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 : heard straight after S2
rapid ventricular filling in early diastole
normal in pregnant
pathological in mitral regurgitation
AKA pathological “gallop”

S4 :heard straight before S4
due to blood forced into stiff hypertrophic ventricles
seen in LVH / aortic stenosis

Erbs point is where heart sounds best heard

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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
What are intermediate lesions and its constituents
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*
26
What are fibrous plaques and their constituents
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
27
Nature of the plaque in stable angina
Fibrous cap is strong & less prone to rupture If plaque prone to rupture —> prothrombotic state; platelet adhesion + accumulation; **progressive lumen narrowing**
28
Percentage of lumen narrowing in stable angina
>70% is when symptoms start to develop
29
Signs and symptoms of stable angina
**Central crushing chest pain radiating to the neck & jaw** Dyspnoae Fatigue Sweating
30
Investigation & diagnosis of stable angina
1st line: ECG : Resting - normal Exercise induced (Ischaemic) - change Gold standard: CT angiography - stenoses atherosclerotic arteries (>70% occlusion)
31
1st line investigation for stable angina
1st line: ECG : Resting - normal Exercise induced (Ischaemic) - change
32
Gold standard investigation for stable angina
Gold standard: CT angiography - stenoses atherosclerotic arteries (>70% occlusion)
33
Treatment for stable angina
Remember RAMP for stable angina management **R**efer to cardiologist; **A**dvise on lifestyle modification, **M**edical Tx, **P**rocedural 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
34
What procedural interventions are there for stable angina
*given if pharmacological intervention unsuccessful* _Revascularisation_ **PCI** - balloon stent via femoral artery to coronary artery **CABG** - bypass graft (LAD bypassed using great saphenous vein)
35
Give a positive and negative for PCI
+ve : Less invasive -ve : High risk of restenosis
36
What is restenosis
a gradual re-narrowing of the stented segment that occurs requiring further procedural treatment
37
What type of CCB is used in stable angina
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.*
38
Give a positive and negative of CABG procedure
+ve: Good prognosis -ve: more invasive + longer recovery time
39
Clinical classification of unstable angina
Cardiac chest pain at rest Cardiac chest pain with crescendo pattern New onset angina
40
Occlusion for unstable angina
partial occlusion of minor coronary artery (>90%)
41
Type of infarction in unstable angina
None - ischaemia only
42
ECG finding in unstable angina
Normal May show some ST depression / T wave inversion
43
Troponin levels in unstable angina
Normal
44
Level of occlusion for NSTEMI
Major partial occlusion (>90%) / total occlusion of minor coronary artery
45
Type of infarction in an NSTEMI
Subendothelial infarct I.e. area furthest away from the occlusion dies
46
ECG finding for NSTEMI
ST depression T wave inversion **no Q waves! - seen in STEMI, only after some time**
47
Troponin levels for NSTEMI
Raised Due to infarct obviously
48
Level of occlusion in STEMI
Complete occlusion of major coronary artery
49
Type of infarction in STEMI
Transmural infarction
50
ECG finding of STEMI
ST segment elevation Pathological Q waves - develop after some time
51
Troponin levels seen in STEMI
Raised
52
Signs and symptoms of ACS
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
53
What is a silent MI
**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
54
Investigations & diagnosis of ACS
ECG Bio markers CT coronary angiogram
55
Treatment for ACS
_**Acute - remember MONAC**_ - **M**orphine - **O**xygen (if SATs <94%; COPD: 88-92%) - **N**itrates (GTN spray) - **A**spirin - **C**lopidogrel 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**_ **A**spirin **A**atorvastatin (life) **A**CEi (life) **B**eta blocker (life)
56
Role of alteplase
Thombolytic agent - activates plasmin to break down fibrin
57
In what conditions is troponin elevated in…
MI But also… Myocarditis PE Aortic dissection Sepsis Chronic renal failure
58
Complications of ACS
**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)
59
Define heart failure
Inability for the heart to pump sufficient Oxygen in order to meet the demand of the tissue metabolism **A syndrome** not a diagnosis
60
Causes of heart failure
**IHD** - most common Hypertension Valvular heart disease (aortic stenosis) Arrythmias (AF)
61
Risk factors for heart failure
Age (>65y/o) Smoking Obesity **Previous MI** Male > female
62
Pathophysiology of heart failure
**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**
63
Classification of heart failure
Time classified: acute / chronic Ejection fraction (normal EF = 50-70%)
64
> 40% ejection fraction suggests what
_Preserved ejection fraction_ (Heart pump function is preserved) **Diastolic failure** - Filling issues due to **stiffness** E.g. hypertrophic cardiomyopathy, Ventricular hypertrophy
65
What can cause diastolic heart failure
hypertrophic cardiomyopathy, ventricular hypertrophy
66
What does < 40% ejection fraction suggest
_Reduced ejection fraction_ Heart pumping has failed **Systolic heart failure** - reduced C.Output due to **inability** to pump E.g. IHD
67
Give a cause for Systolic heart failure
**IHD**
68
Left sided heart failure causes what
Results in **pulmonary vessel backlog** - therefore, **pulmonary oedema**
69
What does right sided heart failure cause
Causes backlog in systemic venous system - leading to **peripheral oedema**
70
Cardinal signs of heart failure
**Dyspnoea Fatigue Ankle oedema**
71
Signs / symptoms of heart failure
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
72
What classification describes severity of heart failure
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**
73
Key marker found in Heart failure
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*
74
Investigation / diagnosis of heart failure
**Bloods** - Raised BNP ECG - Abnormal: may show signs of LVH **Chest X-ray** - **_ABCDE_** •**A**lveolar ‘batwing’ oedema • kerley **B**-lines •**C**ardiomegaly •**D**ilated upper lobes • pleural **E**ffusion Echocardiogram - shows dimension of heart chambers
75
Types of treatment available for heart failure
Conservative Pharmacological Surgical
76
Type of conservative treatment for HF
Lifestyle ∆’s (Reduce BMI, exercise, diet, smoking + alcohol cessation)
77
Pharmacological treatment for HF
**_L.A.B.A_** - first line medical Tx **A**CEi - ramipril **ß** Blocker - atenolol + **A**ldosterone antagonist - Spironolactone **L**oop diuretic - Furosemide *Consider cardiac resynchronisation therapy (to improve AV conduction)*
78
Surgical treatment for heart failure
Consider revascularisation, valve surgery Heart transplant = last resort
79
Role of BNP
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**
80
Define Cor pulmonale
Right sided heart failure **caused by** respiratory disease.
81
Cause of Cor pulmonale
Remember it is RHF due to **a resp disease** • COPD - most common cause • PE • Interstitial lung disease • CF
82
Pathophysiology of cor pulmonale
**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**.
83
Signs / symptoms of cor pulmonale
Raised JVP Cynosis **peripheral oedema** 3rd Heart sound Murmurs : **Tricuspid** regurg - **Pan systolic**
84
Define abdominal aortic aneurysm
Permanent aortic dilation exceeding 50% where diameter > 3cm > 5.5cm is urgent (significant rupture risk) Rupture - surgical emergency!
85
Risk factor for aortic aneurysm
Idiopathic Connective tissue disorder — **Marfan syndrome**, Ehler danlos synderom **Smoking**(biggest RF), obesity, HTN (those RF for atherosclerosis)
86
Pathophysiology for aortic aneurysm
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
87
Signs / symptoms of AAA
Asymptomatic till increased rupture risk / ruptured **Sudden epigastric pain** radiating to flank Pulsatile mass in abdomen Hypotensive + tachycardic
88
Differential diagnosis for AAAneurysm
**Acute pancreatitis** • Non-pulsatile + more associate with Grey turner (flank discolouration) / Cullen Sx (superficial oedema/bruising)
89
Investigation & diagnosis of AAA
1st line + diagnostic **ABDO USS**
90
Tx for AAA
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)
91
Complication of abdominal aortic aneurysm
**Rupture** Stabilise: ABCDE, fluids + transfusions Then, consider surgery • AAA graft surgery; replacing weakened walls with graft • 100% mortality if not treated immediately
92
Define aortic dissection
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**
93
Who is aortic dissection most commonly seen in
50-70y/o **men**
94
Risk factors for aortic dissection
HTN (most common) Connective tissue disorder - Marfan syndrome, EDS FHx AAA Trauma Smoking
95
Common locations of aortic dissection
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
96
Types of aortic dissection + the classification
**_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
97
Pathophysiology of aortic dissection
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
98
Signs and symptoms of aortic dissection
**Sudden onset ripping/tearing chest pain** Anterior pain - ascending Posterior pain - descending Hypotension/shock Syncope Diastolic murmur Radial pulse deficit
99
Differential diagnosis of aortic dissection
**MI** Central crushing chest pain with gradual worsening intensity
100
Investigation & diagnosis of aortic dissection
**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
101
Treatment for aortic dissection
**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
102
Give 3 complications of aortic dissection
(Haemorrhagic) Cardiac tamponade Ischaemic stroke Pre-renal AKI
103
Types of beta blockers used in aortic dissection
Esmolol / labetolol
104
Define hypertension
Abnormally high BP ≥ 140/90 mmHg (clinical) ≥ 135/85 mmHg (ambulatory / home readings)
105
Types of hypertension
Primary (Essential) - idiopathic HTN (95% of cases) Secondary - known underlying cause
106
Causes of hypertension
Primary = idiopathic Secondary = **Remember ROPE** **R**enal disease **O**besity **P**regancy / eclampsia **E**ndocrine disorder: - Conn’s (most common cause of HTN) - Phaemochromocytoma - Cushing’s
107
Risk factors for hypertension
Older age Obesity Black ethnicity Smoking Diabetes Increased salt intake FHx
108
Describe the different stages of HTN
1) 140/90 … 135/85 2) 160/100 … 150/95 3) 180/120 - **start immediate Tx**
109
Pathophysiology of HTN
Ultimately all mechanisms stimulate RAAS + SNS (increasing cardiac output) + TPR … Increasing BP
110
Signs / symptoms of HTN
**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
111
Investigation & diagnosis of hypertension
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)
112
Treatment for hypertension
——— **< 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——
113
What do you give if ACEi is contraindicated
ARB - Candesartan
114
4th line for HTN has you add which drug and what drug is given if contraindicated
In 4th line, the 4th drug given is **K+ sparring diuretic** But **if K+ > 4.5, give ∂/ß blocker**
115
If Px is Black & has T2DM, what is 1st line treatment
ACEi Because T2DM takes precedence over being black
116
A 60y/o black man has hypertension and T2DM, what is the first line treatment
ACEi Having T2DM takes precedence
117
Complications for hypertension
Heart failure CKD IHD Cerebrovascular accident risk increases
118
Define DVT and a PE
**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
119
Risk factors for DVT ± a PE
Remember **Virchow’s Triad**: • _Hypercoagulability_ Pregnant **Antiphospholipid syndrome** DIC • _Venous stasis_ Immobility Long haul flights Surgery • _Endothelial injury_ Trauma / Surgery Smoking HTN
120
What can a PE cause / lead to
**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*
121
Give 3 conditions that present with pleuritic chest pain
PE Pneumothorax Pneumonia
122
Differential diagnosis between: PE, Pneumothorax, Pneumonia
Do CxR: PE - normal Pneumonia + pneumothorax - diagnostic
123
Signs / symptoms of DVT
**Unilateral, swollen, warm + oedematous calf** with dilated superficial veins.
124
What is phlegmasia cerulea dolens
Complete occlusion of a large being —> severe DVT Severe ischaemia —> presents a s cyanosis (blue, not red like DVT)
125
Which scoring system is used in DVT / PE
Wells score
126
Diagnosis + investigation of DVT
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
127
Is D-dimer specific or sensitive
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
128
Conditions D-dimer can be elevated in
**DVT / PE** Heart failure Pneumonia Pregnancy Malignancy
129
Treatment for DVT
**DOAC** - Rivaroxaban / Apixaban **LMWH** - if DOAC is contraindicated (e.g in renal impairment ) + mobilisation, compression stockings (unless contraindicated - Peripheral Arterial Disease)
130
Differential diagnosis for DVT
_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*
131
Complication of DVT
PE
132
Signs and symptoms of PE
**Sudden onset pleuritic chest pain** Dyspnoea ± haemoptysis (streaky blood) Tachycardic + tachypnoea (respiratory alkalosis), hypotensive, increased JVP + *evidence of DVT : swollen, red, oedematous & tender leg*
133
Prophylaxis for VTE: DVT/PE
LMWH - Enoxaparin Warfarin DOAC
134
Diagnosis + investigation of PE
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
Treatment for pulmonary embolism
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
Define pericarditis
Inflammation of the pericardium ± effusion; typically acute, can be chronic
137
Cause / aetiology of pericarditis
**Idiopathic** **Viral** - Coxsackie virus (most common cause) **Bacterial** - TB **Autoimmune** - SLE, Rheumatoid.A (common) **Dressler’s syndrome** (>2 weeks post MI)
138
Pathophysiology of pericarditis
• 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
Signs and symptoms of pericarditis
**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
What is constrictive pericarditis
Late complication of acute pericarditis + there’s a sign of poor heart prognosis. Granulation tissue formation in pericardium —> impaired diastolic filling.
141
Investigation and diagnosis of pericarditis
**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
Treatment of pericarditis
Idiopathic + viral: NSAID’s (aspirin) + Colchicine (anti inflammatory - used in gout too) + antibiotic if bacterial (R.I.P.E Abx for TB)
143
Complication of pericarditis
Pericardial effusion Cardiac tamponade Myocarditis Constrictive pericarditis
144
Define pericardial effusion
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
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Types of effusion and their causes
_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
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Signs and symptoms of pericardial effusion & cardiac tamponade
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
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Investigation and diagnosis of pericardial effusion + cardiac tamponade
ECG : may show electrical CxR : big globular heart **Echo : diagnostic**
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Treatment of pericardial effusion + cardiac tamponade
Pericardial effusion - Tx underlying cause (NSAIDs + Colchicine —> pericarditis) Cardiac tamponade - urgent pericardiocentesis
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Define Peripheral vascular disease
Essentially IHD of lower limb arteries. Males
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Risk factor for Peripheral vascular disease
Smoking HTN Ageing Obesity CKD T2DM
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Pathophysiology for peripheral vascular disease
**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!!
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Define peripheral arterial disease
Peripheral arterial disease (PAD) refers to the **narrowing of the arteries** supplying the limbs and periphery, reducing the blood supply to these areas
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Define intermittent claudication
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
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Define critical limb ischaemia
Critical limb ischaemia is the **end-stage of peripheral arterial disease** Pain at rest; non-healing ulcers + gangrene
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Difference between PVD & PAD
Pretty much the same thing
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Risk factors for PVD
Same as atherosclerosis: Smoking HTN Ageing Obesity CKD T2DM
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Define acute limb ischaemia
**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.*
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Define gangrene
the death of the tissue, *specifically due to an inadequate blood supply.*
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Features of limb ischaemia
**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
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Mention 3 things that can occur if blood vessels to a region is occluded in PVD
1) Irreversible nerve damage (within 6hrs) 2) Irreversible muscle damage (6-12hrs) 3) Skin ∆’s are last to appear **therefore likely to be gangrenous**
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Investigations and diagnosis of PVD
_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)
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What classification used in PAD/ PVD
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
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Treatment for PVD
**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
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Complications of PVD
Amputation Permanent limb weakness Rhabdomyolysis (increased ca2+ and k+ release in blood - Arrhythmias / AKI) Risk of Cerebrovascular accident + CKD
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Define virulence
Ability of microbe to cause damage to host
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Define infective endocarditis
Inflammation of the endocardium - causative bacteria; colonise abnormally in the endothelium (leading to vegetation)
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Cause of infective endocarditis
**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**
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Types of infective endocarditis
Acute S. Aureus; high virulence. Sx onset days-weeks Subacute S. Viridans; lower virulence. Sx onset weeks-months
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Risk factors for infective endocarditis
**Male**, elderly; with **prosthetic valves** Young **IVDU** Young with congenital heart defect **Rheumatic heart disease**
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Pathophysiology of infective endocarditis
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)
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Signs and symptoms of infective endocarditis
**FEVER + NEW MURMUR = I.ENDOCARDITIS** Symptoms: vague; fever, fatigue, SoB Signs: **ROTH SPOTS JANEWAY LESIONS SPLINTER HAEMORRHAGES OSLER NODES**
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What criteria is used in infective endocarditis
DUKE criteria
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Investigation and diagnosis of infective endocarditis
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*
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Treatment of infective endocarditis
Staph Aureus: vancomycin + rifampicin Strep Viridans: Benzylpenicillin + gentamicin *For 4 - 6 weeks* Surgery —> remove valve if incompetent & replace with prosthetic
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Complication of infective endocarditis
Heart failure Aortic root abscess Septic emboli (± sepsis)
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The effects of regurgitation of heart muscle
**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
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When are murmurs best heard
Remember “RILE” Right side valve defect —> Inspiration Left side valve defect —> Expiration *A.R-M.S - Diastolic murmur A.S-M.R - systolic murmur*
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Most common valve disorder
Aortic stenosis
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Normal area of aortic valve vs. Pathological
3-4cm normal Sx at 1/4 lumen size
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Effects of aortic stenosis on heart
Results in LV dilation + hypertrophy
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What causes aortic stenosis
Ageing calcification Rheumatic heart disease
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Signs / symptoms of aortic stenosis
**Remember S.A.D** **S**yncope (exertional) **A**ngina **D**yspnoea (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)
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Investigation and diagnosis of aortic stenosis
ECG CXR **ECHO (Gold standard)** - shows LV size + function, aortic valve area (Doppler derived)
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Treatment of aortic stenosis
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
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Type of sound heard in a hypertrophic cardiomyopathy
Causes S4 (sound just before S1) *Associated with sudden death in young men*
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Define aortic regurgitation
Leaky aortic valve, insufficient
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What causes aortic regurgitation
Congenital bicuspid valve Rheumatic heart disease Connective tissue disorders; Marfan’s / Ehler’s Danlos **INFECTIVE ENDOCARDITIS**
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Signs and symptoms of aortic regurgitation
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
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Investigation and diagnosis aortic regurgitation
ECG CXR **Echo (Gold standard)** - evaluate aortic valve, root and dimension
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Treatment of aortic regurgitation
Consider IE prophylaxis Surgical valve replacement is symptomatic
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Differential diagnosis for aortic regurgitation
Infective endocarditis
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Define mitral stenosis
Mitral lumen 4-6cm Symptoms appear at < 2cm
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Risk factors for mitral stenosis
Rheumatic fever Hx men ageing
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Causes of mitral stenosis
Rheumatic heart disease - *most common, post strep. Pyogenes infection* Valve calcification - *seen in older Px* Infective endocarditis
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Pathophysiology of mitral stenosis
Rheumatic heart disease causes mitral reactive inflammation; over the years its exacerbated with calcification —> leading to left atria hypertrophy
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Signs / symptoms of mitral stenosis
**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 *
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Investigation and diagnosis for mitral stenosis
ECG - may show AFib / p mitrale - ‘m’ shaped p wave seen in LA enlargement CXR - LA enlargement (Gold standard) - echocardiogram
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Treatment for mitral stenosis
Surgical - Percutaneous balloon valvotomy (a stent) - Mitral valve replacement
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Define mitral regurgitation
Insufficient mitral valve function
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Causes of mitral regurgitation
**myxomatous mitral valve** (most common; mass of cells in valves connective tissue making leaflet heavier & prolapse) Connective tissue disorders; Marfan / Ehlers Danlos
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Risk factors for mitral regurgitation
Females Older Decreased bmi Prior MI Connective tissue disorder
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Signs / symptoms of mitral regurgitation
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)
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Investigation and diagnosis of mitral regurgitation
ECG CXR Gold standard - Echocardiogram
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Treatment for mitral regurgitation
ACEi, BBlockers + monitoring using Echo If severe - valve replacement / repair
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Mitral stenosis murmur
Mid diastolic low pitched ‘rumbling’ murmur Loud S1
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What might malar flush indicate
Mitral stenosis
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Which valvular heart disease might cause atrial fib
Mitral stenosis
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Which valvular disease might cause congestive heart failure
Mitral regurgitation
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Mitral regurgitation murmur
Pan-systolic high pitched whistling murmur Radiates to axilla With S3 heart sound
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Aortic stenosis murmur
Ejection systolic high pitched crescendo-decrescendo murmur Radiates to the carotids Slow-rising pulse with narrow pulse pressure
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Aortic regurgitation murmur
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)
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Where are the 4 valve murmurs heard from
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)
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Define tachycardia
> 100 bpm
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Types of tachycardia
_Supraventricular tachycardia (SVT)_ *Atrial fib* *Atrial flutter* *AVRT* (non-junctional) - *wolff-Parkinson’s white syndrome* *AVNRT* _Ventricular tachycardia_ *prolonged QT syndrome* *Ventiricular fibrillation*
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What is the most common SVT
AVNRT - re-enterant pathway goes through AVN
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Difference between AVRT and AVNRT
AVRT - re-enterant pathway through accessory pathway (Bundle of kent) AVNRT - re-enterant pathway goes through AVN
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Define bradycardia
< 60 bpm
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Types of bradycardia
*Bundle branch block* - RBBB / LBBB *1˚/2˚/3˚ heart blocks*
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Atrial fib rhythm
Irregularly irregular
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Causes of atrial fibrillation
**Heart failure, HTN** 2˚ to mitral stenosis Idiopathic
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Risk factors for atrial fibrillation
60+ Valvular heart defect Hx of MI T2DM HTN
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Pathophysiology of atrial fib
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
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Signs / symptoms of atrial fibrillation
**Palpitations Irregularly irregular pulse** Chest pain Syncope Hypotensive *Sx can be paroxysmal (episodic), persistent (> 7 days), permenant - sinus rhythm unrestorable*
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Investigation and diagnosis of atrial fibrillation
ECG (diagnostic) - irregularly irregular, narrow QRS complex No P waves
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Treatment of atrial fibrillation
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
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Which scoring system is used in Atrial Fib
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
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What does CHADS VASc stand for
Congestive heart failure HTN Age > 75y/o (2 points) DM type2 Stroke (2 points) Vascular disease Age 65-74y/o Sex category = female
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Complication of atrial fibrillation
Heart failure Ischaemic stroke
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Define atrial flutter
Irregular regular atrial firing *Less common and less severe that atrial fib*
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Risk factor of atrial flutter
Same as atrial fib: 60+ Valvular heart defect Hx of MI T2DM HTN
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Causes of atrial flutter
Similar to atrial fibrillation - **Heart failure, HTN** 2˚ to mitral stenosis Idiopathic
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Pathophysiology of atrial flutter
Fast atrial ectopic firing causes atrial spasm but not as uncoordinated as A. Fib Pathway typically from around tricuspid annulus (opening of valve)
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Signs and symptoms of atrial flutter
Dyspnoea, palpitations… Irregularly regular
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Investigation and diagnosis of atrial flutter
ECG (diagnostic) - F wave ‘Saw-tooth’ pattern Often seen with 2:1 block (2 P waves for every QRS )
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Treatment of atrial flutter
Acute: unstable —> DC synchronised cardioversion Stable —> rhythm / rate control (ß-blocker) with oral anticoagulation (prevent thromboemboli) Radiofrequency ablation
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Define Wolff Parkinson’s white (AVRT)
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
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Signs / symptoms of AVRT
Palpitations, dyspnoea, dizziness
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Investigation and diagnosis of AVRT
_ECG_ **Slurred delta waves Short PR interval Wide QRS**
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Treatment of AVRT
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
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Define long QT syndrome
Ventricular tachyarrhythmia; usually congenital channelopathy disorder *Where mutations affects cardiac ion channels therefore heart conduction* - QT interval > 480ms
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Causes of long QT syndrome
Romano ward syndrome (autosomal dominant) Jarvell-Lange-Neilson syndrome (autosomal recessive) Hypokalaemia + hypocalcaemia (non-inherited) Drugs - Amiodarone, magnesium
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Define Torsades de pointes
Polymorphic ventricular tachycardia in patients with prolonged QT Rapid irregular QRS complex which ‘twist’ around baseline, can cease spontaneously or develop to ventricular fibrillation
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Define ventricular fibrillation
Shapeless rapid oscillations on ECG Px becomes pulseless + goes into cardiac arrest (no effective cardiac output)
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1st line treatment for ventricular fibrillation
**Electrical defibrillation** Non-synchronised as patient is pulseless
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Define Primary AV block
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
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Cause of primary av block
Drugs (ß-blocker, CCB, Digoxin—> blocks AVN conduction) Post MI SLE
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Complication of primary AV block
Atrial fibrillation
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Define secondary AV block
When some P waves conducted and others aren’t 2 types: Mobitz 1 (Wenkebach’s) Mobitz 2
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Define Mobitz 1
Mobitz 1 (2˚ AV block) **PR prolongation until a QRS is dropped** (PR interval *progressively* elongates)
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Causes of AV block mobitz 1
Drugs - ß-blocker, CCB, Digoxin Previous MI SLE
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Treatment for Mobitz type 1
No Tx unless v. Symptomatic - syncope / reduced consciousness Give Tx: Pacemaker
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Define mobitz 2
Persistent PR interval prolongation with random dropped QRS
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Causes of mobitz type 2
Drugs - ß-blocker, CCB, Digoxin Previous MI Rheumatic fever
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Signs / symptoms of secondary AV block mobitz 2
Syncope SoB Chest pain
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Treatment of mobitz 2
Pacemaker
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Define tertiary AV block
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)
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Cause of tertiary AV block
Acute MI HTN Structural heart disease
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Tx for 3˚ AV block
IV atropine + Permanent pacemaker
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Define bundle branch block
Blocking of the bundle of His 2 types: RBBB LBBB
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Cause of RBBB
Pul emboli IHD Ventricular Septal Defect *RV later activated than LV*
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Dx of RBBB
ECG: **MarroW** - “M” in V1 (RSR wave) - “W” in V2 (deep S wave) Hear: Wide physiological S2 splitting heart sound
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Cause of LBBB
IHD Valvular disease *LV is activated later than RV*
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Dx of LBBB
ECG: **WilliaM** - “W” in V1 (RSR wave) - “M” in V2 (deep S wave) Hear: Reversed S2 splitting heart sound
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Define cardiomyopathy
Disease of the myocardium (muscular / conduction defects) Types: Hypertrophic Dilated Restrictive
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Which cardiomyopathy is most common cause of death in young people
Hypertrophic cardiomyopathy
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Most common cardiomyopathy
Dilated
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Cause of hypertrophic cardiomyopathy
Familial (inherited) - autosomal dominant mutation of sarcomere protein (troponin T, myosin B) Exercise Aortic stenosis
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Pathophysiology for hypertrophic cardiomyopathy
Thick non-complaint heart = leads to impaired diastolic filling Therefore, reducing C.O
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Sx of hypertrophic cardiomyopathy
May present with **sudden death** Chest pain Palpitations SoB Syncope
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Investigation and diagnosis of hypertrophic cardiomyopathy
Echocardiogram (definitive) Abnormal ecg Genetic testing
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Treatment for hypertrophic cardiomyopathy
ß blocker CCB Amiodarone
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Cause of dilated cardiomyopathy
Familial: Autosomal dominant - cytoskeleton gene mutation IHD Alcohol
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Pathophysiology of dilated cardiomyopathy
Thin cardiac walls poorly contract therefore reduced CO
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Sx of dilated cardiomyopathy
SoB Heart failure Atrial fib Thromboemboli
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Investigation and diagnosis of dilated cardiomyopathy
ECG Echo (definitive)
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Treatment for dilated cardiomyopathy
Treat underlying cause like AFib / HF
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Cause of restrictive cardiomyopathy
Granulomatous disease (sarcoidosis / amyloidosis) Idiopathic Post MI
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Pathophysiology of restrictive cardiomyopathy
Rigid fibrotic myocardium fills poorly + contracts poorly Reducing CO
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Sx of restrictive cardiomyopathy
If severe: Dyspnoea, S3+4 Oedema, congestive heart failure Narrow pulse pressure
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Investigation + diagnosis of restrictive cardiomyopathy
ECG Echo Cardiac catheterisation (definitive)
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Tx for restrictive cardiomyopathy
None; Consider transplant Px typically die within a year
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Define shock
Medical emergancy - hypoperfusion, life threatening, due to acute circulation on failure Leads to tissue hypoxia + risk of organ dysfunction
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General Sx to recognise shock
Skin; pale, cold, sweaty Reduced GCS Increased capillary refill time Decreased urine output Prolonged hypotension
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Define hypovolaemic shock
As a result of **fluid loss** — dehydration Or As a result of **blood loss** — trauma / GI bleed
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Sx of hypovolaemic shock
Hypotension + tachycardia Confusion Clammy pale skin
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Treatment for hypovolaemic shock
ABCDE *Airway Breathing (give O2) Circulation Disability Exposure* **IV Fluids**
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Define Septic shock
Due to uncontrolled bacterial infection
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Sx of septic shock
Pyrexia Warm peripheries Bounding pulse Tachycardic
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Treatment for septic shock
Broad spec antibiotics
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Define cardiogenic shock
Due to heart pump failure; MI, cardiac tamponade, pulmonary embolism
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Sx of cardiogenic shock
Sx of heart failure — (ankle) Oedema, SoB and fatigue Increased JVP, S4
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Treatment of cardiogenic shock
ABCDE + Treat underlying cause
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Define anaphylactic shock
Due to **IgE mediated type 1 hypersensitivity** vs allergen; Histamine release - constriction causes excess vasodilation and bronchoconstriction Leads to **decreased MAP and hypoxia**
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Sx of anaphylactic shock
Hypotension + tachycardia **Urticaria** **puffy face + flushing of the cheeks** Dyspnoea
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Treatment of anaphylactic shock
IM adrenaline - for SNS activation; stress response Inflammatory response dampens down
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Define neurogenic shock
Due to spinal cord trauma E.g. RTA - get disrupted SNS but intact PsNS
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Sx of neurogenic shock
Hypotension + **Bradycardia** Hypothermic
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Treatment for neurogenic shock
ABCDE + **IV Atropine** (blocks fatal tone; allows more PsNS inhibition, more chance for SNS to work)
299
Which organs at highest risk of failure
Kidney Lungs Brains Heart
300
Define rheumatic fever
A systemic response to ß haemolytic group A strep - Almost exclusively I developing countries only
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Causes of rheumatic fever
Post strep pyogenes infection (group A, ß haemolytic strep) - typically **pharyngitis** **50%** of cases affect the heart —> **Rheumatic heart disease**
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Pathophysiology of rheumatic disease
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
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Signs and symptoms of rheumatic fever
**New murmur** - mitral stenosis **Arthritis** Pyrexia **Syndentiams chorea** - uncoordinated jerky movements
304
Investigation and diagnosis of of rheumatic fever
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
Treatment for rheumatic fever
Antibiotics: **IV benzylpenicillin** then phenoxypenicillin for 10 days For syndenhams chorea: Haloperidol
306
What are Aschoff bodies
Histological finding for rheumatic heart disease from valves
307
What conditions make up tetralogy of Fallot
1) Ventricular Septal Defect 2) Over-riding aorta 3) Right ventricular hypertrophy 4) Pulmonary stenosis *Right ventricular outflow obstruction*
308
What does Px with tetralogy of Fallot present as
**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
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Investigation and diagnosis of tetralogy of Fallot
Echo CXR - boot shaped heart
310
Treatment for tetralogy of Fallot
Full surgical repair within 2 years of life
311
Define coarctation of aorta
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
Sx of coarctation of aorta
**Scapular bruits** - HTN in collaterals Upper body hypertension
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Investigation and diagnosis of coarctation of aorta
CXR : **Notched ribs** - dilated intercostal vessels CT angiogram
314
Treatment for coarctation of aorta
Surgical repair or stenting
315
What is the most common inherited heart defect
Bicuspid aortic valve *Typically tricuspid, Px ends up with bicuspid valve instead which degenerates quicker than normal + becomes regurgitative earlier*
316
Define atrial septal defect
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
What’s Eisenmenger syndrome
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
Investigation / test for atrial septal defect
ECHO
319
Tx for atrial septal defect
Spontaneous closure sometimes / surgical
320
Define ventricular septal defect
Shunt of blood L—R (non-cynotic; just like atrial septal defect)
321
Sx of ventricular septal defect
Small VSD: asymptomatic Large VSD: exercise intolerant, failure to thrive, harsh pansystolic murmur
322
Investigation and diagnosis of ventricular septal defect
ECHO
323
Treatment for ventricular septal defect
Spontaneous closure / surgical
324
Define atrioventricular septal defect
Hole in the middle of the heart *Essentially, no atria*
325
What is atrioventricular septum associated with
Down syndrome
326
Sx of atrioventricular septal defect
Shortness of breath Exercise intolerance Eventually leads to Eisenmenger syndrome
327
Define patent ductus arteriosus
When the ductus arteriosus fails to close post birth Blood shunts from aorta —> pulmonary trunk; risk of pulmonary overload + Eisenmenger
328
Sx of patent ductus arteriosus
Dyspnoea Failure to thrive Machine like murmur
329
Investigation and diagnosis of patent ductus arteriosus
Echo CXR ECG
330
Tx for patent ductus arteriosus
Prostaglandin inhibitor - indomethacin May induce closure Otherwise consider closure
331
3 cardinal signs of aortic stenosis
Syncope Angina Dyspnoea