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Phase 2a Gold Standard > Cardiology > Flashcards

Cardiology Flashcards

1
Q

CVD risk factors (modifiable) (9)

A

Obesity
Hypertension
Smoking
Sedentary lifestyle
High LDL cholesterol
Poor diet
Alcohol drinking
Cocaine use
Uncontrolled DM

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2
Q

CVD risk factors (non-modifiable) (7)

A

Age
Male gender
Ethnicity (South Asian, African, Caribbean)
Family history
Menopause
Genetic predisposition (hyperlipidaemia)
Socioeconomic status

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3
Q

Normal blood pressure ranges and hypertension staging

A

90/60 - 120-80

Prehypertension - 120/80 +
Stage 1: 140/90 +
Stage 2: 160/100 +
Stage 3 >180/120

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4
Q

Describe the 3 characteristic features of typical stable angina

A
  • Central crushing chest pain that can radiate to jaw, shoulders or left arm
  • Caused by exertion
  • Is relieved by GTN spray or rest

Can also be caused by heavy meals, cold weather, strong emotion.

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5
Q

Other causes of an angina exacerbation

A

heavy meals, cold weather, strong emotion.

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6
Q

Give some primary preventions of cardiovascular disease

A

QRISK3 score (10 year risk calculator of MI or stroke)
Patients with CKD or T1DM taking statins
Checking lipids, LFTs, BP regularly

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7
Q

Pathophysiology of stable angina

A

Usually caused by atherosclerosis, narrowing of coronary arteries (>70% stenosis) causes reduced blood flow to heart, which is unable to meet the metabolic demands of the muscle on exertion (myocardial ischaemia). This usually subsides with rest.

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8
Q

Pathogenesis of atherosclerotic plaque formation

A
  • High LDL causes them to deposit and oxidise in tunica intima, activating endothelial cells which present leukocyte adhesion molecules.
  • Leukocytes move into intima and attract monocytes (macrophages/T helper cells)
  • Macrophages take up oxidised LDL and form foam cells, which release IGF-1 causing smooth muscle to migrate to intima from media.
  • Smooth muscle proliferation forms fibrous cap.
  • As foam cells die they release lipid content, growth factors and cytokines, growing plaque.
  • Plaque either occludes vessel or ruptures, triggering platelet aggregation and clotting.
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9
Q

Signs/symptoms of stable angina

A
  • Central crushing chest pain which may or may not radiate to left arm, neck and jaw. (<5 mins long)
  • Pain is provoked by exertion or stress
  • Pain is relieved by rest/nitrates

May cause sweating, dyspnoea, fatigue, palpitations and syncope

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10
Q

Investigations for stable angina

A
  • 12 lead ECG: Normal (may show ST depression, ruling out NSTEMI/STEMI)
  • CT coronary angiography (GOLD) to highlight stenosis
  • FBC, TFT, LFT, HbA1C to rule out causative pathologies
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11
Q

Management of stable angina

A
  • Acute relief of symptoms: sublingual GTN spray
  • Lifestyle changes (lose weight, exercise, lipid/diabetes/HTN management)
  • Long term treatment: Beta blocker e.g. propanolol (CI: Asthma) or CCB e.g. amlodipine (CI: Heart failure) (must be non rate limiting so doesnt cause bradycardia)
    Then dual therapy if needed
  • Long term prevention may be added: 3As (Aspirin, atorvastatin, ACEi (Ramipril))
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12
Q

If pharmacologically unsuccessful, what surgical options are available to treat angina? With pros and cons

A
  • Percutaneous coronary intervention (PCI) - Balloon stent opens vessel. (less invasive, but higher risk of stenosis)
  • Coronary artery bypass graft (CABG) - chest opened along sternum, taking graft vein from patient’s leg and sewing onto artery to bypass stenosis. (better outcomes, more invasive/greater risks. Leaves midline sternotomy scar)
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13
Q

What 3 conditions make up Acute Coronary Syndrome

A
  • Unstable angina
  • NSTEMI
  • STEMI
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14
Q

Occlusion, infarction, ECG, troponin features in ACS conditions

A
  • Unstable Angina: Partial occlusion, no infarction (just ischaemia), ECG usually normal (can show ST depression/T wave inversion), troponin normal
  • NSTEMI: Major occlusion, subendothelial infarction, ST depression/T wave inversion/Pathological Q waves, troponin elevated
  • STEMI: Total occlusion, transmural infarction, ST elevation/T wave inversion/New LBBB, troponin elevated
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15
Q

ACS signs/symptoms

A

Central crushing chest pain that may or may not radiate to left arm and neck. Symptoms continue at rest and last >~20 mins

  • Dyspnoea, sweating, nausea, palpitations, anxiety (impending sense of doom in MI)
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16
Q

Investigations in ACS

A
  • ECG - see ECG changes cards (if ST elevation or new bundle branch block, STEMI)
  • CT coronary angiography - assess occlusion/stenosis
  • Troponin T - raised in STEMI, NSTEMI (no ST elevation but troponin = NSTEMI)
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17
Q

What are troponins, give alternative causes of raised troponin

A

Cardiac muscle proteins. Released from cardiac muscle in severe ischaemia/infarction.

Alternative causes of raised troponin:
- Chronic renal failure
- Sepsis
- Myocarditis
- Aortic dissection
- Pulmonary embolism

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18
Q

Other imaging warranted in cases of MI

A

Chest X ray - check for pulmonary oedema
Echocardiogram - assess heart damage

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19
Q

Treatment of NSTEMI or unstable angina

A

1 - Acute management: MONAC (AB)
M - Morphine
O - Oxygen (if saturation falls below 94%)
N - Nitrates (GTN spray)
A - Aspirin (dual antiplatelet with C)
C - Clopidogrel (P2Y12 inhibitor) or ticagrelor
(A)- anticoagulant (LMWH) may be needed
(B) - Beta blocker may be needed

2 - Risk stratification:
GRACE Score conducted to calculate 6 month risk of repeat MI or mortality.
If risk is medium or high (>3%), or patient unstable, conduct PCI (percutaneous coronary intervention)

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20
Q

STEMI treatment

A

1 - Acute management: MONAC (AB)

2 - Surgical intervention needed!
- <12 hours since symptom onset and PCI available within 2 hours: PCI. If not, thrombolysis with alteplase, with anticoagulant such as unfractioned heparin. Aspirin/ticagrelor may also be given

Coronary angiography and ECG to assess success of treatment

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21
Q

Complications of MI

A

DREAD
D - Dressler’s syndrome
R - Rupture of heart septum or papillary muscles
E(fgh) - Heart Failure
A - Arrhythmia/Aneurysm
D - Death

Mitral regurgitation
Cardiac arrest

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22
Q

Secondary prevention of CVD

A

Pharmacological: 4A
- Aspirin (+- clopidogrel)
- Atenolol (Beta blocker)
- Atorvastatin
- ACEi (Ramipril)

Lifestyle:
- Exercise
- Diet change (Mediterranean best)
- Smoking cessation
- reduced alcohol intake
- Diabetes/HTN control
- Cardiac rehabilitation

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23
Q

Side effects of statins

A
  • Myopathy (creatine kinase must be checked if any muscle pain/weakness)
  • Type 2 diabetes
  • Haemorrhagic stroke
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24
Q

Aspirin MoA

A

Antiplatelet: COX-1 inhibition - preventing synthesis of thromboxane A2

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25
Q

Clopidogrel/ticagrelor MoA

A

Antiplatelet: P2Y12 receptor inhibitor (inhibit binding of ADP to P2Y12 receptor)

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26
Q

LMWH MoA

A

Antiplatelet: glycoprotein IIb/IIIa receptor antagonist

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27
Q

What are GRACE score variables

A

GRACE score calculates 6 month risk of repeat MI or death using:
- Age
- Heart rate
- Creatinine
- Cardiac arrest at admission
- ST segment deviation
- Abnormal cardiac enzymes
- Killip class symptoms (JV distention, Pulmonary oedema, Cardiogenic shock)

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28
Q

Give the types of angina

A

Angina: Myocardial ischaemia leading to central chest pain or tightness
- Stable (pectoris): Induced by effort, resolved by rest
- Unstable (crescendo): Occurs at rest, increases in intensity
- Decubitus: Precipitated by lying flat
- Prinzmetals (variant): caused by coronary artery spasm

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29
Q

Define prinzmetal angina with investigations and treatments with 2 contraindicated medications

A
  • Angina due to coronary artery spasm (can occur even in normal healthy arteries)
  • Pain occurs at rest
  • ECG shows ST elevation during pain which resolves as pain subsides
  • CCB + long-acting nitrates
  • Beta blockers and aspirin contraindicated; can cause increased spasm or aggravate pain respectively
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30
Q

Define Dressler’s syndrome with symptoms and treatment

A
  • Occurs between 2-10 weeks after an MI. Myocardial damage causes autoimmunity against heart, causing pericarditis.
  • Pleuritic chest pain and pericardial rub on auscultation. May have fever and recurrent infection
  • Treatment with NSAID or steroids
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31
Q

Define pericarditis

A

Inflammation of the pericardium of the heart

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32
Q

Causes of pericarditis (bacterial and viral)

A

Bacterial: TB, pneumonia, rheumatic fever
Viral: Coxsackie, EBV, HIV, CMV (most common)
MI (Dressler’s)

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33
Q

Signs/symptoms of pericarditis

A

Signs
- Pericardial rub on auscultation on left sternal edge as patient leans forward (Squeaky to and fro sound)
- Chest pain that is sharp, central and pleuritic, that is exacerbated by lying flat or inspiration, and is relieved by sitting forwards.

Symptoms: May present with symptoms of effusion or cardiac tamponade (more detail on individual cards)

PE: Dyspnoea, raised JVP, peripheral oedema, tachycardia, tachypnoea
Cardiac tamponade: Beck’s triad, pulsus paradoxus, coughing

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34
Q

Investigations for pericarditis

A

ECG - PeRicardiTiS
- Widespread saddle shaped ST elevation
- PR depression, followed by T wave flattening and eventual inversion
Chest X ray: “Water-bottle heart” (cardiomegalic) may indicate pericardial effusion
Auscultation: Pericardial rub when patient leans forwards (left sternal edge)

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35
Q

Management of pericarditis

A

Analgesia e.g. ibuprofen, and/or colchicine
Treat underlying cause (E.g. antibiotics if Bacterial)

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36
Q

Complications of pericarditis

A

Pericardial effusion
Cardiac tamponade
Myocarditis
Constrictive pericarditis

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37
Q

If pericarditis persists for weeks/months, what is it called?

A

Constrictive (chronic) pericarditis

Caused by fibrosis of serous pericardium, forming an inelastic shell around the heart, making it difficult for the ventricles to contract

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38
Q

Signs in constrictive pericarditis

A

Kussmaul’s sign - raised JVP with inspiration
Pulsus paradoxus - Drop in BP during inspiration greater than 10mmHg

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39
Q

Imaging of constrictive pericarditis

A

CXR: Small heart with pericardial calcification
Echocardiogram: Thick calcified pericardium

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40
Q

Definition of pericardial effusion

A

Accumulation of fluid in pericardial sac usually secondary to pericarditis (same causes)

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41
Q

Signs/symptoms of pericardial effusion

A

Ewart’s sign: Large effusion compressing lower left lobe, causes bronchial breathing at left base
- Dyspnoea, raised JVP, peripheral oedema, tachycardia, tachypnoea

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42
Q

Investigations in pericardial effusion

A

ECG: Low QRS complex voltage
CXR: Enlarged, globular heart

GOLD: Transthoracic Echocardiogram: echo-free zone around heart, heart “dancing” in fluid

Pericardiocentesis may diagnose cause (bacterial culture/ ZN stain) and is possible treatment (cardiac tamponade)

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43
Q

Define cardiac tamponade

A

Severe pericardial effusion, raising intrapericardial pressure enough to impair ventricular filling

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44
Q

Signs/symptoms of cardiac tamponade

A
  • BECKS TRIAD
    - Hypotension
    - Distended jugular veins (+- raised JVP)
    - Muffled S1 and S2 heart sounds
  • Pulsus paradoxus (BP drops more than 10mmHg on inspiration)
    Tachycardia
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45
Q

Investigations in cardiac tamponade

A

Same as pericardial effusion
Echocardiogram diagnostic

Urgent pericardiocentesis to determine cause (bacterial culture, ZN stain, viral serology)

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46
Q

Management and complications of cardiac tamponade

A

Emergency pericardiocentesis and drainage

Complications:
Cardiac arrest
Constrictive pericarditis

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47
Q

What is Becks triad

A

Suggests cardiac tamponade
- Hypotension
- Distended jugular veins (+- raised JVP)
- Muffled S1,S2 heart sounds

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48
Q

What 2 symptoms strongly suggest endocarditis

A

Fever + new murmur

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49
Q

Definition of and risk factors for infective endocarditis. Which valves are most affected

A

Infection of the endocardium usually affecting valves (native or prosthetic)

Mitral valve most affected, tricuspid most in IV drug use

  • Poor oral hygiene (viridians streptococci)
  • Elderly male
  • Rheumatic heart disease
  • Regurgitative valve
  • Prosthetic valves
  • IV drug use
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50
Q

Pathophysiology of infective endocarditis

A
  • Abnormal/damaged endocardium causes platelet deposition (nonbacterial thrombotic endocarditis)
  • Bacteria added (infective endocarditis) which use adhesins to adhere to platelets and each other, causing vegetations.
  • These can detach and deposit elsewhere (septic emboli)
  • Causes regurgitation in valve
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51
Q

Causes of infective endocarditis

A

Usually bacterial, can be fungal

Viridians streptococci
Staph Aureus
Staph epidermidis
Strep bovis (colon cancer)

Rare gram negative (HACEK group)
- Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

SLE, malignancy

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52
Q

Main hand signs of Infective Endocarditis (4)

A

Splinter Haemorrhages (under nails)
Janeway lesions (painless plaques on palms/soles)
Osler’s nodes (Painful nodules on fingers/toes)
Clubbing

(Roth’s spots are the other main sign, white centred retinal haemorrhages!)

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53
Q

Signs/symptoms of infective endocarditis

A

Symptoms:
Fever, rigors, night sweats, weight loss, splenomegaly

Signs
Splinter haemorrhages, janeway lesions, osler’s nodes, roth’s spots, clubbing, petechiae (haemorrhage under skin), septic emboli

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54
Q

What is the scoring system for infective endocarditis

A

Modified Duke’s criteria.
2 major criteria. 1 major, 3 minor. 5 minor.

Major:
- Positive blood cultures from 2 separate cultures drawn >12 hours apart. OR all of 3 or majority of 4+ positive cultures with over an hour between first and last.
- Echocardiogram evidence of endocardial involvement (vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation)

Minor:
- Predisposition (cardiac lesion, IV drug use)
- Fever >38C
- vascular/immunological signs (janeway lesions, conjunctival petechiae, septic embolism/ glomerulonephritis, osler nodes, roth spots, rheumatoid factor)
- Positive culture that doesnt meet major
- Positive echocardiogram that doesnt meet major

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55
Q

Major Dukes Criteria

A
  • Positive blood cultures from 2 separate cultures drawn >12 hours apart. OR all of 3 or majority of 4+ positive cultures with over an hour between first and last.
  • Echocardiogram evidence of endocardial involvement (vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation)
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56
Q

Minor Dukes Criteria

A
  • Predisposition (cardiac lesion, IV drug use)
  • Fever >38C
  • vascular/immunological signs (janeway lesions, conjunctival petechiae, septic embolism/ glomerulonephritis, osler nodes, roth spots, rheumatoid factor)
  • Positive culture that doesnt meet major
  • Positive echocardiogram that doesnt meet major
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57
Q

Investigations in Infective Endocarditis

A

Use Modified Duke’s Criteria!

  • Blood cultures: 3 sets, different sites, at least an hour apart, when fever is highest
  • TRANSOESOPHAGEAL echocardiogram: mobile, valvular vegetations if >2mm

Others:
FBC - normochromic, normocytic anaemia
ESR/CRP - high
CXR - Cardiomegaly
ECG - Long PR
Urinalysis

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58
Q

Treatment of Infective Endocarditis

A

Empirical: Amoxicillin if native, Vancomycin, Gentamicin, Rifampicin if prosthetic

Staph native: Flucloxacillin (1st), vancomycin + rifampicin (2nd)
Staph prosthetic: Flucloxacillin, Gentamicin, Rifampicin

Strep: benzylpenicillin (+gentamicin if prosthetic)

HACEK: Amoxicillin (+gentamicin if prosthetic)

Surgery to remove infected tissue and replace valve if severe sepsis, heart failure, perivalvular abscess

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59
Q

Complications of Endocarditis

A

Valve regurgitation, rupture or fistula
Septic embolisation
Congestive heart failure

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60
Q

Hypertension staging - hospital vs ambulatory

A

Stage - Clinical Reading - Ambulatory Reading

1 - >140/90 - >135/85
2 - >160/100 - >150/95
3 - >180/120

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61
Q

Define the white coat effect

A

A discrepancy of >20/10mmHg between the clinical reading and average daytime ABPM, usually due to the stress of being in hospital

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62
Q

What are the types of hypertension

A

Primary (essential) - No underlying or known cause

Secondary - known cause

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63
Q

What factors could contribute to essential hypertension

A
  • Genetic susceptibility
  • Excessive sympathetic nervous system activity
  • High salt intake
  • Na+/K+ membrane trnasport abnormalities
  • RAAS abnormalities
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64
Q

Give examples of secondary hypertension

A

Renal:
- CKD
- Glomerulonephritis
- Renal artery stenosis

Endocrine:
- Primary hyperaldosteronism
- Cushing’s syndrome
- Phaeochromocytoma
- Hyperthyroidism
- Acromegaly

Pregnancy (pre-eclampsia)

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65
Q

Describe malignant hypertension

A

BP >180/120mmHg
Includes signs of retinal haemorrhage and/or papilloedema
Requires emergency treatment

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66
Q

Who should be offered antihypertensive treatment

A

Stage 1 - Those with:
- Target organ damage
- Established CVD
- Diabetes
- Renal disease
- 10 year CVD risk of >20%

Anyone at Stage 2 or higher

HTN screening every 5 years, more often if borderline. Every year in T2DM

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67
Q

Hypertension treatment

A

<55 or with T2DM
1) ACEi (ARB if ACEi not tolerated)
2) ACEi + CCB or Thiazide like diuretic

> 55 or Black African/Caribbean
1) CCB
2) CCB + ACEi or Thiazide like diuretic

3) ACEi + CCB + Thiazide like diuretic
4) (3) + alpha or beta blocker or K+ sparing diuretic if K+ <4.5mmol/L

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68
Q

Complications of HTN

A

Atherosclerosis!!!

4 Cs

Coronary artery disease
Cerebrovascular event
CVD
CKD
Hypertensive retinopathy

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69
Q

ECG in atrial flutter

A

Sawtooth-like F waves (p wave after p wave)

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70
Q

Give normal pathway of electrical signals in heart

A

SAN > Atria > AVN > Bundles of His > Purkinje fibres > L/R bundle >Ventricles

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71
Q

Give the types of tachycardia and bradycardia

A

Bradycardia
- Bundle branch blocks (LBBB,RBBB)
- Heart blocks (1°, 2° (Mobitz 1,2), 3°(complete)
- Sinus bradycardia

Tachycardia
Supraventricular
- AF (Fibrillation and Flutter)
- AVRT (WPW), AVNRT
Ventricular
- Ventricular ectopic
- Prolonged QT syndrome
- Torsades de Pointes

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72
Q

Define sinus tachycardia

A

Heart rate >100bpm but normal sinus rhythm

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73
Q

Pathophysiology of bundle branch blocks

A

Blocked side gets impulses late, meaning ventricles do not contract together.

Left bundle branch block causes abnormal Q waves (as left responsible for initial ventricular activation)

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74
Q

Causes and sign on auscultation of RBBB and LBBB

A

RBBB:
- PE, cor pulmonale, IHD, Atrial/ventricular septal defect
- Wide physiological splitting of S2 heart sound

LBBB:
- IHD, HTN, Cardiomyopathy, fibrosis
- Reverse splitting of S2 heart sound

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75
Q

ECG of RBBB and LBBB

A

RBBB - MaRRoW
- QRS looks like an M in V1 and V2, looks like an W in V4-V6
- Tall late R wave V1, Slurred S wave V6

LBBB - WiLLiaM
- QRS looks like W in V1 and V2, looks like an M in V4-V6
- Deep S wave in V1, tall late R wave in V6

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76
Q

What are the 4 cardiac arrest rhythms?

A

VT VF PE A
(Shockable)
- Ventricular tachycardia
- Ventricular fibrillation
(Non-shockable)
- Pulseless electrical activity
- Asystole

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77
Q

Risk factors for Bradycardia

A

Increasing age (>70)
Hypothyroidism
Hyper/hypo kalaemia, calcaemia
Drugs (Beta blockers, non dihydropyridine CCB, adenosine)
Infections (Typhoid, diptheria)

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78
Q

Pathophysiology of bradycardia/AV blocks

A

Bradycardia (<50bpm) usually due to sinus node or AV node conduction dysfunction

Types of AV blocks
- 1st degree: Delayed conduction through AV node, every A impulse still causes V contraction. (PR >0.2s)
- Mobitz type 1/Wenckebach: Atrial impulse becomes weaker until it doesn’t trigger Ventricular (PR increases until QRS complex drops) then resets
- Mobitz type 2: Disease of His-Purkinje system causes intermittent failure of AV conduction, causing missing QRS. Usually a set ratio of p waves to QRS. E.g. 2:1 ratio, after every 2nd p wave there is a QRS drop (QRs drop, no PR change)
- Third degree: Complete heart block. No relationship between QRS and P waves

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79
Q

Signs/symptoms of AV Blocks

A

Signs:
- Cushings triad for raised intracranial pressure: Bradycardia, hypertension, apnoea (temporary cessation of breathing)
- JVP: Cannon A waves (complete heart block, due to atrial contraction against closed tricuspid)

Symptoms:
Bradycardia, Dizziness, Fatigue, Dyspnoea, Syncope

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80
Q

Management of bradycardia/ AV blocks

A

If unstable Atropine 500mcg

Then pacemaker can be installed

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81
Q

What are the types of supraventricular tachycardia?

A

AF AF AVRT(WPWS) AVNRT

Caused by electrical signals reentering atria from ventricles

Atrial Fibrillation
Atrial Flutter
AVRT (Wolff-Parkinson White Syndrome)
AVNRT

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82
Q

Define and give risk factors for Atrial fibrillation

A

Most common arrhythmia. SAN causes uncoordinated, rapid, irregular atrial contraction.

Increasing age
DM
Rheumatic Fever
Obesity
Excessive alcohol
Hyperthyroid
HTN/Cornary artery disease
Congestive heart failure
Thyroxine/beta agonist usage

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83
Q

Causes of Atrial fibrillation

A

PIRATES
P - PE/COPD
I - IHD and Heart failure
R - Rheumatic heart disease, any valve disease
A - Anaemia, alcohol, age
T - hyperThyroidism
E - electrolytes - Hypo/hyperkalaemia, hypomagnesemia
S - Sepsis/sleep apnoea

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84
Q

Signs/symptoms of atrial fibrillation, as well as course of disease

A

Signs: Irregularly irregular pulse
Hypotension
ECG changes (other card)

Symptoms: fatigue, palpitations, dyspnoea, syncope, chest pain

Course:
Paroxysmal: Self limiting <7 days
Persistent: recurrent, >7 days
Permanent: Continuous, refractory to treatment

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85
Q

Investigations in atrial fibrillation

Including risk score for 1 year risk of stroke after AF and major bleeding risk for patients with AF on anticoagulants

A

1) ECG
- Irregularly irregular rhythm
- Absent P waves
- QRS complex <120ms
- Absent isoelectric baseline
- Fibrillatory waves

Also check TFT, electrolytes, CXR, Transthoracic echocardiogram, troponin T

Check CHA2DS2-VASc and ORBIT/HASBLED score

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86
Q

Complications of atrial fibrillation

A

Ischaemic Stroke
Syncope
MI
Heart failure
Mesenteric ischaemia

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87
Q

What is CHA2DS2-VASc score?

What results give low medium and high score

A

Calculates 1 year risk of stroke in atrial fibrillation patients
CHADS VASc

Congestive heart failure
Hypertension
Age>75 (2pts)
Diabetes Mellitus
Stroke/TIA/Thromboembolism (2pts)
Vascular disease (PAD, MI, Aortic plaque)
Age 65-74
Sex category (female)

0 low
1 moderate
2+ high - oral anticoagulant required

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88
Q

What is the ORBIT score?

A

Calculates major bleeding risk for patients with AF on anticoagulants (similar to HASBLED, replaced in 2021!)

Low Hb (+2)
Age >74
Bleeding history (+2)
eGFR <60
Treatment with antiplatelet agents

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89
Q

Management of AF

A

Rate control and rhythm control

If unstable: emergency electrical synchronised DC cardioversion

  • Rate control first: Beta blocker (atenolol) or rate limiting CCB (Verapamil). Dual if refractory
  • Rhythm control: Amiodarone or electrical cardioversion if persistent (with amiodarone 4 weeks before and 12 months after)
  • Anticoagulation (DOAC or vitamin K) if CHADSVASC>2
90
Q

Atrial flutter definition/ pathophysiology

A

Continuous atrial depolarisation caused by a re-entrant rhythm, where electrical signal recirculates in self perpetuating loop. Atrial contraction goes up to 300bpm. Ventricular contraction every 2 cycles (2:1 AV block)

ECG: Diagnostic, Sawtooth-like F waves (p wave after p wave)

91
Q

Causes of atrial flutter

A

CHD, obesity, COPD, pericarditis, Cardiomyopathy, Heart failure

92
Q

Treatment of atrial flutter

A

Treatment:
If unstable: electrical synchronised DC cardioversion

  • Rate control: 1 Beta blocker (atenolol) or rate limiting CCB (Verapamil). Dual if refractory
  • Rhythm control: Amiodarone or electrical cardioversion
93
Q

ECG in AVRT/AVNRT

A

Short PR
Slurred delta wave
Wide QRS

94
Q

AVRT/AVNRT (Wolff Parkinson White) pathophysiology

A

Congenital accessory conduction pathway (bundle of kent) between atria and ventricles
(In AVNRT re-entrant pathway through AV node)
Type A - +ve delta wave in V1
Type B - -ve delta wave in V1

Treatment: Amiodarone and ablation (surgical removal) of accessory pathway

95
Q

Indications for pacemakers

A

Symptomatic bradycardia, unresponsive to atropine
AV Blocks
Suppression of tachycardia, unresponsive to drugs

95
Q

AVRT/NRT treatment

A

Amiodarone and ablation (surgical removal) of accessory pathway

96
Q

Define ventricular ectopic tachycardia with ECG

A

Premature ventricular beats caused by ectopic electrical discharges

ECG shows random abnormal QRS on background of normal ECG

97
Q

Define long QT syndrome with common causes (3)

A

Long QT = prolonged repolarisation of muscle cells in heart after a contraction. QT >430 males, >450 females

  • Romano-Ward syndrome: Aut Dom inheritance of 1 copy of KCNQ1 gene, causing long QT without deafness
  • Jervell-Lange-Nielsen syndrome: Aut Rec. inheritance of two copies of variant gene, causes deafness and long QT
  • Can also be caused by drugs that block potassium channels (amiodarone, tricyclic antidepressants, erythromycin also hypokalaemia/calcaemia, myocarditis)
98
Q

Types of Long QT syndrome

A

LQT1 - mutation in KCNQ1, causing exertional syncope
LQT2 - mutation in KCNH2, causing syncope in emotional stress
LQT3 - Syncope at night/rest

99
Q

Treatment of Long QT and main 2 complications

A

Beta blocker (propanolol) and implantable cardioverter-defibrillator

  • Torsade de pointes (depolarisation without proper repolarisation. Fixed with magnesium infusion)
  • Cardiac arrest
100
Q

Define heart failure

A

Cardiac output inadequate for body’s metabolic demands

101
Q

How does left heart failure cause right heart failure

A

Left side of heart is unable to pump efficiently, causing blood to back up into pulmonary veins and arteries. This increases pulmonary blood pressure. This pressure is then transmitted back towards the right ventricle.

The dilation of the right ventricle stretches the AV valve, causing a regurgitation into the right atrium during systole. This causes right atrium dilation, which puts further pressure on the right ventricle causing it’s hypertrophy. Eventually neither work efficiently causing right heart failure. RHF causes an increase in blood backing up into general circulation

102
Q

How does right heart failure cause its cardinal symptoms

A

Jugular vein distension - Increased pressure in right atrium is transmitted back to the jugular veins

Hepatomegaly - Increased pressure of the hepatic veins, which usually directly drain into the inferior vena cava

Peripheral pitting oedema - Increased pressure in the systemic venous circulation, forcing fluid out of the blood into surrounding tissues

103
Q

Systolic vs diastolic heart failure. Causes and pathophysiology

A

Systolic:
Caused by: IHD, MI, Cardiomyopathy.
Inability of ventricle to contract normally, reducing cardiac output. Ejection fraction is REDUCED (<40%)

Diastolic:
Caused by: Constrictive pericarditis, cardiac tamponade, HTN, restrictive cardiomyopathy.
Inability of ventricles to relax and fill with blood properly. Ejection fraction PRESERVED (>50%)

104
Q

Signs and symptoms of left heart failure

A

Signs
- Tachypnoea, tachycardia
- Cool peripheries
- Peripheral cyanosis
- Pink frothy sputum/crackles on auscultation
- Wheeze
- Third heart sound
- Displaced apex beat

Symptoms:
- Dyspnoea, Orthopnoea (SOB when lying flat), Paroxysmal nocturnal dyspnoea (SOB at night)
- Fatigue and weakness
- Weight loss

105
Q

Signs and symptoms of right heart failure

A

(usually due to pathology involving lungs/pulmonary vessels e.g. pulmonary stenosis)

Signs (due to backing up of fluid):
- Raised JVP
- Peripheral pitting oedema (thighs, sacrum, abdomen)
- Hepatosplenomegaly
- Ascites
- Facial engorgement
- Pulsing in face/neck (tricuspid regurgitation)

Symptoms:
- Fatigue/weakness
- Swelling in legs/distended abdomen
- Nausea/anxiety
- Nose bleed

106
Q

What is congestive heart failure

A

When both left and right heart failure occur together

107
Q

How might a heart failure patient present on examination?

A
  • Increased resp rate
  • Reduced O2 saturation
  • Tachycardia
  • Hypotension
  • Dyspnoea
  • Oedema in legs

Auscultation:
- 3rd heart sound/ displaced apex beat
- Bilateral basal crackles (that sound wet)

108
Q

How does left heart failure cause pulmonary oedema, and how does this lead to right sided heart failure

A

LV unable to move blood out into body, causing backlog.
This increases blood stuck in LA, pulmonary veins and lungs. They leak fluid as a result and are unable to reabsorb it. This causes pulmonary oedema; lung tissues and alveoli become full of interstitial fluid, interfering with gas exchange, leading to SOB and other symptoms.

Pulmonary HTN puts pressure on right ventricle, meaning it isn’t able to pump as much blood, causing right sided heart failure.

109
Q

Signs of heart failure that suggest an underlying cause

A

Chest pain - ACS
Fever - Sepsis
Palpitations - Arrhythmia

110
Q

Investigations in Heart failure

A

BNP (Brain Natriuretic Peptide) blood test
- Released from stressed ventricles in response to increased mechanical stress
- (NOT specific, also released in tachycardia, sepsis, PE, renal impairment, COPD)

CXR (ABCDE)
- Alveolar Oedmea, Kerley B lines (interstitial oedema), Cardiomegaly, Dilated upper lobe vessels, Pleural effusion

ECG will show wide QRS and may help diagnose causation

Echocardiography is KEY. Measures Ejection fraction, ventricular function, valvular abnormalities

111
Q

Scoring system for heart failure functional limitations

A

New York Heart Association classifications of heart failure

I (Mild) - No limitation on physical activity. Ordinary physical activity doesnt cause fatigue/palpitations/dyspnoea
II (Mild) - Slight limitation n physical activity. Comfortable at rest; dyspnoea on ordinary activity
III (Moderate) - Less than ordinary activity causes dyspnoea, which is limiting. Rest is fine.
IIII (Severe) - Symptoms present at rest, all activity causes discomfort

112
Q

Criteria for congestive cardiac failure

A

Framingham criteria (2 major, 1 major 2 minor)

Major - PNDyspnoea, Crepitations, JV distention, Pulmonary oedema, S3 gallop, Cardiomegaly, weight loss
Minor - Bilateral ankle oedema, nocturnal cough, dyspnoea on exertion, tachycardia, hepatomegaly, pleural effusion

113
Q

3 cardinal non specific signs in heart failure

A

SOB AS FAT
Dyspnoea, Ankle Swelling, Fatigue

114
Q

Pathophysiology of ischaemic, HTN, LV hypertrophy and dilated cardiomyopathy heart failure, and what HF do these cause?

A

Cause systolic failure
- Ischaemic: Myocytes start to die, reducing ability of contraction
- HTN: Arterial pressure increase in systemic circulation means it is harder for LV to pump blood into hypertensive circulation
- LV hypertrophy: increased muscle mass requires increased oxygen supply, more likely muscles will die
- Dilated cardiomyopathy: Heart chambers dilate, become thinner, weaker contractions.

115
Q

Acute management of heart failure

A

Pour SOD

Pour away fluids (Stop fluids)
Sit up
Oxygen
Diuretics
GTN may be needed

116
Q

Management of chronic heart failure

A

ABAS
ACEi (ramipril)
Beta blocker (propanolol)
Aldosterone antagonist (spironolactone)
SGLT2i - empagliflozin

1) ACEi + beta blocker
2) Add spironolactone and SGLT2i if Ejection fraction not controlled with ACEi and BB

117
Q

What should be kept in mind when prescribing for heart failure? (reg ACEi)

A

ACEi contraindicated in Heart valve disease
ARB (candesartan) can be used instead of ACEi
Aldosterone antagonists added if ejection fraction not controlled with ACEi and BB

118
Q

Define abdominal aortic aneurysm

A

Dilatation in the aorta of >50%, or 3cm. Caused by increased stress to vessel wall which weakens it and eventually causes an outpouching of the vessel.

119
Q

Where do abdominal aortic aneurysms occur most commonly, and why?

A

Occur below level of renal arteries (infrarenal aneurysm). Due to the abdominal aorta below this level lacking vasa vasorum in its adventitial layer, which deliver nutrients to the aorta, making it susceptible to ischaemia.

Thickening of the intima also makes it harder for oxygen to diffuse into the tunica media

120
Q

How does atherosclerosis contribute to aneurysm formation?

A

Atherosclerosis is the most important AAA risk factor

Chronic inflammation causes release of matrix proteinases which degrade extracellular matrix in tunica media, weakening the aortic wall

121
Q

2 main differentials for AAA

A

Pseudoaneurysm (ie false aneurysm, does not involve all 3 layers of vessel wall, [E.G. AORTIC DISSECTION] when bleeding into one or 2 vessel layers causes bulging in those layers, resembling an aneurysm)

Inflammatory AAA (younger patients, occurs with smoking, atherosclerosis, vasculitis, presents similarly but with fever.)

122
Q

Most common causes for AAA

A

Atheroma
Trauma
Inflammation
Connective tissue disorder (Ehrling-Danlos, Marfans)

123
Q

True vs False aneurysm

A

True - Stress to vessel wall causes weakening of wall, leading to the occurrence of an outpouching and dilation. Affects all 3 layers

False (Pseudoaneurysm e.g. Aortic dissection) - Defect in vessel wall leads to bleeding into a layer or 2 (Extravascular haematoma). Causes a pulsatile haematoma

124
Q

Risk factors for AAA

A

Increasing age
Male
Smoking
ATHEROSCLEROSIS!!
Hypertension/lipidaemia
Connective tissue disorders (Marfans, Ehlers Danlos)

Diabetes is protective!

125
Q

Signs/symptoms of AAA

A

Mostly asymptomatic until it is about to rupture imminent or occurred (emergency)

Signs
- Pulsatile abdominal mass
- Sudden abdominal pain that radiates to flank

If ruptured:
- Grey turner’s signs: Flank bruising caused by retroperitoneal haemorrhage
- Cullen’s sign - Peri-umbilical bruising

126
Q

What imaging is diagnostic for AAA
(X ray, CT, MRI, CT Angiography, Ultrasound)? + other investigations

A

Abdominal ultrasound

Group and save and crossmatch needed if ruptured to ensure blood for transfusion

Worth doing FBC, U&E, CT angiogram, CRP/ESR to find cause

127
Q

Screening and associated management for AAA

A

Abdominal ultrasound for over 65s

<3cm - Discharge
3-4.4cm - Annual surveillance
4.5-5.4 cm - 3 monthly surveillance
>5.5cm - refer to surgery (Open or Endovascular Aortic Repair (EVAR) or AAA graft surgery if ruptured)

In general, reduce risk factors (lifestyle), underlying cause treatment (Steroids for inflammatory)

128
Q

Complications of AAA

A
  • Aneurysm rupture: Medical emergency with poor prognosis, IMMEDIATE SURGERY
  • Thromboembolism: Thrombus more likely in dilated aneurysm
  • Aortovenous fistula formation
  • Ureteric obstruction
129
Q

Aortic dissection definition + pathophysiology

A

Tear in tunica intima of aorta causes high pressure blood to tunnel into tear, causing pooling between intima and media. This eventually increases diameter of aorta, causing false aneurysm.

130
Q

Risk factors for aortic dissection

A

Similar to RF for AAA

HTN
Smoking
Atherosclerosis
Connective tissue disorders (Ehlers-Danos, Marfans)
Trauma
Pregnancy
Family history!

131
Q

Signs/symptoms of aortic dissection and Marfans and Ehlers Danlos

A

Sudden onset tearing/ripping chest pain that radiates to back.

Signs:
- Weak downstream pulses
- Differences in BP of both arms
- Diastolic murmur due to aortic regurgitation
- Hypertension
- Tachycardia, hypotension as progresses

Marfans: Tall, Arachnodactyly, Hypermobile joints, Narrow face
Ehlers-Danos: Translucent skin, Easy bruising, hypermobile small joints

132
Q

Classification of Aortic dissection

A

Stanford classification

(2/3) Type A: Dissection involves ascending aorta. Aortic arch and Descending aorta may be involved. Proximal to left subclavian artery

(1/3) Type B: Dissection doesnt involve ascending aorta. Only descending, thoracic, abdominal aorta. Distal to left subclavian artery.

133
Q

Investigations for aortic dissection

A

CXR - Widened mediastinum
Transoesophageal echocardiogram

GOLD - CT Angiography (U+E conducted before this)

Cross match needed before transfusion

134
Q

Treatment of aortic dissection

A

Blood transfusion if blood loss
Opioid analgesia if in pain

1 - Beta blocker
- Vasodilator (Sodium nitroprusside)
2- Urgent Surgery (Thoracic endovascular aortic repair (TEVAR))

135
Q

Complications of aortic dissection

A
  • Aortic rupture (emergency, death without surgery)
  • Aortic regurgitation!
  • Renal failure (if blood continues to tunnel till it reaches renal arteries, pressuring those arteries, reducing flow to kidneys)
  • Pericardial tamponade
  • MI
  • Stroke
136
Q

Define PAD with pathophysiology

A

Peripheral Arterial Disease

Arterial obstruction, usually due to atherosclerosis and thrombosis, causing ischaemia of lower limbs. Ischaemic muscles release adenosine causing pain.

3 main patterns;
- Intermittent claudication
- Critical limb ischaemia
- Acute limb-threatening ischaemia

137
Q

Signs/symptoms of PAD

A

6P’s
Pulseless
Paralysis
Pale
Perishingly cold
Pain
Paraesthesia

Usually due to acute limb ischaemia together but some present in PAD

Other signs:
- Ulcers
- Pale, shiny, taut atrophic skin
- Hair loss

138
Q

Classification of PAD

A

Fontaine classification

1 - Asymptomatic - Low ABPI/lack of pulses
2 - Intermittent claudication - Aching/burning on exertion, after walking:
- 2a: >200m, 2b: <200m. Pain never present at rest
3 - Critical limb ischaemia - Rest pain, “dangling over edge of bed for pain relief”. Risk of limb loss
4 - Tissue loss (Ulceration/Gangrene)

139
Q

Site of claudication with associated site of disease
- Unilateral buttock
- Unilateral thigh
- Unilateral calf
- Foot

A

Unilateral buttock - Common iliac
Unilateral thigh - Common femoral or iliac
Unilateral calf - Popliteal or Superficial Femoral
Foot - Peritoneal or tibial

140
Q

What is the Buerger’s test?

A

Test for PAD

Raise patient’s legs 45 degrees. Pallor after 1-2 mins suggests PAD.
Next, have them sit over the edge of a bed with their legs hanging.
In PAD patient, legs will go blue (as ischaemic tissue deoxygenates blood) and then dark red (reactive hyperaemia due to post-hypoxic vasodilation)

141
Q

What is Leriche syndrome

A

PAD causes occlusion of aortoiliac artery

Patient presents with triad of
- Bilateral buttock and thigh claudication
- Absent or decreased femoral pulses
- Erectile dysfunction

142
Q

Investigations in PAD

A

Ankle-brachial pressure index: systolic BP recorded in both arms, posterior tibial, dorsalis pedis and peroneal arteries.
- >1.4 - Abnormally calcified vessels
- 1.2-0.9 - Normal
- 0.9-0.5 - Intermittent claudication
- <0.5 - Critical limb ischaemia
- Absence of pulse in lower extremities suggests acute limb ischaemia

Duplex ultrasound - First line imaging. CT angiography can be done after

143
Q

Management of PAD

A
  • Exercise first line, control risk factors (clopidogrel as prophylaxis)
  • Vasodilator: naftidrofuryl oxalate
  • Surgical interventions if exercise doesnt work. Percutaneous Transluminal Angioplasty or Atherectomy.
  • Amputation if severe
144
Q

Acute limb ischaemia AKA Acute limb-threatening ischaemia definition and main cause

A
  • Sudden decrease in perfusion due to arterial occlusion, resulting in severe ischaemia. MEDICAL EMERGENCY.
  • Caused by thrombosis/embolism (AF, recent MI causing mural thrombus, valvular vegetation)
145
Q

Signs/symptoms of Acute limb ischaemia and management

A

Pale
Pulseless
Paralysis
Paraesthesia
Pain
Perishingly cold

Initially - IV unfractioned heparin
Then: (depends on Rutherford criteria)
1 - Thrombolysis
2 - Thrombolysis or percutaneous thromboembolectomy
3 - Amputation

146
Q

Complications of PAD

A

Progression to critical limb ischaemia
Ulceration/gangrene
Infection/poor tissue healing
Rhabdomyolysis
Permanent limb pain/weakness

147
Q

Define DVT

A

Formation of a blood clot in the deep veins of leg/pelvis (as opposed to superficial arteries in PAD)

148
Q

Risk factors/causes of DVT

A

Increasing age
Smoking
Pregnancy
SLE
Thrombophilias

Immobility (long haul travel, hospitalisation, bed bound)
Synthetic Oestrogen (combined oral contraceptive pill)
Leg fracture

149
Q

What is Virchows triad

A

Triad for thrombosis

1) Hypercoagulability
- Increased platelet adhesion and clotting tendency (pregnancy, obesity, chemotherapy, antiphospholipid syndrome, malignancy)

2) Venous stasis
- Stasis disrupts laminar flow, increasing risk of thrombus formation

3) Endothelial damage
- Damage disrupts anticoagulant secretion by endothelial cells (Smoking, trauma, surgery, inflammation)

150
Q

Signs/symptoms of DVT

A
  • Pitting Oedema
  • Red, tender, swollen calf
  • Distended superficial veins
  • Mild fever
151
Q

What is the Wells score

A

Predicts DVT
Highly sensitive but not very specific

DVT likely 2 points
DVT unlikely 1 point or less

Some point factors include:
- pitting oedema
- active cancer
- Distended superficial veins
- calf swelling
- previous DVT
- localised tenderness
- recent bedriddenness

If alternative diagnosis equally likely take 2 from points

If DVT unlikely (<1), conduct D Dimer, if positive ultrasound
If DVT likely, do both D dimer and ultrasound

152
Q

What is a possible cause of recurrent venous thromboembolism

A

Antiphospholipid syndrome (or other thrombophilias)

153
Q

What should a patient be started on if at risk of VTE whilst in hospital?

A

LMWH (enoxaparin) is go to prophylaxis for VTE

154
Q

Investigations in DVT

A

Wells score guides investigations

<=1- Perform D dimer
If positive, do duplex ultrasound
>=2 - Duplex ultrasound of leg, perform D dimer and offer interim anticoagulation

Interim coagulation always offered if results cant be obtained within 4 hours.

155
Q

Management of DVT

A

Initial: If no renal impairment: Offer apixaban (factor Xa inhibtor)

If renal impairment: LWMH, or unfractioned heparin

If cancer, DOAC

156
Q

Preventative advice for DVT

A
  • Wear compression stockings
  • Frequent calf exercises
  • Prophylactic anticoagulation (LMWH) in patients with recent surgery/long immobilisation
157
Q

Define Pulmonary Embolism

A

Sudden onset pleuritic chest pain caused by embolus (most commonly by DVT) lodging in pulmonary vasculature.

Embolus travels through circulation, into right atrium then out of right ventricle into lungs. Blockage leads to ischaemia/infarction of lung tissue. Causes V/Q mismatch severe enough to collapse alveoli

158
Q

Signs/symptoms of Pulmonary embolism

A

Hypoxia (+- cyanosis)
Tachypnoea, tachycardia
Hypotension
Crackles

Pleuritic chest pain, dyspnoea, cough +- haemoptysis, fever, fatigue

159
Q

Investigations for thrombophilias

A

Antiphospholipid antibodies

Thrombophilia screen (Especially indicated in unprovoked DVT/PE)

160
Q

Scoring system for pulmonary embolism

A

Well’s Two-Level PE score
<4, low probability
4+, high probability

161
Q

Contra indication for compression stockings

A

PAD

162
Q

Investigations for Pulmonary embolism

A

D dimer and CT pulmonary angiography 1st and GOLD!

ECG also significant (S1Q3T3)
- Large S wave lead 1
- Large Q wave lead 3
- Inverted T wave in lead 3

  • Also shows sinus tachycardia
163
Q

Management of pulmonary embolism

A

Supportive in hospital (Oxygen, analgesia etc)

Massive PE: Thrombolysis - Alteplase

Non massive:
- Initial: If no renal impairment: Offer apixaban (factor Xa inhibtor)
- If renal impairment: LWMH, or unfractioned heparin
- If cancer, DOAC

164
Q

Complications of pulmonary embolism

A
  • Cor pulmonale
  • Pulmonary infarction
  • Respiratory alkalosis
  • Embolic stroke
165
Q

Define rheumatic fever with pathophysiology

A

Type 2 hypersensitivity reaction; Autoimmune condition caused by antibodies created against Group A beta-haemolytic streptococcus infection (strep pyogenes) (Molecular mimicry)

Rheumatic fever is usually secondary (2-4 weeks) to strep throat (Tonsilitis due to streptococcus)

Rare in West, more common in developing world

Systemic, causes joint pain and carditis.

Repeat exposure can become chronic, leading to fibrosis of valves, causing regurgitations.

166
Q

What can be found histologically on the hearts of people with rheumatic fever

A

Aschoff bodies

167
Q

Scoring system for Rheumatic fever, major and minor signs

A

Revised Jones criteria - Evidence of recent strep infection + 2 major signs or 1 major 2 minor (JONES-FEAR)

Evidence of recent infection: group A strep antigen test, positive throat culture, strep antibodies

Major: JONES
- Joint arthritis
- Organ inflammation (CARDITIS! + Murmurs)
- Nodules under skin
- Erythema marginatum rash - red raised edges, clear middle
- Sydenham’s chorea - involuntary semi purposeful movements

Minor: FEAR
- Fever
- ECG (prolonged PR)
- Athralgia without arthritis
- Raised CRP/ESR

other Sx
- Pericardial rub
- rash
- joint pain
- SOB

168
Q

What murmurs does rheumatic fever cause

A

Acute - Mitral and aortic Regurgitations
Chronic - Mitral stenosis

169
Q

Management and complications of rheumatic fever

A

Oral penicillin V for 10 days, NSAIDs

  • Rheumatic heart disease - Fibrosis of valves leading to regurgitations (Stenoses possible if chronic)
  • Heart failure
  • Infective endocarditis/pericarditis
  • Atrial fibrillation
170
Q

Complications of valve disorders

A

Mitral stenosis - Left atrial hypertrophy
Aortic stenosis - Left ventricular hypertrophy

Mitral regurgitation - Left atrial dilatation
Aortic regurgitation - Left ventricular dilatation

171
Q

Mitral stenosis pathophysiology

A

Narrow mitral valve, difficult to push blood into ventricle. Sx occur when mitral bicuspid valve lumen <2cm². Pressure increases until the valve “snaps” open. Backing up of blood can cause right sided heart failure.

172
Q

Mitral stenosis causes, associated symptoms and valve sounds

A
  • Caused by rheumatic fever and Infective endocarditis
  • Malar flush (due to reduced cardiac output causing vasodilation) and atrial fibrillation (strain on heart). May present with Right heart failure signs.
  • Loud S1 snap and mid diastolic murmur
173
Q

Mitral Stenosis investigations

A

CXR - left atrium enlargement - Double right heart border, splayed trachea, calcified mitral valve
ECG - Atrial fibrillation - p mitrale(tall, long p wave), and tall R waves in V1 if RV hypertrophy
Transthoracic Echocardiogram (GOLD)

174
Q

Mitral stenosis treatment and complications

A

Percutaneous mitral valvotomy
Mitral valve replacement

Right sided heart failure
Atrial fibrillation
Thrombus
Stroke

175
Q

What causes S3 and S4 heart sounds

A

S3 - rapid ventricular filling. Normal in young (15-40), indicates heart failure in older patients

S4 - Heard before S1. Always abnormal. Indicates a stiff or hypertrophic ventricle causing turbulent flow against a contracting atrium.

176
Q

Mitral regurgitation pathophysiology

A

Mitral valve allows blood back into atrium during systolic contraction. Causes congestive heart failure due to reduced ejection fraction and backlog of blood.

177
Q

Mitral regurgitation causes and valve sounds

A
  • Ischaemic heart disease, rheumatic heart disease, connective tissue disorders (Ehlers Danos, Marfan), Infective endocarditis
  • Pansystolic whistling murmur that radiates to axilla with mid systolic click and additional S3 sound
178
Q

Mitral regurgitation investigations

A

ECG - p-mitrale may suggest left atrial enlargement, may show AF
CXR - left sided enlargement and pulmonary oedema
Echocardiogram GOLD

179
Q

Aortic stenosis pathophysiology and causes

A

Aortic valve doesn’t open as easily, preventing flow out of heart. Causes LV hypertrophy and dilatation.

  • Idiopathic age related calcification
  • Rheumatic heart disease
  • Bicuspid valve
180
Q

Aortic stenosis signs and symptoms and valve sound

A

Ejection systolic crescendo-decrescendo murmur radiating to carotids. Ejection click and S4 sound.

Sx
- Slow rising pulse and narrow pulse pressure
- Exertional syncope

181
Q

Aortic regurgitation pathophysiology and causes

A

Diastolic leakage of blood from aorta to left ventricle. Causes heart failure

  • Connective tissue disorders (Ehlers Danlos/Marfans)
  • Idiopathic aging related weakness
182
Q

Aortic regurgitation signs and valve sounds

A

Early diastolic murmur, water hammer pulse, soft S1, S2.
OR Austin-Flint murmur: Rumbling murmur at apex (Severe) due to vibration of mitral valve

  • Corrigan’s pulse: collapsing pulse due to blood pumping out of ventricles and immediately back in.
  • de Musset’s sign: Head bobbing with each beat due to severe bounding (water hammer) pulse
  • Quincke’s sign: Pulsation of capillary beds in finger nails
  • Traube’s sign: Pistol shot femoral pulse
183
Q

Define Tetralogy of Fallot with signs/symptoms

A

Congenital abnormalities cause an increase in deoxygenated blood in circulation. This causes:
- Cyanosis
- Clubbing
- Failure to thrive
- Ejection systolic murmur

184
Q

Risk factors for Tetralogy of Fallot

A
  • Family congenital heart disease history
  • Alcohol consumption during pregnancy
  • Diabetic mother
  • Down syndrome (trisomy 21)
  • Rubella infection
185
Q

4 congenital abnormalities in Tetralogy of Fallot

A

VORP - cause right to left cardiac shunt; blood bypasses lungs.

Ventricular Septal Defect - Blood shunts between ventricles. Oxygenated and deox. mix. Deox more into left than ox into right.

Overriding Aorta - Aorta further right than normal. RV sends deox blood into it

RV Hypertrophy - Due to added resistance of LV, ensures deox blood is shunted to left, rather than the other way.

Pulmonary stenosis - RV outflow obstruction makes it harder for deox blood to reach lungs

186
Q

Explain a Tet spell with the symptoms that come with it

A

Cyanosis exacerbated when infant demands extra oxygen (crying, feeding etc)

  • Reduced oxygen saturation
  • Knees to chest “Squatting” position (femoral arteries partially occluded, increasing systemic vascular resistance and reducing shunt)
  • Respiratory distress
  • Severe cyanosis
  • Syncope
187
Q

Treatment of Tetralogy of Fallot

A
  • Cyanosis managed with prostaglandins (e.g. alprostadil)
  • Tet spells managed with oxygen, morphine, sodium bicarbonate, beta blockers, phenylephrine, and squatting position of child
  • Surgery is definitive
188
Q

What does a chest x ray show in Tetralogy of Fallot

A

Boot shaped heart. Echocardiogram may also be shown

189
Q

Coarctation of the Aorta definition and pathophysiology

A

Narrowing of the aortic arch, strongly associated with genetic condition Turner’s syndrome. This causes reduced blood pressure to arties distal to the narrowing, whilst increasing blood pressure on heart and first 3 branches of the aorta.

190
Q

How is Coarctation of the Aorta diagnosed?

A

In neonates: Weak femoral pulses are first sign. Measuring BP of all 4 limbs will show high BP in limbs supplied before narrowing, low in rest. Systolic murmur may be present.

191
Q

What key organs are at risk of failure from shock?

A

Kidney, Lung, Heart, Brain

192
Q

Define Hypovolaemic shock with signs/symptoms

A
  • Shock due to a low blood volume (Decreased by >20%), can be haemorrhagic or non-haemorrhagic (e.g. dehydration, burns)
  • Considered “Cold” shock (cold clammy skin, confusion, tachycardia, narrow pulse pressure)
  • Treated with ABCDE and IV Fluids
193
Q

Define Cardiogenic shock with causes and symptoms

A
  • Shock caused by decreased pumping of blood around body. Causes cold shock due to lack of flow around body.
  • Caused by MI, pericardial effusion/cardiac tamponade, arrhythmia, myocarditis, pneumothorax etc.
  • Presents with symptoms of heart failure (oedema, JVP increase, S4 sound)
194
Q

Define septic shock with symptoms and treatment

A

Uncontrolled bacterial infection
- pyrexia, warm, flushed skin
- Bounding pulse
- Rigors

Treat with broad spectrum antiobiotics

195
Q

Already ill patient suddenly goes tachycardic, cyanotic, tachypnoic and red. What has happened?

A

Acute respiratory distress syndrome. Lungs cannot provide body’s vital organs with enough O2

196
Q

Pathophysiology of acute respiratory distress syndrome

A
  • Alveolar capillary membrane injury
  • Causes neutrophil invasion
  • Fibroblasts initiate fibrosis
  • Lungs scar and go stiff, less ventilation
197
Q

Consequences of Shock on
Kidney
Lung
Heart
Brain

A

Kidney - Acute tubular necrosis
Lung - Acute respiratory distress syndrome
Heart - Myocardial ischaemia
Brain - Confusion, Coma, Irritability.

198
Q

Define neurogenic shock with symptoms and treatment

A

Due to spinal cord trauma disrupting sympathetic nervous system but not parasympathetic
- Hypotension, BRADYCARDIA, confusion
- IV Atropine

199
Q

Define hypertrophic cardiomyopathy with causes

A

LVH causing thick non compliant heart, leading to impaired diastolic filling.

Caused by autosomal dominant mutation of sarcomere proteins (Beta myosin, Troponin T)

200
Q

Pathophysiology of hypertrophic cardiomyopathy

A

Walls of heart get thick, heavy and hypercontractile.

  • Walls take up more room, less cavity space
  • Walls stiff and less compliant cant stretch to fill with blood
  • Less blood pumped from heart (Decreased stroke volume)
  • Bigger heart requires more oxygen, increased ischaeamia
201
Q

Auscultation sounds of hypertrophic cardiomyopathy
Definitive investigation and treatment

A

Ejection systolic murmur (crescendo-decrescendo)
Bifid pulse
S4 sound (think HTCM - 4 letters)

Sudden death may be first sign

  • Echocardiogram (ECG will show abnormality too)
  • Amiodarone, BB
202
Q

What do Ventricular Septal defect, Atrial septal defect, Patent ductus arteriosus all cause

A

Left to right shunt of blood. Causes excess blood in pulmonary system causing pulmonary hypertension. Usually asymptomatic but in severe cases can lead to right heart failure

203
Q

What is ventricular septal defect and how does it present on examination

A

Congenital hole in ventricular septal wall allowing blood to shunt from left to right ventricles

Loud, pan systolic harsh murmur with palpable thrill

204
Q

What is atrial septal defect and how does it present on examination

A

Congenital hole between atria. Causes blood shunt from left to right.

Ejection systolic murmur.

205
Q

What is Patent Ductus arteriosus and how does it present on examination

A

Connection between aorta and pulmonary artery that doesn’t close

Murmur at left sternal edge, thrill at upper left sternal border

Usually treated surgically in first year of life due to infective endocarditis risk

206
Q

What 2 bacteria are most commonly found in lung abscesses

A

Staph aureus and strep millieri

207
Q

What 3 things can you hear on auscultation of a heart failure patient

A
  • Bilateral basal crackles
  • S3 sound
  • Displaced apex beat
208
Q

Leads showing change, site of heart and coronary artery affected in ECG

A

Septal - V1, V2 - Left anterior descending
Anterior - V3, V4 - Left anterior descending
Inferior - II,III, aVF - Right coronary
Lateral- I, aVL, aVR, V5, V6 - Lateral circumflex

209
Q

What are the criteria for cardiac resynchronisation therapy

A
  1. Bundle branch block
  2. Ejection fraction < 40%
  3. NYHA classification lll
210
Q

Define cor pulmonale

A

Right heart failure that occurs secondary to long standing pulmonary hypertension

211
Q

What does cor pulmonale show on ecg

A

P pulmonale - tall, peaked P wave

212
Q

What rule must be followed when prescribing a beta blocker and CCB

A

CCB must be dihydropyridine (non rate limiting) to not cause bradycardia

213
Q

Resuscitation council guidelines on tachycardia treatment

A

1 - If life threatening/unstable (shock, syncope, MI, Heart failure), Synchronised DC shock up to 3 times. If unsuccessful, amiodarone and go again.

If stable:
2 - If QRS narrow (120ms/0.2s), and regular, give amiodarone. If irregular most likely Afib, rate limit with beta blocker.
2- If QRS normal, valsalva manoeuvres. If unsuccessful, give adenosine (6 then 12 then 18). Then verapamil if still unsuccessful

214
Q

What is the valsalva maneuvre

A

Patient breathes out as hard as they can against a closed airway (blocked mouth and nose)

Helps in Supraventricular tachycardia (Normal QRS)

215
Q

What is a carotid sinus massage and when is it used?

A

Pressure applied to carotid sinus, slowing down or terminating arrhythmia in AVNRT or SVT.

It is contraindicated if history or risk of stroke/TIA or carotid artery disease

216
Q

Resuscitation council bradycardia treatment algorithm

A

Life threatening (syncope, shock, MI, heart failure) - Atropine 500mcg. Can be repeated to max of 3 mg or isoprenaline or adrenaline. If pharmacologically unsuccessful, transvenous pacing

If not life threatening and no recent asystole, mobitz 2 or complete heart block, just observe

217
Q

Causes of Long QT

A

Romano-ward syndrome
Jervell-Lange-Nielsen
Hypokalaemia
Hypomagnesaemia

Other obvious heart problems

218
Q

What is an innocent flow murmur and what are 3 things it can be caused by?

A

No valvular pathology. Have a “blowing” sound and can appear anywhere.

Usually due to increased flow across aortic and pulmonary valves caused by:
- Anaemia
- Pregnancy
- Thyrotoxicosis

219
Q

How should a provoked (bed rest, recent surgery etc) PE be anticoagulated?

A

DOAC (Apixaban) 3 months

220
Q

How should an unprovoked PE be anticoagulated?

A

DOAC (Apixaban) 6 months

221
Q

What are the 4 steps of platelet plug formation?

A
  • Damage to a blood vessel causes exposure of collagen. Von Willebrand Factor (vWF) binds to collagen which acts as a molecular anchor for platelets to join.
  • Platelets adhere to the damaged endothelium via vWF. When platelets adhere, they activate and degranulate– their shape changes and they release chemicals that keep the vessel constricted and draw more platelets to the damaged area. This positive feedback loop continues.
  • The aggregation of platelets results in the formation of a plug that temporarily seals the break in the vessel wall.
  • Following formation of the platelet plug, coagulation is activated to form a fibrin mesh which stabilises the platelet plug.

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