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Finals > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the causes of AF and then split into cardiac and nomn cardiac

A
  • S : sepsis
  • M : mitral stenosis or regurgitation
  • I : IHD
  • T : thyrotoxicosis
  • H : hypertension !
  • Cardiac : HTN, myocarditis, IHD
  • Non cardiac : sepsis, hyperthyroid, alcohol abuse
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2
Q

What are the symptoms of AF?

A

SOB
Palpitations
General fatigue
Dizziness or syncope

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3
Q

What might an ECG show in someone with AF?

A
  • Absent P waves
  • Narrow QRS complex tachycardia
  • Irregularly irregular ventricular rhythm
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4
Q

What is a differential for AF?

A
  • Ventricular ectopics : also shows an irregularly irregular pulse but they disappears when the HR gets past a certain threshold
  • Normal HR on exercise = ventricular ectopic
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5
Q

What are the 2 treatment options for AF?

A
  • Rate control
  • Rhythm control
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6
Q

What is rate control in AF?

A
  • Aims to reduce the HR to <100 to allow more time for the ventricles to fill with blood
  • 1st line = BB (atenolol)
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7
Q

when would rhythm control be used for management of AF ?

A
  • Reversible cause of AF
  • Onset within 48hrs
  • HF
  • Still have symptoms despite rate control
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8
Q

What are the 2 methods of anticoagulation in AF?

A
  • DOAC
  • Warfarin

- DOACS - direct acting oral anticoagulants (apixaban, rivaroxaban and dabigatran)

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9
Q

What is the issue with warfarin as an anticoagulant?

A
  • Requires close monitoring of the pts INR
  • Warfarin is a vit K antagonist
  • Vit K is needed for synthesis of certain clotting factors
  • Warfarin therefor increases prothrombin time
  • INR assesses how anti-coagulated blood is on warfarin by calculating PT time and comparing that to normal healthy patient.
  • Target INR for AF pt = 2-3
  • Warfarin is also affected by other drugs (e.g. antibiotics)
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10
Q

What score is used to assess the risk of stroke in pt with AF?

A

CHA2DS2VASc

  • C : congestive heart failure
  • H : HTN
  • A2 : age (>75) - scores 2
  • D : DM
  • S2 : stroke or previous TIA (scores 2)
  • V : vascular disease
  • A : age (65-74)
  • S : sex (female)
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11
Q

What score is used to assess the risk of a major bleed whilst on anti-coagulants ?

A

ORBIT

  • Older age (>75)
  • Renal impairment (GFR <60)
  • Bleeding previously
  • Iron (low Hb or Haematocrit)
  • Taking antiplatelet medication
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12
Q

What is the cause of angina ?

A
  • Narrowing of the lumen of the coronary arteries due to atherosclerosis.
  • Stress = higher demand for blood and oxygen = less reaches myocardium of the heart.
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13
Q

What are the symptoms of angina

A
  • Chest pain on exertion that may radiate to the left arm, shoulder, jaw or back.
  • Relieved by rest of sublingual glyceral trinitrate
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14
Q

What are the principles of angina management ?

A

RAMPS
- Refer to cardiology
- Advise on diagnosis, management and when to call an ambulance
- Medical Tx
- Procedural or surgical interventions
- Secondary prevention

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15
Q

What are the 3 aims of medical treatment of angina ?

A
  1. Immediate symptomatic relied
  2. Long term symptomatic relief
  3. Secondary prevention
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16
Q

What is used for immediate symptomatic relief of angina and what is advised in regards to taking it ?

A
  • Sublingual glyceral trinitrate (GTN)
  • Take as symptoms start.
  • Another dose after 5 minutes
  • Another dose after 5 minutes.
  • If still present - call an ambulance
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17
Q

What is given for long term symptomatic relief of angina ?

A
  • BB or CCB
  • If using CCB as monotherapy = rate limiting one (verapamil, diltiazem)
  • If using both in combination, use a long acting dihydropyridine CCB (amlodipine, modified release nifedidpine)
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18
Q

What is given for secondary prevention of ACS

A

A : aspirin (75mg)
A : atorvostatin (80mg)
A : ACE (if DM, hypertension, CKD or heart failure also present)
A : already on BB

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19
Q

What 2 surgical interventions can be carried out in severe case of angina

A
  • PCI ( catheter inserted into femoral or brachial artery, balloon and stent placed in area of stenosis).
  • CAGB : open the chest and a graft vessel is attached to the coronary artery
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20
Q

What are the 3 main options for the graft vessel in CABG ?

A
  • Saphenous vein (harvested from the inner leg)
  • Internal thoracic artery
  • Radial artery
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21
Q

What are the 2 benefits of PCI over CABG and 1 negative

A
  • Faster recovery
  • Lower rate of strokes as a complication
  • Higher rate of requiring repeat revascularisation (further procedures)
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22
Q

What is pericarditis and it’s 2 most common causes ?

A
  • Inflammation of the pericardial sac (idiopathic and viral - TB, coxsackie, EBV)
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23
Q

How does pericarditis present

A
  • Pleuritic chest pain (worse on laying down and relived by sitting forward)
  • Low grade fever
  • Possible : cough, SOB
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24
Q

What can be heard on auscultation in pericarditis ?

A
  • Pericardial rub
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25
Q

What is seen on an ECG in pericarditis ?

A

Global :

  • PR depression
  • Saddle shaped ST elevation

Reciprocal :

  • ST depression and PR elevation in aVR
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26
Q

How is pericarditis managed ?

A
  • Combination of NSAIDs (Aspirin/Ibuprofen) and colchicine.
  • All pts should receive transthoracic echon
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27
Q

What advice is given to someone with pericarditis ?

A
  • Avoid strenuous activity un til symptoms resolve or inflammatory markers return to normal
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28
Q

Give 4 other causes of pericarditis

A
  • Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus and rheumatoid arthritis).
  • Injury to the pericardium - (e.g., after myocardial infarction, open heart surgery or trauma)
  • Uraemia
  • Hypothyroid
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29
Q

What is infective endocarditis

A
  • Infection of the endothelium of the heart, usually affecting the valves.
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30
Q

What are the RF for IE

A
  • Previous IE
  • Structural pathology : congenital, prosthetic valves, HCM
  • IVDU
  • Immunocompromised (HIV, cancer).
  • CKD (esp dialysis)
  • Rheumatic disease
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31
Q

What is the most common cause of IE ?

A
  • Staph aureus
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32
Q

How does IE present ?

A
  • Onset of SOB, chest pain
  • Longer history of non specific signs of of infection : fever, fatigue, anorexia, night sweats and muscle aches
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33
Q

What are the specific examination findings in IE ?

A
  • New or changing murmur
  • Splinter haemorrhages
  • Janeway lesions
  • Petechiae
  • Osler’s nodes
  • Roth’s spots on fundoscopy
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34
Q

What are 2 features seen in long standing IE ?

A

Splenomegaly
Finger clubbing

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35
Q

What criteria is used for diagnosis IE?

A
  • Modified Duke’s criteria

(One major plus three minor criteria OR Five minor criteria)

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36
Q

What are the major criteria in the diagnosis of IE ?

A
  • Persistently positive blood cultures
  • Specific imaging findings (e.g., a vegetation seen on the echocardiogram)
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37
Q

What are the minor criteria in diagnosing IE?

A
  • Predisposing heart condition or IVDU
  • Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
  • Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
  • Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
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38
Q

What Ix are used in IE?

A
  • Blood cultures : Three blood culture samples separated by at least 6 hours and taken from different sites.
  • Echo (TOE)
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39
Q

What is the initial blind therapy for native valve IE

A
  • IV amoxacillin +/- low dose gentamicin for 4 weeks
  • If pen allergic or MRSA = IV vancomycin + low dose gent
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40
Q

What is the initial blind therapy for prosthetic valve IE ?

A
  • IV Vancomycin + rifampicin + low-dose gentamicin for 6 weeks
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41
Q

How is proven staphlococci native IE managed ?

A
  • IV flucloxacillin
  • Vancomycin + rifampicin if pen allergic
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42
Q

How is proven staphlococci prosthetic IE managed ?

A
  • Flucloxacillin + rifampicin + low does gentamicin
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43
Q

What kind of genetic condition is HOCM and what does it cause ?

A
  • Autosommal dominant, usually effecting b heavy chain of myosin in the sarcomere
  • LV hypertrophy and interventricular septal hypertrophy leading the LV outflow obstruction
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44
Q

What are people with HOCM at increased risk of?

A
  • Heart failure
  • MI
  • Arrhythmia
  • Sudden cardiac death
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45
Q

If not asymptomatic, how might HOCM present ?

A
  • On exertion : syncope, SOB, chest pain
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46
Q

What is heard on examination in HOCM ?

A
  • Ejection systolic murmur (louder with valsalva manoeuvre, decreases on squatting)
  • Pansytolic murmur due to MR
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47
Q

What are the management options in HOCM?

A

A : Amiodarone
B : BB / verapamil for symptoms
C : Cardioverter defibrillator
D : Dual chamber pacemaker
E : Endocarditis prophylaxis

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48
Q

What are people with HOCM told to avoid ?

A
  • Intense exercise, heavy lifting and dehydration
  • ACEI and nitrates as these decrease preload with worsens the LVOT obstruction.
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49
Q

What is an aortic dissection ?

A

Break in the tunica intima of the aorta, causing blood to pool in the tunica media

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50
Q

What are the RF for aortic dissection

A
  • Increased pressure : HTN (biggest risk factor)
  • Weak aortic wall : marfan’s EDS, aneurysms
  • Male, smoking, poor diet, raised cholesterol
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51
Q

How is an aortic dissection classified based on the stanford system ?

A
  • A : ascending aorta, before brachiocephalic artery
  • B : descending aorta, after subclavian artery
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52
Q

How does an aortic dissection present ?

A
  • Sharp chest pain radiating to the back
  • Weak pulse in the brachial or femoral arteries
  • Differing BP in left and right arm
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53
Q

What is the investigation of choice for an aortic dissection ?

A
  • CT angiogram : shows ‘false lume’
  • CXR can also be done : shows widened aorta/mediastinum
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54
Q

How is an aortic dissection managed SAQ ?

A
  • Trigger emergency protocol (vascular surgeons, anaesthetics etc)
  • Analgesia (morphine)
  • BB (control BP and HR to reduce stress on aortic wall)
  • Surgical intervention
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55
Q

How is a type A aortic dissection usually manged

A
  • Control BP = IV labetalol + surgery
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56
Q

How is a type B aortic dissection managed ?

A
  • BP control (IV labetalol) + supportive
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57
Q

What is the DeBakey system for classifying an aortic dissection ?

A
  • Type I – begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta
  • Type II – isolated to the ascending aorta
  • Type IIIa – begins in the descending aorta and involves only the section above the diaphragm
  • Type IIIb – begins in the descending aorta and involves the aorta below the diaphragm
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58
Q

What are the complications of a backwards tear aortic dissection ?

A

Aortic regurg
Cardiac tampomade
MI - usually inferior due to RCA involvement

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59
Q

What are the complications of a forward tear aortic dissection ?

A
  • Stroke
  • Renal failure (compression of renal arteries)
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60
Q

What is a AAA?

A
  • Dilation of the abdominal aorta with a diameter of >3cm.
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61
Q

What are the RF for a AAA?(6)

A
  • Men
  • Older age
  • Smoking
  • HTN
  • FHx
  • Existing CVD
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62
Q

At what age are men screened for a AAA and what is the follow up monitoring ?

A
  • USS aged 65 yrs : vascular referral if >3cm. Urgent if >5.5cm.
  • Yearly if diameter between 3-4.4cm
  • 3 monthly if diameter between 4.5-5.4cm
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63
Q

What investigations are used to diagnose a AAA and then get more management info ?

A
  • USS
  • CT angiogram for more detailed picture
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64
Q

How does a AAA present ?

A
  • Usually asymptomatic and is incidental or screening finding
  • Non specific abdo pain
  • Pulsatile and expansile mass in the abdomen
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65
Q

How is a AAA classified ?

A
  • Normal : <3cm
  • Small : 3-4.4cm
  • Medium : 4.5-5.4cm
  • Large : >5.5cm
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66
Q

How is the progression of a AAA prevented ?

A
  • Modify reversible RF : stop smoking, better diet and exercise, optimising mx of HTN, DM and hyperlipidaemia
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67
Q

When is a AAA electively repaired ?

A
  • Symptomatic
  • Growing >1cm a year
  • > 5.5cm in diameter
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68
Q

What are the rules around driving with a AAA?

A
  • Patients must :
  • Inform the DVLA if they have an aneurysm above 6cm
  • Stop driving if it is above 6.5cm
  • Stricter rules apply to drivers of heavy vehicles (e.g., bus or lorry drivers)
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69
Q

How does a ruptured AAA present

A
  • Severe abdo pain, radiating to the back or groin
  • Haemodynamic instability
  • Pulsatile and expansive mass in abdomen
  • Collapse
  • Loss of consciousness
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70
Q

What are the modifiable and non-modifiable RF for ACS

A
  • Non : male, increasing age and FHx
  • Modifiable : smoking, hypercholesterolaemia, DM, HTN, Obesity
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71
Q

What are the symptoms of ACS ?

A
  • Chest pain : radiating to jaw/arm
  • N&V
  • Sweating/clamminess
  • Feeling of impending doom
  • SOB
  • Palpitations
  • Lasts >15 minutes at rest
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72
Q

How is unstable angina classified for diagnosis ?

A
  • ACS Sx for >15 minutes
  • Normal troponin
  • Normal / ECG changes (ST depression/T wave inversion)
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73
Q

How is a NSTEMI diagnosed ?

A
  • Raised troponin +/-
  • ECG : ST depression / T wave inversion
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74
Q

How is a STEMI diagnosed ?

A
  • ECG : ST elevation / new LBBB block +/- raised troponin
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75
Q

How does a LBBB show on ECG

A
  • Wide, downwards QRS in lead I
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76
Q

How does a RBBB show on ECG

A
  • Wide, upwards QRS in lead I
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77
Q

What is the immediate managed of ACS before diagnosis ?

A
  • C : call ambulance
  • P : perform ECG
  • A : aspirin (300mg)
  • I : IV morphine (+ anti-emetic)
  • N : nitrate (GTN)
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78
Q

How is a STEMI managed ?

A

PCI or thrombolysis

  • If within 2 hrs of presentation = PCI.
  • If not thrombolysis with streoptokinase/alteplase
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79
Q

How is a NSTEMI managed ?

A
  • B : Base decision for PCI/angiography on GRACE
  • A : aspirin (300mg)
  • T : ticagrelor (180mg stat)
  • M : morphine
  • A : antithrombin with fondaparinux
  • N : nitrate (GTN)
  • O2 is sats below 95% in non COPD
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80
Q

What is the GRACE score for NSTEMI management ?

A

6mnth probability of death following NSTEMI

  • 3% or lower = low risk
  • > 3% = medium to high risk = urgent angiography with PCI (within 72hrs)
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81
Q

What are the 3 aspects of ongoing management following initial management of a MI ?

A
  • Echo to check for functional damage
  • Cardiac rehab
  • Secondary prevention
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82
Q

what is involved in secondary prevention following an MI

A
  • A : aspirin (75mg daily)
  • A : atorvostatin (80mg daily)
  • A : another antiplatelet (ticagrelor/clopidogrel)
  • A : atenolol (or other BB)
  • A : ACEI
  • A : aldosterone antagonist (e.g. spironolactone - for those with clinical HF)
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83
Q

What has to be monitored for patients on both a ACEI and aldosterone antagonist ?

A
  • Renal function : both increase the risk of fatal hyperkalaemia
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84
Q

Give 5 complications of an MI

A
  • D : death
  • R : rupture of septum or papillary muscles
  • E : edema (HF)
  • A arhythmia or aneurysm
  • D : dressler’s
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85
Q

What is Dressler’s ?

A
  • Pericarditis 2/3 wks after an MI
  • Pleuritic chest pain, pericardial rub, low grade fever
  • Global ST elevation or T wave inversion on ECG
  • Tx : NSAIDs or pred if severe
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86
Q

What are the 4 kinds of MI

A
  • Type 1 : A : ACS MI
  • Type 2 : C : can’t cop MI (increased demand/reduced supply = severe anemia, tachycardia, hypotension
  • Type 3 : D : dead my MI (sudden cardiac death or arrest)
  • Type 4 : C : caused by US MI (due to intervention)
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87
Q

what are the non modifiable RF for CVD

A
  • Men
  • Older age
  • Family history
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88
Q

What are the modifiable RF for CVD

A
  • Smoking
  • Raised cholesterol
  • Obesity
  • Poor diet and lack of exercise
  • Excessive alcohol consumption
  • Poor sleep
  • Stress
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89
Q

What medical co-morbidites increase the risk of atherosclerosis (5) ?

A
  • DM
  • HTN
  • CKD
  • Inflammatory conditions (e.g. RA)
  • Atypical antipsychotics
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90
Q

Give 5 causes of HF

A
  • IHD
  • Valvular disease (AS)
  • HTN
  • Arrhythmia (common - AF)
  • Cardiomyopathy
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91
Q

Give 5 key symptoms of left sided HF

A
  • Exertional SOB
  • Fatigue
  • Chronic non productive cough
  • Orthopnoea
  • PND
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92
Q

Give 2 signs of left sided HF

A
  • Coarse crackes at base
  • Hypoxia
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93
Q

Give 3 signs of right sided HF

A
  • Raised JVP
  • Liver conjestion
  • Pitting oedema
94
Q

What 4 things are used for an assessment and diagnosis of HF?

A
  • Clinical assessment
  • NT-proBNP
  • ECG
  • Echo
95
Q

What is seen on a chest X-ray in HF

A
  • A : Alveolar oedema
  • B : Kerley ‘B’ lines
  • C : cardiomegaly
  • D : dilated upper lobe vessels
  • E : effusion
96
Q

What is determined as HF with reduced ejection fraction

A
  • <40%
  • Systolic HF as there is an issue with pumping
97
Q

How is HF with reduced ejection fraction managed ?

A
  • A : ACEI
  • B : BB (bisoprolol)
  • A : aldosterone antagonist (spironolactone)
  • L : loop diuretic (furosemide)
98
Q

How is HF with preserved ejection fraction managed ?

A
  • A : ACEI
  • A : aldosterone antagonist
  • L : loop diuretic (furosemide)
99
Q

What can be added to control HF after ABAL ?

A
  • SGLT2 inhibitor (dapagliflozin)
  • Sacubitril with valsartan (entresto)
  • Ivabradine
  • Digoxin
  • Hydralazine in combination with nitrate
  • Cardiac resynchronisation therapy
100
Q

What is HF defined as ?

A
  • Clinical features of impaired heart function, specifically the function of the left ventricle to pump blood out of the heart and around the body
101
Q

What is the new york heart association (NYHA) classification of the severity of symptoms related to HF ?

A
  • Class I: No limitation on activity
  • Class II: Comfortable at rest but symptomatic with ordinary activities
  • Class III: Comfortable at rest but symptomatic with any activity
  • Class IV: Symptomatic at rest
102
Q

What are the 5 pricinples of management with someone presenting with HF

A
  • R – Refer to cardiology
  • A – Advise them about the condition
  • M – Medical treatment
  • P – Procedural or surgical interventions
  • S – Specialist heart failure MDT input, such as the heart failure specialist nurses, for advice and support
103
Q

What does the urgency and specialist assessment of HF depend on ?

A
  • NT-proBNP result :
  • From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
  • Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks
104
Q

What are the surgical interventions for HF?

A
  • Implantable cardioverter defib
  • Cardiac resynchronisation therapy (EF <35%)
  • Heart transplant
105
Q

What are the symptoms of someone with acute HF (5)

A
  • Sudden worsening of SOB ( worse lying flat).
  • Cough with frothy white or pink sputum
  • Oedema
  • Fatigue
  • Reduced exercise tolerance
106
Q

What are the signs of someone with acute HF? (6)

A
  • Raised RR
  • Reduced O2 sats
  • Tachycardia
  • 3rd heart soung
  • Bilateral basal crackles
  • Hypotension
107
Q

What is the management of acute HF ?

A
  • S : Sit up
  • O : Oxygen - if reduced sats
  • D : Diuretics - furosemide
  • I : IV fluids stopped
  • U : Underlying cause tx
  • M : Monitor fluid balance
108
Q

What 2 specialist medications can be used by ICU in the management of acute HF with hypotension ?

A
  • Positive inotropes (dobutamine) = increases cardiac contractility and so increases CO.
  • Vasopressors (norepinephrine) = vasoconstriction
109
Q

What can of respiratory failure does HF cause

A

Type 1

110
Q

4 H’s and 4 T’s of cardiac arrest

A
  • H : hypoxia
  • H : hypothermia
  • H : hypovolaemia
  • H : hyperkalaemia, hypoglycaemia
  • T : Thrombosis
  • T : Toxins
  • T : Tamponade
  • T : Tension pneumothorax
111
Q

Diagnosis of HTN

A
  • Above 140/90 clinical
  • Confirmed with above 135/85 ambulatory or home readings
112
Q

Secondary causes of HTN

A

ROPED

  • R : Renal disease (most common)
  • O : Obesity
  • P : Pregnancy
  • E : Endocrine
  • D : Drugs (alcohol, steroids, NSAIDs, oestrogen, liquorice)
113
Q

Complications of HTN

A
  • Renal failure
  • Stroke
  • Heart failure
114
Q

Stages of HTN

A
  • 1 >140/90 (135/85)
  • 2 >160/100 (150/95)
  • 3 >180/120
115
Q

what should be calculated in all pts with a new diagnosis of HTN ?

A
  • QRISK -> risk of stroke or MI in next 10 yra
  • > 10% = offer 20mg atorvostatin at night
116
Q

Management of HTN in <55 y/o or T2DM of any age or family origin

A
  1. ACEI (Rampiril)
  2. ACEI + CCB (Amlodipine)
  3. ACEI + CCB + TLD (Indapamide)
  4. ACEI + CCB + TLD + spironolactone if K+ <=4.5 OR Doxazosin/atenolol if >4.5)
117
Q

Management of HTN in >55 y/o or Black African or African-Caribbean family origin

A
  1. CCB
  2. CCB + ARB OR LTD
  3. CCB + ARB + TLD
  4. Add spironolactone or alpha/BB depending on serum potassiujm
118
Q

How do ACEIs work ?

A
  • Inhibits the conversion angiotensin I to angiotensin II = vasodilation, reduced aldosterone release and so reduced sodium and water retention by the kidenys = reduced BP
  • Also reduces K+ excretion, hence the risk of hyperkalaemia with ACEI
119
Q

3 SE of ACEIs

A
  • Cough
  • Angioedema
  • Hyperkalaemia
120
Q

what should be checked be checked before initiating ACEI treatment ?

A

U&Es

121
Q

5 SE of BB

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

122
Q

Contraindications to BB

A
  • uncontrolled heart failure
  • asthma
  • sick sinus syndrome
  • concurrent verapamil use: may precipitate severe bradycardia
123
Q

Treatment targets in HTN

A
  • <80 = <140/90
  • > 80 = <150/90
124
Q

What is malignant HTN and what immediate investigation is required

A
  • BP >180/120 with retinal haemorrhages or papilloedema (swelling of the optic disc)
  • Same day referral for fundoscopy
125
Q

3 causes of aortic stenosis

A
  • Idiopathic-age related calcification : most likely cause if >65.
  • Biscuspid aortic valve : Most likely cause if <65
  • Rheuamtic disease
126
Q

Murmur in aortic stenosis

A
  • Harsh ejection systolic -> 2nd intercostal space, right sternal border
  • Loudest leaning forward on end expiration
  • Cresecendo descendo
  • Radiates to the carotids
127
Q

Other signs of aortic stenosis on examination (4)

A
  • Slow rising pulse
  • Narrow pulse pressure
  • Thrill or heave in aortic area on palpation
  • Apex beat is heaving but undisplaced
128
Q

Causes of aortic regurgitation (5)

A
  • Idiopathic age-related weakness
  • IE
  • Bicuspid aortic valve
  • Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome
  • Rheumatic fever
129
Q

Murmur heard in aortic regurgitation

A
  • Early diastolic soft murmur
130
Q

Other signs of aortic regurgitation on examination (4)

A
  • Thrill in the aortic area on palpation
  • Collapsing pulse = waterhammer pulse
  • Wide pulse pressure (large difference between systolic and diastolic BP’s)
  • Displaced apex beat
  • Nail bed pulsation (Quincke’s sign)
131
Q

what other murmur can be heard in aortic regurgitation

A

-> Austin flint murmur
-> Rumbling, low-pitched mid- diastolic murmur heard at apex
-> Blood flows back over the mitral valve causing it to vibrate

132
Q

Causes of mitral stenosis

A
  • Rheumatic heart disease
  • CHD
  • Carcinoid syndrome
  • SLE
  • Mucopolysaccharidoses
133
Q

Murmur heard in mitral stenosis

A
  • Mid diastolic, low pitched “rumbling” murmur heard at the apex
  • Loudest in the left lateral position
134
Q

Other signs of mitral stenosis on examination (5)

A
  • Tapping apex beat, which is a palpable but undisplaced
  • Malar flush
  • AF : irregularly, irregular pulse
  • Loud S1
  • Left parasternal heave
135
Q

Causes of mitral regurgitation (5)

A
  • Idiopathic weakening of the valve with age
  • IHD
  • Infective endocarditis
  • Rheumatic heart disease
  • Connective tissue disorders, such as Ehlers-Danlos syndrome or Marfan syndrome
136
Q

Murmur in mitral regurgitation

A
  • Pan-systolic, high-pitched “whistling” heard at apex
  • Murmur radiates to left axilla
137
Q

Other signs of mitral regurgitation on examination

A
  • Thrusting and DISPLACED apex beat
  • Possible third heart sound
  • Thrill at apex
  • Wide splitting of the second heart sound
138
Q

Causes of tricuspid regurgitation

A
  • Primary (Valvular) pathology = congenital (Ebstein’s, cleft valve), carcinoid syndrome
  • Secondary : pulmonary HTN, chronic left HF
139
Q

Murmur in tricuspid regurgitation

A
  • Pan systolic murmur with split second heart sound
  • 5th ICS, left sternal border
140
Q

Other signs of tricuspid regurgitation on examination

A
  • Thrill in the tricuspid area on palpation
  • Raised JVP with giant C-V waves (Lancisi’s sign)
  • Pulsatile liver (due to regurgitation into the venous system)
  • Peripheral oedema
  • Ascites
141
Q

Associations with pulmonary stenosis

A

Usually congenital :

  • Noonan syndrome
  • Tetralogy of Fallot
142
Q

Murmur heard in pulmonary stenosis

A
  • Ejection systolic loudest 2nd IC space, left sternal border
  • Widely split second heart sound
143
Q

Other signs of pulmonary stenosis

A
  • Thrill in the pulmonary area on palpation
  • Raised JVP with giant A waves (due to the right atrium contracting against a hypertrophic right ventricle)
  • Peripheral oedema
  • Ascites
144
Q

Scar most commonly seen following surgery to valvular pathology

A
  • Midline sternotomy scar = aortic or mitral velve replacement (Could indicate CABG)
  • AS = most common valvular disease and most common in indication for sugery (followed by mitral regurgitation)
145
Q

what do mechanical valves require ?

A
  • Lifelong anticoagulation with warfarin
  • INR target of 2.5-3.5
146
Q

the ‘click’ heard with mechanical valves is heard when dependent on the valves replaced

A
  • S1 in mitral valve replacement
  • S2 in aortic valve replacement
147
Q

3 major complications of mechanical heart valves

A
  • Thrombus
  • IE
  • Haemolysis causing anaemia
148
Q

Organisms commonly causing IE in mechanical heart valves

A
  • Gram +ve

Staphylococcus
Streptococcus
Enterococcus

149
Q

what is a narrow complex tachycardia and give 4 differentials

A

Definition : fast HR with a QRS complex duration of <0.12 seconds

  • Sinus tachycardia
  • Supraventricular tachycardia
  • AF
  • Atrial flutter
150
Q

what is a supraventricular tachycardia and what is seen on ECG

A

-> Tachycardia not ventricular in origin
-> Narrow QRS complex tachycardia
-> The P waves are buried in the T waves = QRS complex followed by T wave, followed by QRS and so on

151
Q

3 main types of SVT

A
  1. Atrioventricular nodal re-entrant tachycardia (re-entry point back through AVN).
  2. Atrioventricular re-entrant tachycardia (re-entry point is an accessory pathway).
  3. Atrial tachycardia
152
Q

what accessory pathway is present in WPW syndrome, what is seen on ECG and what is the definitive treatment

A
  • Bundle of Kent
  • ECG :
    ~Short PR interval, less than 0.12 seconds
    ~ Wide QRS complex, greater than 0.12 seconds
    ~ Delta wave (Slurred upstroke in QRS complex)
  • Radiofrequency ablation of accessory pathway
152
Q

Stepwise acute management of SVT

A

Step 1: Vagal manoeuvres
Step 2: IV Adenosine bolus
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion

153
Q

Management of acute SVT if life threatening features (syncope, chest pain, shock or HF)

A
  • Synchronised DC cardioversion under sedation or general anaesthesia.
  • IV amiodarone is added if initial DC shocks are unsuccessful.
154
Q

What MUST be avoided in pts with WPW and possible AF or Atrial flutter ?

A
  • Adenosine, verapamil, BB
  • They block the AVN, promoting conduction through accessory pathway
  • Therefore management is procainamide or electrical cardioversion
155
Q

Examples of vagal manoeuvres used in SVT

A

-> Valsalva = blowing into 10ml syringe for 10-15s
-> Carotid sinus massage
-> Diving reflex

156
Q

Explain how adenosine is given for SVT

A
  • Rapid IV bolus into large proximal cannula (e.g. grey cannula into antecubital fossa)
  • 3 attempts (6mg, then 12mg, then 18mg)
157
Q

who must adenosine be avoided in

A
  • Asthma -> risk of bronchospasm
  • COPD
  • Heart failure
  • Heart block
  • Severe hypotension
  • Potential atrial arrhythmia with underlying pre-excitation
158
Q

how can recurrent episodes of SVT be managed ?

A
  • Long-term medication (e.g., beta blockers, calcium channel blockers or amiodarone)
  • Radiofrequency ablation
159
Q

what is a broad complex tachycardia and 4 possible causes ?

A

Definition : fast HR with QRS >012s

  • Ventricular tachycardia or unclear cause (treated with IV amiodarone)
  • Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
  • Atrial fibrillation with bundle branch block (treated as AF)
  • Supraventricular tachycardia with bundle branch block (treated as SVT)
160
Q

what is seen on ECG in atrial flutter ?

A

Sawtooth appearance

161
Q

what does prolonged QT mean is occurring in the heart and what can cause it ?

A
  • Prolonged repolarisation of myocytes after contraction
  1. Torsades de pointes
  2. Long QT syndrome (an inherited condition)
  3. Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
  4. Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia
162
Q

acute management of torsades de pointes

A
  • Correcting the underlying cause (e.g., electrolyte disturbances or medications)
  • Magnesium infusion (even if they have normal serum magnesium)
  • Defibrillation if ventricular tachycardia occurs
163
Q

what is a first degree heart block and what is seen on ECG

A

-> Delayed conduction through AVN
-> However, every P wave is followed by QRS as every atrial contraction is followed by ventricular contraction
-> Prolonged PR interval = >0.2 s

164
Q

Mobitz type 1 heart block

A

-> Conduction trhough AVN takes progressively longer until it fails to lead to ventricular contraction
-> Increasing PR interval until a singular P wave is not followed by a QRS.

165
Q

Mobitz type 2 heart block

A

-> Intermittent failure of conduction through the AVN
-> Usually a set ratio of P waves to QRS comnplex (e.g. 3:1)
-> PR interval remains normal

166
Q

Third-degree heart block

A

-> Complete heart block = no relationship between P waves and QRS complex = risk of asystole

167
Q

What is defined as bradycardia and give 3 causes

A

-> HR <60bpm
-> Medications (e.g. BB)
-> Heart block
-> Sick sinus syndrome (= any condition causing dysfunction in SAN - often idiopathi degnerative fibrosis of SAN).

168
Q

4 conditions with a risk of asystole

A

Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds

169
Q

Management of unstable pts and those at risk of asytole

A
  • IV atropine (first line)
  • Inotropes (e.g., isoprenaline or adrenaline)
  • Temporary cardiac pacing
  • Permanent implantable pacemaker, when available
170
Q

How does atropine work ?

A
  • Antimuscarinic medication
  • Works by inhibiting the parasympathetic nervous system.
171
Q

SE of atropine

A
  • Pupil dilation
  • Dry mouth
  • Urinary retention
  • Constipation.
172
Q

How can the type of pacemaker be determined from an ECG

A
  • Pacemaker intervention = sharp verticle line on all leads on ECG
  • Line before P wave = lead in atria
  • Line before QRS + lead in ventricle
  • A line before either the P wave or QRS complex but not the other indicates a single-chamber pacemaker
  • A line before both the P wave and QRS complex indicates a dual-chamber pacemaker
173
Q

what is an atrial myxoma and 5 common features

A

-> Most common primary cardiac tumour : most occur in left atrium

  • Systemic: dyspnoea, fatigue, weight loss, pyrexia of unknown origin
  • Clubbing
  • Emboli
  • Atrial fibrillation
  • Mid-diastolic murmur, ‘tumour plop’
  • Echo: pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum
174
Q

Brugada syndrome and its ECG changes

A

-> Autosomal dominant inherited cardiovascular disease that may present with sudden cardiac death
-> Convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
-> Partial right bundle branch block
-> ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome

175
Q

what is cardiac tamponade and 3 classical features

A
  • Accumulation of pericardial fluid under pressure
  • Beck’s triad (Hypotension, raised JVP and muffled heart sounds)
176
Q

what is a characteristic of the JVP in cardiac tamponade ?

A

Absent Y descent

177
Q

Dilated cardiomyopathy

A
  • Heart muscle becomes thin and dilated.
  • It may be genetic or secondary to other conditions (e..g, myocarditis, alochol, Coxsackie B virus, wet beri beri,, doxorubicin).
178
Q

Restrictive cardiomyopathy

A
  • Heart becomes rigid and stiff, causing impaired ventricular filling during diastole.
  • Causes : amyloidosis, post0radiotherapy and loeffler’s endocarditis
179
Q

Arrhythmogenic cardiomyopathy

A
  • Genetic condition where the heart muscle is progressively replaced with fibrofatty tissue.
  • It becomes prone to ventricular arrhythmias.
  • It is a notable cause of sudden cardiac death in young people, including high-performing athletes.
180
Q

Takotsubo cardiomyopathy

A
  • Rapid onset of left ventricular dysfunction and weakness.
  • This often follows severe emotional stress, for example, the death of a long-term partner.
  • For this reason, it is known as broken heart syndrome. It tends to resolve spontaneously with time.
181
Q

3 symptoms of severe aortic stenosis

A

SAD

  • S : Syncope
  • A : Angina
  • D : Dyspnoea
182
Q

what 4 features of aortic sclerosis make it distinguishable from aortic stenosis ?

A
  • Normal pulse volume and character
  • Normal pulse pressure
  • Apex undisplaced
  • Softer murmur, less likely to radiate to carotids
183
Q

When controlling BP in a pt >55. When would you consider an ARB over a TLD ?

A

If the pt has a diagnosis of gout
TLD can worsen the condition

184
Q

Action and monitoring of amiodarone

A
  • Blocks K+ channels
  • TFT, LFT, U&E and CXR prior (Risk of PF/pneumonitis)
  • TFT, LFT every 6 mnths
185
Q

Atrial myxoma : what, where, murmur and echo

A
  • Primary cardiac tumour
  • Left atrium
  • Mid-diastolic
  • Echo : pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum
186
Q

Criteria for adding ivabradine to manage HF

A

-> sinus rhythm > 75/min and a left ventricular fraction < 35%

187
Q

Criteria for using sacubitril-vasartan as additional management of HF

A

criteria: left ventricular fraction < 35%

188
Q

When is digoxin considered as additional management of HF ?

A

Coexistent AF

189
Q

when is cardiac resynchronisation therapy used as additional management in HF ?

A

widened QRS (e.g. left bundle branch block) complex on ECG

190
Q

INR 5.0-8.0 but no bleeding

A

Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

191
Q

INR 5.0 - 8.0 with minor blleding

A
  • Stop warfarin
  • Give intravenous vitamin K 1-3mg
  • Restart when INR < 5.0
192
Q

INR >8.0 but no bleeding

A
  • 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
193
Q

INR >8.0 with minor bleeding

A
  • Stop warfarin
  • Give intravenous vitamin K 1-3mg
  • Repeat dose of vitamin K if INR still too high after 24 hours
  • Restart warfarin when INR < 5.0
194
Q

Major bleeding on warfarin (e.g variceal, intracranial)

A
  • Stop warfarin
  • Give intravenous vitamin K 5mg
  • Prothrombin complex concentrate - if not available then FFP*
195
Q

what anticoagulation are pts awaiting PCI given ?

A

-> If not already on oral anticoag = Aspirin + prasugrel
-> Already on oral anticoag = Aspirin + clopidogrel

196
Q

Reversal of dabigatran in bleeding patient (anticoag taken in AF)

A

idarucizumab

197
Q

What should be administered during CPR if PE is suspected cause (e.g. large swollen calf noticed when initiating)

A

-> Thromvolytic drug such as alteplase

198
Q

Explain what medications are used for rate control in AF

A
  • First : BB (CI in asthma)
  • Second : CCB (diltiazem, verapamil)
  • Digoxin (only used in HF)
199
Q

Likely causative organisim of endocarditis (five)

A
  • History of prostatitis - strep faecalis
  • Immunocamprimised - Candida albicans
  • Poo dental hygiene - streptococcus mutans
  • Prostetic valve - strep epidermidis
  • IVDU - staph aureu (most common)
200
Q

What is Takotsubo cardiomyopathy

A

Non ischaemic cardiomypathy associated with transient, apical ballooning of the myocardium -> often triggered by extreme stress

201
Q

what are considered normal varients in athletes and so no intervention would be required?

A
  • Sinus bradycardia
  • Junctional rhythm
  • First degree heart block
  • Mobitz type 1 (Wenckebach phenomenon)
202
Q

If starting a pt on a statin for primary prevention of CVD (20mg) what is the aim for reduction of non-HDL cholesterol ?

A

40%
If not, can increase to 80mg

203
Q

what additional finding on a CT angiography would suggest that the aortic dissection was in the ascending over the descending aorta ?

A
  • Diastolic murmur suggesting aortic regurg
204
Q

management of acute pericarditis

A

ibuprofen and colchicine

205
Q

Signs of dissection on CXR

A
  • Widened mediastinum
206
Q

Preffered investigation for suspected aortic dissection

A

CT angiography chest/abdo/pelvis
If unstable = TOE

207
Q

Endocarditis caused by fully-sensitive streptococci (e.g. viridans)

A

Benzylpenicillin

208
Q

ECG finding in IE suggesting the need for surgical intervention

A

PR prolongation
Suggests aortic root abscess

209
Q

Name two complications of AF

A
  • LV failure
  • Sudden cardiac death
210
Q

3 tests to investigate for en-organ damage in HTN

A
  1. ECG -> LV hypertrophy
  2. Fundoscopy -> hypertensive retinopathy
  3. Urine dip
211
Q

Pt suffers a stroke and is found to have permanent AF. After being on aspirin for 2 weeks, they will be switched to daily clopidogrel. What else should they be prescriped for secondary stroke prevention

A

Apixaban

212
Q

Explain the shocks given in VF

A
  • A single shock for VF/pulseless VT followed by 2 mins of CRP
  • If the cardiac arrest is wintnesses in a monitored pt then given 3 stacked shocks
213
Q

What can adenosine cause and so the pt should be warned about it before administering ?

A

Chest pain

214
Q

What guides surgery for AS

A
  • Symptomatic = valve replacement
  • Asymptomatic but valvular gradient >40mmHg with features such a LV dysfunction = consider suregry
215
Q

If fibrinolysis is given for a STEMI as PCI could not be performed within 120 mins. What should be checked afterwards?

A

Repeat ECG is taken after 90 minutes and transfer for urgent PCI if ST elevation has not resolved

216
Q

What is an important interaction with statin to cause myalgia and increased creatinine kinase

A

Clarithromycin / erythromycin

217
Q

what can furosemide cause

A

Bilateral tinnitus and hearing loss (loop diuretics can cause ototoxicity)

218
Q

if a PE is suspected but the CTPA negative, what is the next step in the management plan

A

Proximal leg vein USS

219
Q

Echo findings in HOCM

A

MR SAM ASH
- Mitral regurgitation
- Systolic anterior motion of anterior mitral valve leaflet
- Asymmetric hypertorphy

220
Q

ECG findings in HOCM

A
  • Left ventricular hypertrophy
  • Non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
  • Deep Q waves
221
Q

what 3 drugs should be avoided in HOCM

A

Nitrates
ACEI
Inotropes

222
Q

Medications that can cause torsades de pointes

A

Macrolides

223
Q

what anti-anginal medications do pts commonly develop tolerance too ?

A

Standard release isosorbide mononitrate

224
Q

What electrolyte and urine derangement can bendroflumethazide cause

A

Hypercalcaemia
Hypocalciuria

225
Q

what can hypothermia cause on ECG

A

J waves

226
Q

Operations a midline sternotomy scar can indicate

A

CABG
Aortic valve replacement
Mitral valve replacement

227
Q

Other scar seen in midline indicates a CABG

A

Saphenous vein harvesting scar on inner thigh

228
Q

Artery and leads affected in each STEMI

A
  • Anterolateral : I, aVL, V3-V6 (LCA)
  • Anterior : V1-V4 (LAD)
  • Lateral : I, aVL, V5-V6 (Circumflex)
  • Inferior : II, III & aVF (RCA)
229
Q

Reversal of digoxin in severe toxicity

A

Digibind

230
Q
A

Finals (92 decks)

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