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Phase 2a > Cardiovascular Diseases > Flashcards

Cardiovascular Diseases Flashcards

1
Q

What is stroke volume?

A

End diastolic volume – end systolic volume

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2
Q

What is cardiac output?

A

Heart rate x Stroke volume

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3
Q

What is the equation for blood pressure?

A

CO x Total peripheral Resistance

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4
Q

What is pulse pressure?

A

Systolic pressure - diastolic pressure

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5
Q

What is mean arterial pressure?

A

diastolic pressure + 1/3PP

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6
Q

What is preload?

A

Initial stretching of the cardiac myocytes prior to contraction

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7
Q

What is afteload?

A

Force against which the ventricles must contract to expel the blood out of the ventricles

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8
Q

What is Ischaemic heart disease?

A

Common but serious condition where the blood vessels supplying the heart are narrowed and blocked. There is an imbalance between the supply of oxygen to cardiac muscle and cardiac demand.

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9
Q

what are the risk factors of IHD?

A

Age, obesity, exercise, diet, htn, smoking, FHX, diabetes

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10
Q

What is the pathophysiology of IHD?

A

Caused by atherosclerosis - formation of this

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11
Q

What is the presentation of IHD?

A

Angina, chest pain (discomfort, heaviness, squeezing), radiation to left arm, shoulder, neck ,jaw.

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12
Q

What investigations are needed for IHD?

A

gold standard - CT coronary angiography
HBA1c - exclude diabetes
FBC - anaemia
May have high LDL

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13
Q

What is the QRISK2 score?

A

predicts risk of CVD in next 10 years

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14
Q

What is the treatment for IHD?

A

Nitrate GTN spray
Beta blocker - Bisoprolol (negatively chronologically/inotropic)
ACEI - Ramipril - vasodilator - BP control
CCB - arteriodilators - Amlodipine
Dual anti platelet - stop platelet aggregation - aspirin/clopidrogel
Statin - simvastin- reduce cholesterol
PCI/CABG

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15
Q

What is PCI and CABG?

A

Percutaneous coronary intervention
Coronary artery bypass surgery

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16
Q

Give 2 advantages and 1 disadvantage of PCI

A
  1. less invasive
    2.convenient and acceptable
  2. high risk of restenosis
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17
Q

Give 1 advantage and 2 disadvantages of CABG

A
  1. good prognosis after surgery
  2. very invasive
  3. long recovery time
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18
Q

What are acute coronary syndromes?

A

Acute Coronary Symptoms (ACSs) encompass a spectrum of unstable coronary artery disease.
Unstable angina, STEMI and NSTEMI

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19
Q

What is an example of a chronic coronary syndrome?

A

Stable angina

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20
Q

What is the definition of angina?

A

Central crushing chest pain/discomfort arising from the heart, brought on with exertion as a result of myocardial ischaemia . Relieved with 5mins rest or GTN spray.

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21
Q

What is the definition of stable angina?

A

Chest pain/ discomfort arising from the heart as a result of myocardial ischaemia, induced by effort and relieved by rest.

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22
Q

What are the signs of stable angina?

A
  • Chest pain comes on with exertion and rapidly resolved by rest or GTN spray
  • Exacerbated by cold weather, anger and excitement
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23
Q

What are the symptoms of stable angina?

A

● Central crushing retrosternal chest pain that radiates to arms, jaw and neck
● Dyspnoea
● Palpitations
● Syncope

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24
Q

What is dyspnoea?

A

Difficulty breathing

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25
Q

What is the pathophysiology of stable angina?

A

Imbalance between the heart’s oxygen demand and supply, usually from an increase in demand(exercise). Limited supply can be due to limited blood flow due to blockages, atherosclerotic plaques or reduced oxygen carrying of blood (anaemia).

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26
Q

Define atherogenesis

A

The development of an atherosclerotic plaque

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27
Q

What is athersclerosis?

A

A hardened plaque built up of fats, cholesterol and other substances in the intimal of an artery, causing the arteries to harden and narrow.

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28
Q

What are the risk factors of atherosclerosis?

A

Age, smoking, obesity, diabetes, htn, FHx

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29
Q

Describe in 5 steps the progression of atherosclerosis?

A
  1. fatty streaks
  2. intermediate lesions
  3. fibrous plaques
  4. plaque rupture
  5. plaque erosion
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30
Q

What are the constituents of the fatty streaks?

A

Foam cells
T-lymphocytes

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31
Q

What are the constituents of intermediate lesions?

A

Foam cells
smooth muscle cells
T - lymphocytes
platelet adhesion
extracellular lipid pools

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32
Q

What are the constituents of a fibrous plaque?

A

fibrous cap overlies lipid core and necrotic debris
smooth muscle cells
macrophages
foam cells
T-lymphocytes

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33
Q

What is the structure of a atherosclerotic plaque?

A

Lipid
Necrotic core
connective tissue
Fibrous cap

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34
Q

Why might a plaque rupture?

A

plaques constantly grow and recede. fibrous cap has to be reabsorbed and redeposited in order to be maintained. if balance shifts, cap becomes weak, plaque ruptures, thrombus formation.

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35
Q

What can cause chemoattractant release?

A

A stimulus such as endothelial injury

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36
Q

What are the functions of chemoattractants?

A

chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release IL-1,6 -> inflammation

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37
Q

Describe the progression of athersclerosis

A

Endothelial injury due to smoking, T2DM
Fatty streak forms - earliest stage-LDL move into endothelium and are phagocytksed by macrophages–> Foam cells
Inflammatory reaction- chemoattractants attract leukocytes, foam cells recruit other inflammatory cells -neutrophils, macrophages, lymphocytes, fibroblasts, platelets
Fibroblasts produce smooth muscle fibrous cap which covers plaque - prone to rupture.

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38
Q

What are the risk factors of stable angina?

A

Obesity
T2DM
HTN
Smoking
Age
MAlE
FHx

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39
Q

What are the investigations of stable angina?

A

12 lead ECG - usually normal
CT angiography - Shows narrowing of coronary artery
Stress ECG- exercise stress test
Bloods - FBC for anaemia, Lipid profile
CXR - check heart size and pulmonary vessels

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40
Q

What is the first line investigation for stable angina?

A

ECG resting = normal
Exercise induced= ischaemia

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41
Q

What is the gold standard for stable angina?

A

CT coronary angiography - looks at the arteries to see if narrowed or athersclerosis has taken place

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42
Q

What is the treatment for stable angina?

A

symptomatic: GTN spray
Lifestyle: weightless, more exercise, quit smoking
Treat underlying conditions: HTN and T2DM

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43
Q

What is the pharmaceutical treatment for stable angina?

A

CCb (amlodipine) or BB

BB+CCB

BB+CCB+ nitrates

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44
Q

What are the revascularistaion treatments?

A

Percutaneous Coronary Intervention - stunting the narrow artery - risk of thrombosis, less invasive, shorter recovery
Coronary Artery Bypass Graft -good prognosis/ longer recovery

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45
Q

What is the definition of unstable angina?

A

An acute coronary syndrome classified by. a crushing cardiac chest pain with crescendo pattern. Symptoms frequently occurring at rest, pain not relieved. Deterioration in previously stable angina.

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46
Q

What is the pathology of unstable angina?

A

Rupture or erosion of the fibrous cap of a coronary artery atheromatous plaque with thrombosis formation, inflammation and vasoconstriction produced by platelet release.

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47
Q

What is the diagnosis and investigations for unstable angina?

A

● History
● FBC – anaemia aggravates it
● Cardiac enzymes (troponin normal) – excludes infarction
● ECG – Normal / ST depression when patient is in pain
● CT Coronary angiography
● Risk assessment (QRISK2) – if low risk do an elective stress test
- Grace score

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48
Q

What is the management/ treatment for unstable angina?

A
  • Risk factor modification
  • PCI/ CABG if risk assessment score high
  • Anti platelet therapy- Aspirin or dual therapy with clopidogrel
  • Anti coagulants -heparin
  • Nitrates
  • BB
  • Statins
  • ACE inhibitors
    -CCB
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49
Q

Describe the action of nitrates?

A

Venodilaters-> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand

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50
Q

What are the symptoms of unstable angina?

A

Same as stable angina, but occurs at rest.

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51
Q

What is a myocardial infarction?

A

Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to complete occlusion of an artery by thrombus

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52
Q

What is the epidemiology of an MI?

A

Most common cause of death in developed countries
1/3 cases occur at night

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53
Q

What is the pathology of a MI?

A

● Almost always due to a rupture of an atherosclerotic plaque which leads to clot formation which then occludes one of the coronary arteries causing myocardial cell death and inflammation
● So basically, plaque rupture, development of thrombosis, total occlusion of coronary artery , myocardial cell death

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54
Q

What is a STEMI?

A
  • ST elevation
  • Tall T waves
  • Might present as a new LBBB (WilliaM) (v1- W shape, v6 M shape)
  • Pathological Q waves
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55
Q

What is a NSTEMI?

A

ST depression and/or T wave inversion

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56
Q

What are the risk factors of an MI?

A

● Age
● Male
● History of premature coronary heart disease
● Diabetes mellitus
● Hypertension
● Hyperlipidaemia
● Family history

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57
Q

What are the symptoms of MI?

A

●Crushing central chest pain similar to that occurring in angina – described as “elephant sitting on chest:
● Sweating
● SOB/Dyspnoea
● Fatigue
● Nausea
● Vomiting

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58
Q

What are the signs of a MI?

A

● Occurs at rest
● Last longer than 20 minutes
● Not relived by GTN spray
● Pain may radiate to left arm, neck and/or jaw
● Pulse and BP may vary between being up or down

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59
Q

What is shown on an ECG for a NSTEMI?

A

ST depression and or T wave inversion

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60
Q

What is shown on an ECG for a STEMI?

A

ST elevation
Tall T waves
LBBB
Pathological Q waves

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61
Q

What are the Investigation for an MI?

A

● Clinical history
● ECG
● CT angiography
● CXR
● FBC
● U&E
● Blood glucose and lipids

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62
Q

What is the management for MI?

A

● Acute (initial management)
o MONAC
▪ Morphine
▪ Oxygen (if sats are <94%)
▪ Nitrates –
▪ Aspirin 300mg – chewed in order to increase absorption
- Clopidogrel -75mg
o Refer for PCI if within 12hr or –>,thrombolysis (IV alteplase) if over 12 hr then conider PCI
-CABG

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63
Q

What is the Grace score for unstable angina and NSTEMI?

A

Predictor of mortality from MI in next 6months - 3 years in patients with ACS

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64
Q

Describe the action of beta blockers

A

Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. myocardial work is reduced and so is myocardial demand = symptom relief

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65
Q

Name 3 beta blockers

A

bisoprolol/ B1-specific
Atenolol
Propanolol - non selective

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66
Q

What are the side effects of BB?

A

bradycardia, tiredness, erectile dysfunction, cold peripheries

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67
Q

When would BB be contraindicated?

A

Asthma

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68
Q

What are the secondary prevention for an MI?

A

o Modification of risk factors

o Aspirin – 75mg daily
o Clopidogrel/ticagrelor -75mg for a year
o Statins -atrovastatin - life
o Beta blocker life–
o ACE inhibitors - life

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69
Q

Name 3 ACEI

A

Ramipril, enalapril, perindopril

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70
Q

Why do ACEI lead to increased Kinin?

A

ACE also converts bradykinin to inactive peptides. So ACEI lead to a build up of bradykinin

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71
Q

What are the side effects due to an increase in kinin?

A

dry chronic cough
rash
anaphylactoid reaction

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72
Q

What are the side effects of ACEI?

A

hypotension, hyperkalaemia, acute renal failure, teratogenic

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73
Q

Name 3 ARBs

A

candesartan, valsartan, losartan

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74
Q

What are MI complications?

A

Heart failure due to ventricular fibrillation
Mitral incompetence
LV wall rupture
Cariogenic shock
LV aneurysm
Dressler’s syndrome – pericarditis following cardiac intervention/surgery

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75
Q

What are the differential diagnosis of chest pain?

A

● Cardiac – ACS, Aortic dissection, pericarditis, myocarditis
● Respiratory – PE, pneumonia, pleurisy, lung cancer
● MSK – rib fracture,
● GORD

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76
Q

what is the definition of heart failure?

A

A clinical syndrome where the heart is unable to pump enough blood/O2 to satisfy the needs of metabolising tissues.

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77
Q

What is the epidemiology of heart failure?

A

Annual incidence of 10% in patients over 65.
50% of patients die within 5 years

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78
Q

What are the causes of Heart failure?

A

● Ischaemic Heart Disease – most common cause in the world
● Hypertension – most common cause in Africa
● Cardiomyopathy
● Valvular heart disease – aortic stenosis
● Congenital heart disease

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79
Q

What are the risk factors of heart failure?

A

● Age – 65+
● Obesity
● Gender – male
● People who have had a previous MI
-smoking

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80
Q

What is systolic heart failure?

A

o Failure to contract
o Ejection fraction <40% (SV/EDV)

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81
Q

What are the causes of systolic heart failure?

A

▪ IHD
▪ MI
▪ Hypertension
▪ Cardiomyopathy

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82
Q

What is diastolic heart failure?

A

o Inability to relax and fill
o There is reduced preload because there is abnormal filling of the LV
o Ejection fraction >50%

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83
Q

What causes diastolic heart failure?

A

aortic stenosis
hypertrophic cardiomyopathy

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84
Q

what is low output HF?

A

Decreased cardiac output, fails to increase with exertion.

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85
Q

What could low output heart failure be due to?

A
  • pump failure - systolic HF, increased heart rate
  • Excessive preload - mitral regurgitation
  • Chronic increased afterload - aortic stenosis, hypertension
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86
Q

What is high output heart failure?

A

When the cardiac output is higher than usual due to an increased peripheral demand - anaemia, pregnancy, hyperthyroidism.

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87
Q

What is the pathology of heart failure?

A

normally raised preload = raised after load = high CO by frank starling law
Failing hearts = low CO due to dysfunctional starling law
- compensatory mechanism activates
-soon compensatory fails and heart undergoes cardiac remodelling
-heart less well adapted to function therefore increased RAAS +SNS will exacerberate fluid overload
- HF affecting both L+R circuits =congetsive HF

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88
Q

What are the compensatory changes during heart failure?

A
  • sympathetic stimulation
    -RAAS
  • Cardiac changes
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89
Q

What happens during sympathetic stimulation?

A
  • Increased Air and noradrenaline
    Improves ventricular function by increasing HR and myocardial contractility
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90
Q

What is the RAAS system?

A
  • Increases ADH, Aldosterone

activation increases Na+ and water retention
increases blood pressure and

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91
Q

What cardiac changes occur?

A

Ventricular dilation - as increased volume of blood remaining after systole, myocardial fibres are stretched and myocardial contraction is restored. leads to myocyte damage.

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92
Q

What are the mechanisms of HF?

A
  1. increased preload
  2. increased after load
  3. salt and water retention - RAAS/SNS
  4. Myocardial remodelling.
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93
Q

what are the 3 cardinal symptoms of HF?

A
  • SOB
  • Fatigue
    -Ankle swelling - fluid retention
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94
Q

What is the presentation of heart failure?

A

3 cardinal signs +

-orthopnoea - dyspnoea worse lying flat
-oedema
3rd, 4th heart sounds
Raised JVP
Bibasal crackles
Hypotensive
tachycardic

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95
Q

What does LHS failure result in?

A

Pulmonary vessel backlog therefore pulmonary oedema

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96
Q

What is the result of RHS failure?

A

results in systemic venous back log - peripheral oedema

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97
Q

What are the investigations for heart failure?

A

CXR - ABCDE
ECG- may show evidence of underlying causes - abnormal
Bloods- BNP high
FBC
Echocardiogram - check chambers

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98
Q

What is CXR - ABCDE?

A

o Alveolar oedema (“Bat’s wings”)
o Kerley B lines (interstitial oedema)
o Cardiomegaly
o Dilated upper lobe vessels of lung
o Effusion (pleural)

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99
Q

What is BNP?

A

o Brain Natriuretic Peptide – not specific as may be raised in acute PE
▪ Secreted by ventricles in response to increased myocardial wall stress
▪ Increased in patients with HF
▪ Levels correlate with ventricular wall stress and severity of HF

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100
Q

What is the management for HF?

A

conservative - lifestyle changes
Pharmacological
-ACEi +BB
-Spironolactone +furosemide
Surgery = revascularisation

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101
Q

Name 2 loop diuretics?

A

furosemide, bumetanide

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102
Q

Name a thiazide diuretic and where does it work?

A

bendroflumethiazide - distal tubules

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103
Q

Name a potassium sparing diuretic

A

spironolactone

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104
Q

Give 5 potential side effects of diuretics

A

hypovolemia
hypotension
reduced serum Na+/K+
Erectile dysfunction
increased uric acid -gout

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105
Q

Name 4 calcium channel blockers

A

amlodipine
felodipine
diltiazem
veramipril

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106
Q

Name 2 dihydropyridines

A

They are a class of calcium channel blockers
Amlodipine/felodipine = arterial vasodilators

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107
Q

How does amlodipine work?

A

It is a dihydropyridine calcium agonist that inhibits the influx of calcium ions into smooth and cardiac muscle. This reduces myocardial contractility, and the formation of electrical impulses reduces.

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108
Q

What are the side effects of amlodipine?

A

Abdominal pain, dizziness, drowsiness, headaches

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109
Q

What is cor pulmonale?

A

Right sided heart failure caused by chronic pulmonary arterial hypertension

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110
Q

What are the causes of cor pulmonale?

A

Chronic lung disease
Pulmonary vascular disorders
Neuromuscular and skeletal diseases

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111
Q

what are the symptoms of cor pulmonale?

A

Dyspnoea
fatigue
syncope

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112
Q

What are the signs of cor pulmonale?

A

Cyanosis
tachycardia
raised JVP
Oedema

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113
Q

What are the investigations for cor pulmonale?

A

Arterial blood gas - hypoxia +/-
Hypercapnia - build up of CO2 in the blood stream

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114
Q

What is the management for cor pulmonale?

A
  • treat underlying cause
  • give oxygen to treat respiratory failure
  • treat cardiac failure - diuretics
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115
Q

What is the definition of an aneurysm?

A

An aneurysm is a permanent localised dilation of an artery to twice normal diameter. They may be asymtpmatic or cause symptoms.

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116
Q

What is a true aneurysm? What arteries are most affected?

A

Affects all 3 layers (intimal, media and adventitia)
Have different shapes – saccular or fusiform

▪ Abdominal aorta – most common
▪ Iliac, popliteal and femoral
▪ Thoracic

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117
Q

What is a false aneurysm?

A

● False aneurysm
o Collection of blood under adventitia only (outer layer)
o Can happen after trauma

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118
Q

What are the causes of an aortic aneurysm?

A

● Atheroma – persistent inflammation weakens the arterial wall
● Trauma
● Connective disorders
o Marfan’s – gene coding for fibrillin-1 affected (fibrillin-1 used in ECM structure)
o Ehlers-Danlos syndrome – affects gene that usually alter the structure, production or processing of collagen or proteins that interact with collagen

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119
Q

What are the risk factors of AAA?

A

● Smoking
● Family History
● Age
● Male
● HTN
● Trauma
● COPD
● Hypercholesterolaemia

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120
Q

What are the symptoms of AAA?

A

●Asymptomatic - unruptured
Epigastric pain radiating to flank
Pulsatile mass in abdo
Hypotensive
Tachycardic

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121
Q

What are the signs of AAA?

A
  • pulsatile abdominal swelling - normal but if diameter is >5.5cm it suggests it is unruptured
  • expansile aorta - suggests aortic rupture - epigastric pain and hypovolaemic shock
  • hypotension
  • collapse
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122
Q

what investigations are used for AAA?

A
  • abdominal ultrasound
  • CT and or MRI angiography
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123
Q

What is the management for AAA?

A

Non ruptured:
aSx +<5.5 cm = monitor
Sx +>5.5 or growing rapidly = surgery (Endovascular repair, or open surgery)

Ruptured:
- stabilise ABCDE
-Fluids + transfusion
AAA graft surgery -emergency

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124
Q

What is the pathology of an AAA?

A

Smooth muscle, elastic and structural degeneration of all 3 layers. With leukocyte infiltrate

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125
Q

What is an aortic dissection?

A

A tear in the intimal layer of the aorta which leads to blood dissecting / collecting through the media

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126
Q

What is the epidemiology of an aortic dissection?

A
  • affects males more than females
    Most common emergency affecting the aorta
  • common presentation 50-70
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127
Q

What is the pathology of an aortic dissection?

A

Blood dissects media and intima and pools in false lumen which can propagate forwards or backwards decreasing perfusion to end organs ; organ failure + shock

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128
Q

What is the classification of aortic dissection?

A

Type A- proximal to left subclavian artery (ascending arch)
Type B- distal to left subclavian (descending thoracic)

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129
Q

What are the most common location of AD?

A
  1. sinotubular junction -where aortic root becomes tubular aorta
  2. just distal to left subclavian artery
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130
Q

What are the causes of aortic dissection?

A
  • chronic hypertension
  • pregnancy
  • connective tissue disorders
    -aneurysms
    -infection
    -atherosclerosis
    -trauma
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131
Q

What are the symptoms of aortic dissection?

A

Abrupt onset of severe tearing central chest pain
Shock/ hypotension
-new aortic murmur/ regurgitation
-low left arm peripheral pulse
-neurological signs - affected carotid perfusion - syncope
-cardiac tamponade

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132
Q

What are the investigations for aortic dissection?

A
  • CT/MRI angiography confrims diagnosis
    -CXR - shows widened mediastinum/ aorta
  • Transoesophageal echocardiogram - shows intimal flap and false lumen and classifies into A and B
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133
Q

What is the treatment for AD?

A

Surgical. -open repair / EVAR
Medical - BB - esmolol or labetolol
Beta and alpha blockers - prevents reflex tachycardia and low BP
-vasodilator - sodium nitroprusside

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134
Q

What are the complications of AD?

A
  • cardiac tamponade
    aortic regurgitation
    pre renal AKI
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135
Q

What is cardiac Arrhythmia?

A

An abnormality of cardiac rhythm. They can lead to sudden death, syncope, HF, dizziness, palpitations or no symptoms at all.

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136
Q

What is bradycardia?

A
  • slow heart rate
    -<60bpm
  • More likely to cause symptomatic arrhthymias
  • normal during sleep and in well trained athletes
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137
Q

What is tachycardia?

A
  • fast heart rate
  • > 100bpm
  • subdivided into:
    supra ventricular tachycardias - arise from the atrium or AV junction
    Ventricular tachycardias- arise from ventricles
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138
Q

What are supra ventricular tachycardias and what are the 4 types?

A

Any tachycardia which arises from the atrium or the AV junction.
- Atrial fibrillation
-Atrial flutter
- AV nodal re-entry tachycardia
-AV reciprocating tachycardia

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139
Q

What is atrial flutter?

A

An irregular organised atrial rhythm at a rate of 250-350bpm.

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140
Q

What does atrial flutter look like on an ECG?

A

p wave produces a saw tooth pattern - definitive diagnosis

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141
Q

what are the causes of atrial flutter?

A
  • idiopathic
  • coronary heart disease
  • hypertension
  • pericarditis
    -AF
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142
Q

what is the clinical presentation of an atrial flutter?

A

Palpitations, syncope, fatigue
Dyspnoea

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143
Q

what is the treatment for an atrial flutter?

A

Beta blocker/ bisoprolol ( suppress further arrhythmias) - rate control

+anticoagulation medication

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144
Q

What is AV nodal re-entry tachycardia (AVNRT)?

A

The most common type of SVT, sudden episodes of an abnormally fast heartbeat

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145
Q

What are the risk factors for AVNRT?

A
  • exertion
  • alcohol
  • caffeine
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146
Q

what is the presentation of AVNRT?

A

Regular rapid palpitations, abrubt onset and sudden termination
SOB

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147
Q

What does AVNRT look like on an ECG?

A

P waves not visible ( or seen before or after QRS immediately)
Normal QRS

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148
Q

What is AV reciprocating tachycardia (AVRT)?

A

A tachycardia with an accessory pathway for impulse conduction - often hereditary

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149
Q

What is the best known type of AVRT?

A

Wolf Parkinson white syndrome
- where there is an accessory pathway for conduction - bundle of Kent. A pre excitation syndrome excites ventricles earlier than typical pathway - causing delta waves

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150
Q

What is the presentation of AVRT?

A
  • palpitations
  • dizziness
  • dyspnoea
151
Q

What does AVRT look like on an ECG?

A

Shortened PR interval
Delta wave
QRS wide

152
Q

What is the management of AVNRT and AVRT?

A

If stable- Valsalva, carotid massage
OR
IV adenosine

-surgery- radio frequency dilation

153
Q

What is atrial fibrillation?

A

Irregularly irregular atrial rhythm, 300-600bpm

  • mc cardiac arrhythmia
154
Q

what is the epidemiology of AF?

A
  • most common arrhythmia - 5-10% of patients over 65
155
Q

What are the causes of AF?

A
  • idiopathic
  • heart failure
  • hypertension
  • mitral stenosis
156
Q

What are the risk factors of AF?

A
  • 60+
  • past MI
  • diabetes
  • high bp
  • structural heart disease
157
Q

what is the pathophysiology of AF?

A

Rapid reentrant ectopic foci (300-600 bpm firing rate) causing atrial spasm
Causes atrial blood to pool instead of pump efficiently to ventricles there low cardiac output and high risk of thromboembolic events

158
Q

What is the presentation of AF?

A
  • asymptomatic
  • palpitations
    -syncope
    -irregularly irregular pulse
    -hypotensive
159
Q

What is shown on an ECG for AF?

A
  • irregularly irregular pulse
  • no p waves
  • normal QRS
160
Q

What is the management for AF?

A

Rate control - bisoprolol (BB) or CCB = veramipril
+ anticoagulant
- cha2ds2 - vasc score

161
Q

What are the main effects of digoxin?

A

bradycardia, reduced atrioventricular conduction,

162
Q

What are 4 potential side effects of digoxin?

A

nausea, vomiting, diarrhoea, confusion

163
Q

What is the CHADS2WASc score?

A

used to calculate stroke risk in AF to consider anticoagulation if 2-3

164
Q

How do you calculate a regular heart rhythm?

A

Count the number of large squares within one interval R-R
Divide by 300

165
Q

How do you calculate an irregular heart rhythm?

A

Count the number of complexes on the rhythm strip and times by 6

166
Q

What are the intrinsic causes of bradycardia?

A
  • acute ischaemia
  • infarction of SAN
  • sick sinus syndrome.

Treat with atropine

167
Q

What are the extrinsic causes of bradycardia?

A

Drug therapy - beta blockers, digoxin
Hypothyroidism
Hypothermia

168
Q

What is a heart block?

A

A block at any level of the conduction system in which conduction seizes

169
Q

What are the 2 places which can be blocked?

A
  • block in AVN or bundle of his = AV block
  • block in lower conduction system = Bundle branch block
170
Q

what is a first degree heart block?

A

This is the result of a delayed AV conduction
causes prolonged PR interval >0.22s on the ECG

171
Q

What is a first degree heart block caused by?

A

LEV’s disease
IHD - scar tissue
Hypokalaemia
Myocarditis

172
Q

what is the presentation of a first degree heart block?

A

Asymptomatic

173
Q

What is a second degree heart block?

A

Occurs when some atrial impulses fail to reach the ventricles, AV node block
When some P waves conducted others aren’t

174
Q

What are the two forms of second degree heart block?

A

Mobitz Type 1 (Wenckebach)
Mobitz Type 2

175
Q

What is Mobitz Type 1?

A
  • Generally caused by AV node block
  • Progressive PR interval prolongation until a QRS drops
176
Q

What is the presentation of Mobitz 1?

A

light headedness, dizziness, syncope,

177
Q

What is Mobitz Type 2?

A

PR interval persistently prolonged With random dropped QRS

178
Q

what is the presentation of Mobitz Type 2?

A

Chest pain, SOB, syncope and postural hypotension

179
Q

What is a 3rd degree heart block?

A

Occurs when there is a complete dissociation between atrial and ventricular activity.
Atria and ventricles beat independently of each other

180
Q

What are the causes of a 3rd degree heart block?

A

Acute MI
Hypertension
Structural heart disease

181
Q

What are the symptoms of a 3rd degree heart block?

A

syncope
dyspnoea
chest pain
confusion

182
Q

what does a 3rd degree heart block look like on an ECG?

A

P waves and QRS occur independent
Narrow QRS if above bifurcation of bundle of His
Broad QRS if below the bifurcation of bundle of his

183
Q

What is the treatment for a 3rd degree block?

A

IV atropine

184
Q

What does a shortened PR interval suggest?

A

P wave is originating from somewhere closer to the AV node, so the conduction takes less time
Atrial impulse getting there via a shortcut (accessory pathway), can be associated with a delta wave - wolf Parkinson white syndrome.

185
Q

What does a broad width of a QRS complex show?

A

A broad QRS complex occurs if there is an abnormal depolarisation sequence – for example, a ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle.A bundle branch block results in a broad QRS complex because the impulse gets to one ventricle rapidly down the intrinsic conduction system then has to spread slowly across the myocardium to the other ventricle.

186
Q

What is the P wave?

A

atrial depolarisation

187
Q

What is the PR interval and how long should it last?

A

AVN conduction delay

0.12s-0.2s

188
Q

What is the QRS complex?

A

vent depolarisation and atrial repolarisation
0.08s - 0.1s

189
Q

What is the ST segment?

A

isovolemic ventricular relaxation

190
Q

What is the T wave?

A

ventricular repolarisation

191
Q

What is S1 sound?

A

mitral and tricuspid close

192
Q

What is S2 sound?

A

aortic and pulmonary close

193
Q

What is S3 sound?

A

Rapid ventricular filling
- early diastole
-normal in young/preggo
-pathological in mitral regurgitation +heart failure

194
Q

What is S4 sound?

A

pathological ‘gallop’
- due to blood forced in to stiff hypertrophic ventricle (LVH and aortic stenosis)

195
Q

What is a bundle branch block?

A

Complete block of a bundle of HIS, associated with a wide QRS complex with an abnormal pattern ,usually symptomatic.

196
Q

What is a Right bundle branch block?

A

Right bundle doesn’t conduct, impulse spreads from left ventricle to right.
Results in an R wave in V1 and a slurred S wave in V5/6 (MaRRoW)

197
Q

What are the causes of RBBB?

A

Pulmonary embolism
IHD
Congenital heart disease
Atrial/ ventricular septal defects

198
Q

What is left bundle branch block?

A

Slurred S wave in V1, and R wave in V5/6 (WiLLiaM)

199
Q

what are the causes of LBBB?

A

IHD
valvular disease

200
Q

what are the symptoms of Bundle branch block?

A

syncope

201
Q

what is the treatment for BBB?

A

cardiac pacemaker

202
Q

What is the definition of hypertension?

A

High blood pressure, >140/90 mmHg on at least two readings on separate occasions.

203
Q

What are the causes of hypertension?

A

95% idiopathic
Secondary causes, hypertension due to another underlying cause :
- renal disease
-obesity
-pregnancy
-endocrine - conn’s/crushinh

204
Q

what is stage 1 hypertension?

A

140/90 mmHg 135/85ABPM

205
Q

What is stage 2 hypertension?

A

160/100 mmHg. 150/95ABPM

206
Q

What is malignant hypertension?

A

When high blood pressure causes damage to your organs, this is an emergency. 180/110mmHg

207
Q

What are the risk factors of hypertension?

A

alcohol intake, sedentary lifestyle, DM, age , FHx, ethnicity, male

208
Q

What is the pathology of hypertension?

A

All mechanism will increase RAAs system and SNS activity and TPR therefore blood pressure increases as BP =COxTPR

209
Q

What is the presentation of hypertension?

A

Mainly asymptomatic unless malignant :
- papilloedema
- headache
- visual disturbances
-haematuria

210
Q

What are the investigations for hypertension?

A

Take BP - if >140/90, confirm using ambulatory BP for 25hr - if 135/85 -confirms diagnosis
if still high do Qrisk2 to decide treatment
If stage 2 - start treatment
Urinalysis- check kidney function
Bloods- glucose, creatinine,eGFRLFTs - check organ damage

211
Q

What is the treatment for Hypertension?

A
  • First line, ace inhibitor (ramipril) or angiotensin receptor blocker (candesartan) or if >55 and black calcium channel blocker( amlodipine)
  • Second line: Ace inhibitor + CCB
    Third line: ACEi + CCB + Diuretics (bendroflumethiazide or furosemide)
    Fourth line: ACEI + + CCB + Thiazide + BB if k+<4.5 or spironolactone if k+>4.5
212
Q

What does an ACEI do?

A

stop angiotensin 1 from converting ton angiotensin 2 - to stop vascular growth and salt retention.

213
Q

What does a beta blocker do?

A

Block the release of the stress hormones adrenaline and noradrenaline in certain parts of the body. This results in a slowing of the heart rate and reduces the force at which blood is pumped around your body.

214
Q

What does ARB do?

A

Reduces the action of angiotensin 2

215
Q

What do calcium channel blockers do ?

A

reduce the amount of calcium entering cells of the heart and blood vessel walls. This is significant because calcium is necessary to contract the muscular linings of blood vessels

216
Q

What is peripheral vascular disease?

A

A slow and progressive circulation disorder, leading to claudication of vessels, commonly caused by atherosclerosis.

217
Q

What are the risk factors of PVD?

A

Smoking
diabetes
HTN
sedentary lifestyle
Hyperlipidaemia
Age

218
Q

Which arteries can be affected?

A

● Hip or buttocks pain – aorta or iliac arteries
● Thigh – common femoral artery
● Upper 2/3rd of calf – superior femoral artery
● Lower 1/3rd of calf – popliteal artery
● Foot – tibial or peroneal artery

219
Q

What is intermittent claudication?

A

Nerve pain caused by a release of adenosine in response to muscle ischaemia/partial occlusion. pain in lower limbs, relieved on rest.

220
Q

What are the symptoms of PVD?

A

cramping pain in calves, thighs and buttocks on exercise, relieved on rest.
Skin change on leg - colour/ulceration
Buerger test positive
Lack of lower leg pulse

221
Q

What are the signs of PVD?

A
  • absent pulses
  • punched out ulcers
    -postural colour change (buergers test)
    -6P’s of limb ischaemia
222
Q

What are the 6P’s of limb ischaemia?

A

pain, pallor, pulseless, perishing cold, paraesthesia, paralysis

223
Q

What is the Buerger’s test?

A

Elevate both legs to an angle of 45 degrees, and hold, observe the colour of the feet, pallor indicates ischaemia
Then sit up and hang the legs down, gravity aids blood flow and colour returns in the ischaemic leg

224
Q

What are the investigations for PVD?

A
  • Ankle brachial pressure index (ABPI)
    Normal is 1-1.2,
    PVD = 0.5-0.9- intermittent claudication
    <05. -critical limb ischemia - occlusion big - blood supply barely enough
    -Colour duplex ultrasound imaging - degree of stenosis
225
Q

What is the management for PVD?

A

For intermittent - modify RF- ACE-i, diet, exercise, stations, antiplatelet

Chronic limb ishcemia = Revascularisation surgery - PCI

acute Critical limb ischemia = surgical emergency - PCI otherwise amputation

226
Q

What is critical leg ischaemia?

A

a severe blockage in the arteries of the lower extremities, which markedly reduces blood-flow. Serious form of PVD.

227
Q

What are the causes of CLI?

A

thrombosis
emboli
graft occlusion
trauma

228
Q

What are the symptoms of CLI?

A

Pain in thighs, calves, feet and buttocks
Ulcers - more likely on limb with a poor blood supply

229
Q

What are the signs of CLI?

A

Foot pain at rest, relieved by hanging it out side of the bed at night.
6p’s

230
Q

What is the treatment for CLI?

A

surgical embolectomy
Local thrombolysis

231
Q

What is Pericarditis?

A

Inflammation of the pericardium with/ without effusion

232
Q

What is the pericardium?

A

The pericardium is the fibrous fluid filled sac that surrounds the muscular body of the heart and the roots of the aorta, pulmonary vessels and the superior and inferior vena cave.

233
Q

What is the pericardium made up of?

A

Two main layers:
- external fibrous layer
- internal serous layer which is divided into outer parietal layer and internal visceral layer.

234
Q

What is the pericardial cavity?

A

In between the outer and inner serous layers, is the pericardial cavity which contains 50ml of lubricating serous fluid

235
Q

What is the epidemiology of pericarditis?

A

Most commonly secondary to viral infection or MI

236
Q

What is the pathology of pericarditis?

A

Pericardium becomes acutely inflamed and rub against each other and excaberate further inflammation. May be dry - no extra fluid or become effusive - with extra fluid

237
Q

What are the causes of pericarditis?

A
  • idiopathic
  • infection:
    Viral- coxsackie-mc
    Bacterial - TB
    Fungal - Histoplasma s
  • MI -from dressers syndrome
    -Autoimmune: sjorgens, SLE,RA -common
    -Malignancy
    -trauma
238
Q

What are the symptoms of pericarditis?

A

Central chest pain - severe/ sharp and pleuritic- radiate to left shoulder -relieved sitting forward

Pericardial friction rub heard on auscaltation

239
Q

What are the signs of pericarditis?

A
  • Pericardial friction rub heard by auscultation
  • Chest pain worse on inspiration and lying flat
    Relieved by sitting forward
  • Raised jvp
240
Q

What are the investigations for pericarditis?

A

ECG - diagnostic
- concave, saddle shaped, ST segment elevation
- PR depression
CXR - bottle water shaped silhouette, may show cardiomegaly in case of effusion

241
Q

What is the management for pericarditis?

A

NSAIDs–>aspirin
Colchicine - inhibits migrations of neutrophils to site of inflammation to reduce risk of occurrence
- Abx for bacteria

242
Q

What are the complications of Pericarditis?

A

Pericardial effusion
Cardiac tamponade
Chronic constrictive pericarditis

243
Q

What is pericardial effusion?

A

Accumulation of fluid in the pericardial sac

244
Q

What is cardiac tamponade?

A

When there is enough pericardial effusion in the pericardium that it restricts diastolic ventricular filling and causes reduced BP and CO

245
Q

What are the signs and symptoms of pericardial effusion/ cardiac tamponade?

A
  • Beck’s triad:
    S1+S2 are soft
    -hypotension
    -elevated JVP

-Pulsus paradoxus - a fall in bp on inspiration of more than 10mmHg

246
Q

What are the investigation of pericardial effusion/ cardiac tamponade?

A

Echocardiography - diagnostic, shows free space around heart
CXR - shows globular heart

247
Q

How do you diagnose either pericardial effusion or cardiac tamponade?

A
  • CXR – globular heart
    -ECG – low voltage QRS complexes and sinus tachycardia

Echo - diagnostic

248
Q

What is the management for pericardial effusion/ cardiac tamponade?

A

NSAID’s + colchicine
Tamponade requires emergency pericardiocentesis

249
Q

What is constrictive pericarditis?

A

Persistent inflammation of acute pericarditis causes the heart to be encased with a rigid fibrotic pericardial sac which prevents adequate diastolic filling of ventricles

250
Q

What are the signs and symptoms of constrictive pericarditis?

A
  • jugular venous distention
    -dependent oedema
    -hepatomegaly
  • Kussmauls sign - JVP rises paradoxically
    pulses paradoxus
251
Q

What are the investigations for constrictive pericarditis?

A

CXR - normal heart and pericardial calcification
CT/MRI diagnostic - shows pericardial thickening and calcification

252
Q

What is the treatment for constrictive pericarditis?

A

surgical excision of pericardium

253
Q

What is infective endocarditis?

A

An infection of the endocardium, heart valves and/ or other endocardial lines structures within the heart

254
Q

What is the epidemiology of infective endocarditis?

A

Disease of the elderly, young IV drug users, young congenital heart disease, poor dental hygiene
more common in males

255
Q

What are the causes of IE?

A

Staphylococcus aureus( IVDU, Diabetes, Surgery) - most common cause
Streptococcus viridian’s (dental problems) - gram positive, alpha haemolytic and optochin resistant

256
Q

What is the pathophysiology of IE?

A

abnormal cardiac endothelium = have increases platelet deposition ; bacteria adheres to this and causes vegetations
- typically around valves causing regurgitation therefore aortic and mitral insufficiency causing a risk of heart failure

257
Q

What are the symptoms of IE?

A

Fever
- newly developed ventricular arrhythmias or conduction disturbances
-sepsis

258
Q

What are the signs of IE?

A

Splinter haemorrhages on anil beds of fingers
Roth spots - retinal haemorrhages with white or clear centres
Janeway lesions - haemorrhages and nodules in fingers
Osler nodes in fingers
Clubbing

259
Q

What is the diagnosis for IE?

A

Use Duke’s criteria: -2 major or 1 major +2 minor
3 cultures from different spots, over 24hr and its persistently positive - major criteria
Evidence of IE on echo/TOE - major criteria
minor criteria:
- pyrexia
-predisposing factors
-septic emboli
-1+ve blood cultures
-IVDU

260
Q

What is definitive IE?

A

2 majors, 1major + 2 minor

261
Q

What investigations are done for IE?

A

Echocardiogram/Transoesophageal Echo - gold standard
ECG

262
Q

What is the treatment for IE?

A

S.aureus = vancomycin + rifampicin

S.Viridians= Benzylpenicillin + gentamicin
- surgery - replace any valve that’s infected

263
Q

What is valvular heart disease?

A

When any valve in the heart is damaged or diseased. The valves may become incompetent, stenotic or both. Abnormal valves produce turbulent blood flow, which is heard as a murmur.

264
Q

What are the most common valvular problems?

A

aortic stenosis, mitral stenosis, mitral regurgitation, aortic regurgitation

265
Q

What is aortic stenosis?

A

narrowed aortic valve

266
Q

what is the pathology of aortic stenosis?

A

Due to the narrowing there is obstructed LV emptying, a pressure gradient develops between the LV and the aorta, increased after load, LV hypertrophy.
This results in increased myocardial oxygen demand, relative ischaemia of the myocardium and consequent angina, arrhythmias.

267
Q

What are the causes of aortic stenosis?

A

-ageing calcification
-congenital bicuspid valve - normally tricuspid

268
Q

What are the symptoms of aortic stenosis?

A

Exertional syncope
Angina
Dyspnoea - due to HF

269
Q

What are the signs of aortic stenosis?

A

narrow pulse pressure and slow rising pulse
Heart sounds:
- soft or absent 2nd heart sound, prominent 4th heart sound
Ejection systolic crescendo decrescendo murmur radiating to carotids

270
Q

What are the investigations for aortic stenosis?

A

Echocardiography - diagnostic -LV size, function and valve area
CXR - normal heart zine, LVH, may be valvular calcification
ECG -

271
Q

What is the management for aortic stenosis?

A

Aortic valve replacement / Trancutaneous aortic valve replacement

272
Q

What is mitral stenosis?

A

Narrowing of valve between left chambers, obstruction of LV inflow that prevent proper filling during diastole

273
Q

What is the pathology of mitral stenosis?

A

RHD causes mitral valve inflammation - over years exacerberated by calcification

274
Q

What are the causes of mitral stenosis?

A

Rheumatic heart disease
IE
valve calcification

275
Q

What are the symptoms of of mitral stenosis?

A

dyspnoea
Malar cheek flush
A wave ob JVP
S1 sound
Low pitched mid diastolic murmur
- louder when patient on left hand side and at apex

276
Q

What are the signs of mitral stenosis?

A

Malar flush
Low volume pulse
tapping apex beat
Heart sounds:
- loud first heart sound at apex
Diastolic murmur - Hurd when blood flows over the valve, rumbling at apex when patient is lying on their left with expiration

277
Q

What are the investigations for mitral stenosis?

A

echocardiogram -GS- check valve area, gradient, mobility
CXR - LA enlargement
ECG - AF and LA enlargement

278
Q

What is the treatment for mitral stenosis?

A

Percutaneous mitral balloon valvotomy
Mitral valve replacement

279
Q

What is mitral regurgitation?

A

Valve won’t close properly, so back flow of blood from LV to LA during systole

280
Q

What are the causes of mitral regurgitation?

A

Myxomatous mitral valve
Connective tissue disorders

281
Q

What are the risk factors of mitral regurgitation?

A

Female
Lower BMI
Advanced age
Previous MI

282
Q

What is the pathology of mitral regurgitation?

A

Pure volume overload due to leakage from LV to LA - LA dilation
Compensatory mechanisms:
-LA enlargement
-Increased contractility
-Progressve LA dilation and RV dysfunction due to pulmonary hypertension
-Progressive LV volume overload leads to dilation and HF

283
Q

What are the symptoms of mitral regurgitation?

A

exertion dyspnoea
Soft S1 = prominent S3 in severe case
Pain systolic blowing murmur radiating to axilla

284
Q

What are the signs of mitral regurgitation?

A

-Collapsing pulse with wide pulse pressure
-displaced apex beat
Heart sounds:
- soft first sound
-pansystolic murmur at apex radiating to axilla
-Diastolic blowing murmur at left sternal border

285
Q

What are the investigations for mitral regurgitation?

A

CXR - enlarged LA and LV
Echocardiogram - estimation of LA,LV size and function
ECG

286
Q

What is the treatment for mitral regurgitation?

A

Vasodilators - ACEI
+ BB

Valve replacement

287
Q

What is aortic regurgitation?

A

Valve doesn’t close properly, leakage of blood into LV during diastole due to ineffective computation of aortic cusps.

288
Q

What are the causes of aortic regurgitation?

A

Congenital bicuspid aortic valve
Rheumatic heart disease
IE
Connective tissue disorders

289
Q

What is the pathology of aortic regurgitation?

A

combined pressure and volume overload -> LV dilation and LVH

290
Q

What are the symptoms of aortic regurgitation?

A

Early diastolic blowing murmur
collapsing pulse

291
Q

What are the signs of aortic regurgitation?

A

-Collapsing (water hammer) pulse
- wide pressure pulse
- Quincke’s sign - capillary pulsation in nail beds
-De mussels sign - head nodding with each heart beat

292
Q

What are the investigations for aortic regurgitation?

A

Echocardiogram
ECG - shows evidence of LVH
CXR- shows a large heart

293
Q

What is the treatment for aortic regurgitation?

A

Vasodilators - ACEI
Surgical - replace valve

294
Q

What is pulmonary stenosis?

A

Narrowing of the outflow of the high ventricle, usually at birth, right ventricular failure as neonate.
Treat - Shunt/ bypass blockage/ open valvotomy

295
Q

What are the types of congenital heart defects?

A

Bicuspid aortic valve
Atrial septal defect
Ventricular septal defect
Coarctation of the aorta
pulmonary stenosis

296
Q

What is the bicuspid aortic valve?

A

Typically aortic valve has 3 cusps but in BAV there are only 2. Can lead to aortic stenosis/ regurgitation. And pre-disposes an individual to IE, aortic dilation/ dissection.

297
Q

What is the epidemiology of BAV?

A

affects 1-2% of births

298
Q

What investigations are used for BAV?

A

Echocardiogram

299
Q

What is the management for BAV?

A

Surgical valve replacement

300
Q

What is an atrial septal defect?

A

Abnormal connection between the two atrium, affect higher in the septum, may not present until adulthood.

301
Q

What is the epidemiology of atrial septal defect?

A

affects 40-60 years
M>F

302
Q

What is the pathology of atrial septal defects?

A

Pressure slightly higher in LA than RA causes a left to right shunt. Increased flow into right heart and lungs. As heart compliance falls with age the shunt increases causing heart failure/SOB at 40. If untreated = RV hypertrophy, pulmonary hypertension(eisenmenger’s complex), increase risk of IE

303
Q

If there is a large atrial septal defect, what would happen?

A

● Significant increased flow through the right heart and lungs in childhood
● Right heart dilatation
● SOB on exertion
● Increased chest infections
● If any stretch on the right heart should be closed

304
Q

If there is a small atrial septal defect, what would happen?

A

● Small increase in flow
● No right heart dilatation
● No symptoms
● Leave alone
● NB. The shunt on small to moderate sized defects increases with age

305
Q

What is Eisenmenger’s complex?

A
  • can occur in ASD or VSD
    -Shunt reversal due to pulmonary hypertension
    -Causes deoxygenated blood to skip lungs and go back around the body. Cyanosis/clubbing/syncope
    -Poor prognosis needs transplant
    GOES BLUE
306
Q

What is the presentation of an atrial septal defect?

A
  • pulmonary flow murmur
  • fixed split second heart sound
    -dyspnoea
  • exercise intolerance
  • atrial arrhythmias
307
Q

What are the investigations for an atrial septal defect?

A

Echo - right side hypertrophy of heart and pulmonary arteries

308
Q

What is the management for ASD?

A

surgical closure
Percuatenous, key hole technique

309
Q

What is an atrio-ventricular septal defect?

A

Instead of 2 separate AV valves, there is one big malformed one, usually leaks to a greater or lesser degree. Can be complete or partial.

310
Q

What is a complete defect?

A
  • breathlessness as neonate
  • poor weight gain
    -poor feeding
  • torrential pulmonary blood flow
    -needs repair, but repair is surgically challenging
311
Q

What is a partial defect?

A
  • can present in late adulthood
    -Presents similar to ASD/VSD:
    - Dyspnoea
    - tachycardia
    - exercise intolerance
    -left alone if no right heart dilation
312
Q

what is the treatment fro atrio-ventricular septal defects?

A

Pulmonary artery banding, band reduces flow to lungs to reduce pulmonary hypertension
Surgical repair

313
Q

What is ventricular septal defect?

A

Hole between ventricles, high pressure LV and low pressure RV so left to right shunt.

314
Q

What does a large ventricular septal defect look like?

A
  • very high pulmonary blood flow leads to pulmonary hypertension = eisenmengers complex
  • small breathless baby
    -increased respiratory rate
    -tachycardia
    -big heart on chest x-ray
315
Q

What does a small ventricular defect look like?

A

-could be asymptomatic
-loud systolic murmur
-normal heart rate/size
-risk of endocarditis

316
Q

What is the management for VSD?

A

Surgical closure
prophylactic antibiotics

317
Q

What is a patent ductus arteriosus?

A

DA is persistent communication between the proximal left pulmonary artery and descending aorta. Lung circulation is overloaded = pulmonary hypertension and right sided cardiac failure due to RV hypertrophy. - lead to eisenmenger syndrome

318
Q

What is the presentation for patent ductus arteriousus?

A

machine like murmur
failure to thrive
Dyspnoea

319
Q

What is the management for patent ductus arteriosus?

A

surgical or percutaneous closure
Indomethacin - can be given to stimulate duct closure

320
Q

What is coarction of the aorta?

A

Aorta is narrowed at the site of the ductus arteriosus.
Blood diverted massively through aortic branches therefore increased perfusion to upper body vs lower body

321
Q

What are the long term problems with coarctation of the aorta?

A

HTN
early CAD/ strokes
Aneurysm

322
Q

What is the presentation of coarctation of aorta?

A

Upper body HTN
Scapular bruits - htn in collaterals

323
Q

What investigations do you do for coarctation of aorta?

A

CXR - notched ribs -dilated intercostal vessels

CT angiogram

324
Q

What is the management for coarctation of aorta?

A

surgical repair
percutaneous repair
balloon dilation

325
Q

What is tetralogy of fallot?

A

Ventricular septal defect with RV outflow obstruction (pulmonary stenosis), overriding aorta and RVH
Right to left shunt = cyanosis

326
Q

What does tetralogy of fallot consist if ?

A
  • VSD
    -An overriding aorta
    -RV outflow obstruction - pulmonary stenosis
    -RV hypertrophy
327
Q

What are the symptoms of tetralogy of fallot?

A

Infants often seen in knee to chest squatting position, increases preload and after load therefore improves cyanosis

328
Q

What are the sings of tetralogy of fallot?

A

toddlers may squat - increases TPR
central cyanosis
low growth and birthweight
dyspnoea in exertion
clubbing
systolic ejection murmurs

329
Q

what are the investigations for tetralogy of fallot

A

Echo/CXR - boot shaped heart

330
Q

What is the management for tetralogy of fallot?

A

children - knee to chest position and O2
Full surgical treatment during first 2 years of life

331
Q

What is cardiomyopathy?

A

Group of diseases of the myocardium that affect mechanical or electrical function of the heart.

332
Q

What are the risk factors of cardiomyopathy?

A
  • FHx
    -HTN
    -obesity
    -DM
    -Previous MI
333
Q

What are the types of cardiomyopathy?

A

Hypertrophic, Dilated and restrictive

334
Q

What is hypertrophic cardiomyopathy?

A

Characterised by hypertrophy - ventricular hypertrophy causing obstruction of the outflow tracts. Thick non compliant heart - impaired diastolic filling = reduced CO

335
Q

What are the causes of hypertrophic cardiomyopathy?

A

Autosomal dominant mutation of sacromere proteins

336
Q

What is the presentation of hypertrophic cardiomyopathy?

A

Angina, dyspnoea, palpitations, syncope, sudden death

337
Q

What are the investigations for hypertrophic cardiomyopathy?

A

ECG - abnormal
Genetic testing

Echo - definitive

338
Q

What is the treatment for hypertrophic cardiomyopathy?

A

Amiodarone - anti-arrhythmic
CCB - amlodipine
BB-atenolol

339
Q

What is dilated cardiomyopathy?

A

Dilation of ventricles /thin walls, weak contraction, low CO

340
Q

What are the causes of dilated cardiomyopathy?

A

Auto dom familial - cytoskeleton gene mutation
Alcohol, IHD

341
Q

What is the presentation of dilated cardiomyopathy?

A
  • heart failure symptoms
    -SOB
    -arrhthymias
    -thromboemboli
342
Q

What are the investigations for dilated cardiomyopathy?

A

ECG
Echo

343
Q

what is the treatment for dilated cardiomyopathy?

A

Underlying condition
HF and AF treated in normal way

344
Q

What is restrictive cardiomyopathy?

A

Scar tissue replaces the normal heart muscle and the ventricles become rigid + fibrotic leading to poor contraction and reduced CO

345
Q

What are the causes of restrictive cardiomyopathy?

A

Granulomatous disease:
Amyloidis - misfolded protein
Sarcoidosis - formation of granulomas in heart wall
idiopathic
- idiopathic
-post MI

346
Q

What is the presentation for restrictive cardiomyopathy?

A

Dyspnoea
Narrow pulse pressure
Oedema
Congestive HF
3rd/4th heart sound

347
Q

What are the investigations for restrictive cardiomyopathy?

A

ECG
ECHO
Cardiac catheterisation- definitive

348
Q

What is rheumatic fever?

A

Systemic infection common in developing countries. A systemic response to B haemolytic group A streptococci .

349
Q

What are the causes of rheumatic fever ?

A

Post strep pyogenes infection (group A Haemolytic strep)- typically pharyngitis

350
Q

What is the pathology of Rheumatic fever ?

A

M protein from S.pyogenes reacts with valve tissue of heart; antibodies vs this cross link results in auto-antibody mediated destruction/inflammation - mostly affects mitral valve

351
Q

What is the presentation of rheumatic fever?

A

Major: New murmur, Arthritis, sydenham’s Chorea, erythema nodosum
Minor: Pyrexia, raised ESR/CRP, arthralgia

352
Q

What are the investigations for rheumatic fever?

A

CXR - cardiomegaly / heart failure
ECHO- extent of valvular damage
Jones Criteria - Recent S.pyogenes + 2major or 1major + 2minor

353
Q

What is the treatment for rheumatic fever?

A

Abx; IV benzylpenicillin, then phenoxypenicillin for 10 days
Chorea- Haloperidol

354
Q

What is shock?

A

Medical emergency - hypo-perfusion, life threatening , due to acute circulation failure leading to tissue hypoxia and a risk of organ dysfunction

355
Q

What is cardiogenic shock?

A

Pump failure- heart isn’t pumping enough blood/oxygen to organs

356
Q

What are the causes of cariogenic shock?

A

MI
Cardiac tamponade
Pulmonary embolism

357
Q

What is the presentation of cariogenic shock?

A

HF signs
oedema
Raised JVP
S4

358
Q

What is the treatment for cariogenic shock?

A

ABCDE resuscitation
Underlying cause

359
Q

What is hypovolaemic chock?

A

Reduced preload - low blood volume due to blood loss/fluid loss

360
Q

What are the causes of hypovolameic shock?

A

trauma
GI bleeding
fractures
burns
dehydration

361
Q

what is the presentation of hypovolaemic shock?

A

skin - cold pale clammy
tachycardia
hypotension
confusion

362
Q

What is the treatment for hypovolaemic shock?

A

ABCDE
IV Fluids
Breathing - Give O2

363
Q

What is septic shock?

A

Due to uncontrolled bacterial infection

364
Q

What is the presentation of septic shock?

A

Pyrexic
Warm peripheries
tachycardia

365
Q

What is the management for septic shock?

A

Broad spec Abx
ABCDE

366
Q

What is anaphylactic shock?

A

Due to Ig mediated Type 1 hypersensitivity against an allergen; causing histamine release - which causes vasodilation + bronchoconstriction

367
Q

What is the presentation of anaphylactic shock?

A

swollen tongue, lips
warm peripheries
wheezing/SOB
upper airway obstruction
hypotension
tachycardia

368
Q

What is the treatment for anaphylactic shock?

A

Adrenaline - 500mcg IM injected, then antihistamine and hydrocortisone if necessary.

369
Q

Why is a second dose of adrenaline needed?

A

Adrenaline has a short half-life therefore a second dose may be required if the symptoms aren’t reducing and getting worse.

370
Q

What is the blood test to confirm anaphylaxis?

A

serum mast cell tryptase

371
Q

What is neurogenic shock?

A

Nervous system damaged so can’t control BP - typically caused by spinal cord injury above T6

372
Q

What is the presentation of neurogenic shock?

A

hypotension
bradycardia
confused
hypothermic

373
Q

What is the treatment of neurogenic shock?

A

ABCDE
IV atropine

374
Q

What are the key organs at risk of failure fro shock?

A

Kidney
Lung Heart
Brain

Phase 2a (9 decks)

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