P waves (occasionally after QRS) Normal QRS 40-60bpm.

Answer 13

Usually result of complete AV Block therefore regular P waves seen. May be SAN Failure --> No P waves. Wide QRS 20bpm

Answer 14

Abnormal P wave | Normal QRS

Answer 15

P wave buried in QRS or sometimes immediately before/after QRS. May be negative. Normal QRS

Answer 16

No P waves | Wide QRS and abnormal T waves.

Answer 17

``` AV Nodal Re-entrant tachycardia AVRT Atrial Tachycardia Atrial Flutter Atrial Fibrillation ```

Answer 18

P wave absent or immediately before/after QRS. Normal QRS Episodic tachycardia with abrupt onset and termination; can be associated with symptoms of chest discomfort, dyspnoea, dizziness, or anxiety. Sensation of regular rapid pounding in the neck is suggestive of AV node re-tenrty.

Answer 19

P waves usually visible between QRS complexes. QRS may be narrow or wide. Accessory conduction bundle. May have suggestions of secondary cardiomyopathy - S3 gallop, RV heave, laterally displaced point of maximal impulse. ECG: Delta wave. WPW = Congenital accessory conduction pathways between atria and ventricles leading to AVRT. Can lead to LAD if right sided accessory pathway + vice versa. Type A = left sided pathway with dominant R in V1. - Medical management = sotalol (avoid if AF). - Definitive management = radiofrequency ablation of accessory pathway.

Answer 20

- Abnormally shaped P waves. - Normal QRS complexes - Rate > 150bpm - May be associated with AV block.

Answer 21

'Saw-toothed' baseline as atria contract @ 300 bpm. ``` AVN can't conducted >200. therefore AV block occurs. - 2:1 (150), 3:1 (100), 4:1 (75). Normal QRS. - Flutter waves may be visible following carotid sinus massage or adenosine ```

Answer 22

No P waves - irregular line | Irregularly irregular QRS.

Answer 23

VT Torsades VF

Answer 24

No P waves Regular, wide QRS No T waves Non-sustained VT is an ectopic ventricular rhythm with wide QRS complex, rate faster than 120 bpm, lasting for 3 beats and spontaneously resolving.

Answer 25

Torsades de pointes (twisting of the points) is a form of polymorphic VT associated with long QT interval. It may deteriorate into VF. Causes of Long QT (normal QT = 430ms in males and 450ms in males) - Congenital (Romano-Ward) Drugs - Antiarrhythmics: amiodarone, sotalol, class 1a - Tricyclic antidepressants - Antipsychotics - Chloroquine - Terfenadine - Erythromycin - Myocarditis Electrolyte abnormalities - hypocalcaemia, - hypokalaemia, - hypomagnesaemia - Hypothermia - Sub Haemorrhage Management with MgSO4 IV. if Torsades ``` Otherwise management = Avoid drugs that prolong QT or other precipitants. Beta blockers (sotalol may exacerbate QT syndrome). ```

Answer 26

Shapeless, rapid oscillations and no organised complexes.

Answer 27

VT more likely if - Hx - recent infarction - Atrioventricular dissociation - Broad QRS complexes (>140ms) - Concordant QRS direction in V1-V6 - Fusion and capture beats.

Answer 28

P mitrale | P pulmonale

Answer 29

Peaked P wave. Due to RAH (Pulmonary HTN, Tricuspid stenosis)

Answer 30

Broad, bifid P waves | - LAH (Mitral stenosis)

Answer 31

RVH LVH Narrow Broad

Answer 32

``` Tall R wave in V1 (Right for R1) Deep S wave in V6 RAD Normal QRS width May be T wave inversion in V1-V3 ``` - Aetiology from Cor pulmonale

Answer 33

- S wave in V1 and - R wave in V6 > 35mm - May be LAD - May be T wave inversion in II, aVL, V5, V6. ``` - Aetiology? HTN AS COA H(o)CM ```

Answer 34

Accessory conducting bundle Short PR interval Slurred upstroke of QRS called a Delta wave (V3/V4) Can establish re-entrant circuit --> SVT (antidromic AVRT) AF + WPW --> irregularly irregular broad QRS complex.

Answer 35

Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac death. Presents with a RBBB block. Coved ST elevation in V1-V3 MAnagement: implantable cardioverter-defibrillator

Answer 36

Reverse Tick Sign - Down-sloping ST depression - T wave inversion

Answer 37

SI QIII TIII (rare). - Deep S wave in Lead 1 (RAD) - Pathological Q wave in III inverted T wave in III. (a hole in myocardium) - T wave inversion in III. Right ventricular strain - RAD (S wave in I) - Dominant R wave and T wave inversion in V1-V3

Answer 38

Tall Tented T waves Widened QRS Absent P waves

Answer 39

In Hypokalaemia U have no Pot and no T, but a long PR and a long QT. ``` Small T waves ST Depression Prolonged QT interval >600ms Prominent U wave Sine wave present ``` Due to furosemide therapy?

Answer 40

DIVISIONS - Drugs (ABCD) = Antiarrhythmias (Amiodarone), B-blockers Ca-channel blockers (verapamil) Digoxin - Ishaemia/Infarction Inferior MI - Vagal Hypertonia Athletes, Vasovagal syncope, Carotid sinus syndrome - Infection Viral myocarditis Rheumatic fever Infective endocarditis - Sick sinus syndrome Structural damage or fibrosis of SAN, AVN or conducting tissue. PC - SVT alternating with either sinus f ± arrest or SA/AV block. Rx; bradyarrhythmia: pace Tachyarrhythmias: amiodarone. ``` - Infiltration: restrictive/dilated cardiomyopathy. Autoimmune Sarcoid Haemochromatosis Amyloid Muscular dystrophy ``` - O Hypothyroidism Hypokalaemia Hypothermia - Neuro: increased ICP - Septal defects: primum ASD - Surgery or catheterisation

Answer 41

- Sinus Bradycardia - 1st degree heart block: PR >200ms - Second degree heart block Wenkebach/Mobitz I Mobitz II - Complete Heart block Junctional: narrow QRS @ 50bpm Ventricular: broad QRS @ 40bpm Complete = Syncope, heart failure, bradycardia, wide pulse pressure, JVP: cannon waves. Bizarre wide inverted T waves seen in Stokes-Adams attack. (Syncope due to bradycardia)

Answer 42

If asymptomatic and rate >40: no management needed. Urgent/rate <40bpm (hemodynamically unstable, pale, sweating cold), syncope, heart failure MI. - Medical Atropine 0.6-1.2g (max 3g) IV Isoprenaline IVI. Can give up to 6 doses. Then use - Pacing: External If haemodynamically stable - Look for MI - Check TSH/infection - Check medications Elective - Permanent Pacing :Mobitz II, Complete AV block, Sick Sinus, AF, Drug-resistant tachyarrhythmias First degree heart block - PR >0.2. Asympomatic doesnt need treatment Second degree - Type 1 Mobitz Wenckebach - progressive prolongation of PR until dropped beat. - Type 2 - PR interval constant bu P wave is not followed by QRS.

Answer 43

Rate >100bpm, QRS width <120ms.

Answer 44

- Sinus Tachycardia - Atrial (AF, Atrial Flutter, Atrial Tachy) - AVRT - AVNRT

Answer 45

- If patient is compromised --> sedate + DC cardioversion = Shock, syncope, myocardial ischaemia, heart failure. = 3 shocks. - Otherwise ID rhythm and Rx according (if irregular rhythm = AF = Different Rx) - Vagal manoeuvres (carotid sinus massage, valsalva (supine + exhale forcefully against a closed glottis after normal inspiratory effort) transiently increased AV block and may unmask underlying atrial rhythm. - If manoeuvres unsuccessful, give adenosine while recording rhythm strip 6mg, then repeat again 12mg, then again 12 mg. Half-life of adenosine is 10s. Contraindicated in asthmatics - verapamil - -> Transient AV block, unmasking atrial rhythm - -> Cardioverts AVNRT/AVRT to sinus rhythm

Answer 46

- Assess with ABCDE - Give oxygen - Monitor ECG, BP, SpO2, record ECG - Treat reversible causes If patient is unstable/MI/shock --> DC shock. Then consider amiodarone 300mg IV over 10-20 mins + repeat shock. If stable and QRS narrow, is rhythm regular? Yes - Use vagal manoeuvres, then 6mg adenosine IV bolus if unsucessful, give 12mg, then a further 12mg, continuous ECG monitoring. Consider lidocaine but use with caution in severe left ventricular impairment. Can also use procainamide. No - Irregular narrow complex tachy - AF - Control rate with B-blocker, consider digoxin/amiodarone. if sinus rhythm restored probs Re-entry paroxysmal SVT. If not restored - Possible atrial flutter - Control rate with B-blocker + Seek expert help.

Answer 47

MOA: temporary AVN block SEs: Transient chest tightness, dyspnoea, flushing, headache, bronchospasm Relative CIs: **asthma**, 2nd/3rd degree heart block. Interactions - fx of drug increased by dipyridimole - fx decreased by theophylline. Adenosine half-life is less than 10 sec, central route or large-calibre vein needed. Insert large-bore 16G cannula. Patients with SVT are treated with IV Adenosine

Answer 48

1st line: B-B - AVRT: flecainide wpw - AVNRT: verapamil

Answer 49

Control rate with B-blockers (metoprolol) or digoxin - If onset <48hrs cardioversion with amiodarone or DC shock - Consider anticoagulation with DOAC

Answer 50

- AF/fduke with WPW or Hx of WPW. --> VF. | - Use Amiodarone or flecainide.

Answer 51

Definition: Rate >100bpm, QRS width >120ms.

Answer 52

VT Torsades de Pointes SVT with BBB VT can be monomorphic - caused by MI Polymorphic: TdP.

Answer 53

Most important cause - Hypokalaemia Then Hypomagnesaemia I'M QVICK - Infarction (esp with ventricular aneurysm) - Myocarditis - QT interval increased - Valve abnormality: mitral prolapse, AS - Iatrogenic: Digoxin, antiarrhythmics, catheter - Cardiomyopathy (dilated) - Potassium decreased, Mg decreased, Oxygen decreased, acidosis

Answer 54

- Check the pulse? If no pulse start CPR (30:2) - Then get O2 and IV Access - Check for adverse signs (BP <90, HF, Chest Pain, decreased consciousness, HR >150) - If there are adverse signs - Must consider cardioversion! (sedation --> synchronised cardioversion: 1. 200 2. 300 3. 360 Then give Amiodarone (300mg over 20-60m, then 900mg over next 23hr. Give adrenaline at the same time. at the 3rd shock. Then every 3-5 mins. If no adverse signs - Correct electrolyte problems - Decreased K?: max 60mM KCL @ 20mmol/h - Decreased Mg: 4ml 50% MgSO4 in 30mins ``` Then assess the rhythm - Regular (ie VT) Amiodarone or lignocaine 50mg over 2mins - Irregular Dx is usually: AF with BBB Pre-excited AF: flec/amio Torsades de pointes: MgSO4 2g IV over 10mins ``` - Failure - Synchronised Cardioversion If in Asystole/PEA: give adrenaline 1mg. Treat with 2 mins of CPR.

Answer 55

LA Loses refractoriness before the end of atrial systole --> recurrent, uncoordinated contractions @300-600bpm. Promotes atrial re-entry. - Atrial contraction responsible for 25% of Cardiac output, therefore often triggers heart failure. - General guide - offer rate control as first-line for AF except in those with reversible causes of AF, though with HF and AF, New onset AF.

Answer 56

Common - IHD - Rheumatic Heart Disease - Thyrotoxicosis - HTN Others - Alcohol - Pneumonia - PE - Post-op - Hypokalaemia - RA

Answer 57

- Asymptomatic - Chest pain - Palpitations - Dyspnoea - Faintness

Answer 58

- Irregularly irregular pulse - Pulse deficit: difference between pulse and HS Fast AF --> Loss of diastolic filling --> no palpable pulse - Signs of LVF

Answer 59

- ECG - Holter Monitor - records ECG for 24,48,72hrs. - If this doesn't work can use an external loop recorder - FBC, U+E, TFTs, Trop - Consider TTE: structural abnormalities

Answer 60

Patient's symptoms are from rapid ventricular response, therefore dramatic improvement when ventricular rate is slowed. 1) Aim to prevent systemic embolisation 2) choose rate or rhythm - Haemo unstable --> Emergency cardioversion. IV Amiodarone 2nd line. - Treat underlying cause. When stable - 1) Control Ventricular Rate 1st line - BB or CCB (Bisoprolol, Dilitiazem or verapamil or metoprolol). (slow AVN conduction and reduce rate). 2nd line - Digoxin or amiodarone. -2) Embolisation prevention with antithrombolitic therapy - anticoagulate with LMWH or DOAC - dabigatran/apixaban -3) Cardioversion: only if acute AF Electrical cardioversion or pharmacological 1st: Flecainide (if no structural heart disease) - 200-300mg 2nd: Amiodarone -150mg IV over 10 mins, 1mg/min infusion for 6hrs. If structural heart disease present. Long-term anticoagulation not needed if sinus restored no RFs (0 CHADSVAS) + low recurrence risk.

Answer 61

- Self-limiting, <7 days, recurs. - Anticoagulate: use CHADSVAS - Management: pill in pocket 'Flecainide, propafenone' - Prevention: B-Blocker, Sotalol (rhythm control) , amiodarone, or CCB (diltiazem, verapamil).

Answer 62

>7 days, may recur even after cardioversion.

Answer 63

Try rhythm control first-line if - Symptomatic or CCF - Presenting first time with lone AF - Secondary to treated precipitant. Has a reversible cause. Rate control favour - Older than 65 - History of IHD

Answer 64

TTE first: structural abnormalities - Anticoagulate with warfarin for >3weeks - Pre-Rx >4 weeks with sotalol or amiodarone if increased risk of failure - Electrical or pharmacological cardioversion. - >4 weeks anticoagulation afterwards (target INR 2.5) Maintenance antiarrhythmic - Not needed if successfully treated precipitant - 1st line - B-Blocker (bisoprolol, metoprolol) - 2nd line: amiodarone Other options for rhythm control - Radiofrequency ablation of AV node - Maze procedure - Pacing Rate control (target <90) - 1st line: B-Blocker or rate limiting CCB (not both) - 2nd line: add digoxin (don;t use as monotherapy) - 3rd line: consider amiodarone

Answer 65

- Failed cardioversion/unlikely to succeed - AF > 1yr, valve disease, poor LV function - Patient doesnt want cardioversion - -> Rate control

Answer 66

CHA2-DS2-VAS score determines the necessity of anticoagulation in AF? Do remember that if a patient with AF has a stroke or TIA - anticoagulant of choice should be warfarin or direct thrombin or factor Xa inhibitor such as Apixaban. Most times it is rivaroxaban A patient with an acute stroke should have anticoagulation started 2 weeks after the event. This is due to the haemorrhagic transformation. They should then be on lifelong anticoagulation to prevent risk of stroke.

Answer 67

Assess haemodynamic stability + need for emergent cardioversion . Then evaluation? Cardioversion? --> Yes or No depending on haemodynamic stability. If AF <48hr cardiovert, if unknown, anticoagulate for 4 weeks before DC current. Pre-cardioversion anticoag not required if transoesophageal echo shows no thrombus in left atrial. Rate control --> use beta blockers or CCB as fast line (<80bpm). Consider digoxin or diltiazem Anticoagulation - Use CHAD2DS2-VASc score and risk of bleeding with HAS-BLED score - >2 is anticoagulate. If anticoagulating - Consider Warfarin, or DOACs (Dabigatran, Rivaroxaban, Apixaban). If no - offer no treatment (previously offered aspirin)

Answer 68

``` CCF HTN Age >75 (2 points) DM Stroke or TIA (2 points) ``` VAS - Vascular - Age (65-75) - Sex: female Warfarin CI in AF (Bleeding diathesis, decreased platelets, BP >160/90, poor compliance. Dabigatran may be cost-effective alternative. 0: aspirin 300mg > or equal 1: Warfarin (target INR = 2-3)

Answer 69

Likelihood of haemorrhage and anticoagulation bleeding risk.

Answer 70

``` HTN Abnormal Renal Function + liver Function Stroke Bleeding Labile INR Elderly (Older than 65) Drugs + alcohol. ``` >3 or more indicates patient has a high likelihood of haemorrhage

Answer 71

ACS = Unstable angina + evolving MI Divided into - ST Elevation or New Onset LBBB (STEMI) - NSTEMI (myocardial damage) - Unstable angina (no presence of myocardial damage)

Answer 72

Incidence 5/1000 for STEMI

Answer 73

Plaque rupture, thrombosis and inflammation. | Rarely due to coronary spasm

Answer 74

``` HTN DM Smoking Increased cholesterol Obesity ```

Answer 75

Age Male FH (MI <55yrs)

Answer 76

- Acute central/left chest pain > 20mins - Radiates to left jaw or arm - Nausea - Sweating - Dyspnoea - Palpitations Can also get silent MIs in elderly/diabetics - Syncope - Delirium - Post-op oliguria/hypotension Patient presenting with chest pain - Give GTN, Aspirin and do ECG. Refer patient with current chest pain or chest pain in last 12 hrs with abnormal ECG (emergency). Chest pain 12-72hrs ago, refer to hospital for same day assessment. chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

Answer 77

- Anxiety - Pallor swearing - Pulse tachy/brady - BP Hyper/hypo - 4th heart sound - Signs of LVF (basal creps, increased JVP, 3rd HS) - PSM: Papillary muscle dysfunction/rupture (MR)

Answer 78

- Angina - Peri/endo/myocarditis - Dissection - PE, pneumothorax, pneumonia - Costochondritis - GI e.g GORD, spasm - Anxiety

Answer 79

ECG STEMI sequence - Normal - ST Elevation + hyperacute (tall) T waves (often first sign) - Q waves, full-thickness infarct - Normalisation of ST segment - T wave inversion - New onset LBBB also = STEMI New ST elevation at the J point in two contiguous leads with cut off points: >0.2mV in men or >=0.15mV in women in leads V2-3. ST elevation of >2mm in 2 or more anterior leads ST elevation of greater than 1mm in greater than 2 consecutive inferior leads (II, III, aVF, avL).

Answer 80

- ST depression - T wave inversion - Deep arrowhead T wave inversion in the anterior leads is a sign of Wellen's Syndrome. Trop is raised at this stage + no ischaemic damage yet.

Answer 81

A subendocardial infarct (below the endocardium)

Answer 82

II, III, AVF

Answer 83

I, aVL, V4-V6

Answer 84

V1,2,3 reciprocal. Changes to see are - ST depression - Tall, broad R-waves - Upright T-wave

Answer 85

``` Troponin T/1 - Myofibrillar protein linking actin and myosin - Elevated from 3-12hr therefore need 12hr trop to exclude MI - Peak at 24hrs - Baseline from 5-14 d FBC, U+E, glucose, lipids, clotting ``` Creatinine Kinase remained elevated for 3-4 days. Troponin remains elevated for 10days. CK-MB can the be used to find a re-infarction of 4-10 days.

Answer 86

Cardiomegaly Pulmonary Oedema Widened mediastinum: aortic rupture. Don't forget CCTA (coronary angiogram)

Answer 87

- Typical symptoms + ST elevation (?LBBB) - Typical rise of biomarkers of myocardial necrosis with at least (ischaemic symptoms, pathological Q waves, ECG Changes indicative of ischaemia - coronary angio

Answer 88

- Typical symptoms - no ST elevation - +VE) trop

Answer 89

- Typical symptoms - no ST elevation - ve trop.

Answer 90

- Oxygen? - Morphine - Aspirin 300mg (limit platelet activation) - clopidogrel/ticagrelor and - unfractionated heparin. PCI is gold-standard treatment for STEMI. If you can't do that, use thrombolysis with tPA or tenecteplase. Repeat ECG 90 mins later. (if no access to PCI within 90 mins, within 12 hr of symptoms and no contraindications to thrombolysis = alteplase/reteplase Contraindications - active internal bleeding, intracranial neoplasm, aortic dissection, pregnancy, head injury, coagulation disorders. Secondary Prevention: - ACE - B-blocker - Statin - Dual antiplatelet (aspirin + (clopi or ticagrelor or prasugrel)) consider continuing for up to 12 months. Post ACS = add ticagrelor to aspirin + stop ticagrelor after 12 months. Post PCI = add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months

Answer 91

(M)OGA - Oxygen, - GTN (nitrates - avoid in hypotension) , - Aspirin (300mg) + clopidogrel/Ticagrelor (antiplatelet ADP binding) In some patients: - Fondaparinux (activates antithrombin III) offered to patients who are not at a high risk of bleeding + who are not having angiography within next 24hrs. - IV glycoprotein IIb/IIIa receptor antagonist (eptibibatide or tirofiban) - those with intermediate or higher risk of adverse cardiovascular events). Assess need for invasive or conservative approach - Consider PCI/CABG in patients who have a predicted 6 month mortality above 3% - Give it in 96 hrs. MI: secondary prevention All patients should be on dual antiplatelet therapy (aspirin + ticagrelor or prasugrel) , ACEi, B-Blocker and Statin. Lifestyle Suggestions: Diet, exercise, sexual activity may resume 4 weeks after an uncomplicated MI. NICE: Add ticagrelor to aspirin, stop ticagrelor after 12 months Post PCI: add prasulgrel or ticagrelor to aspirin, stop second antiplatelet after 12 months. Aldosterone antagonist: patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction. Treatment with aldosterone antagonist eplerenone.

Answer 92

STEMI: 30 day mortality ~15% NSTEMI: overall mortality ~ 1-2%

Answer 93

Ventricular fibrillation is the most common cause of death in patients with MI. Post PCI experiencing pain - or haemodynamically unstable - urgent coronary artery bypass = continuing MI. Death Passing PRAED St Death: VF, LVF, CVA Pericarditis Rupture: myomalacia cordis/cardiac tamponade, papillary muscle (MR) - Can lead to a flash pulmonary oedema Septum - VSD Arrhythmias = (Tachy = AF, flutter, ventricular (premature ventricular contractions common after acute MI - no management) - sustained VT, consider cardioversion or amiodarone/lignocaine), (VT, VF)) - Brady (AV block, ventricular brady) Aneurysm Embolism Dressler's Syndrome

Answer 94

- Occurs Early - Mild fever - Central chest pain/change in pain - Relieved by sitting forward - Pericardial friction rub ECG - Saddle-shaped ST elevation - ± PR depression Rx - NSAIDs: Ibuprofen - Echo to exclude effusion

Answer 95

Cardiac Tamponade: - Left ventricular free wall rupture Beck's triad (low BP, High JVP, muffled heart sounds) Pulsus paradoxus (BP drop greater than 10mmHg on inspiration) - Need emergency pericardiocentesis + thoracotomy. Papillary muscle/chordae rupture --> Leads to mitral regurg - PSM - Pulmonary oedema Septum - PSM - increased JVP - Heart failure

Answer 96

- 4-6 weeks - LVF - Angina - Recurrent VT - Systemic emboli ECG: Shows persistent ST elevation Management: **Anticoagulate + consider excision** Embolisms arise from LV mural thrombus, consider warfarin for 3 months after large anterior MI.

Answer 97

Pleuro-pericarditis - Due to auto-antibodies vs myocyte sarcolemma. Presentation - 2-6 weeks - Fever - Pleural pain - Recurrent pericarditis - Pleural effusion - Anaemia - Increased ESR Management - NSAIDs - Steroids if severe

Answer 98

- 12 lead ECG - O2 - 2-4L for 94-98% - IV access (bloods for FBC, U+E, Glucose + lipids) - Brief assessment of Hx of CVD + risk factors. Thrombolysis CIs, CV exam. - Management 1) Antiplatelet Aspirin 300mg PO (then 75mg/d) + Clopidogrel/ 300mg PO (then 75mg/d) or Prasugrel/Ticagrelor 2) Unfractionated heparin: enoxaparin IV then SC or LMWH Add on: 3) Analgesia - Morphine 5-10mg IV - Metoclopramide 10mg IV 4) Anti-ischaemia - GTN 2 puffs or 1 tablet SL - B-B atenolol 5mg IV (CI asthma, LVF) Admit to CCU for monitoring - Arrhythmias - Continue meds except CCBs Aim for Primary PCI or Thrombolysis

Answer 99

Primary Percutaneous Coronary Intervention - Rx of choice if <12hr - angioplasty and stenting - + GP IIb/IIIa antagonist (tirofiban) if high risk Delayed PCI, DM, Complex procedure Complications - Bleeding - Emboli - Arrhythmia

Answer 100

- Without access to PCI - Contraindicated beyond 24hr from pain onset - ECG criteria- ST elevation >1mm in 2+ limbs OR >2mm in 2+ chest leads. New LBBB. Posterior: Deep ST 'depression' and tall 'R' waves in V1-V3.

Answer 101

AGAINST - Aortic dissection - GI bleeding - Allergic reaction previously - Iatrogenic: recent surgery - Neuro: cerebral neoplasm or CVA hx - Severe HTN - Trauma inc CPR

Answer 102

Streptokinase Alteplase Tenecteplase Activate plasminogen to form plasmin. This in turn degrades fibrin and helps breakup thrombi.

Answer 103

Bleeding Stroke Arrhythmia Allergic reaction

Answer 104

- ACEi: Start w/i 24hrs (lisinopril 2.5mg) - B-blocker: e.g bisoprolol 10mg OD (or CCB) - Cardiac rehabilitation (group exercise) - DVT prophylaxis until fully mobile (continue for 3 mont if large MI) - Statin: regarless of basal lipids (atorvastatin) Give advice - Stop smoking - Diet: oil fish, fruit, veg, decreased sat fats - Exercise: 30 mins OD - Work: return in 2m - Sex: avoid for 1 month - Driving: avoid for 1 mon Continue clopidogrel for 1 year following STEMI, continue aspirin indefinitely.

Answer 105

- 12 lead ECG + Admit to CCU - O2 2-4L + SPO2 of 94-98 - IV access + FBC bloods - Brief assessment (Hx of CVD/Risk factors) + CV exam. - Antiplatelet (aspirin 300mg PO then 75/d) and Clopidogrel (300mg PO) - Anticoagulate (Fondaparinux 2.5mg SC) - Analgesia (morphine 5-10mg IV) + metaclopramide (10mg IV) - Anti-ischaemia (GTN: 2 puffs or 1 tablet, B-blocker atenolol (CI in asthma and LVF), IV GTN if pain continues. Assess the CVS risk: using the GRACE/TIMI score (Estimates admission-6 month mortality for patients with acute coronary syndrome) Intermediate-High Risk - Persistent/recurrent ischaemia, ST depression, DM, POSITIVE trop - GPIIb/IIIa antagonist (tirofiban) should be given to patients who have high/intermediate risk + who are scheduled to undergo angiography. - Angiography (±PCI) w/i 96hs - Clopidogrel 75mg/d for one yr Low Risk - No further pain, flat or inverted T wave or normal ECG (negative trop) - May discharge if 12hr trop is negative - Outpatient test: angio, perfusion scan, stress echo. Continuing Therapy: address risk factors - ACEi (lisinopril 2.5mg) - B-blocker (bisoprolol 10mg OD) or CCB - Cardiac Rehabilitation (physio) - Stop antithrombotic therapy when pain free (but give 3-5d) - Statin (atorvastatin 80mg). Continue clopidogrel for 1yr following NSTEMI. Continue aspirin indefinitely.

Answer 106

Atherosclerosis --> myocardial ischaemia NICE defines anginal pain - 1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms 2. precipitated by physical exertion 3. relieved by rest or GTN in about 5 minutes - patients with all 3 features have typical angina - patients with 2 of the above features have atypical angina - patients with 1 or none of the above features have non-anginal chest pain

Answer 107

- Mostly atheroma - Anaemia - AS - Tachyarrhythmias - Arteritis

Answer 108

- Smoking - DM - High cholesterol - HTN - Obesity

Answer 109

- Age - Gender - FH (<55yr) - Genetic (hyperlipidaemia)

Answer 110

- Central Chest tightness or heaviness - Brought on by exertion, relieved by rest - May radiate to one/both arms, neck, jaw, teeth - Other ppt: emotion, cold weather, heavy meals.

Answer 111

Stable: induced by effort Unstable: occurs at rest/minimal exertion Decubitus: induced by lying down Prinzmetal's/variant: occurs during rest - Due to coronary spasm - ST elevation during attack: resolves as pain subsides Rx: CCB + long-acting nitrates Syndrome X: angina pain + ST elevation on exercise test but no evidence of coronary atherosclerosis - perhaps small vessel disease.

Answer 112

- AS - Aortic Aneurysm - GI: GORD, spasm - Musculoskeletal

Answer 113

Bloods: FBC, U+E, lipids, glucose, ESR, TFTs ECG: usually normal - May show ST depression, flat/inverted T waves, Past MI - Perfusion scan - CT coronary Ca score - Angiography (allows for angioplasty and stenting) - For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes): 1st line: CT contrast-enhances coronary angiography. recommended for typical angina, atypical angina, non-cardiac chest pain but a positive resting ECG. 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) 3rd line: invasive coronary angiography Examples of non-invasive functional imaging - myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or stress echocardiography or first-pass contrast-enhanced magnetic resonance (MR) perfusion or MR imaging for stress-induced wall motion abnormalities

Answer 114

Lifestyle (Smoking/weight loss etc) Medical: 2ndry prevention Aspirin 75mg OD, ACEi (ramipril, captopril) , Statins, simvastatin, AntiHTN (beta-blockers - propranolol,atenolol) Anti-anginals: prevents angina episodes. All patient should receive sublingual glyceryl trinitrate 1st (B-Blocker (Atenolol 50mg-100mg OD) or CCB (Verapamil 80mg TDS, then consider amlodipine) Use a rate-limiting CCB, then use a long-acting dihydropyridine CCB. non-dihydropyridine = verapamil, diltiazem 2. Try max dose of the monotherapy 3. If either B-B or CCB doesnt control try both. If both use nifedipine (verapamil + beta blocker = heart block) If patient can't take CCB or the B-B try: - ISMN (isosorbate mononitrate) 20-40mg BD (8hr washout) or slow-release nitrate - Ivabradine - Nicorandil (potassium channel activator with vasodilatory effect). - Ranolazine Patients develop tolerance to ISMN - take a second dose after 8hrs, rather than 12 hrs. Modified release doesn't lead to tolerance. ``` Interventional: PCI - Poor response to medical Rx - Refractory angina but not suitable for CABG - Complications Re-stenosis (20-30% at 6 mo) Emergency CABG MI (<2%) Death ( ```

Answer 115

Indications - LMS disease - Triple Vessel Disease - Refractory Angina - Unsuccessful angioplasty Complications - MI - Stroke - Pericardial tamponade or haemothorax - Postperfusion syndrome - Post-op AF - Non-union of sternum - Graft Stenosis

Answer 116

CO is inadequate for the body's requirements despite adequate filling pressures.

Answer 117

Prevalence: 2% @ 50yrs --> 10% @ 80yrs

Answer 118

Reduced CO initially --> Compensation - Starling effect dilates heart to enhance contractility. - Remodelling --> Hypertrophy - RAS and ANP/BNP release - Sympathetic activation Progressive decreased in CO --> decompensation - Progressive dilatation --> impaired contractility + functional valve regurgitation. - Hypertrophy --> relative MI - RAS activation --> Na and fluid retention --> increased venous pressure --> oedema - Sympathetic excess --> increased afterload --> decreased CO.

Answer 119

Due to this low output: the cardiac output decreased and fails to increase with exertion. - The pump failures: Systolic failure --> impaired contraction (mainly due to ischaemia/MI), or a dilated cardiomyopathy, HTN, Myocarditis. Diastolic Failure --> Impaired filling (due to pericardial effusion/tamponade/constriction. But also cardiomyopathy: restrictive, hypertrophic). Arrhythmias --> Bradycardia, heart block, tachycardias, or anti-arrhythmics (beta-blockers or verapamil).

Answer 120

AR, MR, fluid overload. Initial stretching of the myocytes before contraction.

Answer 121

The pressure the heart must work against once contracting? - AS - HTN - HOCM

Answer 122

- Increased needs - the heart needs to pump harder to meet the needs of the body. --> RVF initially, then LVF Anaemia, AVM, Thyrotoxicosis, Thiamine Deficiency (beri beri), Pregnancy, Paget's.

Answer 123

- LVF - Cor pulmonale - Tricuspid and pulmonary valve disease

Answer 124

Anorexia and Nausea

Answer 125

Increased JVP + jugular venous distension Tender smooth hepatomegaly Pitting Oedema Ascites

Answer 126

1st: IHD 2nd: Idiopathic dilated cardiomyopathy 3rd: Systemic HTN 4th: Mitral and aortic valve disease Specific Cardiomyopathies

Answer 127

``` Fatigue Extertional dyspnoea Orthopnoea + PND Nocturnal cough (± pink, frothy sputum) Wt loss and muscle wasting ```

Answer 128

- Cold peripheries ± cyanosis - Often in AF - Cardiomegaly with displaced apex - S3 + tachycardia = gallop rhythm (blood back and forth through atria + ventricles) - Wheeze (cardiac asthma) Bibasal creps - Cardiac cachexia - Venous congestion of GI organs leading to early satiety. -

Answer 129

``` Acute - New onset or decompensation of chronic - Peripheral/pulmonary oedema - ± evidence of peripheral hypoperfusion = Give Furosemide. GTN IV. ``` Chronic - Develops/progresses slowly - Venous congestion common - Arterial pressure maintained until v.late

Answer 130

Framingham Criteria for CCF - 2 major or 1 major + 2 minor. Major - PND (paroxysmal nocturnal dyspnoea) - + ve abdominojugular reflux - Neck Vein Distension - S3 - Basal Creps - Cardiomegaly - Acute Pulmonary Oedema - increased CVP (>16cmH20) (central venous pressure) - Weight loss > 4.5kg in 5d sndry to management. Minor - Bilateral ankle oedema - SOBOE - Increased HR > 120 - Nocturnal cough - Hepatomegaly - Pleural effusion - 30% decrease in vital capacity

Answer 131

Suspected HF? 1. ECG + Tests to consider (CXr, Lipid, Renal, Thyroid, HbA1c, peak flow etc) Still suspected HF? 2. NT-proBNP (regardless of previous MI) 3. Echo Bloods: FBC, U+E, BNP (raised but not specific), TFTs, glucose, lipids. ``` CXR - ABCDE Alveolar shadowing Kerley B lines (demonstrate expansion of the interstitial space by fluid) Cardiomegaly (Cardiothoracic ratio >50%) Diversion (upper lobe) Effusion Fluid in the Fissures ``` ECG - Ischaemia - Hypertrophy - AF Echo - the key investigation - Global systolic and diastolic function. Systolic failure echo shows dilated left and/or right ventricle with LOW ejection fraction. With pure diastolic heart failure LVEF is normal, but evidence of LVH and of abnormal diastolic filling patterns. - Ejection fraction normally ~60%. Low EF = 40%. - Focal/global hypokinesia - Hypertrophy - Valve Lesions - Intracardiac shunts

Answer 132

Secreted from ventricles in response to - Increased pressure --> Stretch - Tachycardia - Glucocorticoids - Thyroid - RV overload - Hypoxaemia - Renal dysfunction - Sepsis - COPD - Diabetes - Cirrhosis

Answer 133

- Increased GFR, and decreased renal Na reabsorption | - Decreased preload by relaxing smooth muscle

Answer 134

Heart failure - >2000 = 2WW - Increased BNP (>400) supports a diagnosis of abnormal ventricular function. = 6WW. - Intermediate value (100-400) is grey zone, may be due to COPD etc. - Low (<100) can rule out decompensated heart failure. - BNP also increased in RHF: cor pulmonale/PE. Causes of falsely low BNP - Aldosterone antagonist, ACEi, ARB, Beta-blockers, Diuretics.

Answer 135

- 1. No limitation of activity - 2. Comfortable @ rest, dyspnoea on ordinary activity - 3. Marked limitation of ordinary activity - 4. Dyspnoea @ rest, all activity --> discomfort.

Answer 136

- Manage primary risk factors + treat precipitants/causes. - Specific management - Offer annual influenza vaccine - Offer pneumococcal vaccine Primary and Secondary CVS risk factors - Stop smoking - Decreased salt intake - Optimise weight: increased or decreased (dietician) - Supervised group exercised based rehab programme - Aspirin - Statins

Answer 137

- Underlying causes Valve disease Arrhythmias Ischaemia - Exacerbating factors Anaemia Infection Increased BP.

Answer 138

- General principles Newly diagnosed patient need congestion and volume overload control - If patient is anxious or distress consider morphine. (also has vasodilator properties). - Those with low LVEF (add ACEi, B-Blockers, Aldosterone Antagonist (spironolactone) Therefore - ACEi, B-B --> decrease mortality.) 1st line: ACEi/ARB + B-B (watch K on ACEi) ACEi/ARB: lisinopril/captopril 2.5-40mg OD/6.25-50mg TDS. ARB in Class II-IV if tolerated? ``` B-B: Carvedilol (3.125mg BDS) /Bisoprolol 1.25mg orally) Start low, go slow Wait >2 weeks between increments Switch stable pt taking B-Blocker for a comorbidity to a B-B licensed for heart failure. B-B is good therapy for COPD. ``` Consider diuretics for fluid overload - Furosemide in Acute HF.

Answer 139

Get advise - Spironolactone (watch K carefully (also on ACEi) (recommended in those with II-IV with LVEF <35%. Can cause hyperkalaemia. - ACEi + ARB (if cannot tolerate ACEi, use ARB). - Vasodilators: hydralazine + ISDN nitrate (for those who cannot be given ACE/ARB-II)

Answer 140

- Digoxin (especially in those with AF. Used with ACEi, B-B, Diuretics. - Consider ivabradine (already on ACEi, B-B, Aldosterone antagonist), HR >75 + LVEF <35% - Consider ICD: 1) Prevention of sudden cardiac death in patients with non-ischaemic + ischaemic heart failure. 2) Secondary prevention to prolong survival in patients with current or prior symptoms of heart failure with history of cardiac arrest/VF. 3) Asymptomatic patients with an LVEF less than 30% NYHA class I. - Cardiac Resynchronisation therapy ± ICD. - When refractory to optimal medical treatment. Used where LVEF <30% with a LBBB. Involves simultaneous activation of both right and left ventricles. Enhances ventricular contraction + reduced degree of functional mitral regurg.

Answer 141

Monitoring - BP: may be V low - Renal function - Plasma K - Daily weight Use amlodipine for comorbid HTN or angina - Avoid verapamil, dilitiazem, nifedipine (short acting)

Answer 142

- Cardiac resynchronisation ± ICD | - Heart transplant

Answer 143

- Reduced CO, Tissue Hypoperfusion, increased pulmonary pressure. - Presents with dyspnoea, decreased exercise tolerance, swelling or legs + generalised fatigue.

Answer 144

- Sit up - Oxygen (15L/min via reservoir mask) - Target SpO2: 94-98% - IV access + monitor ECG (bloods for FBC, U+E, trop, BNP, ABG) + check for arrhythmias. - Diamorphine 2.5-5mg IV/Metoclopramide 10mg (makes patient more comfortable + pulm venodilators --> decrease preload --> optimise position on starling curve). - Treat fluid overload - Loop diuretics (Furosemide/Bumetanide (40-160mg). - Treat with vasodilators (lower left ventricular filling pressure + symptomatic improvement. GTN (5mg - 2 puffs unless SBP <90) OR 5micrograms/min IV and increase by 5-20 every 3-5 mins. - If worsening CPAP, more furosemide or increase infusion. - BiPAP is not used in acute pulmonary oedema (matches person's respiration) - Haemofiltration/dialysis.

Answer 145

- CXR: Looking for ABCDE - ECG: MI, Arrhythmias, pulsus alternans (upstroke of pulses is weak then strong) - shows in heart failure. - Consider Echo

Answer 146

Consider Inotropes or vasopressor - Milrinone (25-50micro IV) or Dobutamine (5-15 micro) If in shock. 2nd/3rd line: Can also consider Intra-aortic balloon pump and left ventricular assist device

Answer 147

``` Cardiogenic and Non-cardiogenic: - Cardiogenic MI, Arrythmias, fluid overload: renal/iatrogenic - Non-cardiogenic - ARDS: sepsis, post-op, trauma - Upper airway obstruction - Neurogenic: head injury ```

Answer 148

- Dyspnoea - Orthopnoea - Pink Frothy Sputum

Answer 149

- Distressed, sweaty, cyanosed - Increased HR/ Increased RR - Increased JVP - S3/ gallop rhythm - Bibasal creps - Pleural effusions - Wheeze (cardiac asthma)

Answer 150

- Asthma/COPD - Pneumonia - PE

Answer 151

- RR - HR - BP - JVP - urine output - ABG

Answer 152

- Daily Weights - DVT prophylaxis - Repeat CXR - Change to oral furosemide or bumetanide - ACEi + B-B if heart failure - Consider Spiro - Consider digoxin + warfarin (esp if in AF).

Answer 153

Inadequate tissue perfusion primarily due to cardiac dysfunction. In Cardiogenic shock - PAOP high, Cardiac Output Low, SVR high. In Hypovolaemia - PAOP low, cardiac output low, SVR high.

Answer 154

MI HEART - MI - Hyperkalaemia (inc electrolytes) - Endocarditis (valve destruction) - Aortic Dissection - Rhythm disturbance - Tamponade Obstruction - Tension pneumothorax - Massive PE

Answer 155

- unwell: pale, sweaty, cyanosed, distressed. - Cold clammy peripheries - Increased RR + increased HR - Pulmonary oedema

Answer 156

- O2 15L/min on a reservoir mask with a target SpO2 of 94-98%. - IV access + ECG (need an ABG + standard bloods) - Diamorphine + metoclopramide 10mg IV - Correct any arrhythmias, Electrolyte disturbances, acid-base abnormalities (MI needs angioplasty or CABG, tamponade needs drainage, PE needs thrombolysis) - Ix (CXR, Echo, CT Thorax (dissection/PE)) - Consider need for dobutamine (in hypotension + No MI) Used to treat reversible heart failure related to shock.

Answer 157

Accumulation of pericardial fluid within the pericardial space increasing intra-pericardial pressure, restricting cardiac filling and decreasing cardiac output.

Answer 158

- Trauma (presents with classic Beck triad signs). - Lung/breast Ca (Subacute - most common). - Pericarditis (scarred pericardium) - MI (regional/local effusion) - Bacteria (TB) (subacute)

Answer 159

- Beck triad: Hypotension, raised JVP and muffled heart sounds. - Kussmaul's sign: Increased JVP on inspiration (inspiration increases venous return to right heart) and volume of right side decreased). When the pericardium is stretched, this is greater exaggerated leading to pulsus paradoxus. Rare sign in cardiac tamponade. (inspiratory drop systemic bp of >10). Difference between Cardiac Tamponade + Constrictive Pericarditis? - CP = X+Y JVP, no Pulsus paradoxus, and pericardial calcification.

Answer 160

Echo: Diagnostic ECG - Electrical alternans CXR: Globular heart

Answer 161

- ABCs - give fluid. Do NOT dry these patient. - Pericardiocentesis (under echo guidance (if effusion present less than 1 month, echo shows effusion larger than 20mm). - Paraxiphoid - 15 degree angle

Answer 162

Essential HTN is over >140/90 with no secondary cause. ACC Guidelines: Average of 2 or more seated measurements: Normal BP: Systolic BP 120-129 mmHg and diastolic BP <80 Grade 1 HTN: Systolic BP 140-159 or Diastolic BP 90-99. ABPM of 135/85 Grade 2 HTN: systolic BP 160-179 or diastolic BP 100-109 mmHG. ABPM of 150/95 Grade 3 HTN: Systolic BP >180 or Diastolic BP >110 Malignant HTN: BP >180/110 + papilloedema and/or retinal haemorrhage. Chest pain due to increased workload on the heart. Nosebleeds, haematuria due to kidney failure. Isolated SHT: SBP >140, DBP <90.

Answer 163

``` PREDICTION - Primary: 95% - Renal (RAS System): RAS, GN, APKD, PAN - Endo: increased T4, Cushing's, Phaeo, Acromegaly, Conns (5-10%) Congenital adrenal hyperplasia - Drugs: cocaine, NSAIDS, OCP, MOAi, - ICP increased - CoA - Toxaemia of Pregnancy - Increased Viscosity - Overload with fluid - Neurogenic: Diffuse axonal injury, spinal section ```

Answer 164

Increased HR: Thyrotoxicosis Radio-femoral delay: CoA Renal Bruits: RAS Palpable Kidneys: APKD Paroxysmal Headache, tachycardia, sweating, palpitations, labile or postural hypotension: phaeo Conns: Excess aldosterone therefore retaining salt HTN and losing K. Acromegaly: Coarse facial appearance, spade hands, large tongue, excess sweating.

Answer 165

CANER - Cardiac: (IHD, LVH --> CCF, AR, MR) - Aortic: (aneurysm, dissection) - Neuro: (CVA: ischaemic, haemorrhagic). Encephalopathy (malignant HTN). - Eyes: (hypertensive retinopathy) - Renal (proteinuria, CRF)

Answer 166

hypertensive retinopathy - 1. Tortuosity and silver wiring - 2. AV nipping (tight constrictions) - 3. Flame (retinal) haemorrhages (copper wiring) and cotton wool spots (ischaemic changes) , exudates - 4. Papilloedema 3 + 4 = malignant hypertension

Answer 167

- 24hr ABPM - confirm HTN in those found with elevated clinic reading. NICE recommends taking two readings during the consultations. If both at >140/90 then offer ABPM or HBPM. Use HBPM if ABPM declined. If at ABPM/HBPM >= 135/85 (stage 1). treat if <80 + any of the following - target end organ damage, CVS, Renal disease, diabetes. If ABPM/HBPM >150/95 offer drug treatment regardless of age. - Urine: Haematuria, Alb:cr ratio (end organ damage) - Bloods: FBC, U+E, (renal insufficiency, hypokalaemia suggesting Conn's (Hyperaldosteronism) eGFR (end organ damage) Glucose (metabolic syndrome) Fasting lipids (high LDL, Low HDL) - 12 lead ECG: LVH, old infarct (rule out CAD) - Calculate 10yr CV risk

Answer 168

Do ABPM to confirm Dx before management - Lifestyle Increase exercise, decrease smoking/ETOH, salt, decrease caffeine.

Answer 169

<80 yr, Stage 1 HTN (>135/90) - via ABP and one of the following: - Target organ damage (LVH/retinopathy) - 10yr CV risk >20% - Established CVD - DM - Renal Disease Anyone with Stage 2 HTN (>160/100) Severe/malignant HTN (specialist referral) Consider specialist opinion if <40yr with stage 1 HTN and no end organ damage.

Answer 170

Age <80 - Clinic = 140/90. - ABPM/HBPM = 135/85 Age >80 - Clinic = 150/90 - ABPM/HBPM = 145/85 If end-organ damage <130/80. Otherwise <140/90.

Answer 171

patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotension receptor blocker (ACE-i or ARB): (A) because renoprotective. If <55 or T2DM 1st Line <55 = ACEi or ARBs - lisinopril 10mg OD (increase to 30-40mg). - Candesartan 4mg OD (max 32 mg OD) - Captopril, losartan. NOT recommended in pregnancy. Avoid all ACEi ARBS in pregnanc

Answer 172

patients >= 55-years-old or of Afro-Caribbean origin: Calcium channel blocker (C) 1st line >55/Black - CCB or Thiazide-like diuretics. CCB = Nifedipine MR 30-60, Amlodipine 2.5mg orally once daily initially. Diltiazem: 120-180mg orally. Peripheral vasodilators. May also be helpful in Raynaud's, coronary artery spasm If diabetic - use ACEi (ramipril). Thiazide-Like Diuretics: - Hydrochorothiazide (12.5 to 25mg. - Chlortalidone - 12.5mg, - indapamide 1.25mg orally. Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule. Blocking Na Cl symptoms. Use this instead of traditional Diuretics Adverse effects - Dehydration, postural hypotension, gout, impaired glucose tolerance, impotence. can also cause agranulocytosis, photosensitivity rash, pancreatitis.

Answer 173

if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic. if already taking a Calcium channel blocker add an ACE-i or ARB A+C or A+ D - ACEi or ARB - !!use ARBs over ACEi in blacks!! + Either CCB or Diuretics. - Can also be used as a low-dose 1st line therapy. Remember ACEi is ok in CKD, just not AKI. A potassium above 6mmol should prompt cessation of ACEi in a patient with CKD.

Answer 174

A + C + D + consider Spiron or a/b blocker (hydralazine = a or labetalol (b). Consider adding Spiro if the K was below 4.5 Consider adding alpha or beta blocker if above 4.5 e.g carvedilol (beta-blocker)

Answer 175

Consider Beta-blockers - Cardioprotective effects in patients with CAD. Decreases myocardial wall stress and lessens myocardial oxygen demand. Then consider CCB Then B-B + CCB Then B-B + ACE/ARB

Answer 176

HTN emergency Systolic is usually >180 and diastolic >120 + risk factors. May have dizziness/headache, cardiac symptoms (SOB, palpitations), oliguria (end organ renal damage), fundoscopy abnormal - Controlled decreased in BP over days to avoid stroke - 1st line Labetalol IV 20mg. - 2nd line = nicardipine long acting CCB If LV failure or Pulmonary oedema - GTN + Furosemide (peripheral dilator IV) OR Clevidipine (CCB that increases stroke volume and coronary vasodilatory activity). - 2nd line = Nitroprusside + furosemide. (arterial and venous vasodilator reducing afterload and preload.

Answer 177

- Senile calcification (60yr+) = commonest - Congenital: bicuspid valve (40-60yrs), William's syndrome - Rheumatic fever (Strep autoimmune inflammation reaction triggered by prior Strep infection. leads to inflammation + calcification). - Subvalvular: HOCM

Answer 178

- Triad: Angina, dyspnoea, syncope (esp with exercise) - LVF: PND, orthopnoea, frothy sputum - Arrhythmias - Systemic emboli if endocarditis - Sudden death

Answer 179

- Slow rising pulse with narrow PP (taking time to get through the stenosis, pushing harder therefore narrow pressure) - due to reduced stroke volume due to narrow valve - Aortic thrill (palpable murmur) - Apex: (forceful, non-displaced) pressure overload. - Heart Sounds Quiet A2 (aortic valve closing) Early systolic ejection click if pliable (young) valve) S4 (forceful atria contraction vs hypertrophied ventricle) Murmur - ESM (crescendo/decrescendo). Loudest in the right upper sternal border. - Right 2nd ICS - Sitting forward in end-expiration - Radiates to carotids - Gallavardin's phenomenon - Mimic Mitral Regurg (holosystolic murmur present at apex of heart)

Answer 180

- Quiet/absent A2 - S4 (indicative of left ventricular hypertrophy) - Narrow pulse pressure - Decompensation: LVF

Answer 181

Coronary artery disease MR - Gallavardin's phenomenon Aortic Sclerosis - Valve thickening: no pressure gradient Turbulence --> murmur - ESM with no radiation and normal pulse. - HOCM ESM murmur which increases in intensity with valsalva (AS decreases with valsalva)

Answer 182

Stenosis - Valve narrowing due to fusion of the commissures - Narrow PP, slow rising - Forceful apex - ESM radiating --> carotids - ECG: LVF Aortic stenosis - Valve thickening - ESM with no radiation.

Answer 183

- Bloods: FBC, U+E, Lipids, Glucose - ECG: LVH, LV strain, Tall R, ST depression, T inversion in V4-V6 LBBB or complete AV block (septal calcification) May need pacing - CXR Calcified AV (esp on lateral film) LVH Evidence of failure Post-stenotic aortic dilatation - Echo + Doppler: Diagnostic Thickened, calcified, immobile valve cusps Severe AS (Stage D): Pressure gradient >40mmHg, Jet velocity >4m/s, Valve areas <1cm. - Cardiac Catheterisation + Angiography Can assess valve gradient and LV function Assess coronaries in all pt planned for surgery. - Exercise Stress Tet Contraindicated if symptomatic AS May be useful to assess ex capacity in asymptomatic patient.

Answer 184

If asymptomatic then observe patient If symptomatic then valve replacement If asymptomatic but valvular gradient >40mmHg then consider surgery. Medical - Optimise RFs: Statins, antihypertensives, DM - Monitor: regular f/up with echo - Angina: B-blockers - Heart failure: ACEi and diuretics - Avoid nitrates due to profound hypotension ``` Surgical - Poor prognosis if symptomatic Angina/syncope: 2-3 yr LVF: 1-2 yrs - Indications for valve replacement Severe symptomatic AS Severe asymptomatic AS with reduced EF (<40%) Severe AS undergoing CABG or other valve Op ``` -Valve types Mechanical valves last longer but need anticoagulation: young patient Bioprosthetic don't require anticoagulation but fail sooner (10-15yrs) REMEMBER: needs long-tern antibiotic prophylaxis for endocarditis.

Answer 185

Balloon Valvuloplasty - Limited use in adults as complication rates is high, and restenosis occurs in 6-12 months. Transcatheter Aortic Valve Implantation (TAVI) - Folded Valve deployed in aortic root - increased perioperative stroke risk cf. replacement - Decreased major bleeding - Similar survival @ 1 yr - Little long-term data Transfemoral rather than a transthoracic approach.

Answer 186

Acute (18%) - Infective endocarditis (56%) - Type A aortic dissection (44%) (ascending part of aorta) - alongside an Inferior MR. Chronic - Congenital: bicuspid aortic valve (22%) - Rheumatic heart disease - Connective tissue: Marfan's, Ehler's Danlos - Autoimmune: Ank Spond, Ra

Answer 187

LVF: Exertional Dyspnoea, PND, Orthopnoea Arrhythmias (esp AF) --> palpitations - Forceful heart beats Angina

Answer 188

- Collapsing Pulse (water hammer or Corrigan's pulse) - Arterial pulse shows rapid rise and a quick collapse resulting in widened pulse pressure >50 mmHg. - Wide Pulse Pressure - Apex: displaced (volume overload) in order to overcome later volume - Heart Sounds (Soft/Absent S2) - inadequate closure of aortic valve in severe AR ± S3. - Thrill (increased stroke volume) - Murmur Early diastolic murmur URSE (Upper Right sternal edge) + 3rd left IC parasternal Sitting forward in end-expiration ± ejection systolic flow murmur. Murmur occurs after S1 due to flow of increased stroke volume across a non-stenotic aortic valve. Early peaking, crescendo-decrescendo systolic sound, best heard at second right intercostal space. ± Austin-Flint Murmur Soft, rumbling mid to late diastolic murmur heard best at apex. It produced by the abutment of an aortic regurg jet against the left ventricular endocardium. Different to a mitral stenosis by absence of an opening snap and loud S1. Underlying cause - High-arched palate - Spondyloarthropathy - Embolic phenomena

Answer 189

- Corrigan's Sign: carotid pulsation due to increased stroke volume. For collapsing pulse (feel the forearm) - De Musset's: Head nodding - Quincke's: capillary pulsation in nail bed. - Traube's: pistol-shot sound over femorals - Austin-Flint Murmur: Rubling MDM @ apex due to regurgitant jet fluttering the anterior mitral valve cusp = severe AR. - Duroziez's - Systolic murmur over the femoral artery with proximal compression. Diastolic murmur with distal compression.

Answer 190

- Wide PP - Collapsing pulse - S3 - Long Murmur - Austin Flint murmur - Decompensation: LVF

Answer 191

- There is a left ventricular volume and pressure overload - Increase in left ventricular volume and pressure causes an increase in wall tension - Therefore wall undergoes hypertrophy. - Systolic hypertension occurs due to increased stroke volume due to regurgitant and forwards stroke volume. Volume overload related to severity of leak results in an increase in left ventricular end-diastolic volume. - Low diastolic volume as less blood is present in diastole. - Increased in systolic as more blood is being sent out. - If your diastolic is so low, you're gonna see syncope too - Diastole also supports the coronary arteries, therefore angina.

Answer 192

Bloods: FBC, U+E, Lipids, Glucose - ECG: LVH (R6 + S1 >35mm) - CXR - Cardiomegaly, Dilated ascending aorta, pulmonary oedema. - Echo: Aortic valve structure and morphology (e.g bicuspid) Evidence of infective endocarditis (e.g vegetations) Severity Jet width (>65% of outflow tract = severe Regurgitant jet volume Premature closing of the mitral valve LV function: ejection fraction, end-systolic dimension Cardiac Catheterisation - Coronary artery disease - Assess severity, LV function, root size

Answer 193

Medical - Optimise RF: Statins, anti-hypertensives, DM - Monitor: regular f/up with echo - Decreased systolic HTN: ACEi (relax blood vessels + volume to reduce systolic bp), CCB Decreased afterload --> Decreased regurgitation ``` Surgical - Definitive therapy - Indicated in severe AR if: Symptom of heart failure Asymptomatic with LV dysfunction, decreased EF/increased ES dimension Can use TAVI or surgery. ```

Answer 194

- Rheumatic Fever (95%) - receive inflammatory damage. Years later, fusion of the mitral leaflet commissures and thickening of leaflets + sub-valvular apparatus causes mitral stenosis. - Prosthetic Valve - Carcinoid Syndrome - Congenital (rare)

Answer 195

- Valve narrowing --> increased left atrial pressure --> Loud S1 and atrial hypertrophy --> AF. - -> Pulmonary oedema and PHT --> loud P2, PR. - -> RVH --> left parasternal heave - -> Tricuspid regurg --> large v waves (represents filling of the right atrium when the tricuspid is closed) - venous filling. - -> RHF --> increased JVP, oedema, Ascites.

Answer 196

- Dyspnoea (increased left atrial pressure results in pulmonary congestion) - Fatigue - Chest pain - AF --> Palpitations + emboli - Haemoptysis: rupture of bronchial veins due to sudden increases in pulmonary venous pressure.

Answer 197

- Symptoms manifest when orifice <2cm (normally 4-6) - AF, low volume pulse due to left atrial enlargement. - Malar flush (decreased CO -->> backpressure + vasocontrisction). Also due to CO2 retention + vasodilatory effects. - JVP may be raised late on Prominent a waves: PHT (right atria contraction) or stenosis of tricuspid valve. Large v waves: TR Absent a waves: AF - Neck vein distension due to pulmonary HTN - Left parasternal heave (RVH 2ndry to PHT) - Apex: Tapping (palpable S1), non-displaced. S1 is loud as high gradient holds it open until ventricular systole closes it. - Heart sound Loud S1, Loud P2 (if PHT). Early diastolic opening snap. - Murmur Rumbling MDM Apex Left lateral position in end expiration Radiates to the axilla ± Graham Steell murmur (EDM 2ndry to pulmonary regurg).

Answer 198

- Mitral facies - Longer murmur - Opening snap closer to 2nd heart sound High LA pressure focing valve open early - Decompensation: RVF

Answer 199

Pulmonary HTN Emboli: TIA, CVA, PVD, Ischaemic colitis Hoarseness: rec laryngeal N.palsy = Ortner's Syndrome (due to the enlarged left atrium encroaching upon the left recurrent laryngeal nerve. Dysphagia = Left atria encroaching on oesophagus. Bronchial obstruction

Answer 200

- Bloods: FBC, U+E, LFTs, glucose, Lipids - ECG AF, P mitrale (if in sinus) = left atrial enlargement showing bifid P waves, RVH with strain: ST depression and T wave inversion in V1-V2. - CXR LA enlargement Pulmonary oedema: ABCDE Mitral valve calcification - Echo + Doppler Severe MS Valve orifice <1.5cm Pressure gradient >10mmHg Pulmonary artery systolic pressure >50mmHg. - Use TOE to look for left atrial thrombus if intervention considered. May see a hockey stick-shaped mitral deformity. Cardiac Catherisation - Assess coronary arteries

Answer 201

Asymptomatic patients with severe disease usually do not require therapy. Medical - Optimise RFs: Statins, Anti-hypertensives, DM - Monitor: regular f/up with echo - Consider prophylaxis vs rheumatic fever: e.g Pen V - AF: rate control + anticoagulate - Diuretics provide symptom relief (furosemide - 40mg orally.) Reduce left atrial pressure + relieve mild symptoms. ``` Surgery - indicated in symptomatic severe MS - Percutaneous Balloon valvuloplasty Management of choice Suitability depends on valve characteristics - Pliable, minimally calcified - CI if left atrial mural thrombus ``` - More severe MS = valvotomy/commissurotomy: valve repair (open valve repair) - Valve replacement if repair not possible.

Answer 202

- Mitral valve prolapse - LV dilatation: AR, AS, HTN - Annular calcification --> contraction (elderly) - Post- MI: papillary muscle dysfunction/rupture - Rheumatic fever - Infective endocarditis - Connective tissue: marfan's, Ehlers-Danlos.

Answer 203

- Chronic MR can be mild with asymptomatic. - With progression, cardiac hypertrophy occurs, increasing left ventricular end-diastolic volume. Left atrial enlargement. - Acute MR = Acute disruption of mitral valve leaflets, chordae tendineae, papillary muscle following MI, infective endocarditis, rheumatic fever.

Answer 204

- Dyspnoea - Fatigue - AF --> palpitations + Emboli - Pulmonary congestion --> HTN + oedema

Answer 205

- AF - Left parasternal heave due to RVH - Apex: displaced Volume overload as ventricle has to pump forwards SV and regurgitant volume = Eccentric hypertrophy - HS Soft S1 S2 not heard separately from murmur Loud P2 (if PTH) - Murmur Blowing PSM Apex Left lateral position in end expiration Radiates to the axilla

Answer 206

- Larger LV - Decompensation: LVF - AF

Answer 207

- AS - TR - VSD

Answer 208

Bloods: FBC, U+E, glucose, lipids ECG: AF, P mitrale (unless in AF), LVH CXR: LA and LV hypertrophy, Mitral valve calcification, pulmonary oedema. Echo - Doppler echo to assess MR severity: multiple criteria Jet width (vena contracta) >0.7 cm = severe Systolic pulmonary flow reversal Regurgitant volume >60ml - TOE to assess severity and suitability of repair cf. replacement. - First line is Transthoracic echo Cardiac catheterisation - Confirm diagnosis - Assess CAD

Answer 209

- Medical Optimise RF: statins, Anti-HTN, DM Monitor: regular f/up with echo AF: rate control and anticoagulate Also anticoag if: hx of embolisation, prosthetic valve, additional MS. Drugs to decrease afterload can help with symptoms - ACEi or B-B (captopril+ metoprolol/atenolol) (if LVEF >60%) or LVESD <45mm. If less than 60% use surgery (valvuloplasty, annuloplasty (tighten ring) mechanical valve + anticoag, bioprostheses. - Diuretics Surgery - Valve replacement or repair - Indications Severe symptomatic MR (EJ 30% or more) + medical treatment. Severe asymptomatic MR with diastolic dysfunction: Decreased ejection fraction (<60%)

Answer 210

Most common valve problem (5%). | - Systolic prolapse or billowing of one or both mitral valve leaflets into the left atrium.

Answer 211

Primary MVP is due to myxomatous degeneration eg Marfans, Ehlers-Danlos, osteogenesis imperfecta. In MVP, progressive changes result in mitral regurg that worsens over time. Produces volume overload of the left ventricles + atrium.

Answer 212

- Usually asymptomatic - Autonomic dysfunction: atypical chest pain, palpitations, anxiety, panic attack - MR: SOB, fatigue.

Answer 213

- Mid-systolic click + late systolic murmur (due to mitral regurg). Decreasing the preload, or afterload, the click and murmur occur earlier in systole. Squatting or increasing afterload with handgrip the click + murmur occur later.

Answer 214

MR Cerebral emboli Arrhythmias --> sudden death

Answer 215

- B-B may relieve palpitations + chest pain. Aspirin + warfarin for severe mitral regurg - Surgery if severe (commonest reason for MV surgery)

Answer 216

Occurs when blood flows backwards through tricuspid valve. Mainly during systole.

Answer 217

- Functional: RV dilatation - Rheumatic fever - Infective endocarditis - Carcinoid Syndrome Can also be due to rheumatoid arthritis, Marfans, tricuspid valve prolapse.

Answer 218

Tricuspid valve develops dysfunction with elevation of right ventricular systolic/diastolic pressure, right ventricular cavity enlargement. If longstanding leads to reduced cardiac output, elevate right atrial pressure, leading to atrial distension and AF. Present with ascites symptoms of dyspepsia or indigestion.

Answer 219

- Fatigue (right-sided heart failure) - Hepatic pain on exertion - Ascites and oedema peripherally. - Palpitations (AF)

Answer 220

``` Increased JVP with giant V waves - V regurg together RV heave Murmur - PSM - LLSE in inspiration (Carvallo's sign) - Pulsatile hepatomegaly - Jaundice ```

Answer 221

LFTs - Cardiac Cirrhosis Echo - TOE, TTE assessment of L/R heart EF. ECG - AF CXR - Cardiomegaly, pleural effusion, presence of pacemaker.

Answer 222

- treatment of underlying cause (endocarditis, rheumatic valvulitis, carcinoid). - Close follow up - Medical treatment (management of HF) Diuretics, ACEi, digoxin - Surgical: valve replacement. or annuloplasty.

Answer 223

- Rheumatic Fever (with MV and AV disease). Group A streptococcus antigens cross react and lead to an inflammatory response of the host tissue. Requirement case of group A streptococcal pharyngitis? - Rare condition defined by an abnormally elevated pressure gradient across the tricuspid valve - Can be due to Carcinoid heart disease (intestinal tumour mets to liver).

Answer 224

- Fatigue - Dyspnoea (Concomitant mitral stenosis present in >95% of cases of rheumatic TS). - Ascites - Oedema

Answer 225

- Large A waves (hallmark of TS). Due to a poorly compliant right ventricle (increasing the impedence against which the right atrium has to eject blood) STANosis. - Opening Snap - Murmur EDM LLSE in inspiration. Can be similar to MS. If right heart signs involved, must have high index of suspicion. Murmur increases in intensity with inspiration and squatting.

Answer 226

- Medical: diuretics - fluid and sodium restriction + diurectics to treat right heart failure. If carcinoid somatostatin analogues. - Surgical: repairs, replacement. Percutaneous balloon tricuspid dilatation For Rheumatic fever - intractable RHF or low CO following initial illness. Surgical Valve here is primary treatment in severe disease.

Answer 227

- Any cause of pulmonary HTN. (MS, Pulmonary Disease/Pulmonary HTN). Endocarditis. Rheumatic Heart disease, carcinoid heart disease. - PR 2ndry to MS = Graham-Steell murmur Signs - Murmur: Decrescendo EDM @ ULSE. Inx - ECG (RV dilation + RBBB + RAD, (tall R wave in R1). - TTE + Doppler - CXR

Answer 228

- Results in volume overload + dilation of right ventricle and RVH. LEads to equalisation of pulmonary artery pressure with PV pressure in diastole. - Further more, right-sided stroke volume decreases, leading to peripheral oedema, dyspnoea and easy fatigability.

Answer 229

Non-severe - Medical management of heart failure - May need inotropic support Surgery - If symptomatic with pulmonary valve replacement ± anticoagulation.

Answer 230

- Majority are congenital - Noonans, Williams,Alagille - Also Carcinoid, endocarditis.

Answer 231

Main pathophysiological consequence of PS is RV strain and increase in RV pressure, there is an increase in hypertrophy. Mild to moderate obstruction will be tolerated, but can then present with cyanosis, syncope in severe disease. Eventually, RV cannot cope with stenosis, so patient gets jugular venous distension, peripheral oedema, hepatomegaly, ascites.

Answer 232

Dyspnoea Fatigue Ascites Oedema

Answer 233

- Dysmorphia of Williams, Noonans etc. - Large A waves (large - Rheumatic fever - Dyspnoea - Chest pain - Fatigue - RV heave - Ejection click, soft P2 (loudest over left upper sternal border. Long and harsh murmur peaking later in systole. - Murmur ESM ULSE --> L shoulder - Signs of RHF

Answer 234

``` - ECG P pulmonale (peaked P wve in II and V1 - V3) RAD RBBB - CXR Prominent pulmonary arteries: post-stenotic dilatation - Echo with doppler - Catheterisation: diagnostic ```

Answer 235

MIld disease: Observation Moderate - Percutaneous balloon pulmonary valvuloplasty, surgical valvuloplasty, endocarditis prophylaxis prior to high risk procedures.

Answer 236

Cardiac valves develop vegetations composed of bacteria and platelet-fibrin thrombus.

Answer 237

Cardiac disease --> Subacute Normal valves --> acute. - Prosthetic valves - Degeneration valvulopathy - VSD, PDA, CoA - Rheumatic Fever - Dental caries - Post-op wounds - IVDU (tricuspid valve) - immunocompromised (inc DM)

Answer 238

Culture +ve Strep viridans (>20%) second most common. Also strep mitis and strep sanguini. Classically linked to poor dental hygiene. - S. bovis - linked to colorectal cancer - Staph aureus (coagulase +ve) = IVDU - most common cause - S. epidermidis (coagulate negative) - Patients with previous prosthetic valve. Enterococci Pseudomonas S. haemolyticus/capitis both coagu negative but rare Culture -ve (HACEK) or Right sided - Haemophillis - Actinobacillus - Cardiobacterium - Eikenella - Kingella - Coxiella - Chlamydia Non-infective - SLE - Marantic

Answer 239

- Fever, rigors* (really important) - Night sweats - Weight loss - Anaemia - Splenomegaly* - Clubbing* - Embolic phenomena Abscesses in brain, heart, kidney, spleen, gut and lung (if right sided) Janeway lesions - painless palmar macules (septic emboli from left-sided valves)

Answer 240

``` - new/changing murmur (MR: 85%, AR 55%) (TR murmur often absent) In IVDU it is tricuspid - AV block - LVF ```

Answer 241

- Micro haematuria due to GN - Vasculitis - Roth Spots: Boat shaped retinal haemorrhages with pale centre - Splinter Haemorrhages - Osler Nodes = painful, purple papules on finger pulps.

Answer 242

Duke's Criteria?

Answer 243

Major - 1. +ve blood culture Typical organism in 2 separate cultures or Persistently +ve cultures e.g 3 >12hr apart. - 2. Endocardium involved +ve echo (vegetation, abscess, valve dehiscence or New valvular regurgitation

Answer 244

Minor 1. Predisposition: cardiac lesion, IVDU 2. Fever >38 3. Emboli: Septic infarcts, splinters, Janeway lesions 4. Immune phenomenon: GN, Osler nodes, Roth Spots, Rheumatoid Factor 5. +ve blood culture not meeting major criteria

Answer 245

``` 2 major OR 1 major + 3 minor OR 5 minor ```

Answer 246

Bloods - N chromic, Normocytic anaemia - Increased ESR/CRP - +ve IgG RF (immune phenomenon) - One of the criteria in the Duke's diagnostic criteria - Culture x3, >12hr apart - Serology for unusual organism Urine: Micro Haematuria ECG: AV block Echo: - TTE detects vegetations >2mm - TOE is more sensitive (90-100% vs 50-60%)

Answer 247

- Supportive care (ABCDE) - May need other supportive management - Take blood cultures - BROAD Empirical Antibiotics Native valve endocarditis (NVE): amoxicillin + gentamicin NVE with severe sepsis, penicillin allergy or suspected methicillin-resistent staphylococcus aureus (MRSA): vancomycin + gentamicin NVE with severe sepsis and risk factors gram negative infection: vancomycin + meropenem Prosthetic valve endocarditis: vancomycin, gentamicin + rifampacin When confirmed endocarditis on native valve (Strep) - Benpen ± gentimicin Methicillin-sensitive staph - Consider Nafcillin/oxacillin + Clindamycin HACEK organisms - Ceftriaxone ± gentamicin Fungi: Flucystosine IV + fluconazole PO - Amphotericin if flucytosine resistance or Aspergillus. Consider surgery - Heart failure - Emboli - Valve Obstruction - Prosthetic valve Prophylaxis - ABx prophylaxis solely to prevent IE not recommended ie for dental procedures, upper GI and lower GI tract procedures. GU tract. Mortality - 30% with Staph - 14% with bowel flora - 6% with sensitive streps Infective endocarditis causing congestive cardiac failure is an indication for emergency valve replacement surgery. - Other indications = CCF, Overwhelming sepsis, recurrent embolic episodes, pregnancy.

Answer 248

Acute rheumatic fever is an autoimmune disease that may occur following a group A streptococcal throat infection. If can affect multiple systems, including joints, hearty, brain and skin. Only the effects on the heart can lead to permanent illness. Chronic changes are referred to chronic rheumatic heart disease and without long-term penicillin secondary prophylaxis, acute rheumatic fever can recur, leading to damage of the cardiac valvular tissue.

Answer 249

Group A beta-Haemolytic Strep (pyogenes)

Answer 250

5-15 yrs Rare in west. Common in developing world. Only 2% of population susceptible.

Answer 251

- Ab cross reactivity following S.pyogenes infection. T2 hypersensitivity reaction (molecular mimicry) - Abs vs M protein in cell wall - Cross reaction with myosin, muscle glucogen and SM cells. - Pathology: Aschoff bodies and Anitschokow myocytes.

Answer 252

Revised Jones Criteria - Evidence of GAS infection plus 2 major criteria or 1 major + 2 minor

Answer 253

There is a low and high risk population criteria. Low risk major: JONES = Joints, Carditis, Nodules, Erythema marginatum, Syndenam Chorea. - PanCarditis (clinical and/or subclinical) - Polyarthritis - Chorea - Erythema Marginatum - Subcutaneous nodules

Answer 254

- Fever (>38.5/38) - Polyarthralgia - Elevated inflammatory markers (ESR >60 and/or CRP >28.57 - Prolonged PR interval on ECG. - Previous rheumatic fever

Answer 255

Pancarditis (60%) - Pericarditis: Chest pain, friction pericardial rub (squeaky leather, scratching/rasping). Best heard between apex and sternum - Myocarditis: sinus tachy, AV block, HF, increased CK, T wave inversion. - Endocarditis: murmur MR (most common loudest at apex, radiating to axilla and accentuated when patient is rolled over on their left side), AR, Carey Coombs (pseudo-mitral stenosis because increased flow of regurg volume of blood over mitral valve during diastolic filling of left ventricle)

Answer 256

- Migratory polyarthritis of large joints (esp. knees) - Typically asymmetrical but not always migratory. - Joint swelling, with tenderness, warmth, restricted movement.

Answer 257

- Subcutaneous nodules (2-20%) | - Small mobile, painless nodules on extensor surfaces

Answer 258

- Red, raised edges with central clearing - Trunk, thighs and arms - Smoke rings beneath skin

Answer 259

- Occurs late | - Grimacing, clumsy, hypotonia (Stops in sleep).

Answer 260

- Recent sore throat or scarlet fever - Arthralgia - Pronator sign (turning outwards of arms and palms when held above head)

Answer 261

Bloods: - Strep Ag test or ASOT - Throat culture for Beta-haemolytic group A strep. - FBC, - ESR (>60 low risk, >30 high risk) - CRP (28.57 or >3mg/dL) - WBC - Blood cultures (no growth) to exclude bacteraemia ECG - Prolonged PR interval CXR - Demonstrate CCF, chamber enlargement Echo - morphological changes to the mitral/aortic valves and severity of regurgitation, pericardial effusion if pericarditis present

Answer 262

If diagnosis has not established - hold off NSAIDS, give paracetamol. - Bed rest until CRP normal for 2 weeks - Benpen 0.6-1.2mg IM for 10 days. OR single injection of benzylpenicillin. - Analgesia for carditis/arthritis: aspirin/NSAIDs - Add oral pred if: CCF, cardiomegaly, 3rd degree block (1-2mg/kg/day orally for 7 days). - Chorea: Carbamazepine or valproic acid. - AF: add digoxin or amiodarone LONG TERM - Secondary prophylaxis Benzylpenicillin - 900mg IM every 3-4 weeks adults.

Answer 263

-Attacks last ~3 months - 60% with carditis develop chronic rheumatic heart disease - Recurrence ppted by Further strep infection Pregnancy OCP - Valve disease --> Regurg moves on to stenosis. Leads to rheumatic heart disease. Mitral (70%) Aortic (40%) tricuspid (10%) Pulmonary (2%)

Answer 264

Inflammation of the pericardium. - Acute form - new onset inflammation lasting <4-6 weeks. - Can be fibrinous (dry) or effusive with a purulent,serous or haemorrhagic exudate. - Clinical triad of Chest pain, pericardial friction rub and serial electrocardiographic changes. - Constrictive pericarditis impedes normal diastolic filling and can be late complications of pericarditis. Most common disease of the pericardium encountered.

Answer 265

- Causes Viral (90%) : Coxsackie, flu, EBV, HIV Other (also common) : uraemia, RA, SLE, Sarcoid, radiotherapy Bacterial: pneumonia, rheumatic fever, TB, Staph Fungi MI - Dressler's Drugs: penicillin, isoniazid, procainamide, hydralazine

Answer 266

- Pericardium consists of a 2-layer pliable fibroserous sac covering surface of heart.

Answer 267

Central/retrosternal chest pain - Sharp (mimic MI) - Pleuritic - Worse lying down - Relieved by sitting forward - Radiates to left shoulder Pericardial friction rub (high pitch squeaky) Fever Signs of effusion/tamponade

Answer 268

ECG (most useful) : saddle-shaped ST-elevation ± PR depression (very diagnostic feature) Bloods: FBC (WBC) , ESR/CRP raised, Trop (may be increased), urea elevated in uraemic cause, cultures, virology Echo - All patients should have an echo. may show pericardial effusion, absence of LV wall motion. CXR - Normal or water-bottle shaped enlarged cardiac silhouette May take pericardial fluid/ culture

Answer 269

Triage - Major risk = high fever, large pericardial effusion, cardiac tamponade, failure to respond to 7 days NSAIDs. Minor = myocarditis, immunosuppression, trauma, oral anticoagulant. If tamponade - Urgent pericardiocentesis If purulent - need pericardiocentesis + Vanc + ceftriaxone + NSAID If viral = NSAIDS + PPI + Colchicine + exercise restriction - Consider steroids/immunosuppression If recurrent - NSAID + PPI + Colchicine + exercise restriction

Answer 270

Heart encased in a rigid pericardium - impedes normal diastolic filling and can be a late complication of acute pericarditis. Most cases occur 3-12 months after pericardial insult. TB is the main cause in developing countries. In developed countries, it is caused by prior cardiac surgery, radiotherapy and idiopathic pericarditis.

Answer 271

- RHF with increased JVP - Kussmaul's sign: increased JVP with inspiration, Key sign to distinguish this from cardiac tamponade. - Quiet HS - S3 (Pericardial knock) - caused by diastolic filling of ventricle. Heard in left ventricular failure (dilated cardiomyopathy), constrictive pericarditis, mitral regurg - Hepatosplenomegaly - Ascites, oedema

Answer 272

CXR: small heart + pericardial calcification Echo Cardiac Catheterisation

Answer 273

Surgical Excision - pericardiectomy is removal or portion or all of the pericardium.

Answer 274

- Accumulation of transudate, exudate or blood in the pericardial sac. - Can be due to pericardial inflammation. Increased intrapericardial pressure from pericardial effusion (especially when fluid fills up quickly) can compress the cardiac chambers leading to cardiac tamponade.

Answer 275

- Dypnoea - Increased JVP (prominent x descent) - Bronchial breathing @ let base Ewart's sign: large effusion compressing left lower lobe - Signs of cardiac tamponade may be present

Answer 276

``` CXR: enlarged, globular heart ECG - Low-voltage QRS complex - Alternating QRS amplitude (Electrical alterans) - Echo: Echo free zone around heart. ```

Answer 277

Treat cause Pericardiocentesis may be diagnostic or therapeutic - Culture, ZN stain, cytology - Fluid analysed for glucose, protein, lactate dehydrogenase. Cell count, micro, bacterial/viral culture + cytology performed.

Answer 278

Accumulation of pericadial fluid --> increased intra-pericardial pressure --> poor ventricular filling --> decreased CO

Answer 279

- Any cause of pericarditis - Aortic dissection - Warfarin - Trauma

Answer 280

Beck's Triad: decreased BP, increased JVP, quiet heart sounds Pulsus paradoxus: abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as pulsus paradoxus. Kussmaul's sign

Answer 281

ECG: low-voltage QRS ± electrical alternans CXR: Large, globular heart Echo: Diagnostic, echo-free zone around heart

Answer 282

Urgent pericardiocentesis - 20ml syringe + long 18G cannula - 45, just left of xiphisternum, aiming for tip of left scapula - Aspirate continuously and watch ECG Treat cause Send fluid for cytology, ZN stain and culture.

Answer 283

Causes - Idiopathic (~50%) - Viral: coxsackie B, flu, HIV - Bacterial: S.aureus, syphilis - Drugs: Cyclophosphamide, Herceptin, CBZ, phenytoin - Autoimmune: Giant cell myocarditis associated with SLE.

Answer 284

- Flu-like prodrome: fever, sore throat, myalgia. - Dyspnoea, fatigue - Chest pain (may coexist with Bornholm Disease) - Arrhythmia --> palpitations

Answer 285

``` Age <50. Chest pain Soft S1 S4 gallop (CHF) Signs of autoimmune disease Signs of prior viral syndrome ```

Answer 286

ECG - ST-elevation or depression - T wave inversion - Transient AV block Bloods: +ve trop, increased CK

Answer 287

``` Supportive Rx cause - If autoimmune - Methylprednisolone - Giant cell myocarditis Methylprednisolone ```

Answer 288

- LVOT obstruction from asymmetric septal hypertrophy - AD inheritance (50% sporadic) - B-myosin heavy chain mutation commonest - Ask re family hx of sudden death Can be associated with Friedreich's ataxia, and WPW Septal thickening as as well abnormal, thickened collagen. Mostly marked below the aortic valve.

Answer 289

- Angina - Dyspnoea - Palpitations: AF, WPW, VT - Exertional syncope or sudden death - proposed mechanism is VT secondary to ischaemia and this typically occurs in the setting of extreme exertion. - Syncope after exercise due to subaortic hypertrophy og ventricular septum, and functional aortic stenosis.

Answer 290

- Jerky pulse - Pulsus bisferiens - Large a waves - Double Apex beat - This transient interruption in cardiac output occurs when anterior leaflet of the mitral valve is pulled into the left ventricular outflow tract during systole). - Harsh ESM @ LLSE with systolic thrill increased on Valsalva manoeuvre and decreased on squatting. - S4 - contracting against a stiff ventricle.

Answer 291

ECG - HOCM associated with WPW congenital accessory conducting pathway between atria and ventricles leading to AVRT. - Deep Q waves - LVH/LAD/L strain - Abnormal ST waves, T waves. (Non-specific) - ST depression - Giant T wave inversion - Ventricular ectopics, VT, VF CXR - Cardiomegaly Echo - Exercise test ± holter (may be normal or demonstrate ventricular or supraventricular arrhythmia) monitor to quantity risk - LVH, - Asymmetric septal hypertrophy MR SAM ASH - Mitral regurg, systolic anterior motion of mitral valve leaflet, ash.

Answer 292

ABCDE - Amiodarone, Beta blockers, Cardioverter defib, Dual chamber pacemaker, endocarditis prophylaxis Medical - -ve inotropes: 1st - B-B, 2nd verapamil. Negative inotropic and chronotropic agents. Help alleviate obstruction - Amiodarone: arrythmias (blocks potassium) - Anticoagulate: if AF or emboli. Warfarin 2-10mg Non-medical (symptomatic: predominant non-obstructive with preserved systolic function) - Consider ICD if at any stage during therapy they are found to be at a higher risk level. - Sudden cardiac death caused by ventricular arrythmias that can be effectively treated by implantable cardioverter defibs.

Answer 293

- Unknown origin - Familial myxomas have an autosomal-dominant transmission. May present as a component of a Carney's complex (An AD condition comprising myxomas, endocrine tumours, spotty pigmentation of the skin). - Rare, benign cardiac tumour - May be familial, e.g Carney Complex - Cutaneous myxoma, skin pigmentation and endocrinopathy (Cushings).

Answer 294

- Constitutional symptoms: Clubbing, fever, weight loss, increased ESR. - Dyspnoea, syncope, dizziness (Mitral valve obstruction). - Signs similar to mitral stenosis (MDM, systemic emboli, AF) but vary with posture. Diagnosis: Echo Management: Excision

Answer 295

- Rigid walls but not thickened. - Heart restricted from stretching and filling with blood properly. - Much like Constrictive pericarditis

Answer 296

miSSHAPEN - Sarcoid - Haemochromatosis - Amyloidosis - Primary: endomyocardial fibrosis - Eosinophilia (Loffler's eosinophilic endocarditis) - Neoplasia: carcinoid (--> TR and PS) - Post-radiotherapy

Answer 297

``` RVH with raised JVP Kussmaul's sign: increased JVP with inspiration Quiet Heart sounds S3 Hepatosplenomegaly ```

Answer 298

- Catheterisation and treat cause. - Allows for ventriculography to be performed. Ejection fraction, ventricular size, wall motion and left ventricular outflow tract size can be estimated. - Important to distinguish constrictive pericarditis and restrictive cardiomyopathy - use ECG Cardiac MRI, cardiac catheterisation.

Answer 299

- Heart becomes enlarged and cannot pump blood effectively.

Answer 300

DILATE - Dystrophy: muscular, myotonic, glycogen storage disease - Infection: complication of myocarditis, Coxsackie B. - Late pregnancy: peri-, post-partum - Autoimmune: SLE - Toxins: Alcohol (big cause), doxorubicin, cyclophosphamide, DXT - Endocrine: thyrotoxicosis

Answer 301

- LVF and RVF | - Arrhythmias

Answer 302

- Increased JVP - Displaced apex - S3 gallop - decreased BP - MR/TR

Answer 303

- CXR: cardiomegaly, pulmonary oedema - ECG: T inversion, poor progression, wide QRS/LBBB. - Echo: globally dilated, normal or decreased wall thickness, hypokinetic heart + decreased EF - Catheter + biopsy: myocardial fibre disarray. Increased ventricular size on ventriculography - used to form coronary angiogram

Answer 304

- Bed Rest - Medical: diuretics, ACEi, digoxin, anticoagulation - Non-medical: biventricular pacing, ICD - Surgical: heart Tx

Answer 305

No problems at birth - Most eventually develop stenosis ± regurgitation - Pre-disposed to IE/SBE

Answer 306

- Hole connects the atria - Secundum defects high in the septum are commonest - Often asymptomatic until adulthood - LV compliance decreased with age --> increased L--> R shunt. - Pressure difference between atria lower than ventricles therefore emboli has travelled through ASD rather than VSD to cause a stroke. Ostium secundum (70% of ASDs) - associated with Holt-Oram Syndrome - ECG: RBBB with RAD LV compliance increased with age, as LV becomes less compliant and gets more stiff. Therefore the right atrium, ventricle and pulmonary arteries may enlarge due to increased volume load. The Pulmonary and Tricuspid valves may become incompetent due to enlargement of valves annuli.

Answer 307

- Dyspnoea - Pulmonary HTN - Arrhythmia - Chest pain

Answer 308

- AF - Increased JVP - Pulmonary ESM (excess volume of blood crossing pulmonary valve) - Pulmonary HTN --> TR or PR - Fixed splitting of the second heart sound: does not become single with expiration.

Answer 309

- Paradoxical emboli - venous thrombus into a systemic arterial circulation through the ASD and may present as a stroke or TIA. - Eisenmenger's syndrome. Long-standing L--> R shunt due to VSD/ASD/PDA leading to reversal due to PHTN and overall cyanosis. Increased RA pressure: R--> L shunt --> cyanosis

Answer 310

- ECG: Secundum will show Right Axis Deviation (right atrial enlargement where P waves >2.5mm, R waves greater than upper limit for RVH. Crochetage pattern in R wave in inferior limb leads (notch near the apex of R wave) - Echo: Visualisation of the defect: flow pattern and shunt volume ascertained. - CXR: Pulmonary plethora - Normal or enlarged heart with increased pulmonary markings.

Answer 311

- Transcatheter closure - median sternotomy/ or cath lab. - Recommended in adults if high pulmonary to systemic blood flow ratio (>1.5:1) - In L--> R shunt acute consider closure. Normally at age 2-4 + prophylaxis for antibiotics for bacteraemia. In R-->L shunt which is reversible - use corrective closure. For Eisenmenger's syndrome - irreversible shunt therefore avoid pregnancy, dehydration and high altitude. Give pulmonary vasodilators - bosentan/sildenafil. Monitor + treat hyperviscosity due to erythrocytosis to compensate for hypoxaemia - phlebotomy. Consider heart/lung transplant.

Answer 312

- Congenital narrowing of the aorta - Usually occurs just distal to origin of left subclavian - More common in males - Most common at the insertion of the ductus arteriosus, distal to the left subclavian.

Answer 313

Bicuspid aortic valve | Turner's syndrome

Answer 314

- Radio-femoral delay + weak femoral pulse - Hypertension - upper extremity systolic hypertension or murmur. - Systolic murmur/bruit heard best over left scapula

Answer 315

- heart failure | - IE

Answer 316

HTN presenting at young age or resistant to treatment - Diminshed lower extremity pulse - Differntial upper + lower extremity BP. - May have an systolic ejection murmur maximal over back or under left clavicle.

Answer 317

- ECG - infants may show right ventricular hypertrophy. Children may show LVH. - Chest X-ray: cardiomegaly or posterior rib notching, 3 sign. (not seen in young children) - Echo: Discrete narrowing in the thoracic aorta: pressure gradient across narrowing. CT angiogram

Answer 318

- Balloon dilatation + Stenting | - Percutaneous stent implantation in repair of aortic coarctation.

Answer 319

Hole connecting ventricles

Answer 320

Congenital | Acquired: MI

Answer 321

- Risk factors (Down's Syndrome or maternal use of alcohol during pregnancy) - Pansystolic murmur left parasternal region. Does not increase with inspiration. Smaller defect is generally louder. - Best heard on the lower left sternal border. - Left parasternal heave - Larger holes have high pressure PHT. - Failure to thrive - SOB - Recurrent pulmonary infections

Answer 322

- Infective endocarditis (high flow rate of VSD). May need prophylaxis - PHT - Eisenmenger's

Answer 323

ECG - Small: Normal - Large: LVH + RVH This is because of left to right shunting and variable amount of PHT. CXR - Small: mild pulmonary plethora - Large: cardiomegaly + marked pulmonary plethora (also common in Eisenmenger's) Echo - Single most important + useful tst. Colour flow Doppler are usually diagnostic.

Answer 324

- Prophylactic antibiotics: amoxicillin because of IE. - Surgical closure indicated if symptomatic VSD with large shunt. - Preoperatively furosemide Should be corrected to avoid Eisenmenger's Syndrome. Consider pulmonary vasodilators - bosentan/sildenafil

Answer 325

Congenital Cardiac Malformation - Anterior + cephalad deviation of outlet of ventricular septum - 1) Mal-alignment ventricular septal defect - 2) aorta overriding the VSD - 3) Right ventricular outflow tract obstruction (Pulmonary Stenosis) - 4) secondary right ventricular hypertrophy Due to abnormal separation of truncus arteriosus into aorta and pulmonary arteries.

Answer 326

Di-George: Catch 22q11 deletion. Alagille's syndrome: Jagged1 Trisomy: 21, 18, 13

Answer 327

Infants: Hypercyanotic episodes, squatting and clubbing Adult: Often asymptomatic, unoperated: cyanosis, ESM of PS (left sternal border) across narrowed right ventricular outflow tract. Repaired: dyspnoea, palitation, RVF

Answer 328

O2: baby may be hypoxaemic ECG: RVH + RBBB CXR: Coeur en sabot. Boot-shaped heart + normal cardiac silhouette does not rule out cyanotic heart disease. Echo: anatomy + degree of stenosis. Overriding aorta, non-restrictive VSD, RVH.

Answer 329

Surgical closure (usually before 1yr) - Blalock-Taussig Shunt. - Closure of VSD - Correction of pulmonary stenosis Management of hypercyanotic spells - Knees to the chest. Supportive care with B-blockers, Phenylephrine. Profound cyanosis of baby- Alprostadil (Prostaglandin E1) to maintain patency of ductus arteriosus.

Answer 330

- Autosomal Dominant - Characterised by loss of elastic tissue, resulting in musculoskeletal deformities, lens subluxation, aortic dissection and root aneurysms. - Spontaneous mutation in 25% - M =F - Prevalence = 1/5000

Answer 331

Mutation in FBN1 gene on Chr 5 - Encodes fibrillin=1 glycoprotein - Fibrillin-1 is essential component of elastin - Cystic medial necrosis

Answer 332

``` Cardiac - Aortic aneurysm and dissection - Aortic root dilatation --> regurgitation - MV prolapse ± regurgitation (non-ejection systolic click) Ocular - Lens dislocation: superotemporal MSK - High-arched palate - Arachnodactyly (long slender fingers) - Arm-span > height - Pectus Excavatum (excavate = dig hole therefore funnel chest)> - Scoliosis - Pes planus - flat feet - Joint hypermobility ```

Answer 333

- Ruptured aortic aneurysm (sudden, stabbing onset chest pain). LOC, signs of abdominal ischaemia. - Spontaneous pneumothorax - Diaphragmatic hernia - Abdominal hernia

Answer 334

``` - 3/4 organ systems must be involved Family history Lens subluxation MSK findings Aortic dilatation or dissection ```

Answer 335

- MEN-2b - Homocystinuria - Ehlers-Danlos

Answer 336

- Echo (aortic regurg, aortic root dilation, ascending aortic dissection, mitral valve prolapse) . - CT scan - Aortic root dilation or ascending aortic dissection. - Slit lamp examination: ectopia lentis, visualisation of subluxed dislocated lens). Elevated intra-ocular pressure. - Consider CXR (widened mediastinum, scoliosis, pneumothorax). - ECG - Arrhythmias. - MRI - dural ectasia 9dilation of neural canal) - Genetic testing - FBN-1 mutation.

Answer 337

- Refer to ortho, cardio and ophtho - Lifestyle alteration: decreased cardiointensive sports - Beta-blockers slow dilatation of the aortic root (metoprolol, atenolol), then consider ACEi, lorsartan). - Management lens subluxation (spectacles etc) - Regular cardiac echo Surgery when aortic root 4.5cm-5 wide. - Give endocarditis prophylaxis prior to high-risk procedure.

Answer 338

``` Rare heterogeneous group of collagen disorders. 6 subtypes with varying severity. Commonest types (1 and 2) are AD. ```

Answer 339

- Hyperelastic skin - Hypermobile joints - Cardiac: MVP, AR, MR and aneurysms - Fragile blood vessels --> Easy bruising, GI bleeds. (Tissue fragility) - Poor healing

Answer 340

Cutis Laxa: loose skin + hypermobile joints Pseudoxanthoma elasticum: skin laxity Marfan's

Answer 341

MS and Skin manifestations, then Cardio and GI. Joint hypermobility is the only universal symptom.

Answer 342

- Avoid contact sports - Encourage minimise risk of injury. - Genetic counselling - Pain management + physiotherapy.

Answer 343

Mitral valve prolapse. Mitral regurg is also common.

Answer 344

Selective a1-blocker used to treat hypertension.

Answer 345

Ionotropic agents for patients in shock.

Answer 346

- Education + lifestyle such as hydration and salt intake. - Discontinuation of vasoactive drugs e.g nitrates, antihypertensives, neuroleptic agents, dopaminergic drugs - Medication treatment? fludrocortisone, midodrine, head-up tilt sleeping.

Answer 347

Increases renal sodium reabsorption and increase plasma volume.

Answer 348

- Ratio of chest compressions to ventilation is 30:2 - Chest compression are now continued while a defib is charged - Shock at 150J - during VT/VF cardiac arrest, adrenaline 1mg is given once chest compressions have restarted after the 3rd shock and then every other shock. - Amiodarone given at same time as adrenaline whilst still performing CPR (300mg). 2nd dose of amiodarone given after total of 5 defib attempts. - A single shock for VF/Pulseless VT followed by 2 mins of CPR, rather than a series of 3 shocks followed by 1 min CPR. - asystole/pulseless-electrical activity: adrenaline 1mg should be given as soon as possible. Should be treated with 2 minutes of CPR prior to reassessment of the rhythm. - Atropine no longer recommended for routine use in asystole or PEA Important to note difference in management in a patient who has a witnessed or monitored shock in CCU, cath lab or crit care. If here VF or pVT identified, patient should be given 3 successive shocks then CPR given.

Answer 349

Polymorphic VT - Acute treatment is IV Magnesium 2g over 10 mins. - Do not give amiodarone. - Correct electrolyte abnormalities such as hypokalaemia.

Answer 350

<6 years = 150micrograms (0.15ml 1 in 1000) 6-12 years = 300 micrograms (0.3ml 1 in 1000) Adults = 500 micrograms 0.5 1 in 1000, 200mg hydrocortisone, 10mg of chlorphenamine. Can be repeated every 5 mins.

Answer 351

Warfarin is an oral anticoagulant - prevents reduction of Vit K to active form. Affects factors 2, 9, 7, 10. Overdose of warfarin = increased APTT and PT - Major bleeding on warfarin - Stop warfarin, give IV vit K 15mg. Prothrombin complex concentrate - if not available then FFP. Used to reverse warfarin - INR >8.0 minor bleeding Stop warfarin Give intravenous vit K 1-3mg Repeat dose of vit K if INR still too high after 24hr. Restart warfarin when INR <5.0. INR >8 No bleeding - Stop warfarin Give vitamin K 1-5mg by mouth, using the intravenous preparation orally Repeat dose of vitamin K if INR still too high after 24 hours Restart when INR < 5.0 INR 5.0-8.0 Minor bleeding Stop warfarin Give intravenous vitamin K 1-3mg Restart when INR < 5.0 INR 5.0-8.0- No bleeding - Withhold 1 or 2 doses of warfarin - Reduce subsequent maintenance dose Indications? - Venous thromboembolism: target INR = 2.5 - AF, target INR = 2.5 - Mechanical heart valve. Mitral valve requires higher INR than aortic valve. - Bioprosthestic valve = 2.5 for first 3 months. - Recurrent PE = 3.5 LMWH is rapid acting, therefore need LMWH. Factors potentiating warfarin - Liver disease - P450 enzyme inhibitors - Cranberry juice - Drugs displacing warfarin from albumin (NSAIDS) - Inhibiting platelet function: NSAIDs. Side effects - Haemorrhage - Teratogenic, although can be used in breastfeeding mothers. - Skin necrosis - Purple toes Patients taking warfarin should avoid food high in vitamin K, such as sprouts, spinach, kale and broccoli.

Answer 352

Sinus Brady Junctional rhythm First degree heart block Wenckebach phenomenon

Answer 353

Take an ARB over an ACEi.

Answer 354

- Large vessel vasculitis. - Typically occludes the aorta and questions commonly refer to an absent limb pulse. - More common in females and Asian people. Features - Systemic features of a vasculitus e.g malaise, headache. - Unequal blood pressure in upper limbs - Carotid bruit - Intermittent claudication - Aortic regurg Associated with renal artery stenosis. Manage with Steroids

Answer 355

Tear in the tunica intima of the wall of the aorta Associations - HTN - most important - Trauma - bicuspid aortic valve - collagens: Marfan's, ED syndome - Turner's/Noonan's - pregnancy - Syphilis

Answer 356

- Chest pain: typically severe, radiates through to the back and tearing in nature - Aortic regurg - HTN - Other features may result from the involvement of specific arteries. Complications of backward tear - Aortic incompetence/regurgitation - MI: inferior pattern due to right coronary involvement Complications of forward tear - unequal arm pulses and BP - Stroke - Renal failure

Answer 357

Stanford classification - Type A = ascending aorta, 2/3 of cases. ascending aorta to at least the aortic arch. Therefore can lead to MI or Neurological symptoms. - Type B - Descending aorta, distal to left subclavian origin DeBakey - Type I - originates in ascending aorta to at least the aortic arch. Therefore can lead to MI or Neurological symptoms. - Type II - originates in and is confined to the ascending aorta - Type III - origin in the descending aorta, rarely extends proximally but will extend distally. Management - Type A = Surgical management but BP should be controlled at 100-120 SBP whilst waiting. EVAR or Open intervention. - Type B = conservative management, bed rest + reduce bp with IV labetalol Analgesia. If uncomplicated (no end-organ involvement).

Answer 358

Pericarditis

Answer 359

Shingles - pain + paraesthesia often precede vesicular rash seen

Answer 360

Pneumothorax

Answer 361

Pericarditis

Answer 362

Dissecting aortic aneurysm

Answer 363

Flap or filling defect in aortic intima. BLood tracks into medial layer. Tearing intrascapular pain. Type A or B.

Answer 364

Mackler's triad of Boerhaave's syndrome: vomiting, thoracic pain and subcutaneous emphysema. - Spontaneous rupture of oesophagus as a result of repeated episodes of vomiting - Ruptures is usually distally sited + on the left side. - Sudden onset of severe chest pain that may complicate severe vomiting. Treated with thoracotomy + lavage.

Answer 365

Aged less than 80 with stage 1 HTN with one or more of target organ damage, established CVS, renal disease, diabetes or a 10yr CVS risk fo 10% or more.

Answer 366

``` Aortic stenosis Pulmonary stenosis HOCM Atrial septal defect Tetralogy of Fallot ```

Answer 367

Mitral/tricuspid regurg | Ventricular septal defect

Answer 368

Mitral valve prolapse | Coarctation of aorta

Answer 369

``` Aortic regurg (high-pitched blowing) Graham steel (pulmonary regurgitation) ```

Answer 370

``` Mitral stenosis (rumbling) Austin-Flint murmur (severe aortic regurg) ```

Answer 371

HTN - Can drive. If 180 or more cannot. Angioplasty 1 week off driving CABG - 4 weeks off driving ACS - 4 weeks off driving 1 week if treated by angioplasty Angina - Driving must cease if symptoms occur at rest Pacemaker insertion - 1 week ICD - if for Ventricular arrhythmia = 6 months. Successful cathether ablaiton for arrhythmia - 2 days AAA of 6 cm - notify DVLA Lorry - Patient must notify the DVLA, may not drive for at least 6 weeks.

Answer 372

Shortening of the QT J waves (osborne) Can lead to VT

Answer 373

Inhibit action of HMG-CoA reductase. - SE: Myopathy. (more common in simvastatin + atorvastatin than rosuvastatin). This included myalgia, myositis, rhabdomyolisis, asymptomatic raised CK. - Liver impairment: discontinue if transaminases 3x upper limit of normal - May increase risk of intracerebral haemorrhage CI: macrolides + pregnancy Erythromycin + clarithromycin can induce a statin-induced myopathy

Answer 374

All people with CVS Anyone with a 10 yr CVS risk of 10% Patient with T2DM to determine if they need it T1DM more than 10 yrs ago. Take at night. - Primary prevention = Atorvastatin 20mg (10 yr risk >10%, most type 1 diabetes, or CKD eGFR <60, older than 40) - Secondary prevention 80mg Known IHD or CVD, peripheral artery disease. When on statins - Check LFTs at baseline, 3 months and 12 months.

Answer 375

``` Bisoprolol/Beta-blocker - Side effects Bronchospasm Cold peripheries Fatigue Sleep disturbance Erectile dysfunction ``` Contraindications - Uncontrolled heart failure - Asthma - sick sinus - concurrent verapamil use. Beta-blockers can theoretically suppress all of the adrenergic mediated symptoms of hypoglycaemia therefore lead to unawareness of hypoglycaemic events.

Answer 376

Recurrent episodes of collapse + normal resting ECG, 24hr Holter would be pertinent to investigate any underlying arrhythmias.

Answer 377

- Removing the patient from the cold environment and removing any wet/cold clothing, - Warming the body with blankets - Securing the airway and monitoring breathing, - If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient's body - Don't put the person into a hot bath. - Don't massage their limbs. - Don't use heating lamps. - Don't give them alcohol to drink.

Answer 378

Patients with major risk factors should consider wearing anti-embolism stockings. These can either be bought by the patient or prescribed (class I). Clearly if the risk is very high (e.g. a long-haul flight following recent major surgery) then consideration should be given to delaying the flight or specialist advice sought regarding the use of low-molecular weight heparin.

Answer 379

- Buerger's Disease (thromboangiitis obliterans) of small and medium vessel vasculitis that is strongly associated with smoking. - Features include extremity ischaemia: intermittent claudication, ischaemic ulcer, superficial thrombophlebitis. Raynaud's phenomenon.

Answer 380

Verapamil is a highly negatively inotropic calcium channel-blocker; it reduces cardiac output, slows heart rate and may impair atrioventricular conduction. The BNF recommends that verapamil is not given to patients taking beta-blockers because of the risk of hypotension and asystole. Do not give it in VT either

Answer 381

Nitrates are involved in reducing venous return through increased venous capacitance/venous dilatation but also cause large artery dilatation. As a consequence of the reduced venous return, the diastolic filling time is increased. Therefore Decreased ejection time, decreased arterial pressure, decreased LV diastolic pressure and decreased ventricular volume. Avoid in patients with hypotensions SE: Hypotension, tachycardia, headaches and flushing.

Answer 382

Higher probability of causing a prolonged QT interval if administered IV or in combo with other antipsychotic drugs.

Answer 383

``` Antiplatelet = established cardiovascular disease Anticoag = AF, VTE, Valvular heart disease. ``` Stop Antiplatelet - start anticoag. In Post-acute coronary syndrome = much stronger indication for antiplatelet = triple therapy (2 antiplatelets + 1 anti-coag) for 4 weeks - 6 months after event and dual therapy (1 antiplatelet + 1 anticoag) to complete 12 months. VTE - patient on antiplatelets develops VTE they are likely to be given anticoag for 3-6 months.

Answer 384

Postural hypotension Loss of respiratory arrhythmias Erectile Dysfunction T2DM mainly sensory and autonomic neuropathy

Answer 385

Defined as fall of SBP >20mmHg after 3 minutes or at least DBP 10mmHg after 3 mins. Caused by hypovolaemia (venous pooling) After meals autonomic dysfunction: diabetes, Parkinson's. Drugs: Diuretics, antihypertensives, L-dopa, Phenothiazines.

Answer 386

If able to respond - mild airway obstruction: - Encourage patient to cough If serious (cannot respond) - Give up to 5 back-blows - If unsuccessful give up to 5 abdominal thrust - If unsuccessful continue the above cycle. If unconscious - Call for ambulance - Start cardiopulmonary resus

Answer 387

Hypoxia Hypovolaemia Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders Hypothermia Thrombosis (coronary or pulmonary) Tension pneumothorax Tamponade – cardiac Toxins

Answer 388

Do chest compressions in PEA asystole 2 mins of 30:2 then reassess 1mg Adrenaline is given IV immediately in PEA. 1

Answer 389

Pedunculated heterogeneous mass on echo. Atrial myxoma is a benign tumour most commonly occurring in the left atrium. It can present with the triad of mitral valve obstruction, systemic embolisation and constitutional symptoms such as breathlessness, weight loss and fever.

Answer 390

Takayasu's arteritis is a vasculitic disorder generally affecting young Asian women. It affects the aorta and its branches and causes both systemic features and those specific to which vessels coming off of the aorta are affected. It is associated with renal artery stenosis - systemic features of a - vasculitis e.g. malaise, headache - unequal blood pressure in the upper limbs - carotid bruit - intermittent claudication aortic regurgitation (around 20%)

Answer 391

Bradycardia J wave 1st degree heart block Long QT

Answer 392

HTN (systemic or pulmonary) Hyperdynamic states Atrial septal defects without P HTN

Answer 393

Aortic Stenosis

Answer 394

Atrial septal defect

Answer 395

Deep inspiration RBBB Pulmonary stenosis Severe mitral regurg

Answer 396

``` LBBB Severe aortic stenosis Right ventricular pacing WPW PDA ```

Answer 397

Loop diuretics ``` hypotensions hyponatraemia Hypokalaemia hypocalcaemia hyperglycaemia gout Ototoxicity ```

Answer 398

Infective = Coxsackie B, Chagas. Infiltrative = Amyloid Storage = Haemachromatosis Toxicity = Doxorubicin, Alcoholic CM Inflammatory = Sarcoidosis Endocrine = DM, Thyroxicsis Neuromuscular = Friedreich's ataxia, Duchenne-Becker muscular dystrophy

Answer 399

5 days before planned surgery and once the person's INR is less than 1.5

Answer 400

Sleep disturbance ``` Bronchospasm Cold peripheries Fatigue Sleep disturbance Erectile dysfunction ```

Answer 401

O-Devices ``` O- Omeprazole Disulfarim Erythromycin Clarithromycin Ciprofloxacin Isoniazid Cimetidine Allopurinol SSRI Ritonavir Sodium valproate Fluconazole ``` P450 inducers include - PC BRAS - - Phenytoin - Carbamazepine - Chronic alcohol - Barbitone - Rifampicin - St John's Wort - Smoking

Answer 402

Broken Heart syndrome - Takotsubo's apical ballooning syndrome - Described as an octopus trap. - Bottom of the heart does not contract.

Answer 403

Non-specific phosphodiesterase inhibitor and decreased cellular uptake of adenosine. Use as an antiplatelet mainly after an ischaemic stroke.

Answer 404

Inhibits conversation of Angiotensin 1 to II. SE: Cough, angioedema, hyperkalaemia, first-dose hypotension. Cautions: Avoid in pregnancy, with aortic stenosis may result in hypotension. ACEi with potassium >5 needs help. INteractions - pAtients with high-dose diuretics therapy (80mg) - leads to hypotension. Monitoring - U+E. Rise in creatinine + potassium may be expected after starting ACE. Changes in 30% baseline + increased in potassium up to 5.5mmol. If there is a rise of creatinine by >100% or to above 310 micromols or if potassium rises to >5.5 mmol ACEi should be stopped.

Answer 405

Massage carotid artery for 5 seconds. Stimulates baroreceptors + PNS. Increased vagal tone + SA + AV node, leading to decrease in BP and HR> Cardioinhibitory = ventricular pause of >3 seconds. Vasodepressive - Fall of SBP >50mmHg.

Answer 406

These techniques use radiotracers which are extracted by normal myocardium. Examples include: thallium technetium (99mTc) sestamibi: a coordination complex of the radioisotope technetium-99m with the ligand methoxyisobutyl isonitrile (MIBI), used in 'MIBI' or cardiac Single Photon Emission Computed Tomography (SPECT) scans fluorodeoxyglucose (FDG): used in Positron Emission Tomography (PET) scans The primary role of SPECT is to assess myocardial perfusion and myocardial viability. Two sets of images are usually acquired. First the myocardium at rest followed by images of the myocardium during stress (either exercise or following adenosine / dipyridamole). By comparing the rest with stress images any areas of ischaemia can classified as reversible or fixed (e.g. Following a myocardial infarction). Cardiac PET is predominately a research tool at the current time

Answer 407

Yellow vesicles on extensor surfaces - elbows, knees. familial hypertriglyceridaemia lipoprotein lipase deficiency

Answer 408

familial hypercholesterolaemia | remnant hyperlipidaemia

Answer 409

surgical excision topical trichloroacetic acid laser therapy electrodesiccation

Answer 410

Class 3 antiarrhythmic used to treat atria, nodal and VT. Blocks potassium channels which inhibit repolarization. - Long half-life (20-100days) - Give in central veins - Lengthens QT - Interacts with p450 inhibitors. - Numerous long-term adverse effects. Monitor TFTs, LFTs, U+E, CXR prior to treatment TFTs, LFTs every 6 months. ``` Adverse effects - thyroid dysfunction: both hypothyroidism and hyper-thyroidism - corneal deposits - pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis - peripheral neuropathy, myopathy - photosensitivity - 'slate-grey' appearance - thrombophlebitis and injection site reactions bradycardia lengths QT interval ```

Answer 411

Ivabradine indicated for symptomatic relief of angina in patients with HR of >70. Deals with mixed sodium and potassium channels. Slows heart rate via SAN. Most common side effect is the transient luminous phenomenon. Also headaches and Heart block. Affects by CYP450 inducers or inhibitors.

Answer 412

If surgery can wait 6-8hr = give 5mg vit K IV. Ig surgery can't wait - 25-50 units Stop warfarin before elective or emergency surgery

Answer 413

Bipap = Breathing + sucking away excess CO2, therefore used in T2RF or mechanical resp failure. CPAP is just continous - so mostly in low O2. Pushing more O2 in.

Answer 414

Activates antithrombin III

Answer 415

- Grade 1 - Very faint murmur, frequently overlooked - Grade 2 - Slight murmur - Grade 3 - Moderate murmur without palpable thrill - Grade 4 - Loud murmur with palpable thrill - Grade 5 - Very loud murmur with extremely palpable thrill. Can be heard with stethoscope edge - Grade 6 - Extremely loud murmur - can be heard without stethoscope touching the chest wall

Answer 416

Clotting in arterial system is mainly platelet driven. Clotting in venous system /AF is blood stasis, not due to damage of endothelium, therefore mostly clotting factor driven.