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Phase 2 > Cardio > Flashcards

Cardio Flashcards

1
Q

What are the risk factors for atherosclerosis (7)

A
  • Increasing age
  • Smoking
  • Diabetes
  • High cholesterol
  • Hypertension
  • Family history
  • Obesity
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2
Q

Describe the pathophysiology of atherosclerosis formation

A
  • 1st stage (fatty streaks) - Endothelial damage causes attraction and accumulation of lipid laden macrophages and T-lymphocytes in the vessel wall
  • 2nd stage (intermediate lesions) - Layers of lipid laden macrophages and T-lymphocytes in the vessel wall with platelet aggregation and adhesion
  • 3rd stage (fibrous plaques) - Dense fibrous cap formed on the lesions with fibrin filling of lesion. Prone to rupture and partially occlude arteries
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3
Q

What is stable angina

A
  • Chest pain or exercise that is a result of reversible myocardial ischaemia
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4
Q

What are the risk factors for stable angina (7)

A
  • Obesity/sedentary lifestyle
  • Smoking
  • Hypertension
  • High cholesterol
  • Diabetes
  • Family history
  • Increasing age
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5
Q

How might stable angina present (3)

A
  • 1) Central crushing chest pain radiates to jaw/right arm
  • 2) Brought on by exercise
  • 3) Relived by rest/GTN
  • 3/3 = typical angina, 2/3 = atypical angina, 1/3 = non-anginal pain
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6
Q

How do you diagnose stable angina (3)

A
  • ECG (may be normal or show ST depression)
  • CT Ca scoring (shows up as white)
  • Exercise ECG
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7
Q

How do you treat stable angina (7)

A
  • Lifestyle modification
  • Beta blockers (reduces HR and contractility by increased filling time hence sec. load on heart)
  • GTN spray (dec. afterload by arterial vasodilation and cornary artery vasodilation)
  • Aspirin
  • Statins (simvastatin)
  • CCB (verapamil)
  • PCI/revasc./CABG
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8
Q

What are the types of acute coronary syndrome (ACS) (3)

A
  • STEMI (complete major coronary artery blockage)
  • NSTEMI (partial major or complete minor coronary artery blockage)
  • Unstable angina (<24hrs onset, symptoms at rest, worsening of stable)
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9
Q

How might ACS present (6)

A
  • Acute severe central crushing chest pain, radiates to arm/neck/jaw
  • Sweating
  • Nausea and vomiting
  • Shortness of breath
  • Palpitations
  • Tachycardic and hypotensive
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10
Q

How do you diagnose ACS (3)

A
  • ECG (STE/STD/ tall T)
  • Raised troponin/CT-MB
  • Trans-thoracic echo
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11
Q

How do you treat ACS acutely (8)

A
  • MOANA
  • Morphine
  • Oxygen
  • Aspirin/clopidogrel
  • Nitrates
  • Atenolol
  • PCI (must be in 120 mins)
  • CABG
  • Fibrinolysis
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12
Q

How do you manage ACS (7)

A
  • Lifestyle modification
  • Statins
  • Beta blockers
  • ACE inhibitors
  • Aspirin
  • Warfarin
  • CCB
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13
Q

What are the potential complications of ACS (3)

A
  • Arrhythmia
  • Pericarditis
  • Heart failure
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14
Q

What is the definition of heart failure

A
  • Inability of the heart to deliver sufficient blood, hence oxygen to metabolising tissues
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15
Q

What are the main causes of heart failure (4)

A
  • Ischaemic heart disease (most common)
  • Valvular disease
  • Cardiomyopathy
  • Hypertension
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16
Q

What are the risk factors for heart failure (5)

A
  • Increasing age
  • Previous MI
  • Male
  • Obesity
  • African
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17
Q

Describe the pathophysiology of heart failure

A
  • As heart begins to fail various compensatory physiological changes occur
  • Sympathetic input increases HR and contractility
  • Renin-angiotensin system increases venous return hence increasing contractility
  • However as failure progresses the changes become pathophysiological eg. inc. HR and contractility means increased work load causing myocardial ischaemia
  • This is known as decompensation
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18
Q

How might heart failure present (5)

A
  • Triad of shortness of breath, fatigue and ankle oedema
  • Ascites
  • Cold peripheries/cyanosis
  • Hypotension/tachycardia
  • Bi-basal crackles
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19
Q

How do you classify heart failure symptoms

A
  • New york heart association classification
  • Class 1 - asymptomatic
  • Class 2 - symptoms on moderate exercise
  • Class 3 - symptoms on mild exercise
  • Class 4 - symptoms at rest
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20
Q

How do you diagnose heart failure (3)

A
  • CXR (cardiomegaly)
  • Brain natriuretic peptide (released by ventricles in response to strain)
  • Echo
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21
Q

How do you treat heart failure (6)

A
  • Lifestyle change
  • Diuretics (spironalactone (k+ sparing)/ furosemide)
  • ACE inhibitors/ angiotensin 2 R.B (canderstan)
  • Beta blockers (atenolol)
  • Revascularisation
  • Transplant in young
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22
Q

What is the epidemiology of hypertension (3)

A
  • More common in men
  • Increases with age
  • More common in black people
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23
Q

What are the stages of hypertension (3)

A
  • Stage 1 - >140/90 in clinic or >135/85 at home
  • Stage 2 - >160/100 in clinic or >150/95 at home
  • Severe - >180 syst. and/or >110 dias.
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24
Q

What are the risk factors for hypertension (6)

A
  • Black
  • Increasing age
  • Male
  • Diabetes
  • Smoking
  • High salt diet
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25
Q

How do you diagnose hypertension (2)

A
  • Clinical examination

- 24 hour ambulatory monitoring

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26
Q

How do you treat hypertension

A
  • Aim for 140/90
  • <55 1st line ACE-i or ARB
  • > 55 or afro-Caribbean 1st line CCB
  • 2nd line ACI-i and CCB
  • 3rd line ACE-i and CCB and thiazide diuretic
  • 4th line add Beta blocker or spironalactone
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27
Q

What is atrial fibrillation (AF)

A
  • A chaotic irregular atrial rhythm of 300-600 bpm with irregular ventricular response and hence rhythm
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28
Q

What is the epidemiology of AF

A
  • Most common arrhythmia

- More common in males

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29
Q

What are the causes of AF

A
  • CAD
  • Cardiomyopathy
  • Cardiac surgery
  • Hypertension
  • Heart failure
  • Idiopathic
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30
Q

Describe the pathophysiology of AF

A
  • Rapid irregular depolarisation of the atria with poor contractile response leading to atrial spasm
  • Irregular ventricular response
  • CO decreases due to poor ventricular filling
  • Blood pools in atria and clots causing increased risk of embolism
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31
Q

How might AF present (5)

A
  • Palpitations
  • Chest pain
  • Shortness of breath
  • Fatigue
  • Syncope
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32
Q

How do you diagnose AF

A
  • ECG (absent P waves, irregular, rapid QRS)
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33
Q

How do you treat AF (5)

A
  • Cardioversion (LMW heparin - enoxaparin)
  • Warfarin
  • Anti-arrhythmic (amoidarone)
  • CCB (verapamil) - Blocks AV node
  • Beta blockers (atenolol) - Controls HR
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34
Q

What is atrial flutter

A
  • A rapid regular organised atrial rate 250-350 bpm
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35
Q

What is the epidemiology of atrial flutter (3)

A
  • Often associated with AF
  • More common in males
  • Increases with age
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36
Q

How might atrial flutter present (5)

A
  • Palpitations
  • Syncope
  • Fatigue
  • Chest pain
  • Shortness of breath
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37
Q

How do you diagnose atrial flutter

A
  • ECG (sawtooth)
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38
Q

How do you treat atrial flutter (4)

A
  • Cardioversion (LMW heparin - enoxaparin)
  • Warfarin
  • Anti-arrhythmic (amoidarone)
  • Beta blockers (atenolol) - Controls HR
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39
Q

Describe 1st degree AV block

A
  • P-R enlongation without QRS drop
  • Caused by AV blocking drugs (CCB/BB) and inferior MI
  • Asymptomatic and no treatment
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40
Q

What are the two types of type 2 AV block

A
  • Mobitz I and II
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41
Q

Describe Mobitz I AV block

A
  • Progressive Q-R elongation then QRS drop then reset
  • Caused by inferior MI and AVN blocking drugs (CCB/BB)
  • Syncope, dizziness, fatigue
  • Pacemaker if poorly tolerated
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42
Q

Describe Mobitz II AV block

A
  • P-R interval constant with QRS dropping
  • Caused by inferior MI and AVN blocking drugs (CCB/BB)
  • Syncope, chest pain, SOB and hypotension
  • Pacemaker
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43
Q

Describe type 3 AV block

A
  • No conduction of atrial depolarisation to ventricles
  • Complete block at AV node
  • Ventricular rhythm sustained by spontaneous depolarisation below AV node
  • Syncope, chest pain, SOB and hypotension
  • P completely independent of QRS
  • Pacemaker insertion
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44
Q

What is the epidemiology of mitral valve stenosis (3)

A
  • Normal = 4-6cm symptoms start at <2cm
  • More common in men
  • Usually secondary to rheumatic HD
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45
Q

Describe the pathophysiology of mitral valve stenosis

A
  • Narrowing and stiffening of mitral valve causes decreased blood flow from LA-LV
  • To maintain CO, LA hypertrophy and dilatation occurs
  • This causes secondary PH and PO and PH causes RV hypertrophy/dilatation
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46
Q

How might mitral valve stenosis present (6)

A
  • Progressive shortness of breath/dyspnoea
  • RH failure (ankle oedema/fatigue/SOB)
  • Haemoptysis due to PH
  • Palpitations (AF can occur)
  • Malar flush (pink/purple cheek discolouration)
  • Heart sounds
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47
Q

How do you diagnose mitral valve stenosis (3)

A
  • CXR (stenosed mv and RV/LA hypertrophy)
  • ECG (AF and RV/LA hypertrophy)
  • Echo (gold standard)
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48
Q

How do you treat mitral valve stenosis (4)

A
  • Beta blockers
  • Diuretics for oedema
  • Percutaneous mitral balloon valvotomy
  • Mitral valve replacement
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49
Q

What is the epidemiology of mitral regurgitation (2)

A
  • Due to abnormality in chordae tendinae, LV, leaflets of valve or papillary muscles
  • Most commonly due to myxomatous degeneration (weakening of chordae tendinae)
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50
Q

Describe the pathophysiology of mitral regurgitation

A
  • Systolic leak of blood from LV to LA
  • Leads to LA dialtation and LV hypertrophy/dilatation in an attempt to maintain CO
  • LA dilatation causes PH and RV hypertrophy/dilatation
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51
Q

How might mitral regurgitation present (4)

A
  • Shortness of breath/dyspnoea
  • RV failure (oedema/fatigue/SOB)
  • Raised SV felt as palpitation
  • Heart sounds
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52
Q

How do you diagnose mitral regurgitation (3)

A
  • CXR (LV/LA/RH enlargement)
  • ECG (LV/RV hypertrophy)
  • Echo.
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53
Q

How do you treat mitral regurgitation (3)

A
  • Beta blockers
  • Diuretics
  • Surgery
54
Q

What is the epidemiology of aortic stenosis (3)

A
  • Normal area is 3-4cm symptoms at less than 1
  • Mostly disease of ageing, but also congenital
  • Most common valve disease
55
Q

What are the types of aortic stenosis (3)

A
  • Supravalvular
  • Valvular (most common)
  • Subvalvular
56
Q

Describe the pathophysiology of aortic stenosis

A
  • Decreased blood flow from LV to aorta leads to LV hypertrophy and dilatation in an attempt to maintain CO against increased afterload
  • This also causes relative LV ischaemia causing angina, arrhythmia and failure
57
Q

How might aortic stenosis present (5)

A
  • TRIAD
  • Angina
  • Shortness of breath
  • Syncope
  • Slow rising carotid pulse and decreased pulse amplitude
  • Heart sounds
58
Q

How do you diagnose aortic stenosis (3)

A
  • CXR (LV enlargement + calcified aortic valve)
  • ECG (LV hypertrophy + arrhythmia)
  • Echo.
59
Q

How do you treat aortic stenosis (2)

A
  • Aortic valve replacement

- Transcutaneous aortic valve implantation

60
Q

What is the epidemiology of aortic regurgitation (3)

A
  • Mostly caused by congenital bicuspid aortic valve
  • Also infective endocarditis and rheumatic HD
  • May be associated with aortic stenosis
61
Q

Describe the pathophysiology of aortic regurgitation

A
  • Reflux of blood form aorta to LV
  • LV hypertrophy occurs to maintain CO
  • Due to hypertrophy and decreased perfusion of coronary arteries LV ischaemia and angina occurs
62
Q

How might aortic regurgitation present (6)

A
  • Angina
  • Shortness of breath/dyspnoea
  • Wide pulse pressure
  • Palpitations
  • Syncope
  • Heart sounds
63
Q

How do you diagnose aortic regurgitation (3)

A
  • CXR (LV hypertrophy and aortic root dilation)
  • ECG (LV hypertrophy)
  • Echo
64
Q

How do you treat aortic regurgitation (2)

A
  • ACE-inhibitors

- Valve replacement

65
Q

What are the risk factors for infective endocarditis (5)

A
  • Elderly
  • Congenital heart disease
  • Poor dental hygiene
  • IV drug use/iv cannula
  • Heart surgery/pacemaker
66
Q

What organisms cause infective endocarditis (3)

A
  • Staph. areus (most common)
  • Strep. viridans
  • Pseudomonas aeruginosa
67
Q

Describe the pathophysiology of infective endocarditis

A
  • Combination of organisms in blood and abnormal cardiac endothelium allowing adherence and growth
  • Vegetation grows on valves, most commonly on mitral/aortic (except in iv drug use affects RH)
  • Causes valvular destruction and hence worsening HF
68
Q

How might infective endocarditis present (8)

A
  • Headache/fever/myalgia/sweats
  • Splinter haemorrhage
  • Embolic skin lesions
  • Finger clubbing
  • Osler nodes - tender nodules in the digits
  • Janeway lesions - haemorrhages and nodules in the fingers
  • Roth spots - retinal haemorrhages
  • Petechiae
69
Q

How do you diagnose infective endocarditis (3)

A
  • Transoesophageal echo
  • Blood cultures (3 different sites in 24 hours)
  • FBC (raised ESR/CRP/anaemia)
70
Q

How do you treat infective endocarditis (3)

A
  • Staph. areus vancomycin + Rifampicin
  • Step. viridans Gentamycin + benzylpenicillin
  • Surgery to replace infected valve
71
Q

What is the epidemiology of hypertrophic cardiomyopathy (3)

A
  • 2nd most common cardiomyopathy
  • Autosomal dominant
  • Most common cause of sudden cardiac death in young
72
Q

Describe the pathophysiology of hypertrophic cardiomyopathy

A
  • Ventricular hypertrophy of no other cause
  • Caused by sarcomeric protein gene mutation
  • Ventricles become less compliant leading to decreased filling and hence decreased CO
73
Q

How might hypertrophic cardiomyopathy present (5)

A
  • Angina/chest pain
  • Shortness of breath/dyspnoea
  • Syncope
  • Palpitation/arrhythmia
  • Jerky carotid pulse
74
Q

How do you diagnose hypertrophic cardiomyopathy (3)

A
  • ECG (LV hypertrophy)
  • Echo
  • Genetic testing
75
Q

How do you treat hypertrophic cardiomyopathy (3)

A
  • Anti arrythmic (amoidarone)
  • Beta blocker
  • CCB
76
Q

What is the epidemiology of dilated cardiomyopathy (3)

A
  • Most common cardiomyopathy
  • Autosomal dominant
  • May also be caused by alcohol, ischaemia and thyroid issues
77
Q

Describe the pathophysiology of dilated cardiomyopathy

A
  • Cytoskeletal gene mutations
  • Dilatation of ventricles or all 4 cardiac chambers
  • Thin muscle layer means poor contractility and hence CO is low
78
Q

How might dilated cardiomyopathy present (5)

A
  • Chest pain/angina
  • Shortness of breath/dyspnoea
  • HF (oedema, fatigue, SOB)
  • Palpitations/arrhythmia
  • Raised jugular venous pressure
79
Q

How do you diagnose dilated cardiomyopathy (2)

A
  • CXR (cardiomegaly)

- Echo

80
Q

How do you treat dilated cardiomyopathy

A
  • Treat HF and arrhythmia
81
Q

Describe eisenmengers syndrome

A
  • Initial L to R shunt as left pressure > right pressure
  • This causes increase in pulmonary blood flow, resulting in increased pulmonary artery vascular resistance
  • This initiates an increase in RH pressure above LH pressure
  • This causes the shunt to reverse, so now is R to L
  • This causes cyanosis
82
Q

What is the epidemiology of atrial septal defects (ASD) (3)

A
  • 1/3 of congenital HD
  • Often presents in adulthood
  • More common in women
83
Q

Describe pathophysiology of ASD

A
  • Hole in atrial septum (wall)
  • Shunt from L to R
  • Can reverse with PH (eisenmengers)
84
Q

How might ASD present (4)

A
  • Shortness of breath/dyspnoea
  • Cyanosis
  • Palpitation/arrhythmia
  • Murmur
85
Q

How do you diagnose ASD (3)

A
  • CXR (cardiomegaly/large PA)
  • Echo.
  • ECG (RBBB)
86
Q

How do you treat ASD

A
  • Surgical or percutaneous closure
87
Q

What is the epidemiology of ventricular septal defects (VSD) (2)

A
  • 20% of congenital HD

- Many close spontaneously during childhood

88
Q

Describe the pathophysiology of VSD

A
  • Shunt R to L

- May reverse/ PH (eisenmengers)

89
Q

How might VSD present (5)

A
  • Cyanosis
  • Small skinny baby
  • Raised resp. rate
  • Tachycardia
  • Murmur
90
Q

How do you diagnose VSD (2)

A
  • Echo

- CXR (cardiomegaly)

91
Q

How do you treat VSD (3)

A
  • Small = none
  • Medium = ACE-i and diuretics
  • Surgical closure
92
Q

What is the epidemiology of AVSD (2)

A
  • Associated with downs syndrome

- Instead of two AV valves one large leaky malformed one

93
Q

How might AVSD present (3)

A
  • Cyantic, breathless baby
  • Tachycardia/ raised resp. rate
  • Poor weight gain/feeding
94
Q

How do you treat AVSD

A
  • Surgical repair/PA banding
95
Q

Describe the epidemiology of peripheral vascular disease (2)

A
  • More common in men

- Mostly caused by atherosclerosis

96
Q

Describe Chronic lower limb ischaemia (4)

A
  • Exercise induced
  • Partial blockage causes decreased oxygen delivery caused increased lactic acid production
  • Crampy pains on exercise, relived by rest
  • Cold limbs
97
Q

Describe critical limb ischaemia (4)

A
  • Symptoms at rest, usually nocturnal
  • Relieved by hanging limb out of bed
  • Blood supply barely adequate for normal metabolism
  • May lead to infarct/gangrene
98
Q

Describe acute limb ischaemia (6)

A
  • 6ps
  • Perishing cold
  • Pallor
  • Pain
  • Paralysis
  • Paraesthesiae
  • Pulseless
99
Q

How do you diagnose limb ischaemia (2)

A
  • Colour duplex ultrasound

- CT/MR angiography

100
Q

How do you treat limb ischaemia (6)

A
  • Acute
  • Revasc./thrombolysis
  • Chronic/critical
  • Warfarin/clopidogrel
  • ACE-i/statins
  • Risk factor modification
101
Q

What is patent ductus arteriosus (PDA)

A
  • A persistent connection between the pulmonary artery and the descending aorta
  • Leads to R-L reverse shunt (eisenmengers)
102
Q

How might PDA present (4)

A
  • Breathlessness/dyspnoea
  • Cyanosis
  • Tachycardia
  • Bounding pulse
103
Q

What are the key features of tetralogy of fallot (4)

A
  • Most common cyanotic congenital HD
  • VSD
  • Overriding aorta
  • Pulmonary stenosis
  • RH hypertrophy
    (R-L shunt due to RV pressure increase due to pulmonary stenosis)
104
Q

How might tetralogy of fallot present (4)

A
  • Cyanosis
  • Small baby, slow growth
  • SOB/dyspnoea
  • Murmur
105
Q

How do you treat tetralogy of fallot

A
  • Surgery

- Often pulmonary regurgitation, requiring follow up surgery in adulthood

106
Q

What is the epidemiology of pericarditis (2)

A
  • More common in males

- Usually seen in adults

107
Q

What can cause pericarditis (5)

A
  • Viral
  • Adeno/enteroviruses
  • Bacterial
  • Mycobacterium tuberculosis
  • Trauma
  • Iatrogenic
  • Autoimmune
108
Q

How might pericarditis present (5)

A
  • Sudden onset severe pleuritic chest pain
  • Worse on inspiration/lying relieved by sitting forward
  • Shortness of breath/dyspnoea
  • Fever
  • Pericardial friction rub
109
Q

How do you diagnose pericarditis (2)

A
  • ECG (saddle STE)

- CXR may show effusion

110
Q

How do you treat pericarditis (3)

A
  • Rest
  • NSAIDs
  • Colchicine
111
Q

What is pericardial effusion/cardiac tamponade

A
  • A collection of fluid in the potential space of the pericardial space
  • Often associated with acute pericarditis
  • When a large amount accumulates it decreases ventricular filling - this is cardiac tamponade
112
Q

How might pericardial effusion/cardiac tamponade present (4)

A
  • High pulse with low BP
  • High JVP
  • Pulsus paradoxus
  • Decreased CO
113
Q

How do you diagnose pericardial effusion/cardiac tamponade (2)

A
  • CXR (large globular heart)

- Echo

114
Q

How do you treat pericardial effusion/cardiac tamponade

A
  • Mild resolve

- Pericardial drainage via. pericardiocentesis

115
Q

What is an aneurysm

A
  • A permanent dilatation of an artery to 2x its normal diameter
116
Q

What are the types of aneurysm (2)

A
  • True = all layers

- False = Outer layer only (adventitia)

117
Q

What is the epidemiology of aortic aneurysm (2)

A
  • Increases with age

- More common in males

118
Q

How might an abdominal aortic aneurysm present (5)

A
  • Abdominal/back/groin pain
  • Pulsatile abdominal swelling
  • Hypotension
  • Tachycardia
  • Collapse
119
Q

How do you diagnose abdominal aortic aneurysm

A
  • Abdominal ultrasound
120
Q

How do you treat abdominal aortic aneurysm (3)

A
  • Monitor/treat risk factors (hypertension etc.)
  • Endovascular stent
  • Surgical clipping
121
Q

How might a thoracic aortic aneurysm present (5)

A
  • Neck/back/chest/epigastric sudden onset severe pain
  • Hypotension
  • Collapse
  • Tachycardia
  • Haemoptysis
122
Q

How do you diagnose thoracic aortic aneurysm (2)

A
  • CT/MRI

- Transoesophageal echo

123
Q

How do you treat thoracic aortic aneurysm (2)

A
  • Monitor/treat risk factors (hypertension)

- Surgical clipping

124
Q

What is the epidemiology of aortic dissection (3)

A
  • Elderly
  • More common in males
  • Most common aortic emergency
125
Q

How might aortic dissection present (4)

A
  • Sudden onset severe central chest pain
  • Tearing sensation
  • Hypertension
  • Shock
126
Q

How do you diagnose aortic dissection (2)

A
  • CXR (widened mediastinum)

- Urgent CT/MRI/TOE

127
Q

How do you treat aortic dissection (3)

A
  • Rapid B.P control (iv Beta blocker/GTN)
  • Morphine
  • Surgery/endovascular stent
128
Q

What is shock

A
  • Acute circulatory failure with inadequate perfusion of tissues resulting in generalised hypoxia
129
Q

How might shock present (7)

A
  • Pale
  • Cold/shivering
  • Sweaty
  • Weak/fast pulse
  • Confusion
  • Collapse
  • Increased capillary refill time
130
Q

What can cause shock (4)

A
  • Hypovolaemic
  • Cardiogenic
  • Anaphylactic
  • Septic
131
Q

How do you treat shock

Phase 2 (10 decks)

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