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Osha 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

How are atherosclerotic plaques distributed?

A
  • found in peripheral and coronary arteries
  • focal distribution (small area) along artery length
  • change in flow alters endothelial cell function
  • wall thickness changed leading to neointima (scar tissue)
  • altered gene expression in key cell types
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2
Q

What are fatty streaks and when do they appear?

A
  • earliest type of lesion < 10 years
  • aggregations of lipid laden macrophages and T lymphocytes in the intimal layer of the vessel wall
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3
Q

What is an intermediate lesion?

A
  • no symptoms and walled off
  • foam cells and T lymphocytes
  • vascular smooth muscle cell proliferation from media > intima
  • adhesion and aggregation of platelets to vessel wall
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4
Q

What is a fibrous plaque?

A
  • impedes blood flow
  • prone to rupture
  • covered by dense fibrous cap made of ECM proteins inc collagen, elastin overlying lipid core and necrotic debris
  • may experience symptoms e.g. angina
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5
Q

Describe plaque rupture

A
  • Plaques grow and recede
  • fibrous cap is resorbed and redeposited in order to be maintained
  • if balance shifts in favour of inflammatory conditions, cap becomes weak and plaque ruptures
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6
Q

What is the difference between red and white thrombus?

A
  • Red: contains red blood cells and fibrins
  • White: platelets and fibrinogen
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7
Q

What drugs are commonly used in treatment of atherosclerosis?

A
  • aspirin
  • clopidogrel/ticagrelor - inhibits P2Y12 ADP receptor on platelets
  • statins: reduce cholesterol synthesis by inhibiting HMG CoA reductase
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8
Q

How is acute MI diagnosed?

A
  • ST elevation MI can be diagnosed on ECG
  • Non ST elevation MI is diagnosed retrospectively made after troponin results
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9
Q

What are the 3 acute coronary syndromes?

A
  • STEMI: ST elevation MI
  • NSTEMI: Non-ST elevation MI
  • Unstable angina: prolonged, severe angina, usually at rest possibly with ECG changes
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10
Q

Describe unstable angina:
- occlusion
- infarction
- ECG
- troponin

A
  1. partial occlusion of minor coronary artery
  2. no infarction: ischaemia only
  3. normal ECG, may show ST depression or T wave inversion
  4. normal troponin
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11
Q

Describe NSTEMI:
- occlusion
- infarction
- ECG
- troponin

A
  1. partial occlusion of major coronary artery/total occlusion of minor coronary artery
  2. sub endothelial infarction so area distal to occlusion dies
  3. ST depression, T wave inversion, new LBBB
  4. elevated troponin
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12
Q

Describe STEMI:
- occlusion
- infarction
- ECG
- troponin

A
  1. total occlusion of major c.a.
  2. transmural infarction (full thickness of myocardium)
  3. ST elevation in local leads,
  4. elevated troponin
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13
Q

What are the causes of ACS?

A
  • most common: rupture of an atherosclerotic plaque + consequent arterial thrombosis
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14
Q

What are the risk factors for ACS/IHD?

A
  • age
  • smoking
  • family history
  • diabetes
  • hyperlipidaemia + htn
  • obesity
  • stress
  • male 1.5:1
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15
Q

What are the symptoms of MI?

A
  • unremitting cardiac chest pain radiating to left arm, neck, jaw (crushing/squeezing)
  • usually severe but may be mild or absent
  • associated with sweating, breathlessness, nausea/vomiting
  • dyspnoea
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16
Q

What are the symptoms of unstable angina and how can it be diagnosed?

A
  • cardiac chest pain at rest, with crescendo pattern
  • new onset angina
  • diagnosed by history, ECG and troponin
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17
Q

What is the first line investigation for ACS?

A

12 lead ECG

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18
Q

What is seen on an ECG after an MI?

A
  • hyperactive T waves
  • pathologically steep Q waves
  • LBBB (left bundle branch block - electrical impulse disrupted) (prolonged QRS complex)
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19
Q

What is the gold standard investigation for ACS?

A

CT coronary angiogram

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20
Q

How is ACS managed?

A
  • MONAC if acute
  • coronary reperfusion: PCI (<12h) or thrombolysis w alteplase (>12h)
  • patient should be given aspirin, β blocker
  • 2nd antiplatelet agent e.g. clopidogrel
  • atorvastatin + ACEi
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21
Q

What should patients be offered for secondary prevention of ACS/stable angina?

A
  • lifestyle advice firstly
  • ACE inhibitor/ARB
  • β blocker
  • dual anti platelet therapy
  • statin
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22
Q

How are MIs managed?

A
  • oxygen therapy if hypoxic
  • pain relief (opiates/nitrates)
  • Aspirin (and maybe P2Y12 inhibitor)
  • potentially β blocker, antianginal therapy, angoigraphy
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23
Q

What is troponin?

A
  • protein complex regulating actin:myosin contraction
  • highly sensitive marker of cardiac muscle injury
  • may not represent permanent muscle damage
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24
Q

What is the pathophysiology of stable angina?

A
  • oxygen supply ≠ demand
  • most commonly attributed to IHD
  • impairment of blood flow by proximal arterial stenosis
  • increased distal resistance
  • reduced oxygen carrying capacity of the blood
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25
Q

What are the criteria for stable angina?

A
  • central crushing chest pain radiating to neck/jaw
  • brought on with exertion e.g. walking up hill, cold weather, heavy meal
  • relieved with 5 mins rest/ GTN spray
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26
Q

What are the symptoms of stable angina?

A
  • central crushing chest pain radiating to neck/jaw (worsens with time)
  • nausea
  • sweating
  • fatigue
  • dyspnoea
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27
Q

What is the gold standard investigation for stable angina?

A

CT coronary angiography to highlight any narrowing

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28
Q

What is the management strategy for immediate symptomatic relief of angina?

A
  • GTN spray used as required to cause vasodilation and ease symptoms
  • a second dose is taken after 5 mins if pain hasn’t subsided
  • call an ambulance after another 5 mins if pain hasn’t gone
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29
Q

What medications are used for long term symptomatic relief of angina?

A
  • β blockers (contraindicated by asthma)
  • calcium channel blockers (CCB)
  • lifestyle changes
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30
Q

How do calcium channel blockers work and in which disease are they contraindicated?

A
  • reduce afterload
  • relax smooth muscle cells in arterial walls
  • contraindicated by heart failure
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31
Q

What is a CABG?

A
  • coronary artery bypass graft
  • for multi vessel disease
  • a graft vein is taken from the leg (usually great saphenous vein) or internal mammary artery and sewn on to bypass the stenosis
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32
Q

What is PCI?

A
  • Percutaneous coronary intervention with coronary angioplasty
  • putting a catheter into the brachial or femoral artery
  • contrast injected so stenosis is evident
  • balloon stent can be inserted
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33
Q

Describe the anatomy of the pericardium

A
  • great vessels lie within pericardium
  • 2 layers are continous
  • LA is mainly outside pericardium
  • parietal layer uses fibrous attachments to fix heart in thorax
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34
Q

What is acute pericarditis?

A
  • an inflammatory pericardial syndrome with or without effusion
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35
Q

What factors are used in diagnosis of acute pericarditis and how many factors are needed?

A
  • diagnosis made with 2 of 4 factors:
  • chest pain
  • friction rub
  • ECG changes
  • pericardial effusion
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36
Q

What is the epidemiology of pericarditis?

A
  • 80-90% is idiopathic + seasonal with viral trends
  • higher in young, previously healthy patients
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37
Q

What are the infectious causes of pericarditis?

A
  • MAINLY viral: enteroviruses, herpesviruses (EBV, CMV, HHV-6), adenoviruses
  • bacterial: mycobacterium tuberculosis
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38
Q

What are the non-infectious causes of pericarditis?

A
  • autoimmune: Sjogren, rheumatoid arthritis, scleroderma
  • neoplastic (most common): secondary metastatic tumours
  • trauma (most common): PCI, pacemaker insertion
  • other (rare): amyloidosis, aortic dissection
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39
Q

How does pericarditis present?

A
  • severe chest pain, sharp and pleuritic (not constricting + crushing like IHD)
  • KEY: relieved by sitting forward and exacerbated by lying down
  • rapid onset
  • left ant chest/epigastrium
  • breathlessness, coughing, hiccups
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40
Q

How can pericarditis be investigated?

A
  • pericardial rub: heard around 2nd heart sound, sounds like crunching snow
  • ECG, bloods, CXR, Echo
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41
Q

What is seen on the ECG in pericarditis?

A
  • PR depression
  • concave (saddle shaped) ST elevation
  • similar ECG to acute STEMI
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42
Q

Describe the management of pericarditis

A
  • restricting physical activiity
  • NSAIDs + PPIs
  • colchicine
  • 2nd line: corticosteroids if NSAIDs or colchicine fail
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43
Q

What is cardiomyopathy and what is hypertrophic cardiomyopathy the cause of?

A
  • disease of the heart muscle
  • caused by autosomal dominant mutation of sarcomeric protein genes
  • HCM = most common cause of sudden cardiac death in young people
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44
Q

What is the pathology behind HCM?

A
  • thickening of the cardiac muscle leads to impaired filling of the ventricles (esp LV)
  • this leads to decreased cardiac output
  • can lead to diastolic heart failure
  • may be white areas of fibrosis/scarring of the heart muscle + septum becomes asymmetrically thickened
  • patients with troponin T mutation at greatest risk
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45
Q

What are the risk factors for HCM?

A
  • young + asymptomatic
  • family history of sudden cardiac death
  • history of arrhythmia
  • playing competitive sport
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46
Q

How does HCM present?

A
  • exertion chest pain, dyspnoea
  • palpitations
  • fatigue
  • exertion syncope: suggests LV outflow tract obstruction
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47
Q

What is seen on ECG for HCM?

A
  • diagnosed by ECG: sharp, deep Q waves > 40ms
  • wide P waves
  • T wave inversion
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48
Q

How is HCM managed?

A
  • control arrhythmias with amiodarone
  • control LV function: β blockers and verapamil
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49
Q

What is the cause of dilated cardiomyopathy?

A
  • cytoskeletal gene mutations
  • enlarged ventricular size and systolic dysfunction
  • thin cardiac muscle walls contract poorly > dec CO
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50
Q

How does DCM present?

A
  • dyspnoea
  • fatigue
  • peripheral oedema
  • loud 3rd and 4th heart sounds
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51
Q

How is DCM diagnosed?

A
  • ECG: sinus tachycardia, T wave inversion, ST depression, LBBB
  • CXR: enlarged heart, pleural effusion
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52
Q

How is DCM managed?

A
  • treat reversible causes
  • prophylactic anticoagulation
  • consider pacemaker
  • treat as heart failure
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53
Q

What is restrictive cardiomyopathy?

A
  • reduced compliance of ventricular walls during diastolic filling
  • Commonly affects the LV, but can often affect both.
  • Causes high diastolic filling pressures > pulmonary hypertension
  • reduced CO
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54
Q

What are the symptoms of RCM?

A
  • dyspnoea
  • fatigue
  • pulmonary oedema
  • loud 3rd heart sound
  • AF in 75% of patients
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55
Q

How is restrictive cardiomyopathy diagnosed and managed?

A
  • ECG: T wave and ST changes, pathological Q waves
  • echocardiogram: may have dilated atria or myocardial hypertrophy
  • no treatment, maybe transplant
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56
Q

What is tetralogy of fallot and its 4 features ?

A
  • key issue: interior dislocation of the septum which partially obstructs RVOT and PA
    1. ventricular septal defect: leading to equal ventricular pressures
    2. pulmonary stenosis
    3. overriding aorta
    4. RV hypertrophy
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57
Q

What is the presentation of tetralogy of fallot?

A
  • cyanosis
  • dyspnoea on feeding, crying, exertion
  • failure to thrive
  • murmur
  • fallot spells: sudden onset dyspnoea/cyanosis
  • inc venous return to RV and severe spells > death
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58
Q

How is tetralogy of fallot managed?

A
  • VSD patched
  • PV widened or replaced
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59
Q

What is a ventricular septal defect?

A
  • most common form of congenital heart disease
  • malformation of ventricular septum
  • if LV pressure > RV then blood flows LV to RV
  • inc blood flow through lungs
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60
Q

How does a VSD present?

A
  • loud systolic murmur
  • severe: breathlessness, poor feeding, failure to thrive, tachycardia
  • mild: small inc in pulmonary blood flow, endocarditis risk, asymptomatic
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61
Q

How is a VSD diagnosed and managed?

A
  • gold standard: echocardiogram
  • CXR, ECG
  • percutaneous/open heart surgery, patch application
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62
Q

What is an atrial septal defect?

A
  • congenital heart defect causing a shunting of blood from L to R atria
  • inc flow into right heart and lungs
  • secundum ASD: patent foramen ovale
  • leads to right heart dilation in severe
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63
Q

How does an ASD present?

A
  • pulmonary flow murmur
  • split S2 heart sound due to delayed closure of PV and inc blood volume
  • big pulmonary arteries and heart on CXR
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64
Q

What is an atrio-ventricular septal defect (AVSD)?

A
  • Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves
  • Can be complete or partial
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65
Q

What is a patent ductus arteriosus (PDA)?

A
  • Persistence of the connection between the aorta and pulmonary artery
  • normally rise in PaO2 and decline in prostaglandins close the duct
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66
Q

How does a patent ductus arteriosus present?

A
  • tachycardia and tachypnoea
  • continuous murmur at left sternal edge
  • failure to thrive
  • poor feeding
  • risk of endocarditis
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67
Q

How is PDA diagnosed and managed?

A
  • diagnosis: echocardiogram
  • management: usually closed via cardiac catheterisation
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68
Q

What is coarctation of the aorta and how does this present in severe and mild patients?

A
  • narrowing of the aorta at the site of the ductus arteriosus
  • presents with htn and murmur
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69
Q

How does coarctation of the aorta present?

A
  • right arm hypertension
  • bruits over scapulae and back
  • murmur
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70
Q

How is coarctation of the aorta managed?

A
  • repaired by surgical or percutaneous intervention - narrow section removed
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71
Q

What is an abdominal aortic aneurysm and what is the pathophysiology?

A
  • permanent dilation of the abdominal aorta with a diameter of more than 3cm
  • mostly originate below the renal arteries
  • smooth muscle, elastic and structural degeneration in all 3 layers of the vascular tunica
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72
Q

What are the risk factors for an AAA/TAA?

A
  • men more than women, and at a younger age
  • smoking
  • hypertension
  • family history
  • existing CVD
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73
Q

What is the aetiology of AAAs?

A
  • coarctation of the aorta
  • Marfan’s syndrome
  • aortic surgery
  • 3rd trimester pregnancy
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74
Q

How does AAA present?

A
  • mostly asymptomatic and detected on rupture
  • non-specific abdominal pain
  • Pulsatile and expansile mass in the abdomen when palpated with both hands
  • incidental finding on x-ray, ultrasound or CT
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75
Q

What is the diagnostic investigation for AAA?

A

ultrasound then CT angiogram to guide elective surgery

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76
Q

How are AAAs managed?

A
  • treating reversible risk factors
  • screening yearly/3 monthly
  • surgical: artificial graft: open repair or EVAR (endovascular aneurysm repair) stent
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77
Q

How do TAAs present?

A
  • dilation of thoracic aorta = asymptomatic
  • chest or back pain
  • trachea/L bronchus compression > cough, shortness of breath, stridor
  • same nerve compressions as pericardial effusion
78
Q

How do ruptured aortic aneurysms present?

A
  • severe chest/back pain (TAA)
  • abdo pain radiating to back/groin (AAA)
  • haemodynamic instability
  • collapse
79
Q

How are ruptured aortic aneurysms treated?

A
  • permissive hypotension to decrease blood loss
  • immediate surgery
80
Q

What is pericardial effusion?

A
  • collection of excess fluid in the pericardial sac
  • can be acute or chronic
  • transudates, exudates, blood, pus, gas
  • creates inward pressure on heart making it more difficult to expand during diastole
81
Q

What causes pericardial effusion?

A
  • Transudative: congestive heart failure, pulmonary htn
  • Exudative: infection, autoimmune, injury to pericardium
  • rupture > tamponade: MI, trauma, aortic dissection
82
Q

How does pericardial effusion present?

A
  • chest pain
  • SOB and orthopnoea
  • fullness in chest
  • quiet heart sounds
  • pulsus paradoxus
83
Q

What nerve compressions cause which symptoms in pericardial effusion?

A
  • phrenic nerve compression > hiccups
  • oesophageal compression > dysphagia
  • recurrent laryngeal > hoarse voice
84
Q

What is cardiac tamponade?

A
  • the pericardial effusion is large enough to raise the intra-cardiac pressure
  • inc pressure leads to reduced filling during diastole and decreased CO during systole
85
Q

How is pericardial effusion diagnosed?

A
  • Echo: diagnose and assess size and effect on heart function
  • fluid analysis: protein content, bacterial, viral, tumour markers
86
Q

How is pericardial effusion managed?

A
  • treatment of underlying cause: aspirin, NSAIDs, colchicine, steroids
  • drainage: needle pericardiocentesis or surgical drainage
87
Q

What is a pulmonary embolism and what causes it?

A
  • formation of a blood clot in pulmonary arteries
  • usually results from DVT developed in leg, travelled through venous system and RHS of heart to PAs
  • blocks blood flow to lungs and creates strain on RHS of heart
88
Q

What are the risk factors for DVT/PE?

A
  • immobility
  • recent surgery
  • long haul flights
  • pregnancy
89
Q

How does a PE present?

A
  • shortness of breath
  • cough ± haemoptysis
  • pleuritic chest pain
  • hypoxia
  • tachycardia
  • tachypnoea + breathlessness
  • low grade fever
90
Q

What is aortic stenosis and what are the 3 types and causes?

A
  • narrowing of the aortic valve area
  • symptoms occur when valve area is 1/4 of normal
  • types: supravalvular, subvalvular, valvular
91
Q

What is the pathophysiology of aortic stenosis?

A
  • pressure gradient develops between LV and aorta (inc after load)
  • LV function initially maintained by compensatory pressure hypertrophy
  • LV function declines when compensatory mechanisms are exhausted
92
Q

What are the symptoms of aortic stenosis?

A
  • syncope
  • angina
  • dyspnoea
93
Q

What are the signs of aortic stenosis?

A
  • slow rising carotid pulse with decreased amplitude (little difference between systolic and diastolic)
  • soft/absent 2nd heart sound, S4 aortic gallop
  • crescendo descendo murmur
94
Q

How is aortic stenosis investigated?

A
  • GOLD: Echocardiogram: LV size and function, Doppler derived area and gradient
95
Q

How is atrial stenosis managed?

A
  • vasodilators fairly contraindicated
  • aortic valve replacement, prosthetic requires anticoagulants (healthy patient)
  • TAVI: trans catheter aortic valve implantation (less invasive)
96
Q

What is mitral regurgitation and what causes it?

A
  • back flow of blood from LV to LA during systole
  • LV dilatation
  • myxomatous mitral valve (mass of cells makes leaflets heavier
  • rheumatic heart disease and infective endocarditis
97
Q

What is the pathophysiology of MR?

A
  • volume overload: need a larger SV to compensate for backflow
  • compensatory mechanisms: left atrial enlargement, LV hypertrophy, increased contractility
  • progressive LV overload > dilatation > heart failure
98
Q

How does MR present?

A
  • auscultation: apex beat is displaced downwards and laterally
  • intensity of murmur correlates with severity
  • S3 heart sound
  • exertion dyspnoea
  • heart failure (may coincide with inc haemodynamic burden)
99
Q

What investigations are done for MR?

A
  • ECG: LA enlargement, atrial fibrillation, LV hypertrophy
  • CXR: LA and central PA enlargement
  • GOLD: Echo: size estimation and valve structure
100
Q

How is MR managed?

A
  • rate control for AF: β blockers, CCB, digoxin
  • anticoagulation for AF and flutter
  • nitrates/diuretics
  • valve replacement if serious
101
Q

What is aortic regurgitation and what is its aetiology?

A
  • leakage of blood back from aorta into LV during diastole due to ineffective coming together of aortic cusps
  • bicuspid aortic valve
  • rheumatic fever and infective endocarditis
102
Q

What is the pathophysiology of aortic regurgitation?

A
  • combined pressure and volume overload due to backflow of blood in addition to circulating blood
  • leads to LV hypertrophy and dilatation. Progressive dilation > heart failure
103
Q

How does aortic regurgitation present?

A
  • wide pulse pressure
  • early diastolic blowing murmur at 2nd intercostal space on R sternal border
  • pulmonary oedema, pallor, sweating
104
Q

How is aortic regurgitation investigated?

A
  • GOLD: Echo: evaluate AV and aortic root, measure LV dimension and function
  • CXR: enlarged cardiac silhouette
105
Q

How is aortic regurgitation managed?

A
  • IE prophylaxis as differential diagnosis
  • ACEIs can improve SV and regurgitation
  • surgical valve replacement
106
Q

What is mitral stenosis and what causes it?

A
  • obstruction of LV inflow preventing proper filling during diastole
  • rheumatic carditis
107
Q

What causes dyspnoea in mitral stenosis?

A
  • progressive dyspnoea due to LA enlargement leading to pulmonary congestion
  • inc transmitral pressures > LA enlargement and AF
108
Q

How does mitral stenosis present?

A
  • mitral facies: vasoconstriction causing pink/purple tinge on face
  • low pitched diastolic rumble at apex
  • loud S1
  • opening snap after S2
109
Q

How is mitral stenosis investigated?

A
  • ECG: AF and LA enlargement
  • CXR: LA enlargement and pulmonary congestion
  • GOLD: Echo: mitral valve mobility, gradient, area
110
Q

How is mitral stenosis managed?

A
  • serial echocardiography
  • β blockers, CCBs, Digoxin, diuretics
  • percutaneous mitral balloon valvotomy
111
Q

What is infective endocarditis?

A
  • infection of heart valve(s) or other endocardial lined structures within the heart
  • damages the valves + can cause heart failure
112
Q

What are risk factors for infective endocarditis?

A
  • rheumatic heart disease
  • valvular degeneration/prosthetic valve
  • IV drug use
113
Q

What is the pathophysiology behind infective endocarditis?

A
  • endocardial damage > thrombi formation made of platelets and fibrin
  • valve cusps are avascular preventing normal immune response
  • high pressure makes infection more likely
  • thrombus is colonised by bacteria and these break off and travel round the bloodstream
  • tricuspid most commonly affected due to first contact w blood from body
114
Q

How does infective endocarditis present?

A
  • fever and heart murmur
  • haematuria (blood in urine)
  • splinter haemorrhages
  • Osler’s nodes (nodules on digits)
  • Janeway lesions (haemorrhages and nodules in fingers
  • Petechiae (small purple spots)
  • Roth spots (retinal haemorrhages)
  • malaise
115
Q

What is the Duke criteria?

A
  • major: 2 +ve blood cultures, echo shows vegetation
  • minor: immunological signs, septic emboli, 1 +ve culture, fever, IV drug user
  • present if: 2 major criteria, 1 major & 3 minor or 5 minor
116
Q

How is infective endocarditis investigated?

A
  • Transthoracic echo for vegetations
  • Raised CRP
  • ECG: showing new heart block, ischaemia or infarction
  • FBC, blood cultures, urinalysis
117
Q

How is infective endocarditis managed?

A
  • S. aureus: vancomycin + rifampicin
  • S. viridian: benzylpenicillin + gentamicin
  • surgery if valve incompetent
118
Q

What is aortic dissection?

A
  • tear in inner layer of aorta
  • blood found between intima and media creating a false lumen
  • MC in ascending aorta and aortic arch
119
Q

What are some causes of aortic dissection?

A
  • bicuspid aortic valve
  • coarctation of aorta
  • CABG
  • Ehlers-Danlos/Marfan’s syndrome
120
Q

How is aortic dissection classified?

A
  • R lateral area is most common site
  • Type A: affects ascending aorta, before brachiocephalic artery
  • Type B: descending aorta after L subclavian artery
121
Q

What are the risk factors for aortic dissection?

A
  • hypertension
  • age
  • male
  • smoking
  • poor diet
  • low physical activity
  • raised cholesterol
122
Q

How does aortic dissection present?

A
  • ripping/tearing pain in chest
  • pain in anterior chest if ascending aorta affected or back if descending aorta
  • hypertension > hypotension
  • radial pulse deficit/difference in bp between arms
  • diastolic murmur
  • focal neurological deficit
123
Q

What is a differential diagnosis for aortic dissection?

124
Q

How is aortic dissection diagnosed?

A
  • ECG and CXR exclude MI
  • widened mediastinum
  • 1st: CT/MRI angiogram
  • Gold: TOE shows intimal flap and false lumen
125
Q

How is aortic dissection managed?

A
  • analgesia for pain
  • β blockers to control BP and HR and reduce stress on walls
  • Type A: open surgery replaced with graft
  • Type B: thoracic endovascular aortic repair (TEVAR) using catheterisation
126
Q

What are some common complications of aortic dissection?

A
  • MI, stroke
  • paraplegia
  • cardiac tamponade
  • aortic regurgitation
127
Q

What is heart failure?

A
  • An inability of the heart to deliver blood (and oxygen) at a rate that meets the requirements of metabolising tissues despite normal or increased cardiac filling pressure
128
Q

What is the aetiology of heart failure?

A
  • IHD: MI
  • hypertension: inc strain
  • valvular disease
  • pericarditis/pericardial effusion
  • cardiomyopathy
  • alcohol
129
Q

What is the pathophysiology behind heart failure?

A
  • Heart failure causes a drop in MAP. This is compensated for by inc TPR, RAAS and vasoconstriction.
  • The compensatory mechanisms are not sustainable
  • causes inc afterload, workload and strain on the heart as well as fluid retention
130
Q

What are the different types of heart failure?

A
  • Systolic: inability to eject adequate volumes of blood
  • Diastolic: reduced compliance, filling and ejection
  • LHF: LV failure: ejection <40%
  • RHF: RV failure > pulmonary hypertension
  • Congestive HF: LV and RV failure
  • HFpEF: HF in normal/high CO due to inc metabolic demand
131
Q

What are the signs of heart failure?

A
  • tachycardia
  • 3rd heart sound (unless <25)
  • Raised JVP
  • displaced apex beat
  • peripheral oedema (R side - venous backlog) or pulmonary oedema (L side)
132
Q

What are some symptoms of heart failure?

A
  • dyspnoea
  • fatigue
  • paroxysmal nocturnal dyspnoea
  • cold peripheries
  • cough productive of pink frothy sputum
133
Q

What are the NY heart association classes of heart failure?

A

I: no limitation (asymptomatic)
II: slight limitation (mild HF)
III: Marked limitation (symptomatically moderate)
IV: inability to carry out physical activity without discomfort

134
Q

What investigations are done for heart failure?

A
  • b-type natriuretic peptide
  • ECG
  • CXR
  • Gold: Echo: checks diastolic volume and ejection fraction for heart failure
135
Q

What is ABCDE for heart failure?

A
  • alveolar oedema (batwing opacification)
  • Kerley B lines (interstitial oedema)
  • cardiomegaly
  • dilated upper lobe vessels
  • effusions (pleural)
136
Q

How is heart failure (reduced EF) managed?

A
  • ACEi (ARB if intolerant) and β blockers
  • diuretics: furosemide or spironolactone(K sparing)
  • neurohumoral blockade
137
Q

What is atrial fibrillation?

A
  • uncoordinated, rapid, irregular contraction of the atria
  • An irregularly irregular atrial firing rhythm
  • disorganised activity overriding SAN
  • can lead to heart failure due to poor filling in diastole
  • is a common cause of stroke
138
Q

How does atrial fibrillation present?

A
  • palpitations
  • tachycardia
  • shortness of breath
  • syncope
  • symptoms of associated conditions e.g. stroke, sepsis
139
Q

How is atrial fibrillation recognised on ECG?

A
  • Absent P waves
  • narrow QRS complex tachycardia
  • irregularly irregular ventricular rhythm
140
Q

How is atrial fibrillation managed?

A
  • treat underlying cause
  • rate and rhythm control
  • restore sinus rhythm: electrical/pharmacological cardioversion
141
Q

What is rate control for atrial fibrillation?

A
  • aims to extend diastole and coordinate filling
  • β blocker (1st line), CCB, Digoxin
142
Q

What is rhythm control in atrial fibrillation?

A
  • aims to return patient to a normal sinus rhythm
  • flecanide or amiodarone 1st line cardioversion or electrical using defib
  • long term: β blockers (1st line), dronedarone, amiodarone
143
Q

What are the causes of AF?

A
  • sepsis
  • mitral valve pathology
  • IHD
  • thyrotoxicosis
  • hypertension
144
Q

What is paroxysmal AF and how is it treated?

A
  • comes and goes in episodes <48 hrs
  • anticoagulation based on CHADSVASc score
  • pill in the pocket approach: flecanide
145
Q

What is the CHA2DS2VASc scoring system?

A
  • calculates stroke risk for AF
  • Congestive heart failure/left ventricular dysfunction
  • Hypertension
  • Age ≥75 (+2)
  • Diabetes
  • stroke/TIA (+2)
  • Vascular disease
  • Age 64-74 (+1)
  • Sex category (female)
  • score of ≥2 or ≥1 in men = anticoagulation offered
146
Q

How can AF lead to stroke?

A
  • uncontrolled and unorganised movement leads to stagnating blood, especially in atrial appendage
  • this leads to a thrombus which becomes an embolus
  • can lodge in brain
147
Q

What is atrial flutter?

A
  • A re-entrant rhythm where the electrical signal recirculates in a self-perpetuating loop
  • stimulates atrial contraction at 300bpm
  • signal enters ventricles every 2nd lap due to long refractory period at AV node
  • 150 bpm in ventricle
148
Q

How does atrial flutter present and how is its investigated and treated?

A
  • dyspnoea and palpitations
  • sawtooth appearance on ECG
  • rate/rhythm control
  • radiofrequency ablation
  • anticoagulation
149
Q

What is 1st degree heart block and how does it present on ECG?

A
  • delayed AV conduction through AV node
  • PR interval greater than 0.20 seconds
150
Q

What is 2nd degree heart block?

A
  • some atrial impulses don’t make it through the AV node > ventricles so some P waves aren’t followed by QRS complexes
  • Mobitz T1 and T2
151
Q

What is Mobitz type 1?

A
  • atrial impulses become weaker until they don’t pass through AV node.
  • fails to stimulate ventricular contraction
  • atrial impulse returns to strong and cycle repeats
  • shows as increasing PR interval until P wave no longer conducts to ventricles and QRS is missed then returns on next cycle
152
Q

What is Mobitz type 2?

A
  • failure or interruption of AV conduction
  • leads to missing QRS complexes
  • usually set ratio of P waves:QRS complexes
  • e.g. 3:1 block
153
Q

What is 3rd degree heart block?

A
  • complete heart block
  • no observable relationship between P waves and QRS complexes
  • significant risk of asystole
154
Q

How is heart block treated?

A
  • atropine
  • pacemaker
155
Q

What is supraventricular tachycardia?

A
  • caused by electrical signal re-entering atria from ventricles causing self-perpetuating loop
  • results in narrow complex tachycardia
  • appears on ECG as QRS, T, QRS, T…
156
Q

How is supraventricular tachycardia managed?

A
  • continuous ECG monitoring
  • Valsalva
  • carotid sinus massage
  • adenosine: slows cardiac conduction through AV node
  • same medications as AF
157
Q

What is the home and what is the clinical bp threshold for hypertension?

A

Home: 135/85
Clinic: 140/90
- higher in clinic due to white coat effect

158
Q

What investigations should be done for hypertension?

A
  • urine dip
  • ECG
  • HbA1c
  • renal function
  • fundoscopy: hypertensive retinopathy
  • lipid profile
  • QRISK
159
Q

What are the stages of hypertension?

A
  • 1: 140/90 or 135/85
  • 2: 160/100 or 150/95
  • 3: 180 and/or 110
160
Q

What medications are used to treat hypertension?

A
  • A: ACE inhibitor (ramipril)
  • B: β blocker (bisoprolol)
  • C: calcium channel blocker (amlodipine)
  • D: thiazide-like diuretic (indapamide)
  • ARB: can be used in place of ACEi
161
Q

What are the steps for choosing hypertension medications?

A
  • 1: <55 and non-black use A otherwise use C
  • 2: A+C or A+D or C+D. if black use ARB instead of A
  • 3: A+C+D
  • 4: A+C+D. spironolactone if K below 4.5mmol/l otherwise α/ β blocker
162
Q

What are the types of hypertension and the causes?

A
  • primary: idiopathic: 95% cases
  • secondary: renal disease, obesity, pregnancy, endocrine
163
Q

What is a dihydropyridine?

A
  • Calcium channel blocker
  • e.g. amlodipine
  • affects vascular smooth muscle
  • dilates peripheral arteries
164
Q

What is a phenylalkylamine?

A
  • Calcium channel blocker
  • e.g. verapamil
  • mainly affects heart
  • negatively chronotopic and inotropic
165
Q

How is coronary arterial thrombosis treated?

A
  • aspirin/antiplatelet agent (inhibits platelet function)
  • low molecular weight heparin
  • streptokinase/TPA (generates plasmin, degrades fibrin)
  • catheter directed thrombolysis
166
Q

How is cerebral arterial thrombosis treated and which drug should be avoided?

A
  • aspirin
  • catheter directed thrombolysis
  • reperfusion e.g. stent
  • heparin avoided due to inc risk of bleeding
167
Q

How is venous thrombosis treated?

A
  • DOACs (direct acting oral anticoagulants) e.g. apixaban, rivoraxaban
  • LMWH
  • warfarin
  • for DVT: compression stockings
168
Q

What is the presentation of DVT?

A
  • unilateral
  • leg pain
  • swelling, tenderness
  • warmth
  • discolouration
  • dilated superficial veins
169
Q

How is DVT/PE investigated?

A
  • D-dimer: normal excludes diagnosis but +ve doesn’t confirm
  • Gold: ultrasound
  • PE: CT coronary angiogram/VQ scan
170
Q

What are the causes and signs of cardiogenic shock?

A
  • heart pump failure, MI, cardiac tamponade, PE
  • heart failure signs, raised JVP, 4th heart sound
171
Q

What are the causes and treatment of septic shock?

A
  • uncontrolled bacterial infection
  • ABCDE and broad spectrum antibiotics
172
Q

What are the signs of septic shock?

A
  • pyrexic
  • warm peripheries
  • bounding pulse
  • tachycardia
173
Q

What are the causes of hypovolemic shock?

A
  • blood loss: trauma, GI bleed
  • fluid loss: dehydration
174
Q

What are the symptoms of hypovolaemic shock?

A
  • clammy, pale skin
  • confusion
  • hypotension
  • tachycardia
175
Q

What are the causes of neurogenic shock?

A
  • spinal cord trauma e.g. RTA
  • disrupted SNS, intact PSNS
176
Q

What are the symptoms and treatment of neurogenic shock?

A
  • hypotension, bradycardia, confusion, hypothermia
  • ABCDE, IV atropine
177
Q

What are the general signs of shock?

A
  • confusion
  • skin: pale, cold, sweaty, vasoconstriction
  • prolonged hypotension
  • inc capillary refill time
  • reduced GCS
  • weak, rapid pulse
178
Q

Describe anaphylactic shock?

A
  • IgE mediated type 1 hypersensitivity
  • hypotension, tachycardia, urticaria, puffy face
  • ABCDE, IM adrenaline
179
Q

What is the cause of rheumatic fever?

A
  • systemic response to group A β haemolytic strep
  • post strep pyogenes infection
  • typically pharyngitis
180
Q

What is the pathophysiology behind rheumatic fever?

A
  • proteins from S. pyogenes
  • Abs to bacterial cell wall cross react with heart valve tissue causing Ab mediated destruction/inflammation
181
Q

What are the major criteria of rheumatic fever?

A
  • Joint arthritis
  • nOdules (subcutaneous)
  • New murmur (esp mitral stenosis)
  • Erythema marginatum (rash with raised edges, clear centre)
  • Sydenham’s chorea (uncoordinated jerky movements)
182
Q

What are the minor criteria of rheumatic fever?

A
  • Fever
  • ECG changes (prolonged PR)
  • Arthralgia
  • Raised ESR/CRP
183
Q

What is the diagnosis of rheumatic fever?

A
  • recent strep infection + (2 major criteria) OR (1 major + 2 minor)
  • CXR: cardiomegaly
  • Echo
184
Q

How is rheumatic fever treated?

A
  • IV benzylpenicillin then penicillin V
  • haloperidol
  • bed rest
185
Q

What does right bundle branch block look like on ECG?

A
  • QRS > 0.12s
  • M shape in V1-3
  • W shape in V5-6
  • caused by PE and cor pulmonale
186
Q

What does left bundle branch block look like on ECG?

A
  • QRS > 0.12s
  • W shape in V1-3
  • M shape in V5-6
  • aortic stenosis, IHD, MI
187
Q

What is peripheral arterial disease?

A
  • narrowing of arteries supplying limbs
  • reduced blood supply
  • leads to claudication
188
Q

How does peripheral arterial disease present?

A
  • intermittent claudication
  • crampy pain after walking
  • after stopping and resting, pain disappears
  • calf, thighs, buttocks
189
Q

What are the investigations of peripheral arterial disease?

A
  • ultrasound
  • Ankle brachial pressure index (systolic in leg: arm)
190
Q

What is the management of peripheral arterial disease?

A
  • risk factor modification
  • atorvastatin, clopidogrel
  • endarterectomy, endovascular angioplasty
191
Q

What is MONAC?

A
  • management of acute ACS or MI
  • Morphine
  • Oxygen if sats <94%
  • fast acting Nitrates
  • Aspirin
  • Clopidogrel

Osha 2a (15 decks)

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