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Phase 2a Basic Knowledge > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define atherosclerosis

A

A build up of fatty deposits leading to plaque formation in blood vessel walls causing the hardening and stiffening of the walls

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2
Q

What do the letters in ECGs stand for

A

P : atrial depolarisation
Pr interval : AVN conduction delay
QRS : septal depolarisation + apex depolarisation + outer depolarisation = whole ventricular depolarisation
St segment : isovolaemic ventricular relaxation
T : ventricular repolarisation

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3
Q

ECG paper / box sizes

A

Width :
0.2s = big square
0.04s per small box (5 small squares = 1 big square)

Height :
0.5mV = big square
0.1mV per small square

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4
Q

What chest leads give you an inferior view of the heart

A

AvF, lead II, lead III

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5
Q

Which artery supplies inferior portion of heart

A

RCA

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6
Q

What chest leads show anterior view of heart

A

V1 - V4

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7
Q

What leads show lateral view of the heart

A

V5-V6, lead 1, aVL

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8
Q

What do the 4 heart sounds show

A

S1 : mitral + tricuspid close
S2 : aortic + pulmonary close
S3 : rapid ventricular filling in early diastole
normal in pregnant
pathological in mitral regurgitation
S4 : pathological “gallop”
due to blood forced into stiff hypertrophic ventricles
seen in LVH / aortic stenosis

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9
Q

Categories of ischamic heart disease

A

Angina
Myocardial infarction

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10
Q

What sign is seen as a result of myocardial ischaemia

A

“Angina” (Levine’s sign - fist over chest) central crushing chest pain due to decreased coronary artery blood flow ‘ increased O2 demand

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11
Q

3 characteristics / signs of stable angina pain

A

Central crushing chest pain radiating to the neck and jaw

Brought on by exertion

Relived by 5 mins of rest / GTN spray

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12
Q

Types of angina

A

Stable

Unstable

Prinzmetal

Dont need to know about angina pectoris - but Decubitus is a variant of this angina and it is induced by lying down

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13
Q

Define each type of angina

A

Stable: normal 3 part definition - i.e. about pain & / on exertion, relieved with rest / GTN spray

Unstable: Pain at rest, not relieved by rest or GTN spray

Prinzmetal: Due to coronary Vasospasm (not to do with atherogenesis —> ischaemia)

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14
Q

What can coronary vasospasm cause

A

Prinzmetal angina

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15
Q

What is seen in Px with Prinzmetal angina (ECG)

A

ECG : ST elevation

Seen in cocaine users

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16
Q

What is and when is QRISK score used

A

Predicts risk of CVD in the next 10 years

Score >10% indicates 10prevention - give statins

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17
Q

What should you do with QRISK score of >10%

A

Give statin - atorvastatin

primary prevention

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18
Q

What’s GRACE score and when is it used

A

Predictor of mortality from MI with the next 6months-3years

Used in ACS cases to help guide Tx

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19
Q

What is ACS

A

Umbrella term for :

Unstable angina - severe ischaemia
NSTEMI - partial infarction
STEMI - transmural infarction

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20
Q

Risk factors for IHD

A

Obesity
Smoking
Diabetes mellitus T2
Hypertension
Older age
Male
FHx

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21
Q

Pathophysiology for IHD

A

ATHEROGENESIS - endothelial injury induces cells to signal chemokines (IL-1,IL-6, IFN-¥) to produce…………..

Fatty streaks — intermediate lesions — fibrous plaques

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22
Q

Precursor of a plaque

A

Fatty streaks

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23
Q

What is the constituents of a fatty streak

A

T cells
+
Foam cells (lipid laden macrophages)

Fatty streaks can begin to form in less than 10y/o

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24
Q

Where can fatty streaks be found

A

In intima wall of vessel

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25
Q

What are intermediate lesions and its constituents

A

Essentially bigger fatty streaks as more lipids are taken up..
You see:
T cells +
Foam cells
Smooth muscle cells

platelets also aggregate at & adhere to site of lesions, inside vessel lumen

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26
Q

What are fibrous plaques and their constituents

A

Large lesions with the development of a fibrous cap over the lesion - lipid increased with a necrotic core
You see:
T cells +
Foam cells +
Smooth muscle cells +
Fibroblasts

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27
Q

Nature of the plaque in stable angina

A

Fibrous cap is strong & less prone to rupture
If plaque prone to rupture —> prothrombotic state; platelet adhesion + accumulation; progressive lumen narrowing

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28
Q

Percentage of lumen narrowing in stable angina

A

> 70% is when symptoms start to develop

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29
Q

Signs and symptoms of stable angina

A

Central crushing chest pain radiating to the neck & jaw

Dyspnoae

Fatigue

Sweating

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30
Q

Investigation & diagnosis of stable angina

A

1st line:
ECG : Resting - normal
Exercise induced (Ischaemic) - change

Gold standard:
CT angiography - stenoses atherosclerotic arteries (>70% occlusion)

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31
Q

1st line investigation for stable angina

A

1st line:
ECG : Resting - normal
Exercise induced (Ischaemic) - change

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32
Q

Gold standard investigation for stable angina

A

Gold standard:
CT angiography - stenoses atherosclerotic arteries (>70% occlusion)

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33
Q

Treatment for stable angina

A

Remember RAMP for stable angina management
Refer to cardiologist; Advise on lifestyle modification, Medical Tx, Procedural intervention

Medical Tx:
Immediate symptomatic relief -
GTN sublingual spray

Long term symptomatic relief -
All patients:
CCB (CI : heart failure) / BB (CI : asthma)
CCB + BB
CCB + BB + another anti-anginal (ivabradine / longacting nitrates)

Secondary prevention -
Aspirin
Atorvastatin
ACEi

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34
Q

What procedural interventions are there for stable angina

A

given if pharmacological intervention unsuccessful

Revascularisation

PCI - balloon stent via femoral artery to coronary artery

CABG - bypass graft (LAD bypassed using great saphenous vein)

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35
Q

Give a positive and negative for PCI

A

+ve : Less invasive

-ve : High risk of restenosis

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36
Q

What is restenosis

A

a gradual re-narrowing of the stented segment that occurs requiring further procedural treatment

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37
Q

What type of CCB is used in stable angina

A

Non-rate limiting one - Amlodipine

If others are used(verapamil / diltiazem), causes excessive bradycardia

Dihydropyridine CCBs have predominantly peripheral vasodilatory actions, whereas nondihydropyridine CCBs have significant sinoatrial (SA) and AV node depressant effects and possible myocardial depressant effects with lesser amounts of peripheral vasodilation.

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38
Q

Give a positive and negative of CABG procedure

A

+ve: Good prognosis

-ve: more invasive + longer recovery time

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39
Q

Clinical classification of unstable angina

A

Cardiac chest pain at rest

Cardiac chest pain with crescendo pattern

New onset angina

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40
Q

Occlusion for unstable angina

A

partial occlusion of minor coronary artery (>90%)

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41
Q

Type of infarction in unstable angina

A

None - ischaemia only

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42
Q

ECG finding in unstable angina

A

Normal
May show some ST depression / T wave inversion

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43
Q

Troponin levels in unstable angina

A

Normal

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44
Q

Level of occlusion for NSTEMI

A

Major partial occlusion (>90%) / total occlusion of minor coronary artery

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45
Q

Type of infarction in an NSTEMI

A

Subendothelial infarct

I.e. area furthest away from the occlusion dies

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46
Q

ECG finding for NSTEMI

A

ST depression
T wave inversion

no Q waves! - seen in STEMI, only after some time

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47
Q

Troponin levels for NSTEMI

A

Raised
Due to infarct obviously

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48
Q

Level of occlusion in STEMI

A

Complete occlusion of major coronary artery

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49
Q

Type of infarction in STEMI

A

Transmural infarction

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50
Q

ECG finding of STEMI

A

ST segment elevation
Pathological Q waves - develop after some time

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51
Q

Troponin levels seen in STEMI

A

Raised

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52
Q

Signs and symptoms of ACS

A

Same as stable (more severe) - dyspnoea, chest pain radiating to neck and jaw, sweating + nausea

+

Pain at rest, prolonged with no relief
often described as - ’impeding doom’ +
Palpitations

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53
Q

What is a silent MI

A

Diabetic patients may not experience typical chest pain during an acute coronary syndrome

Due to diabetic neuropathy; don’t feel the anginal pain so could miss the diagnosis and Px could die with sudden collapse

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54
Q

Investigations & diagnosis of ACS

A

ECG
Bio markers
CT coronary angiogram

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55
Q

Treatment for ACS

A

_Acute - remember MONAC_
- Morphine
- Oxygen (if SATs <94%; COPD: 88-92%)
- Nitrates (GTN spray)
- Aspirin
- Clopidogrel
Then…
For unstable / NSTEMI = GRACE score
- low risk : monitored
- high risk : coronary angiogram - may need PCI
For STEMI
- PCI if within 12hr Sx onset / <2hr of first medical contact
- Thrombolysis using alteplase / streptokinase if >12hrs of Sx onset, then consider PCI

_Long-term prevention_
Aspirin
Aatorvastatin (life)
ACEi (life)
Beta blocker (life)

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56
Q

Role of alteplase

A

Thombolytic agent - activates plasmin to break down fibrin

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57
Q

In what conditions is troponin elevated in…

A

MI
But also…

Myocarditis
PE
Aortic dissection
Sepsis
Chronic renal failure

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58
Q

Complications of ACS

A

Acutely (<2 weeks)
H.F - due to ventricular fib
Mitral incompetence
LV wall rupture
Cardiogenic shock

>2 weeks
Dressler’s syndrome (autoimmune pericarditis)
H.F
LV aneurysm (heart becomes saggy)

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59
Q

Define heart failure

A

Inability for the heart to pump sufficient Oxygen in order to meet the demand of the tissue metabolism

A syndrome not a diagnosis

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60
Q

Causes of heart failure

A

IHD - most common

Hypertension

Valvular heart disease (aortic stenosis)

Arrythmias (AF)

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61
Q

Risk factors for heart failure

A

Age (>65y/o)

Smoking

Obesity

Previous MI

Male > female

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62
Q

Pathophysiology of heart failure

A

Normally…
Increased preload = increased afterload (frank starlings law)

But, in failing heart…
Decreased cardiac output due to dysfunctional frank starling law so
1) Compensatory mechanism activation: RAAS + SNS (to temporarily increase BP) - increased aldosterone — increased ADH ; increased Ad/NAd
2) compensation then fails as heart undergoes cardiac remodelling. (Decreasing C.Output)
• Heart becomes less adapted to function so increased RAAS +SNS causes fluid overload
• In response to the increased work of the heart, both left and right circuits are affected - Congestive heart failure

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63
Q

Classification of heart failure

A

Time classified: acute / chronic

Ejection fraction (normal EF = 50-70%)

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64
Q

> 40% ejection fraction suggests what

A

Preserved ejection fraction
(Heart pump function is preserved)

Diastolic failure
- Filling issues due to stiffness
E.g. hypertrophic cardiomyopathy, Ventricular hypertrophy

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65
Q

What can cause diastolic heart failure

A

hypertrophic cardiomyopathy, ventricular hypertrophy

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66
Q

What does < 40% ejection fraction suggest

A

Reduced ejection fraction
Heart pumping has failed

Systolic heart failure
- reduced C.Output due to inability to pump

E.g. IHD

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67
Q

Give a cause for Systolic heart failure

A

IHD

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68
Q

Left sided heart failure causes what

A

Results in pulmonary vessel backlog
- therefore, pulmonary oedema

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69
Q

What does right sided heart failure cause

A

Causes backlog in systemic venous system
- leading to peripheral oedema

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70
Q

Cardinal signs of heart failure

A

Dyspnoea
Fatigue
Ankle oedema

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71
Q

Signs / symptoms of heart failure

A

Oedema
3, 4 heart sound
Increased JVP (backlog in jugular veins) - i.e. RHF
Orthopnoea (worse when lying flat) / paroxysmal nocturnal dyspnoea
Bibasal crackles** (pul. Oedema) - i.e. LHF

Hypotensive + tachycardic

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72
Q

What classification describes severity of heart failure

A

NY heart association class 1-4 of HF severity:
1) No limit on physical activity
2) Slight limit on moderate activity
3) Marked on moderate / gentle activity
4) symptoms even at rest

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73
Q

Key marker found in Heart failure

A

BNP
B type- natriuretic peptide
(> 400µg/mL)

Inactive BNP = NT-proBNP
it is x5 higher than BNP so (> 2000µg/mL) is high level indicating HF

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74
Q

Investigation / diagnosis of heart failure

A

Bloods - Raised BNP

ECG - Abnormal: may show signs of LVH

Chest X-ray - ABCDE
•Alveolar ‘batwing’ oedema
• kerley B-lines
•Cardiomegaly
•Dilated upper lobes
• pleural Effusion

Echocardiogram - shows dimension of heart chambers

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75
Q

Types of treatment available for heart failure

A

Conservative
Pharmacological
Surgical

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76
Q

Type of conservative treatment for HF

A

Lifestyle ∆’s
(Reduce BMI, exercise, diet, smoking + alcohol cessation)

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77
Q

Pharmacological treatment for HF

A

L.A.B.A - first line medical Tx
ACEi - ramipril
ß Blocker - atenolol
+
Aldosterone antagonist - Spironolactone
Loop diuretic - Furosemide

Consider cardiac resynchronisation therapy (to improve AV conduction)

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78
Q

Surgical treatment for heart failure

A

Consider revascularisation, valve surgery

Heart transplant = last resort

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79
Q

Role of BNP

A

Released by ventricular myocardium - opposes affect of RAAS
BNP act on blood vessels, causing them to dilate, or widen.

They also work on the kidneys, causing them to excrete more salt and water.

Reduce the production of adrenaline, angiotensin, and aldosterone.

BNP is therefore secreted when there’s increased pressure on heart - elevated in heart failure

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80
Q

Define Cor pulmonale

A

Right sided heart failure caused by respiratory disease.

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81
Q

Cause of Cor pulmonale

A

Remember it is RHF due to a resp disease

• COPD - most common cause
• PE
• Interstitial lung disease
• CF

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82
Q

Pathophysiology of cor pulmonale

A

Increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries.

This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.

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83
Q

Signs / symptoms of cor pulmonale

A

Raised JVP

Cynosis

peripheral oedema

3rd Heart sound

Murmurs : Tricuspid regurg - Pan systolic

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84
Q

Define abdominal aortic aneurysm

A

Permanent aortic dilation exceeding 50% where diameter > 3cm

> 5.5cm is urgent (significant rupture risk)
Rupture - surgical emergency!

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85
Q

Risk factor for aortic aneurysm

A

Idiopathic

Connective tissue disorder — Marfan syndrome, Ehler danlos synderom

Smoking(biggest RF), obesity, HTN (those RF for atherosclerosis)

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86
Q

Pathophysiology for aortic aneurysm

A

Smooth muscle, elasticity and structural degeneration in all 3 layers of vascular tunic (intima, media, adventitia) with leukocyte infiltration

If not all 3 layers affected - pseudoaneurysm

Note: Most aortic aneurysm = Abdominal (infrarenal), but
Can occur as thoracic
• Main cause = Marfan syndrome / Ehler’s Danlos / Atherogenesis
• Monitor with CT / MRI
• Any Sx: surgery immediately

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87
Q

Signs / symptoms of AAA

A

Asymptomatic till increased rupture risk / ruptured

Sudden epigastric pain radiating to flank
Pulsatile mass in abdomen
Hypotensive + tachycardic

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88
Q

Differential diagnosis for AAAneurysm

A

Acute pancreatitis

• Non-pulsatile + more associate with Grey turner (flank discolouration) / Cullen Sx (superficial oedema/bruising)

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89
Q

Investigation & diagnosis of AAA

A

1st line + diagnostic
ABDO USS

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90
Q

Tx for AAA

A

Conservative management - ∆ modifiable risk factors

aSx and <5.5cm : monitor

Sx, >5.5cm &/ rapidly expanding : Surgery
• Endovascular repair - stent inserted through femoral artery (less invasive)
• Open surgery (more invasive)

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91
Q

Complication of abdominal aortic aneurysm

A

Rupture

Stabilise: ABCDE, fluids + transfusions

Then, consider surgery
• AAA graft surgery; replacing weakened walls with graft
• 100% mortality if not treated immediately

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92
Q

Define aortic dissection

A

Tear in the intima of the aorta resulting in blood dissecting through the media of the aorta, separating the layers apart - due to mechanical wall stress; surgical emergency

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93
Q

Who is aortic dissection most commonly seen in

A

50-70y/o men

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94
Q

Risk factors for aortic dissection

A

HTN (most common)
Connective tissue disorder - Marfan syndrome, EDS
FHx
AAA
Trauma
Smoking

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95
Q

Common locations of aortic dissection

A

1) Sinotubular junction - where the aortic root becomes tubular; near aortic valve. (Ascending aorta)
• Aortic dissection A

2) Distal to left subclavian artery - thoracic descending aorta. (Descending aorta)
• Aortic dissection B

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96
Q

Types of aortic dissection + the classification

A

Stanford’s classification

Type A : Ascending aorta
Sinotubular junction - 2/3 (more common)
Type B : Descending aorta
Distal to left subclavian artery - 1/3

Debakey system

Type I : ascending + descending aorta
Type II : ascending aorta
Type III : descending aorta

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97
Q

Pathophysiology of aortic dissection

A

Blood dissects media + intima, where it pools in a false lumen which can propagate forwards (anterograde) and backwards (retrograde; towards aortic root)
Decreased perfusion to end organ —> organ failure + shock

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98
Q

Signs and symptoms of aortic dissection

A

Sudden onset ripping/tearing chest pain
Anterior pain - ascending
Posterior pain - descending

Hypotension/shock
Syncope
Diastolic murmur
Radial pulse deficit

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99
Q

Differential diagnosis of aortic dissection

A

MI

Central crushing chest pain with gradual worsening intensity

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100
Q

Investigation & diagnosis of aortic dissection

A

CXR shows widened mediastinum (> 8cm = suspicious)

Gold standard -
TOE (Transoesophageal echocardiogram) : shows intima flap / false lumen - more invasive than TTE but is more specific to aortic dissection + v.sensitive;
then classify AD as A / B

OR

CT angiogram : shows intima flap / false lumen / leak or rupture (also v. Specific & sensitive) - used more when Px is haemodynamically stable

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101
Q

Treatment for aortic dissection

A

Surgery - open surgery (type A) / endovascular aortic repair (type B)
— if they’re hypotensive: consider IV fluid, blood transfusion, adrenaline

Medical (prevention) -
1) Special beta blocker : esmolol / labetolol
— ß-Blocker and partial ∂-blockers prevent reflex tachycardia + decrease BP
• Aim: systolic BP (100-120) + HR: ≈ 60
2) Vasodilator : Sodium Nitroprusside

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102
Q

Give 3 complications of aortic dissection

A

(Haemorrhagic) Cardiac tamponade
Ischaemic stroke
Pre-renal AKI

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103
Q

Types of beta blockers used in aortic dissection

A

Esmolol / labetolol

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104
Q

Define hypertension

A

Abnormally high BP

≥ 140/90 mmHg (clinical)
≥ 135/85 mmHg (ambulatory / home readings)

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105
Q

Types of hypertension

A

Primary (Essential) - idiopathic HTN (95% of cases)
Secondary - known underlying cause

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106
Q

Causes of hypertension

A

Primary = idiopathic
Secondary = Remember ROPE
Renal disease
Obesity
Pregancy / eclampsia
Endocrine disorder:
- Conn’s (most common cause of HTN)
- Phaemochromocytoma
- Cushing’s

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107
Q

Risk factors for hypertension

A

Older age
Obesity
Black ethnicity
Smoking
Diabetes
Increased salt intake
FHx

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108
Q

Describe the different stages of HTN

A

1) 140/90 … 135/85
2) 160/100 … 150/95
3) 180/120 - start immediate Tx

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109
Q

Pathophysiology of HTN

A

Ultimately all mechanisms stimulate RAAS + SNS (increasing cardiac output) + TPR … Increasing BP

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110
Q

Signs / symptoms of HTN

A

Mostly aSx
May have pulsatile headaches

Malignant hypertension :
180/120 (usually marked more by diastolic BP ≥ 120)
Px : typically seen in 30-40y/o black males
M.HTN causes:
Heart failure
Blurred vision
Haematoma
Headache

Consider signs of 2º cause

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111
Q

Investigation & diagnosis of hypertension

A

BP reading in hospital (≥140/90)
— Then ABPM for 24hr to confirm diagnosis (≥135/85)

Assess end organ damage
— Fundoscopy (papilloedema)
— eGFR (renal function + risk of diabetes)
— Echo/ECG (heart function; check for LVH)

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112
Q

Treatment for hypertension

A

——— < 55y/o / T2DM ——— ≥ 55y/o / black African———

1 —————ACEi————or———— CCB—————

2 —————————ACEi + CCB—————————

3 ———— ACEi + CCB + Thiazide diuretic —————

4 —— ACEi + CCB + Thiazide ± diuretic + K+ sparring——

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113
Q

What do you give if ACEi is contraindicated

A

ARB - Candesartan

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114
Q

4th line for HTN has you add which drug and what drug is given if contraindicated

A

In 4th line, the 4th drug given is K+ sparring diuretic
But if K+ > 4.5, give ∂/ß blocker

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115
Q

If Px is Black & has T2DM, what is 1st line treatment

A

ACEi

Because T2DM takes precedence over being black

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116
Q

A 60y/o black man has hypertension and T2DM, what is the first line treatment

A

ACEi
Having T2DM takes precedence

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117
Q

Complications for hypertension

A

Heart failure
CKD
IHD
Cerebrovascular accident risk increases

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118
Q

Define DVT and a PE

A

DVT
- Thrombus formation in deep leg vein
When in calf, less concerning - more common
When in thigh, life threatening - less common

PE
- When DVT emobolise and lodges in pulmonary artery circulation

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119
Q

Risk factors for DVT ± a PE

A

Remember Virchow’s Triad:

• Hypercoagulability
Pregnant
Antiphospholipid syndrome
DIC
• Venous stasis
Immobility
Long haul flights
Surgery
• Endothelial injury
Trauma / Surgery
Smoking
HTN

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120
Q

What can a PE cause / lead to

A

Cor pulmonale
(Right sided heart failure due to a resp condition);

Increased PVR —> increased right ventricle strain to overcome it —> RVH —>R.Ventricle fails, 2º to Pulmonary artery pressure

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121
Q

Give 3 conditions that present with pleuritic chest pain

A

PE
Pneumothorax
Pneumonia

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122
Q

Differential diagnosis between: PE, Pneumothorax, Pneumonia

A

Do CxR:
PE - normal
Pneumonia + pneumothorax - diagnostic

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123
Q

Signs / symptoms of DVT

A

Unilateral, swollen, warm + oedematous calf with dilated superficial veins.

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124
Q

What is phlegmasia cerulea dolens

A

Complete occlusion of a large being —> severe DVT

Severe ischaemia —> presents a s cyanosis (blue, not red like DVT)

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125
Q

Which scoring system is used in DVT / PE

A

Wells score

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126
Q

Diagnosis + investigation of DVT

A

Wells score ≥ 2 is likely of DVT

If D-dimer - elevated (1st line) —>
Do Duplex USS (Gold standard - diagnostic)

If D-dimer not elevated - not a DVT/PE

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127
Q

Is D-dimer specific or sensitive

A

Sensitive (95%)
Not specific

Measures clot burden - a small protein released into the blood when a clot is fibrinolysed

  • Will always (95% of the time) be seen in DVT/PE - sensitive
    but can also be raised in other conditions - not specific
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128
Q

Conditions D-dimer can be elevated in

A

DVT / PE

Heart failure
Pneumonia
Pregnancy
Malignancy

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129
Q

Treatment for DVT

A

DOAC
- Rivaroxaban / Apixaban

LMWH - if DOAC is contraindicated (e.g in renal impairment )

+ mobilisation, compression stockings (unless contraindicated - Peripheral Arterial Disease)

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130
Q

Differential diagnosis for DVT

A

Cellulitis

• Skin infection
Typically Staph. Aureus / Strep. Pyogenes

• Tender, inflamed, swollen calf with pronounced demarcation (Bullae: fluid-filled blisters + golden-yellow crust - indicate a staphylococcus aureus)

Typically show leukocytosis - sign of infection on FBC
BUT
Not seen in DVT : D-dimer and D.USS used for DVT diagnosis

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131
Q

Complication of DVT

A

PE

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132
Q

Signs and symptoms of PE

A

Sudden onset pleuritic chest pain

Dyspnoea ± haemoptysis (streaky blood)

Tachycardic + tachypnoea (respiratory alkalosis), hypotensive, increased JVP

+ evidence of DVT : swollen, red, oedematous & tender leg

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133
Q

Prophylaxis for VTE: DVT/PE

A

LMWH - Enoxaparin
Warfarin
DOAC

134
Q

Diagnosis + investigation of PE

A

Wells score ≥ 4 : PE likely

If likely —> CT Pulmonary Angiogram (CTPA - Gold standard) = Diagnostic

This is because CTPA is specific for Pulmonary Embolism

If unlikely (Wells score < 4) —> D-dimer (1st line)
- if raised, do CTPA
- if not raised, not PE

135
Q

Treatment for pulmonary embolism

A

If massive PE (hypotensive:< 90 systolic BP):
Thrombolytics - Alteplase

If non-massive PE:
1st line - DOAC (Rivaroxaban / Apixaban)
• if contraindicated (renal impairment) - give LMWH

136
Q

Define pericarditis

A

Inflammation of the pericardium ± effusion; typically acute, can be chronic

137
Q

Cause / aetiology of pericarditis

A

Idiopathic
Viral - Coxsackie virus (most common cause)
Bacterial - TB
Autoimmune - SLE, Rheumatoid.A (common)
Dressler’s syndrome (>2 weeks post MI)

138
Q

Pathophysiology of pericarditis

A

• Inflamed pericardial layer rub against each other - because of narrowed pericardial space due to the inflammation
• Further exacerbating inflammation

Can either present as:
• Dry - no extra fluid; not as bad because friction doesn’t need to be overcome
• Effusive - extra fluid needed to compensate for friction

139
Q

Signs and symptoms of pericarditis

A

sharp severe pleuritic chest pain with referral to left shoulder tip (at trapezius ridge)

Relieved sitting forward
Worse laying flat or on inspiration

Pericardial friction rub on auscultation - heard when patient leans forward squeaky leather to and fro sound

May show signs of right sided HF (constrictive pericarditis) —> SoB, peripheral oedema, tachycardia (chronic inflammation of pericardium)

140
Q

What is constrictive pericarditis

A

Late complication of acute pericarditis + there’s a sign of poor heart prognosis.

Granulation tissue formation in pericardium —> impaired diastolic filling.

141
Q

Investigation and diagnosis of pericarditis

A

ECG (diagnostic):
- Widespread saddle shaped ST elevation
- PR depression

CXR:
- “Water-bottle” heart (cardiomegalic)
- Pneumonia commonly seen (bacterial pericarditis - TB)

Increased ESR
- Seen in autoimmune pericarditis
Increased WCC
- in infective pericarditis

142
Q

Treatment of pericarditis

A

Idiopathic + viral:
NSAID’s (aspirin)
+
Colchicine (anti inflammatory - used in gout too)

+ antibiotic if bacterial (R.I.P.E Abx for TB)

143
Q

Complication of pericarditis

A

Pericardial effusion
Cardiac tamponade
Myocarditis
Constrictive pericarditis

144
Q

Define pericardial effusion

A

Pericardial effusion
When the potential space of the pericardial cavity fills with fluid. This creates an inward pressure on the heart, making it more difficult to expand during diastole (filling of the heart).

Cardiac tamponade
Where the pericardial effusion is large enough to raise the intra-pericardial pressure. This increased pressure squeezes the heart and affects its ability to function. It leads to reduced filling of the heart during diastole, resulting in decreased cardiac output during systole

145
Q

Types of effusion and their causes

A

Transudative effusion:
Due to increased hydrostatic pressure
Less protein
Transparent fluid
••• Congestive heart failure
••• Pulmonary hypertension

Exudative effusion:
Occur in any inflammatory process; via infection / malignancy
More protein
Cloudy fluid
••• Infection; pneumonia / pancreatitis
••• PE
••• Medication - methotrexate

146
Q

Signs and symptoms of pericardial effusion & cardiac tamponade

A

Sx related to pericarditis (chest pain)

Phrenic nerve compression can cause hiccups
Oesophageal compression may cause dysphagia (difficulty swallowing)
Recurrent laryngeal nerve compression may cause a hoarse voice

For cardiac tamponade:
Beck’s triad - hypotension, increased JVP, muffled s1-s2 sound
Pulses paradoxicus - fall in systolic BP of 10+ mmHg on inspiration (good indicator of cardiac tamponade) —> kussmaul’s sign

147
Q

Investigation and diagnosis of pericardial effusion + cardiac tamponade

A

ECG : may show electrical
CxR : big globular heart

Echo : diagnostic

148
Q

Treatment of pericardial effusion + cardiac tamponade

A

Pericardial effusion - Tx underlying cause (NSAIDs + Colchicine —> pericarditis)

Cardiac tamponade - urgent pericardiocentesis

149
Q

Define Peripheral vascular disease

A

Essentially IHD of lower limb arteries.
Males

150
Q

Risk factor for Peripheral vascular disease

A

Smoking
HTN
Ageing
Obesity
CKD
T2DM

151
Q

Pathophysiology for peripheral vascular disease

A

Intermittent claudication (least severe) —>
Atherosclerotic, partial lumen occlusion, pain on exertion as blood flow < demand

Critical limb ischaemia (more severe) —>
Occlusion is V. Big; blood supply barely adequate to meet metabolic demand
Pain at rest + increased risk of gangrene / infection

Limb ischaemia can be acute / chronic!!

152
Q

Define peripheral arterial disease

A

Peripheral arterial disease (PAD) refers to the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas

153
Q

Define intermittent claudication

A

Intermittent claudication is a symptom of ischaemia in a limb, occurring during exertion and relieved by rest. It is typically a crampy, achy pain in the calf, thigh or buttock

Reduced blood to muscle —> reduced O2 —> ischaemia —> this causes cells to release adenosine (signalling molecule for nerve cells) —> feel the signal as pain —> pain = claudication

154
Q

Define critical limb ischaemia

A

Critical limb ischaemia is the end-stage of peripheral arterial disease
Pain at rest; non-healing ulcers + gangrene

155
Q

Difference between PVD & PAD

A

Pretty much the same thing

156
Q

Risk factors for PVD

A

Same as atherosclerosis:

Smoking
HTN
Ageing
Obesity
CKD
T2DM

157
Q

Define acute limb ischaemia

A

rapid onset of ischaemia in a limb.

Typically, this is due to a thrombus (clot) blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardial infarction.

158
Q

Define gangrene

A

the death of the tissue, specifically due to an inadequate blood supply.

159
Q

Features of limb ischaemia

A

Remember 6P’s - found in both acute and critical (chronic is more limb threatening)

Pain
Pallor
Perishingly cold
Paralysis
Paraesthesia
Pulselessness

In critical limb ischaemia - causes burning pain. It is worse at night when the leg is raised

160
Q

Mention 3 things that can occur if blood vessels to a region is occluded in PVD

A

1) Irreversible nerve damage (within 6hrs)

2) Irreversible muscle damage (6-12hrs)

3) Skin ∆’s are last to appear therefore likely to be gangrenous

161
Q

Investigations and diagnosis of PVD

A

Ankle brachial pressure index (ABPI) = 1st line
[•] < 0.9 indicates PVD
[•] 0.9 - 1.3 = Normal;
[•] 0.5 - 0.9 = intermittent claudication;
[•] < 0.5 = critical limb ischaemia;
[•] When absent / v. Low = high risk of Acute limb ischaemia

Ratio / comparison of systolic BP of lower limb * upper limb

Duplex ultrasound scan
[•] Assesses degree of stenosis

CT Angiography = Gold standard
[•] Highlights arterial circulation

Buerger’s test
[•] +ve
[] Elevate leg 45˚ for a minute; Pallor.lower the leg; reactive hyperaemia (blue initially, then red)

162
Q

What classification used in PAD/ PVD

A

Fontaine’s classification (stages 1-4):
Classification of the pain experienced after a particular distance.

1) Asymptomatic

2) Intermittent claudication:
• 2a - > 200m pain free walking
• 2b - < 200 m

3) Critical limb ischaemia (pain at rest)

4) Ischaemic ulcers —> gangrene formation

163
Q

Treatment for PVD

A

Intermittent claudication
- RF management

Critical limb ischaemia
- Revascularisation surgery (PCI if small; CABG if big occlusion)

Acute limb threatening ischaemia
- Surgical emergency (do within 4-6hrs) —> risk of amputation

164
Q

Complications of PVD

A

Amputation

Permanent limb weakness

Rhabdomyolysis (increased ca2+ and k+ release in blood - Arrhythmias / AKI)

Risk of Cerebrovascular accident + CKD

165
Q

Define virulence

A

Ability of microbe to cause damage to host

166
Q

Define infective endocarditis

A

Inflammation of the endocardium

  • causative bacteria; colonise abnormally in the endothelium (leading to vegetation)
167
Q

Cause of infective endocarditis

A

Staph. Aureus - most common; IVDU / T2DM / Surgery

Strep. Viridans - Poor dental hygiene; Gram +ve haemolytic Optochin resistant strep.

Staph epidermidis - Prosthetic valve / infected IV catheters

168
Q

Types of infective endocarditis

A

Acute
S. Aureus; high virulence. Sx onset days-weeks

Subacute
S. Viridans; lower virulence. Sx onset weeks-months

169
Q

Risk factors for infective endocarditis

A

Male, elderly; with prosthetic valves
Young IVDU
Young with congenital heart defect
Rheumatic heart disease

170
Q

Pathophysiology of infective endocarditis

A

Abnormal / damaged endocardium have increased platelet deposition; bacteria adheres to this & causes vegetation.

  • Around valves - typically mitral valve (highest turbulence; more damage), but in IVDU more so tricuspid valve is affected\
  • causes regurgitation (+ left side more affected so get aortic & mitral insufficiency; increased risk of HF)
171
Q

Signs and symptoms of infective endocarditis

A

FEVER + NEW MURMUR = I.ENDOCARDITIS

Symptoms: vague; fever, fatigue, SoB

Signs:
ROTH SPOTS
JANEWAY LESIONS
SPLINTER HAEMORRHAGES
OSLER NODES

172
Q

What criteria is used in infective endocarditis

A

DUKE criteria

173
Q

Investigation and diagnosis of infective endocarditis

A

Diagnosis made using a DUKE criteria
ECG (prolonged PR —> aortic root abcess)
Increased ESR / CRP + neutrophilia
TOE = gold standard
Blood culture —> over 3 sites over 24hr
- 2 major / 1 major + 2 minor
— Major:
≥2 +ve blood cultures
echo TOE - shows vegetations
— Minor:
IVDU
1 +ve blood culture
Pyrexia
Immunological signs

174
Q

Treatment of infective endocarditis

A

Staph Aureus: vancomycin + rifampicin

Strep Viridans: Benzylpenicillin + gentamicin

For 4 - 6 weeks

Surgery —> remove valve if incompetent & replace with prosthetic

175
Q

Complication of infective endocarditis

A

Heart failure
Aortic root abscess
Septic emboli (± sepsis)

176
Q

The effects of regurgitation of heart muscle

A

Insufficiency + proximal chamber dilation
(Regurgitation - defective valve, floppy)
• Loss of structural chamber integrity + strength

Stenosis causes increase upstream pressure + proximal chamber hypertrophy
(Stenotic - narrowed valve lumens)
• Heart becomes huge and rigid; poorly compliant

177
Q

When are murmurs best heard

A

Remember “RILE”

Right side valve defect —> Inspiration
Left side valve defect —> Expiration

A.R-M.S - Diastolic murmur
A.S-M.R - systolic murmur

178
Q

Most common valve disorder

A

Aortic stenosis

179
Q

Normal area of aortic valve vs. Pathological

A

3-4cm normal

Sx at 1/4 lumen size

180
Q

Effects of aortic stenosis on heart

A

Results in LV dilation + hypertrophy

181
Q

What causes aortic stenosis

A

Ageing calcification

Rheumatic heart disease

182
Q

Signs / symptoms of aortic stenosis

A

Remember S.A.D

Syncope (exertional)
Angina
Dyspnoea (related to heart failure)

- Murmur: Ejection systolic crescendo decrescendo radiating to carotids
- Prominent S4: seen in LVH
- narrow pulse pressure + slow rising pulse (NOT collapsing corrigan’s pulse)

183
Q

Investigation and diagnosis of aortic stenosis

A

ECG
CXR
ECHO (Gold standard) - shows LV size + function, aortic valve area (Doppler derived)

184
Q

Treatment of aortic stenosis

A

Surgical (if Px = symptomatic);

*Healthy Px — open repair / valve replacement (definitive)
In a risky Px (>75y/o) — TAVI; transcutaneous aortic valve implant = less invasive; just a stent valve open

185
Q

Type of sound heard in a hypertrophic cardiomyopathy

A

Causes S4 (sound just before S1)

Associated with sudden death in young men

186
Q

Define aortic regurgitation

A

Leaky aortic valve, insufficient

187
Q

What causes aortic regurgitation

A

Congenital bicuspid valve
Rheumatic heart disease
Connective tissue disorders; Marfan’s / Ehler’s Danlos
INFECTIVE ENDOCARDITIS

188
Q

Signs and symptoms of aortic regurgitation

A

Murmur: Early diastolic blowing murmur (@ right sternal border)

Severe form = Austin flint murmur - a mid diastolic low pitched rumble; Heard when regurgitation is so severe the blood bounces off mitral valve cusps + makes sound

Collapsing corrigon pulse with wide pulse pressure

189
Q

Investigation and diagnosis aortic regurgitation

A

ECG
CXR
Echo (Gold standard) - evaluate aortic valve, root and dimension

190
Q

Treatment of aortic regurgitation

A

Consider IE prophylaxis
Surgical valve replacement is symptomatic

191
Q

Differential diagnosis for aortic regurgitation

A

Infective endocarditis

192
Q

Define mitral stenosis

A

Mitral lumen 4-6cm
Symptoms appear at < 2cm

193
Q

Risk factors for mitral stenosis

A

Rheumatic fever Hx
men
ageing

194
Q

Causes of mitral stenosis

A

Rheumatic heart disease - most common, post strep. Pyogenes infection

Valve calcification - seen in older Px

Infective endocarditis

195
Q

Pathophysiology of mitral stenosis

A

Rheumatic heart disease causes mitral reactive inflammation; over the years its exacerbated with calcification —> leading to left atria hypertrophy

196
Q

Signs / symptoms of mitral stenosis

A

Malar flush
Dyspnoea
A wave on JVP
Associated with AFib - M. Stenosis leads to LA hypertrophy so more chance of embolisation as blood being pumped out harder

Murmur: low pitched, mid-diastolic murmur
- loudest at apex
- best heard on expiration (lying on LHS)
*Loud S1 snap *

197
Q

Investigation and diagnosis for mitral stenosis

A

ECG - may show AFib / p mitrale - ‘m’ shaped p wave seen in LA enlargement
CXR - LA enlargement
(Gold standard) - echocardiogram

198
Q

Treatment for mitral stenosis

A

Surgical
- Percutaneous balloon valvotomy (a stent)
- Mitral valve replacement

199
Q

Define mitral regurgitation

A

Insufficient mitral valve function

200
Q

Causes of mitral regurgitation

A

myxomatous mitral valve (most common; mass of cells in valves connective tissue making leaflet heavier & prolapse)

Connective tissue disorders; Marfan / Ehlers Danlos

201
Q

Risk factors for mitral regurgitation

A

Females
Older
Decreased bmi
Prior MI
Connective tissue disorder

202
Q

Signs / symptoms of mitral regurgitation

A

Exertion dyspnoea (pulmonary hypertension, from back log of blood)

Murmur - pan-systolic murmur - radiating to axilla
- soft S1, prominent S3 if prolonged and lead to heart failure (severe form)

203
Q

Investigation and diagnosis of mitral regurgitation

A

ECG
CXR
Gold standard - Echocardiogram

204
Q

Treatment for mitral regurgitation

A

ACEi, BBlockers + monitoring using Echo

If severe - valve replacement / repair

205
Q

Mitral stenosis murmur

A

Mid diastolic low pitched ‘rumbling’ murmur

Loud S1

206
Q

What might malar flush indicate

A

Mitral stenosis

207
Q

Which valvular heart disease might cause atrial fib

A

Mitral stenosis

208
Q

Which valvular disease might cause congestive heart failure

A

Mitral regurgitation

209
Q

Mitral regurgitation murmur

A

Pan-systolic high pitched whistling murmur

Radiates to axilla
With S3 heart sound

210
Q

Aortic stenosis murmur

A

Ejection systolic high pitched crescendo-decrescendo murmur

Radiates to the carotids

Slow-rising pulse with narrow pulse pressure

211
Q

Aortic regurgitation murmur

A

Early diastolic ‘rumbling’ murmur
With collapsing pulse (aka corrigans pulse)

Austin flint murmur heard best at apex of the heart (severe for of aortic regurgitation)

212
Q

Where are the 4 valve murmurs heard from

A

Pulmonary: 2nd I.C.S left sternal border

Aortic: 2nd I.C.S right sternal border

Tricuspid: 5th I.C.S left sternal border

Mitral: 5th I.C.S mid clavicular line (apex area)

213
Q

Define tachycardia

A

> 100 bpm

214
Q

Types of tachycardia

A

Supraventricular tachycardia (SVT)
Atrial fib
Atrial flutter
AVRT (non-junctional) - wolff-Parkinson’s white syndrome
AVNRT

Ventricular tachycardia
prolonged QT syndrome
Ventiricular fibrillation

215
Q

What is the most common SVT

A

AVNRT
- re-enterant pathway goes through AVN

216
Q

Difference between AVRT and AVNRT

A

AVRT - re-enterant pathway through accessory pathway
(Bundle of kent)

AVNRT - re-enterant pathway goes through AVN

217
Q

Define bradycardia

A

< 60 bpm

218
Q

Types of bradycardia

A

Bundle branch block
- RBBB / LBBB

1˚/2˚/3˚ heart blocks

219
Q

Atrial fib rhythm

A

Irregularly irregular

220
Q

Causes of atrial fibrillation

A

Heart failure, HTN

2˚ to mitral stenosis

Idiopathic

221
Q

Risk factors for atrial fibrillation

A

60+
Valvular heart defect
Hx of MI
T2DM
HTN

222
Q

Pathophysiology of atrial fib

A

Rapid re-entrant ectopic foci (over 300 beats) causes atrial spasm - not coordinating contraction like normal .
This leads to atrial blood pooling instead of pumping efficiently to the ventricles
So, decreased CO and increased risk of thromboembolic events

223
Q

Signs / symptoms of atrial fibrillation

A

Palpitations
Irregularly irregular pulse

Chest pain
Syncope
Hypotensive

Sx can be paroxysmal (episodic), persistent (> 7 days), permenant - sinus rhythm unrestorable

224
Q

Investigation and diagnosis of atrial fibrillation

A

ECG (diagnostic) - irregularly irregular, narrow QRS complex

No P waves

225
Q

Treatment of atrial fibrillation

A

Acute / unstable - (syncope, shock, chest pain, heart failure):
DC synchronised cardioversion

If stable (/prevent further episodes) - ß-blockers/CCB (like verapamil) + anticoagulant

Surgical radiofrequency ablation - restores normal rhythm by targeting misfiring heart tissue and killing it

226
Q

Which scoring system is used in Atrial Fib

A

CHA2DS2 VASc score is used
Because high stroke risk + anticoagulation needed

HASBLED score
Assesses risk of major bleeds in AF patients on anticoagulant
≥ 3 score (max 9) - regular reviews required

227
Q

What does CHADS VASc stand for

A

Congestive heart failure
HTN
Age > 75y/o (2 points)
DM type2
Stroke (2 points)

Vascular disease
Age 65-74y/o
Sex category = female

228
Q

Complication of atrial fibrillation

A

Heart failure
Ischaemic stroke

229
Q

Define atrial flutter

A

Irregular regular atrial firing

Less common and less severe that atrial fib

230
Q

Risk factor of atrial flutter

A

Same as atrial fib:

60+
Valvular heart defect
Hx of MI
T2DM
HTN

231
Q

Causes of atrial flutter

A

Similar to atrial fibrillation -

Heart failure, HTN

2˚ to mitral stenosis

Idiopathic

232
Q

Pathophysiology of atrial flutter

A

Fast atrial ectopic firing causes atrial spasm but not as uncoordinated as A. Fib
Pathway typically from around tricuspid annulus (opening of valve)

233
Q

Signs and symptoms of atrial flutter

A

Dyspnoea, palpitations…
Irregularly regular

234
Q

Investigation and diagnosis of atrial flutter

A

ECG (diagnostic) - F wave ‘Saw-tooth’ pattern

Often seen with 2:1 block (2 P waves for every QRS )

235
Q

Treatment of atrial flutter

A

Acute: unstable —> DC synchronised cardioversion

Stable —> rhythm / rate control (ß-blocker) with oral anticoagulation (prevent thromboemboli)

Radiofrequency ablation

236
Q

Define Wolff Parkinson’s white (AVRT)

A

AVRT - means an accessory pathway exists for impulse conduction, not re-entry though the AVN.

Hereditary

Most common example of AVRT = Wolff Parkinson’s white; accessory pathway for conduction I.e. via bundle of Kent.
- pre-excitation syndrome (excites ventricles earlier than typical pathway) - seen as delta waves

237
Q

Signs / symptoms of AVRT

A

Palpitations, dyspnoea, dizziness

238
Q

Investigation and diagnosis of AVRT

A

ECG

Slurred delta waves
Short PR interval
Wide QRS

239
Q

Treatment of AVRT

A

1st line:
Valsalva (blow into syringe vs. Resistance) /
Carotid massage

2nd:
IV adenosine (will temporarily cease conduction) - warn patient as they will “feel like they’re dying”

3rd:
Consider surgical radiofrequency ablation of bundle of Kent

240
Q

Define long QT syndrome

A

Ventricular tachyarrhythmia; usually congenital channelopathy disorder

Where mutations affects cardiac ion channels therefore heart conduction
- QT interval > 480ms

241
Q

Causes of long QT syndrome

A

Romano ward syndrome (autosomal dominant)
Jarvell-Lange-Neilson syndrome (autosomal recessive)

Hypokalaemia + hypocalcaemia (non-inherited)

Drugs - Amiodarone, magnesium

242
Q

Define Torsades de pointes

A

Polymorphic ventricular tachycardia in patients with prolonged QT
Rapid irregular QRS complex which ‘twist’ around baseline, can cease spontaneously or develop to ventricular fibrillation

243
Q

Define ventricular fibrillation

A

Shapeless rapid oscillations on ECG

Px becomes pulseless + goes into cardiac arrest (no effective cardiac output)

244
Q

1st line treatment for ventricular fibrillation

A

Electrical defibrillation

Non-synchronised as patient is pulseless

245
Q

Define Primary AV block

A

PR prolongation (> 200ms) - every P wave is followed by a QRS

Asymptomatic / stable, therefore no Tx

Causes:
drugs (ß-blocker, CCB, Digoxin—> blocks AVN conduction)
Post MI
SLE

Complication: atrial fibrillation

246
Q

Cause of primary av block

A

Drugs (ß-blocker, CCB, Digoxin—> blocks AVN conduction)
Post MI
SLE

247
Q

Complication of primary AV block

A

Atrial fibrillation

248
Q

Define secondary AV block

A

When some P waves conducted and others aren’t

2 types:
Mobitz 1 (Wenkebach’s)
Mobitz 2

249
Q

Define Mobitz 1

A

Mobitz 1 (2˚ AV block)
PR prolongation until a QRS is dropped (PR interval progressively elongates)

250
Q

Causes of AV block mobitz 1

A

Drugs - ß-blocker, CCB, Digoxin
Previous MI
SLE

251
Q

Treatment for Mobitz type 1

A

No Tx unless v. Symptomatic
- syncope / reduced consciousness

Give Tx: Pacemaker

252
Q

Define mobitz 2

A

Persistent PR interval prolongation with random dropped QRS

253
Q

Causes of mobitz type 2

A

Drugs - ß-blocker, CCB, Digoxin
Previous MI
Rheumatic fever

254
Q

Signs / symptoms of secondary AV block mobitz 2

A

Syncope
SoB
Chest pain

255
Q

Treatment of mobitz 2

A

Pacemaker

256
Q

Define tertiary AV block

A

Complete AV dissociation
I.e. atria and ventricles beat independently of each other

  • ventricular escape rhythm is what sustains the heartbeat

SAN (best - 60-100)
—> AVN (then takes over: 40-60)
—> If dysfunctional, ventricular pacemakers take over (Worst firing rate: 20-40)

257
Q

Cause of tertiary AV block

A

Acute MI
HTN
Structural heart disease

258
Q

Tx for 3˚ AV block

A

IV atropine
+
Permanent pacemaker

259
Q

Define bundle branch block

A

Blocking of the bundle of His

2 types:

RBBB
LBBB

260
Q

Cause of RBBB

A

Pul emboli
IHD
Ventricular Septal Defect

RV later activated than LV

261
Q

Dx of RBBB

A

ECG: MarroW
- “M” in V1 (RSR wave)
- “W” in V2 (deep S wave)

Hear: Wide physiological S2 splitting heart sound

262
Q

Cause of LBBB

A

IHD
Valvular disease

LV is activated later than RV

263
Q

Dx of LBBB

A

ECG: WilliaM
- “W” in V1 (RSR wave)
- “M” in V2 (deep S wave)

Hear: Reversed S2 splitting heart sound

264
Q

Define cardiomyopathy

A

Disease of the myocardium (muscular / conduction defects)

Types:
Hypertrophic
Dilated
Restrictive

265
Q

Which cardiomyopathy is most common cause of death in young people

A

Hypertrophic cardiomyopathy

266
Q

Most common cardiomyopathy

A

Dilated

267
Q

Cause of hypertrophic cardiomyopathy

A

Familial (inherited) - autosomal dominant mutation of sarcomere protein (troponin T, myosin B)

Exercise

Aortic stenosis

268
Q

Pathophysiology for hypertrophic cardiomyopathy

A

Thick non-complaint heart = leads to impaired diastolic filling

Therefore, reducing C.O

269
Q

Sx of hypertrophic cardiomyopathy

A

May present with sudden death

Chest pain
Palpitations
SoB
Syncope

270
Q

Investigation and diagnosis of hypertrophic cardiomyopathy

A

Echocardiogram (definitive)
Abnormal ecg
Genetic testing

271
Q

Treatment for hypertrophic cardiomyopathy

A

ß blocker
CCB
Amiodarone

272
Q

Cause of dilated cardiomyopathy

A

Familial: Autosomal dominant - cytoskeleton gene mutation

IHD

Alcohol

273
Q

Pathophysiology of dilated cardiomyopathy

A

Thin cardiac walls poorly contract therefore reduced CO

274
Q

Sx of dilated cardiomyopathy

A

SoB
Heart failure
Atrial fib
Thromboemboli

275
Q

Investigation and diagnosis of dilated cardiomyopathy

A

ECG
Echo (definitive)

276
Q

Treatment for dilated cardiomyopathy

A

Treat underlying cause like AFib / HF

277
Q

Cause of restrictive cardiomyopathy

A

Granulomatous disease (sarcoidosis / amyloidosis)
Idiopathic
Post MI

278
Q

Pathophysiology of restrictive cardiomyopathy

A

Rigid fibrotic myocardium fills poorly + contracts poorly

Reducing CO

279
Q

Sx of restrictive cardiomyopathy

A

If severe:

Dyspnoea, S3+4
Oedema, congestive heart failure
Narrow pulse pressure

280
Q

Investigation + diagnosis of restrictive cardiomyopathy

A

ECG
Echo
Cardiac catheterisation (definitive)

281
Q

Tx for restrictive cardiomyopathy

A

None;
Consider transplant

Px typically die within a year

282
Q

Define shock

A

Medical emergancy - hypoperfusion, life threatening, due to acute circulation on failure
Leads to tissue hypoxia + risk of organ dysfunction

283
Q

General Sx to recognise shock

A

Skin; pale, cold, sweaty

Reduced GCS

Increased capillary refill time

Decreased urine output

Prolonged hypotension

284
Q

Define hypovolaemic shock

A

As a result of fluid loss — dehydration
Or
As a result of blood loss — trauma / GI bleed

285
Q

Sx of hypovolaemic shock

A

Hypotension + tachycardia

Confusion

Clammy pale skin

286
Q

Treatment for hypovolaemic shock

A

ABCDE

Airway
Breathing (give O2)
Circulation
Disability
Exposure

IV Fluids

287
Q

Define Septic shock

A

Due to uncontrolled bacterial infection

288
Q

Sx of septic shock

A

Pyrexia
Warm peripheries
Bounding pulse
Tachycardic

289
Q

Treatment for septic shock

A

Broad spec antibiotics

290
Q

Define cardiogenic shock

A

Due to heart pump failure; MI, cardiac tamponade, pulmonary embolism

291
Q

Sx of cardiogenic shock

A

Sx of heart failure — (ankle) Oedema, SoB and fatigue
Increased JVP, S4

292
Q

Treatment of cardiogenic shock

A

ABCDE
+
Treat underlying cause

293
Q

Define anaphylactic shock

A

Due to IgE mediated type 1 hypersensitivity vs allergen;
Histamine release - constriction causes excess vasodilation and bronchoconstriction

Leads to decreased MAP and hypoxia

294
Q

Sx of anaphylactic shock

A

Hypotension + tachycardia
Urticaria
puffy face + flushing of the cheeks
Dyspnoea

295
Q

Treatment of anaphylactic shock

A

IM adrenaline - for SNS activation; stress response
Inflammatory response dampens down

296
Q

Define neurogenic shock

A

Due to spinal cord trauma
E.g. RTA
- get disrupted SNS but intact PsNS

297
Q

Sx of neurogenic shock

A

Hypotension + Bradycardia
Hypothermic

298
Q

Treatment for neurogenic shock

A

ABCDE
+
IV Atropine (blocks fatal tone; allows more PsNS inhibition, more chance for SNS to work)

299
Q

Which organs at highest risk of failure

A

Kidney
Lungs
Brains
Heart

300
Q

Define rheumatic fever

A

A systemic response to ß haemolytic group A strep
- Almost exclusively I developing countries only

301
Q

Causes of rheumatic fever

A

Post strep pyogenes infection (group A, ß haemolytic strep)
- typically pharyngitis

50% of cases affect the heart —> Rheumatic heart disease

302
Q

Pathophysiology of rheumatic disease

A

M protein from S. Pyogenes reaches heart valve tissue; antibodies attack this ‘cross-link’ (molecular mimicry)resulting in autoantibody mediated destruction ± inflammation

  • mitral valves most affected (70% just mitral; 25% mitral and aortic)
  • typically thickens leaflets; mitral stenosis
303
Q

Signs and symptoms of rheumatic fever

A

New murmur - mitral stenosis
Arthritis
Pyrexia
Syndentiams chorea - uncoordinated jerky movements

304
Q

Investigation and diagnosis of of rheumatic fever

A

CXR - cardiomegaly / heart failure / mitral stenosis
Echo - details extent of valvular damage

Jones criteria: recent pyogenes infection
+
2 major
or
1 major + 2 minor

305
Q

Treatment for rheumatic fever

A

Antibiotics:
IV benzylpenicillin then phenoxypenicillin for 10 days

For syndenhams chorea:
Haloperidol

306
Q

What are Aschoff bodies

A

Histological finding for rheumatic heart disease from valves

307
Q

What conditions make up tetralogy of Fallot

A

1) Ventricular Septal Defect
2) Over-riding aorta
3) Right ventricular hypertrophy
4) Pulmonary stenosis Right ventricular outflow obstruction

308
Q

What does Px with tetralogy of Fallot present as

A

Cyanotic; VSD with RV outflow obstruction (therefore, oxygen systemically shunted)

Infants often seen in knee to chest squatting position - increases preload + afterload, therefore improves cyanosis
So can Px in clinic if put into the squat position they become less cyanotic

309
Q

Investigation and diagnosis of tetralogy of Fallot

A

Echo
CXR - boot shaped heart

310
Q

Treatment for tetralogy of Fallot

A

Full surgical repair within 2 years of life

311
Q

Define coarctation of aorta

A

Aorta narrows at or just distal to ductus arteriosus
Blood is diverted massively through aortic arch branches, so increased upper body perfusion vs lower body

312
Q

Sx of coarctation of aorta

A

Scapular bruits - HTN in collaterals
Upper body hypertension

313
Q

Investigation and diagnosis of coarctation of aorta

A

CXR : Notched ribs - dilated intercostal vessels
CT angiogram

314
Q

Treatment for coarctation of aorta

A

Surgical repair or stenting

315
Q

What is the most common inherited heart defect

A

Bicuspid aortic valve

Typically tricuspid, Px ends up with bicuspid valve instead which degenerates quicker than normal + becomes regurgitative earlier

316
Q

Define atrial septal defect

A

Aka patent foreman Ovale

Shunt of blood L—>R, therefore NOT CYNOTIC
May overload right side circulation; right ventricular hypertrophy (if severe; Eisenmenger syndrome)

317
Q

What’s Eisenmenger syndrome

A

When pulmonary hypertension causes reversal shunt; R—>L shunt of blood

So deoxygenated blood is pumped systemically

In younger Px the heart is more compliant… but… in older, more shunting so causes dyspnoea

318
Q

Investigation / test for atrial septal defect

A

ECHO

319
Q

Tx for atrial septal defect

A

Spontaneous closure sometimes / surgical

320
Q

Define ventricular septal defect

A

Shunt of blood L—R (non-cynotic; just like atrial septal defect)

321
Q

Sx of ventricular septal defect

A

Small VSD: asymptomatic

Large VSD: exercise intolerant, failure to thrive, harsh pansystolic murmur

322
Q

Investigation and diagnosis of ventricular septal defect

A

ECHO

323
Q

Treatment for ventricular septal defect

A

Spontaneous closure / surgical

324
Q

Define atrioventricular septal defect

A

Hole in the middle of the heart
Essentially, no atria

325
Q

What is atrioventricular septum associated with

A

Down syndrome

326
Q

Sx of atrioventricular septal defect

A

Shortness of breath
Exercise intolerance
Eventually leads to Eisenmenger syndrome

327
Q

Define patent ductus arteriosus

A

When the ductus arteriosus fails to close post birth
Blood shunts from aorta —> pulmonary trunk; risk of pulmonary overload + Eisenmenger

328
Q

Sx of patent ductus arteriosus

A

Dyspnoea
Failure to thrive
Machine like murmur

329
Q

Investigation and diagnosis of patent ductus arteriosus

A

Echo
CXR
ECG

330
Q

Tx for patent ductus arteriosus

A

Prostaglandin inhibitor - indomethacin
May induce closure
Otherwise consider closure

331
Q

3 cardinal signs of aortic stenosis

A

Syncope
Angina
Dyspnoea

Phase 2a Basic Knowledge (13 decks)

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