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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Arthrogenesis RF

  • Modifiable
  • Non modifiable
A

Modifiable

  • High cholesterol
  • Smoking
  • Alcohol
  • Obesity
  • Sedentary lifestyle
  • Hyperlipidaemia
  • HTN
  • DM

Non mod

  • Male
  • Family hx
  • Age
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2
Q

Atherosclerosis pathogenesis

A

-Endothelial injury
-endothelial dysfunction
-endothelium releases chemoattractants
-Leukocytes accumulate and migrate into vessel walls releasing inflamm cytokines
IL-6
IL-1
IFN-Gamma
LDL - can pass in and out of arterial wall when in excess
Accumulation leads to glycation and oxidation

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3
Q

Stages of atherogenesis

A
  1. fatty streak
  2. Intermediate lesions
  3. Fibrous plaques
  4. Rupture of fibrous plaque
  5. Erosion
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4
Q

Complonents of Fatty streak

A

Foam cells and T-lymphocytes

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5
Q

Components of Intermediate lesions

A

Foam cells
T lymphocytes
Vascular SM
Aggregated platelets

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6
Q

Fibrous plaque components

A 
Central necrotic tissue 
Foam cells 
T - lymphocytes 
Vascular SM 
Fibrous cap - Fibrin+Elastin
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7
Q

Primary prevention of CVD

A 
- QRISK 3 Score 
If score >10% innitate STATINS
- Stop Smoking 
-Stop drinking Alcohol 
-Tx Co-morbidities 
- Diet 
-Excercise 
-Weight Loss
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8
Q

Secondary prevention of CVD

A 
After CVD development 
A - Asprin + Clopidogrel (12m)
A - Atorvastatin 
A - Atenolol - Bisoprolol (Titrated) 
A - ACEi (Titrated) - Ramipril

Titrated to max tolerable dose

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9
Q

Complications of atherosclerosis

A
  • TIA
  • MI
  • Peripheral vascular disease
  • Strokes
  • Chronic Mesenteric Ischaemia
  • Angina
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10
Q

What is stable angina

A 
Chest pain due to reversible myochardial Ischaemia 
Mismatch in O2 demand and supply
Exacerbated by excercise
Relieved by rest +GTN Spray 
Radiation: Neck,Jaw,Arm 
Exacerbating factors:
- Cold weather 
- Emotion 
- Heavy meal
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11
Q

Types of Angina

A

Stable
Unstable
Prinzmetal - C.A vasospasm
Decubitus - Precipitated by lying flat

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12
Q

Causes of Myochardial Ischaemia

A
  • Decrease B.F –> Atheroma
  • Decrease O2 carrying capacity –> Anaemia
  • Decrease O2 availability –> Hypoxia
  • Increase distal resistance –> L.V hypertrophy
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13
Q

What percentage occlusion does a rapid decline in perfusion occur

A

Diameter stenosis > 70%

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14
Q

Stable angina Investigations

A

ECG

  • ST depression/ T-wave inversion
  • Excercise ECG - ST depression

Bloods
- FBC/U+E/HbA1c/LFT

CT Coronary Angiogram

  • GOLD - Diagnostic
  • Shows narrowing
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15
Q

Stable Angina Management

A

Secondary prevention

  • Weight loss
  • Diet
  • Smoking/Alcohol
  • Hyperlipidaemia –> Statins
  • 75mg Asprin

Short term Sx relief
- GTN Spray
5mins - repeat - pain - 999

Long term sx relief
- Bisoprolol
-CCB –> Amlodopine
Either or used in combo if sx not controlled

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16
Q

What are the methods for revascularisation

A
  • Percutaneous Coronary Intervention

- Coronary Artery Bypass Graft

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17
Q

PCI

  • Procedure
  • Advantages
  • Risks
A
  • Ballon inflated in stented vessel + Stent (Drug eluting)
  • DAPT (Asprin + Clopidogrel) Decrease risk of instent thrombosis

A:
Less invasive
Short recovery

D:
DAPT
Risk of stent thrombosis
Not for compex cases

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18
Q

CABG

  • Procedure
  • Advantages
  • Disadvantages
A

Use ITA to bypass stenosis in LAD/RCA

A:
Good prognosis
Complex cases

D:
Invasive
Risk - Stroke,Bleeding
Long recovery - Hospitalised

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19
Q

What is ACS

A

Umbrella term for Unstable angina and MI
- Result of rupture of a fibrous cap –> Platelet aggregation –>thrombus formation from an atherosclerotic plaque blocking a coronary artery

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20
Q

Dx STEMI

A

ST elevation
New LBBB
Tall T-waves/T-wave inversion
Pathalogical Q-wave

Troponin T+I elevated
Creatnine Kinase elevated

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21
Q

Dx NSTEMI

A

Normal ECG
ST depression
T-wave inversion
Pathalogical q-wave

Troponin T+I elevated

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22
Q

Dx Unstable Angina

A

ST - depression
T- wave inversion
NO PATHOLOGICAL WAVES

NORMAL TROPONIN LEVELS

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23
Q

RF for ACS

A 
Male 
Obese 
HTN 
Smoking 
Family Hx
Age 
High cholesterol 
DM
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24
Q

Describe the cardiac enzymes

A

Troponin T+I

  • Myocardial necrosis
  • > 30ng/l –> MI
  • Rises 3-12hrs after chest pain onset

Creatnine Kinase MB

  • Low accuracy present in normal individuals
  • Determines re-infarction as levels fall slower than troponin
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25
Q

ACS Sx + signs

A

Acute central chest pain >20mins

  • Nausea
  • Sweating
  • Vomitting
  • S.O.B
  • Feeling of impending doom
  • Pain radiating to arms/neck/jaw

Signs:

  • HR
  • BP
  • Reduced 4th Heart sound
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26
Q

Signs of silent MI + who experiences them

A
  • Elderley and DM pts
    Syncope
    Pulmonary oedema
    Vomitting
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27
Q

Alternative causes of raised troponins

A

Sepsis
Myocarditis
Aortic dissection
PE

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28
Q

NSTEMI and UA initial Tx

A 
M- Morphine (5-10mg)
O- 02 (SaO2<90%/S.O.B)
A- Asprin (300mg)
     \+Clopidogrel 
N - Nitrates - GTN spray

Additional:
Beta blockers
Anticoagulant
- LMWH (Enoxaparin)

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29
Q

Risk stratification NSTEMI

A

GRACE

  • 6m risk of death or repeat MI after NSTEMI
  • High risk if score>10%
  • Consider PCI to tx CAD

TIMI
- Thrombolysis In MI
Risk of dying from a heart event for pts with NSTEMI/UA

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30
Q

STEMI Patho

A 
Plaque rupture
thrombus 
occlusion 
Infammation
Myocardial cell necrosis
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31
Q

STEMI Sx + signs

A

Sx

  • Central chest pain
  • Radiates to arm/neck…
  • Sweating
  • S.O.B
  • Palpitations

Signs

  • Clammy
  • Pale
  • 4th heart sound
  • Pansystolic murmur
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32
Q

Acute STEMI managment

A

Morphine
Oxygen
Asprin + Ticagrelor (180mg)
Nitrates - GTN

B- Blocker
- Ensure no: HF/HB/COPD/Shock

STEMI ECG + PCI availabel in 2hrs?
Yes –> PCI
NO –> Fibrinolysis

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33
Q

Fibrinolysis

A

STREPTOKINASE
Plasminogen activation factors given
Plasmin cleaves fibrin to its degradation products breaking up the thrombus

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34
Q

STEMI Secondary management

A 
Asprin 
Antiplatelets - Clopidogrel 
Atorovostatin - (80mg)
ACEi - Titrated slowly
Atenolol - CI --> CCB

Lifestyle

  • Stop smoking + alcohol
  • Cardiac rehabilitation
  • Optomise tx for other conditions - DM/HTN
  • Mediterranian diet
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35
Q

Advice following STEMI

A

Quit job if:

  • Airline pilots
  • Drivers

Can return to work in 2 months

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36
Q

Differential Dx STEMI

A 
Cardio:
ACS
Aortic dissection 
Pericarditis 
Myocarditis

Lungs:
PE
Pneumonia
Pneumothorax

GI:
Oesophageal spasm

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37
Q

STEMI Complications

A
  • AV block
  • Cardiogenic shock
  • LV failure
  • PE
  • Pericarditis
  • Cardiac tamopnade
  • Mitral regugitation
  • Ventricular septal defect
  • Dresslers syndrome
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38
Q

ECG Leads visualisation

A

1 - Lateral –> Circumflex

2 - Inferior –> RCA

3 - Inferior –> RCA

aVR - Neutral
aVL - Circulflex
aVF - RCA

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39
Q

ECG chest leads

  • Heart area
  • Vessel
A 
SEE ALL LEADS 
V1 - Septal --> LAD
V2 - Septal --> LAD
V3 - Anterior --> RCA
V4 - Anterior --> RCA
V5 - Lateral --> Circumflex
V6 - Lateral --> Circumflex
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40
Q

Rules for ECG

A
  • All waves -ve in aVR
  • PR interval = 120-200ms
  • QRS <110ms
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41
Q

Heart failure defenition

A

CO inadequate to meet body’s requirements

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42
Q

Types of HF + Causes

A

Systolic

  • Failure to contract
  • EF <40%
  • IHD/MI/Cardiomyopathy
Diastolic 
- Inability to relax and fill 
- Normal EF as total volume decreased
- Reduced pre-load
- Tamponade
  Restrictive cardiomyopathy
  Constrictive pericarditis
  Obesity 
   HTN
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43
Q

Calculation for EF

A

= SV/Total volume

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44
Q

HF Causes

A 
IHD
HTN
Cardiomyopathy 
Arrhythmias --> Atrial fibrillation
Aortic stenosis 
Mitral regrug
Chronic lung disease
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45
Q

Types of output in HF and causes

A

HIGH

  • Anaemia
  • Pregnancy
  • HTN
LOW
- Decreased CO that fails to increase with exertion 
- Pump failure 
Systolic failure  due to decreased HR - Anti - arrhthmic drugs
- Excessive pre-load
FLuid overload
Mitral regurg
-Chronic increased afterload
Aortic stenosis 
HTN
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46
Q

How does HF occur

A

As heart begins to fail compensatory changes occur

Overtime these compensatory changes get overwhelmed causing pathological development

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47
Q

Compensatory changes in HF

A
  • Sympathetic stimulation
    Increased afterload through peripheral vasoconstriction and Increasing HR/contractility
  • RAAS
    Salt and water retention
    Increases afterload and preload through increased volume and vasoconstriciton
-Cardiac 
Ventricualr dilatation 
Ventricular remodelling 
  - Myocyte hypertrophy 
  - Interstitial fibrosis
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48
Q

Why is increased preload beneficial in HF

A

Failure of heart muscle means blood remain after systole resulting in increased preload
This stretches the myocardium
Frank starling
Maintains CO for a short period

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49
Q

Left sided HF Sx

A 
Exertional dyspnoea
Fatigue
Paroxusmal noctural dyspnoea
Cough - Frothy sputum 
Breathlessness 
Orthopnea
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50
Q

Left sided HF sings

A
  • Crepitations in lung bases
  • Tachycardia
  • Heart murmur
  • Pulmonary oedema
  • Cardiomegaly (Displaced apex beat)
  • 3rd/4th Heart sound
  • Reduced BP
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51
Q

Rght sided HF causes

A
  • Pre-existing LVF
  • Pulmonary stenosis
  • Cor pulmonale
  • Atrial/ventricular septal defect
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52
Q

Right sided HF Sx

A
  • Nausea

- Anorexia

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53
Q

Right sided HF Signs

A
  • Raised JVP
  • Hepatosplenomegaly
  • Ascites
  • Weigth gain (fluid)
  • Pitting oedema
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54
Q

Cause of paroxysmal noctural dyspnoea

A
  • Decreased adrenaline at night
  • Resp centres less responsive
  • Fluid settles over large S.A
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55
Q

What is used to classify severuty of Sx in HF

A 
New york Heart classification 
1. Asymptomatic 
2. Slight limitation 
    Comfortable at rest
3. Marked limitations 
    Limiting dyspnoea 
4. Dyspnoea present at rest
    Activtiy leads to discomfort
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56
Q

HF investigations

A

Bloods:
- Brain natriuretic peptide
Levels correlate with severity
- FBC/LFT/U+E/TFTs

ECG

  • Shows underlying causes
  • Ischaemia
  • LV hypertrophy
  • Arrhythmias

If BNP + ECG abnormal –> Echo

Echo - TTE

  • Assess cardiac chamber dimensions
  • Valvular disease
  • Wall abnormalities

CXR

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57
Q

Changes in CXR for HF

A 
A - Alveolar oedema 
B - Kerley B- lines
C - Cardiomegaly 
D - Dilated upper lobe vessels 
E - Pleural effusion
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58
Q

HF management

- Lifestyle

A 
Education 
Loose weight 
Stop smoking 
Decrease Alcohol 
Diet
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59
Q

HF Management Notes

A

Avoid exacerbating factors eg: Verapamil/ NSAIDs

Tx exacerbating factors
eg: Infection/ Anaemia

Annual flu and one off Pneumococcal vax

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60
Q

Acute HF tx

A
  • 100% O2
  • Nitrates - GTN
  • IV opiates - Diamorphine
  • IV furosemide (fluid overload)
  • Consider inotropic drugs
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61
Q

Chronic HF tx

A 
A - ACEi/ARB
B- Betal blocker 
A - Aldosterone antagonist 
      (Spirinolactone)
If A + B don't control sx
L - Lood diuretics 
     Digoxin

Consider CCB - Amlodopine fro vasodialtion

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62
Q

HF RF

A
  • Age>65
  • African desecent
  • Previous MI
  • Obesity
  • Men of Lack of protective effect from oestrogen resulting in early onset IHD
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63
Q

Why does HTN lead to HF

A
  • Increase arterial pressure
  • harder to pump in to HTN system
  • L.V hypertrophy
  • Increase O2 demand and decreased supply from C.A
  • Weaker contractions
  • Systolic failure
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64
Q

Why does dilated cardiomyopathy lead to HF

A
  • Chmaber grows to increase increase preload
  • Increase contraction and strength via FSM
  • Overtime muscles get thin and weak
  • Systolic failure
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65
Q

How do:

- Aortic stenosis, HTN and hypertrophic cariomyopathy lead to HF

A
  • Concentric myocyte hypertophy
  • Muscle crowds in to chamber doom
  • Diastolic failure
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66
Q

How does restrictive cariomyopathy lead to HF

A
  • Muscle stiffer and less compliant
  • Cant’t fill and stretch
  • Diastolic failure
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67
Q

How does IHD lead to HF

A

C.A atherosclerosis

MI

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68
Q

What is Cor pulmonale

A

Right sided HF caused by rep disease

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69
Q

Cor pulmonale causes

A
  • COPD
  • PE
  • CF
  • Interstitial lung disease
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70
Q

Cor pulmonale patho

A

Diseased lung leads to hypoxia

  • Hypoxic pulmonary vasoconstriciton
  • Increase pulmonary B.P
  • Harder for R.V to pump in against
  • Hypertrophy and failure
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71
Q

Acute HF

A

New onset/ Decompensated chronic HF

Charecterised by pulmonary and/or peripheral oedema without signs of peripheral hypoperfusion

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72
Q

Chronic HF

A

Devlops slowly
Venous congestion is common
Arterial pressure maintained until late

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73
Q

HTN diagnostic BP

A

Clinic = 140/90

Ambulatory BP = 135/85

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74
Q

HTN - Primary

A 
Essential HTN
- Unknown cause 
- Multifactoral 
genetic susceptibility 
obesity 
sedentary lifestyle
old age
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75
Q

HTN - Secondary

A

R - Renal disease
CKD - DM nephropathy
Renal artery stenosis
Glomerulonephritis

O - Obesity

P - Pregnancy induced HTN

E - Endocrine

  • Conn’s syndome
  • Cushings syndrome - Hypersecretion of corticosteroids enhances vasoconstrictive effects of adrenaline
  • Phaemochromocytoma

Aorta coarctation

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76
Q

Drugs assosciated with HTN

A 
Coricosteroids - Prednisolone 
EPO
Alcohol 
Ecstacy
Cocaine 
Contraceptive pill (Oestrogen)
NSAIDs
Vasopressin
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77
Q

HTN RF

A 
Age 
Male 
DM
Afro-carribean 
Obeaity 
Alcohol 
High salt diet 
Fam hx
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78
Q

HTN Complications

A

IHD
HF
Stroke
Haemorrhage

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79
Q

HTN CP

A

Headache
Visual disturbances
Usually asymptomatic apart from malignant HTN

Signs:
Bilaterral retinal haemorrhages and exudates
Papilloedema

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80
Q

HF main causes (3)

A

IHD
Dilated CM
HTN

81
Q

HTN Histological changes and untreated results

A

Fibrinoid necrosis of the vessel wall in untreated results in end organ damage

Renal - Haematuria/Proteinuria/Progressive Kidney disease

Brain -
Cerebral oedema/Haamorrhage

Retina -
Cotton wool spots/ hard exudates/papilloedema

CV
HF/Aortic dissection

82
Q

Diagnosing HTN

A

*Pt has BP >140/90
*Offer ABPM
Calculate Qrisk2 and look for end organ damage
- Fundoscopy - haemorrhage
- Urinalysis - Protein/blood
- Blood tests - eGFR
*ABPM <135/85 NO tx
* ABPM >135/85
tx if Qrisk2>20% or EOD
*ABPM >150/95
TX

83
Q

When should you always treat HTN

A

If there is end organ damage

84
Q

Tests for EOD

A 
Urine analysis 
*A:C - Proteinuria 
*Dipstick - Haematuria 
ECG/Echo - LV hypertophy 
Fundoscopy 
Bloods - HbA1c/eGFR/Lipids
85
Q

Stage 1 HTN

A

Clinic = >140/90

Ambulatory = >135/85

86
Q

Stage 2 HTN

A

Clinic > 160/100

Ambulatory >150/95

87
Q

Stage 3 HTN

A

BP > 180/110

Immediate ant-HTN tx

88
Q

BP equation

89
Q

HTN Tx

- Lifestyle

A 
Reduce alcohol 
reduce salt intake 
Excercise 
Loose weight 
Smoking cessation - CVD risk
90
Q

HTN tx

- Additional pharamacological tx

A

Statins - Reduce CVD risk

Optomise glycaemic control in pts with DM HbA1c<53mmol/mol

91
Q

HTN Tx pathway

A

<55y/o –> HIGH renin
>55y/o or Black –> LOW renin

A - ACEi
B-ARB
C - CCB
D - Diuretics

Add:
Spirinolacone
Alpha-blocker - hydralazine
Beta-blocker

92
Q

HTN treatment targets

A

Under 80 BP<140/90

Over 80 BP <150/90

93
Q

Common causes of chest pain

A

Angina
ACS
Pericarditis - Sharp pain aggrevated by movement, respiration and changes in posture
Aortic dissection - Severe chest pain radiating to back
GORD - Exacerbated by lying down
MSK - tender to palpate over affected areas
PE - dyspnoea/ Tachycardia/ Hypotension

94
Q

What is Bradycardia

A

Slow HR <60bpm

95
Q

What is tachycardia

A

Fast HR>100bpm

96
Q

Sinus arrhythmia

A
  • Results from fluctuations in autonomic tone
    Inspiration –> fall in PNS tone and HR quickens
    Expiration –> HR falls

Children and YA
Predictable changes in HR

97
Q

Sinus bradycardia

  • When is it normal
  • Extrinsic causes
  • Intrinsic causes
A
  • Sleep and athletes
  • Extrinsic
    Beta- blockers
    Anti- arrhythmic drugs
    Hypothyroidism
  • Intrinsic
    MI –> Acute ischaemia of SAN
98
Q

Sever symptomatic bradycardia tx

99
Q

Heart Block common causes

A

CAD
Cardiomyopathy
Fibrosis of conducting tissue

100
Q

Heart Block - AVN

- First degree

A
  • Delayed AV conduction
  • Every atrial impulse leads to ventricular contraction
  • Long PR interval (>0.2secs)
101
Q

Hear block - AVN

- Second degree

A

Some atrial impulses do not make it through AVN to ventricles

  • Mobitz type 1
  • Mobitz type 2
102
Q

HB - Mobitz type 1

  • Defenition
  • Causes
A

Wenckebach phenomenon

  • Longer-longer- longer- drop
  • Progressive PR interval elongation until beat is dropped and impulse fails to move through to ventriles
  • Absent QRS complexes

Causes:

  • AVN Blocking drugs
  • Inferior MI
103
Q

Mobitz type 2

  • defenition
  • causes
  • risks
  • Tx
A
  • QRS compexes dropped without PR interval prolongation
  • Specified ratio (Pwaves:QRS)

Causes:
- Inferior infarction

Risk:
Asystole

tx-
Pacemaker

104
Q

3rd degree HB

  • defenition
  • risks
A
  • P waves completely independent of QRS complexes
  • Ventricular contractions maintaind by escape rhythms
  • Risk of asystole

Causes:
HTN
Endocarditis
IHD –> MI

105
Q

Aropine

  • MOA
  • Indications
  • S/E
A
  • Inhibits PNS
  • Mobitx type 2
  • Complete HB

S/E

  • Pupil dilatation
  • Urinary retention
  • Dry eyes
  • Constipation
106
Q

RBBB

  • Causes
  • ECG findings
  • Oscultation
A

RBB no longer conducts
Late activation of R.V

Causes:

  • healthy individuals
  • PE
  • R.V Hypertrophy
  • IHD
  • Congenital HD (Fallot’s)

MaRRoW

  • M - QRS - V1
  • W - QRS - V6

Splitting of S2

107
Q

LBBB

  • causes
  • ECG findings
A

Late activation of L.V
Abnormal Q waves

Causes:

  • Aortic stenosis
  • HTN
  • Cardiac surgery

WiLLiaM
W - QRS - V1
M - QRS - V6

108
Q

Sinus tachycardia

A
  • Excercise
  • Excitement
  • Fever
  • Pain
  • Anaemia
  • HF
109
Q

Narrow comlex tachy

A

QRS <120ms

  • A.Fibrillation
  • A.Flutter
  • SVT
110
Q

Broad complex tachy

A

QRS >120ms

- VT

111
Q

What is AVNRT

- ECG

A

AV nodal re-entrant tachycardia

  • Fast HR caused by electrical signals that loop back on themselves
  • Narrow complex tachycardia
  • Self perpetuating electrical loop where the re-entry point is back through the SAN

ECG:

  • QRS –> T-wave–>QRS
  • No Pwave visible as Atria and ventricles recieve impulses at the same time
112
Q

What is AVRT

A

AV re-entrant tachycardia
- Re-entrant loop via accessory pathway
Wolff - parkinson white syndrome
- Incomplete atria and ventrical separation during development

113
Q

Wolff - Parkinson white syndrome

  • defenition
  • bundle name
  • ECG chnages
  • CP
  • Tx
A
  • Accessory electrical pathway connecting atria and venticles
  • Bundle of Kent

ECG

  • Short PR interval
  • Wide QRS complex
  • Delta wave
-CP
Palpitations 
dizziness 
syncope 
dyspnoea
114
Q

SVT Tx

A
  1. Vagal manoevers
    - carotis massage
    - Valsalva manoevere
    - Breath hold
  2. Adenosine
    complete HB for 1/4sec
  3. Direct current cardioversion
115
Q

WPWS Tx

A

Radiofrequency catheter ablation of accessory pathway

116
Q

Adeosine

- CI

A

Slows cardiac conduction through AVN
Resets sinus rhythm

  • brief asystole

CI

  • HB
  • COPD
  • HF
117
Q

Shockable heart rhythms

118
Q

Ventricular fibrillation

  • Defenition
  • ECG
  • Tx
A
  • Rapid and irregular ventricular activation with no mechanical effect –> NO CO
  • Pt is pulseless, unconscious and resp stops –> C.A
  • Usually caused by ventricular ectopic beats

ECG:

  • Shapeless rapid oscillations
  • No organised complexes

Tx:

  • Electrical defib
  • Cardioverter - defibrillators
119
Q

AF

  • Defenition
  • Causes
A

Chaotic irregular atrial rhythm - 300-600bpm
Intermitent response from AVN so irregular ventricular rate

Sepsis
Mitral stenosis 
IHD 
Thyrotoxicosis 
HTN
120
Q

Risk of AF

A

Embolic stroke

121
Q

AF CP

A

Sx

  • chest pain
  • palpitations
  • dyspnoea
  • faintness

Signs

  • irregular pulse
  • No p waves on ECG
  • Rapid irregular QRS rhythm
122
Q

AF DD

A

Atrial flutter

Ventricualr ectopics

123
Q

AF Dx

A

ECG

  • No p waves
  • rapid irregular QRS complexes
124
Q

AF TX

A

Acute - alcohol toxivity/chest infection
tx provoking cause

  • Cardioversion
  • LMWH - Enoxaparin - thromboembolism
  • Cadioversion fails –> Anti-arrhthmic - Amioderone
125
Q

What are most patients with AF usually on

126
Q

What is used to calculate the risk of stroke therfore the need for anti-coag

A 
CHA2-DS2-VASc Score
C - CCF
H - 
A2 - Age >75
D - DM
S2 - Stroke
V - Vascular disease 
A - Age (65-74)
Sc - - Female 
1 = consider asprin or anticoag
2 = oral anti-coag required
127
Q

Atrial flutter

  • Definition
  • causes
A

Abnormal but organised atrial rhythm
250-350bpm

Idiopathic
HTN
HF
Pericarditis
COPD
Obesity 
CHD
128
Q

Atrial flutter CP

A 
Palpitations 
chest pain 
dizziness
syncope 
fatigure
breathlessness
129
Q

Atrial flutter Dx

A

saw-tooth like atrial flutter waves - F waves

- if not visiable –> carotid sinus massage

130
Q

Atrial flutter

A
  • radiofrequency catheter ablation
  • IV Amioderone - sinus rhythm
  • B-blocker - suppresses arrhthmias
131
Q

Aneurysm defenition

A

permanent dilation of artery 2x normal diameter

132
Q

Aneurysm
Symmetrical
Asymetrical

A
  • Fusiform

- Saccular

133
Q

True aneurysm

A 
- dilations involving all 3 layers of arterial wall
Aorta - A + T
Iliac 
popliteal 
femoral
134
Q

False aneurysm

A

hole in B.V allows leakage
blood collects in adventitia
surrounding tissue acts as wall

135
Q

Where do most aneurysms occur specifically

A

40% - T
60% - A
* below branching of renal artery but above aortic birfucation
- less elastine so weaker

136
Q

AAA RF

A 
HTN
Familh hx
smoking 
male 
trauma 
hyperlipidaemia 
Male 
atherosclerotic damage
137
Q

AAA CP

A

unruptured - no sx

  • pain: abdo/back/loin
  • pulsatile abdo swelling

ruptured

  • abdo pain
  • pulsatile abdomen
  • collapse
  • tachy
  • hypotension
138
Q

AAA DD

A

GI bleed
ischaemic bowel
perforated ulcer
appendicits

139
Q

AAA Dx

A
  • US

- CT/MRI

140
Q

AAA Tx

A

RF-
smoking cessation
BP control
Statind

small <5.5cm - monitered

open surgical repair
Endovascular stenting

141
Q

TAA

  • Ascending
  • descending
A
  • Marfans/ HTN

- secondary to atherosclerosis

142
Q

TAA CP

A

asymptomatic

  • chest pain
  • aortic regurgitation
  • compression of local structures –> IVC
  • Cardiac tamponade
143
Q

TAA Dx

A
  • Transoesophageal echocariography
  • US
  • CT/MRI
144
Q

Aortic dissection defenition

A
  • Tear of tunica intima
  • blood flows between layers of aorta wall increasing diameter of vessel
  • collects in false lumen
145
Q

AD causes + RF

A 
HTN
Stress
Pregnancy - increase B.V
coarctation of aorta
Aneuryrsm
Trauma - shearing forces

RF:
Ehlers danlos
Marfans

146
Q

AD CP

A
  • Tearing chest pain
  • pain radiates to back and arms
  • HTN
  • Hypotension
  • shock
  • absent peripheral pulses
147
Q

AD DD

A 
MI 
ACS
Aortic regurgitation 
MSK pain 
Pericarditis
148
Q

AD Diagnosis

A

CXR - widened mediastinum

CT scan

Transoesophageal echo

MRI

149
Q

What law is applied to aortic dissections

A

Laplaces law

  • increase diameter
  • increase tension
150
Q

Aortic aneurysm complications

A
  • Aortic insufficiency
    pulls on valve as it dilates
    blood flows back to ventricles during diastole
  • high pitched cough
    LRL nerve stretched
  • Blood clots
    blood polls in extra lumen space
  • Headache + can’t flex neck fowards
    bleeding into SA space
    increases pressure
    irritates meninges
151
Q

Aortic Dissection tx

A
  • analgesia - morphine
  • resuscitation
  • surgery
    replace arch
    surgical stenting
  • control HTN - B-blockers
    - GTN
152
Q

What is peripheral vascular disease

A

Partial blockage of peripheral vessels by an atherosclerotic plaque resulting in insuffecient perfusion of lower limb

153
Q

Peripheral vascular disease RF

A 
Smoking 
obesity 
HTN 
DM 
Sedentary lifestyle 
High cholesterol
154
Q

Peripheral vascular disease symptoms

A 
Pain 
Pallour 
Perishingly cold 
Pulseless
Paralysis 
Parasthesia
155
Q

Pericardium function

A

Promotes cardiac efficiancy
- limited dilation

Aids atrial filling

  • creates a closed chamber
  • Decrease external friction

Anatomically fixes heart to sternum and diaphragm

156
Q

Acute pericarditis aetiology

  • Infectious
  • non infectious
A
  • Infectious
    Viral
  • coxsackie viruses
  • EBV / HIV/ Mumps

bacterial
- Mycobacterium TB

Fungal
- Histoplasa spp –> immunocompromised

  • Non infectious
  • Rhemuatoid arthiritis
  • Uraemia
157
Q

Acute pericarditis clinical presentation

A 
Fever 
chest pain  
- worse with deep breathing 
- relieved by sitting and leaning foward 
Hiccups 
pericardial friction rub - auscalltation 
tachycardia 
pain radiates to arm - trapezius ridge
158
Q

Acute pericarditis DD

A 
Pneumonia 
angina 
MI 
Aortic dissection 
Pneumothorax
159
Q

Acute pericarditis diagnosis

A
  • ECG
    saddle shaped ST elevation –> ALL leads
    PR segment depression

-CXR
rule out effucion (>300ml to be detectable)

160
Q

Acute pericarditis tx

A
  • NSAIDs
  • Colchicine –> 3m course
    S/E - Nausea and diarrhoea
161
Q

How does pericardial effusion lead to tamponade

A

large volume of fluid collects in pericardial sac
ventricullar filling compramised so decrease in CO
Cardiac tamponade

162
Q

Pericardial effusion presentation

A 
chest pain 
dyspnoea 
muffled heart sounds 
compression of local structures 
- Hiccough - phrenic nerve - spasm of diaphragm 
- nausea - diaphragm
163
Q

cardiac tamponade presentation

A 
increase pulse 
decrease BP 
Increase JVP 
Kussmauls sign 
Pulsus paradoxus - large decreases S.V and Systolic BP during inspiration
164
Q

Pericardial effusion diagnosis

A

CXR - large globular heart
ECG - low voltage QRS complex
Electrical alternans - Diff heights QRS complexes
Echo - echo free zone

165
Q

Cardiac tamponade diagnosis

A 
CXR - Big globular heart 
ECG - Low voltage QRS 
           Electrical altercans 
Echo - Echo free zone 
            Diastolic collapse - R.A/R.V 
Bck's triad - Falling BP 
                    Rising JVP 
                    Muffled heart sounds
166
Q

Pericardial effusion tx

A

analgesia
pericardiocentisis –> Send fluid for culture
- ZN stain/ TB culture / Cytology

167
Q

constrictive pericarditis presentation

A 
Kussmauls sign 
right HF signs 
Ascites 
Oedema 
Diffuse apex beat
168
Q

Constrictive pericarditis diangosis

A

CXR - small heart + calcification
ECG - low voltage QRS
Echo - small ventricular cavaties with normal wall thickness
CT/MRI - distinguish from restrictive CM

169
Q

Where does infective endocarditis occur (3)

A
  • valves with congenital/aquired defects
    RS endocarditis more common in IVDU
  • Normal valves with virulent organisms
  • Prosthetic valves/ pacemakers
170
Q

Which organism most commonly causes infective endocarditis and descibe it

A 
Viridans streptococci 
Gram +ve 
alpha haemolytic 
optochin resistant 
low virulence
171
Q

Where is viridans step found and what type of valves are at risk

A

found in mouth

attacks previously damaged valves

172
Q

Where is S.aureus found and which groups of people are at risk from infective endocarditis caused by it

A

Skin

IVDU
diabetic
surgery

Attacks healthy or previously damaged valves (Tricuspid)

173
Q

S. epidermidis

  • valves
  • route of entry
A
  • Prosthetic

- Valve surgery/ IV catheter - HOSPITAL

174
Q

RF for infective endocarditis

A 
IVDU 
Poor dental hygeine 
Dental treatement 
Prosthetic valve
Pacemaker
Cardiac surgery 
congenital heart defects
175
Q

Infective endocarditis presentation

A

systemic features of infection

  • malaise
  • fever
  • night sweats
  • weight loss

Signs:

  • Spliter haemorrhage (Septic emboli deposit)
  • Janeway lesions
  • Oslers nodes - fingers and toes
  • Roth spots - eyes
  • Glomerulonephritis
  • Arrhythmias
  • HF
  • PE/Stroke/MI
  • Murmur - turbulent flow past damged valve
176
Q

what presentation of a pt requires infective endocarditis ruling out

A

Heart murmur and fever

177
Q

Infective endocarditis diagnosis

A

Blood cultures - 3 from 3 different sites
- take before Abx

Blood test -
High ESR and CRP
Neutrophilia

Echo - Transoesophageal

ECG -
Long PR intervals

178
Q

Infective endocarditis initial tx

A

Presuming not staph

- Benzylpenicillin + Gentamycin

179
Q

Criteria for infective endocarditis diagnosis

A

Duke’s classification

180
Q

Tx for suspected staphylococcus infective endocarditis

A

Vancomycin swapped for penicillin

181
Q

Infective endocarditis preventions

A
  • Abx prophylaxis to high risk groups before procedure
    Prosthetic valves
    Hx of transpalnt
    Hx of IE
  • Good oral health
  • Inform pts of IE sx
182
Q

Aortic valve ausculltation

A

2nd intercostal space - Right sternal edge

183
Q

Aortic stenosis aetiology

A
  1. Ageing - Degeneration and calcification of normal valve
  2. Congenital - Clacification of congenital bicuspid valve
  3. Rheumatic heart disease - scar tissue formation
184
Q

Aortic stenosis patho

A

narrowing of valve = obstructed L.V emptying
Increase pressure gradient between aorta and L.V resulting in increased afterload
Increase L.V pressure
Compensatory L.V hypertrophy
- Increased myocardial demand
- relative ischaemia –> Angina / Arrhythmia

185
Q

Aortic stenosis presentation

A

Angina
Syncope - exertional
HF

Signs:

  • Dizziness
  • Decrease carotid pulse - SLOW RISING
  • Decrease intensity of 2nd heart sound
  • Murmur
186
Q

Aortic stenosis diagnosis

A
  1. Echo - diagnostic
    L.V hypertorphy
  2. CXR
    - Calcified aortic valve
    - L.V hypertrophy
  3. ECG
    - L.V hypertrophy
    - Depressed ST Segments
187
Q

Aortic stenosis tx

A
  1. Trancutaneous aortic valve implantation - cracks calcification
  2. Aortic valve replacement

Infective endocarditis prophylaxis

188
Q

Aortic regurg aetiology

A

Rheumatic fever
IE
Bicuspid aortic valve

189
Q

Aortic regug presentation

A

exertional dyspnoea
palpitations
angina

Signs:
collapsing pulse 
wide pulse pressure 
Ascites 
displacement of apex beat
190
Q

Aortic regurg diagnosis

A

CXR -
enlarged cardiac silouhette
Aortic root enlargement

ECG -
L.V hypertrophy - tall R waves
Inverted t waves

Echo

191
Q

Mitral regurg aetiology

A
  1. mitral valve prolapse
  2. papillary muscle damage - post MI
  3. IE
  4. LSHF
  5. Rheumatic fever
192
Q

Mitral regurg presentation

A

Exerional dyspnoea
fatigue
palpitations

signs:
AF
Apex beat displaced laterally
Soft S1

193
Q

Mitral regug diagnosis

A
  • ECG - Severe MR
    AF
    LV hypetrophy + LA enlargement
  • CXR - LA enlargement
  • Transoesophageal echo
194
Q

Mitral regurg tx

A

Mild - serial echos

Meds:
ACEi
B- blockers - HR control for AF
Diuretics for overload

195
Q

Mitral valve stenosis aetiology

A
  1. rheumatic fever
    - commisural fission
  2. IE
  3. Mitral annular calcification
    - elderly
    - end stage renal disease
196
Q

Mitral stenosis presentation

A

Progressive dyspnoea

  • pulmonary HTN + Congestion
  • worse with excercise/pregnancy

Dysphagia and hoarse voice
- pressure on local structures

Fatigue
chest pain
palpitations

197
Q

Mitral stenosis signs

A

Malar flush
Low volume pulse
S1 - loud snap

RSHF

  • Increae JVP
  • Ascites
  • Peipheral oedema
198
Q

Mitral stenosis diagnosis

A

ECG:

  • LA enlargement - Bifid P wave
  • AF

CXR

  • LA enlargement
  • Pulmonary congestion

ECHO - GOLD

199
Q

why is lidocaine effective in VT tx

A

Blocks inactivation gate of the sodium channel

Phase 2a (11 decks)

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