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Phase 2a Green Conditions > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Pathophysiology of IHD

A
  • primarily caused by atherosclerosis
  • when 70-80% sclerosed → exertional symptoms → angina
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2
Q

What is the mechanism of atherosclerotic plaque formation?

A
  1. fatty streaks
  2. intermediate lesions
  3. fibrous plaques of advanced lesions
  4. plaque rupture → infarction
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3
Q

What is an atherosclerotic plaque?

A

complex lesion consisting of:

  • lipid
  • necrotic core
  • connective tissue
  • fibrous cap
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4
Q

What are the major cell types involved in atherogenesis?

A
  • endothelium
  • macrophages
  • smooth muscle cells
  • platelets
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5
Q

What arteries does atherogenesis affect most commonly?

A
  • LAD
  • circumflex
  • RCA
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6
Q

Risk factors of IHD

A
  • family history
  • age
  • South Asian
  • smoking
  • poor nutrition
  • sedentary lifestyle
  • alcohol
  • stress
  • HTN
  • obesity
  • DM
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7
Q

Presentation of angina

A
  • constricting discomfort in front of chest, neck, shoulders, jaw or arms
  • precipitated by physical exertion
  • relieved by rest/GTN spray (5 mins)

normal exam

  • typical angina = all 3
  • atypical angina = 2
  • non anginal pain = 1/none
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8
Q

Investigations for IHD

A
  • ECG usually normal
  • lipid profile → high LDL
  • FBC
  • HbA1c

GOLD STANDARD = CT coronary angiography

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9
Q

Treatment of IHD

A
  • antiplatelet therapy → aspirin/clopidogrel
  • lipid lowering thearpy → statin
  • good hypertensive/glycaemic control
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10
Q

Treatment for angina

A
  • symptomatic relief = GTN spray
  • long term symptomatic relief = beta blocker/CCB
  • secondary prevention = AAA
  • PCI/CABG if extensive damage
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11
Q

What is the secondary prevention for angina?

A

AAA

  • aspirin
  • atorvastatin
  • ACEi
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12
Q

What surgical interventions are available for angina?

A
  • percutaneous coronary intervention
  • coronary artery bypass graft → preferred in patients with diabetes, >65
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13
Q

What is ACS?

A

Acute Coronary Syndrome
- thrombus from an atherosclerotic plaque blocking a coronary artery

  • unstable angina = ischaemia
  • STEMI = complete occlusion
  • NSTEMI = partial occlusion → subendocardial infarction
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14
Q

Presentation of ACS

A
  • central constricting chest pain radiating to jaw/arms
  • sweating
  • SOB
  • >20 mins
  • unstable angina → pain not relieved by rest or GTN spray
  • silent MI → in diabetics
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15
Q

ECG changes in ACS

A

STEMI
- ST segment elevation

NSTEMI/unstable angina

  • ST depression
  • deep T wave inversion
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16
Q

How do you differentiate between unstable angina and NSTEMI?

A
  • unstable angina = troponin normal
  • NSTEMI = troponin abnormal
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17
Q

Immediate management of ACS

A

MONAC

  • morphine
  • oxygen
  • nitrate
  • aspirin
  • clopidogrel
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18
Q

Management of STEMI

A

PCI within 120mins
- clopidogrel/prasugrel and aspirin

Fibrinolysis if not PCI eg alteplase
- ticagrelor and aspirin

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19
Q

Management of NSTEMI/unstable angina

A
  • GRACE score
  • fondaparinux

low risk

  • ticagrelor
  • aspirin

medium/high risk

  • angiography and PCI
  • prasugrel and aspirin
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20
Q

What is the GRACE score?

A
  • assess for PCI in NSTEMI
  • gives 6 month risk of death and repeat MI after having a NSTEMI
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21
Q

Secondary prevention of ACS

A

ACAB

  • ACEi
  • clopidogrel
  • aspirin and atorvastatin
  • beta blocker
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22
Q

What are the post MI complications

A

DREAD

  • death
  • rupture of heart septum/papillary muscles
  • edema (HF)
  • arrhythmias and aneurysms
  • Dressler’s syndrome
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23
Q

Definition of HTN

A
  • >140/90 in clinic (be aware of white coat HTN)
  • >135/85 with ABPM/home readings
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24
Q

Pathophysiology of HTN

A

95% idiopathic = essential HTN
rest = underlying cause → ROPE
- renal disease
- obesity
- pregnancy (pre-eclampsia)
- endocrine (Conns)

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25
Q

Risk factors for HTN

A
  • >65
  • family history
  • Afro-caribbean
  • alcohol intake
  • DM
  • sedentary lifestyle
  • sleep apnoea
  • smoking
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26
Q

Investigations for HTN

A
  1. clinic BP >140/90
  2. offer ABPM or home readings
  3. ABPM >135/95 = diagnosis confirmed
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27
Q

Stages of HTN

A
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28
Q

Further investigations for HTN

A
  • urine ACR, dipstick, bloods
  • ECG
  • hypertensive retinopathy → fundus examination
  • HbA1c
  • lipids
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29
Q

What medications can be used to treat HTN?

A

ABCDA

  • ACEi → ramipril
  • beta blocker → bisoprolol
  • CCB → amlodipine
  • diuretic (thiazide like) → indapamide
  • ARB → candesartan

ARB used instead of ACEi if

  • not tolerated (dry cough)
  • patient is black
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30
Q

When to offer medical management of HTN

A
  • stage 2 HTN
  • <80, stage 1 HTN, QRISK score 10%+, complications
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31
Q

NICE guideline treatment for HTN

A
  1. <55 and non-black = ACEi, >55 or black = CCB
  2. ACEi and CCB, alternative ACEi and D, CCB and D, if black use ARB not ACEi
  3. ACEi and CCB and D
  4. ACEi and CCB and D and additional
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32
Q

Definition of HF

A
  • CO is inadequate for body’s requirement
  • inability of heart to deliver blood and O2 at a rate the body needs to meet demand
  • physiological changes occur to maintain CO
  • eventually overwhelmed and become pathophysiological
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33
Q

Types of HF

A
  • systolic = inability of ventricles to contract normally
  • diastolic = inability of ventricles to relax and fill normally
  • can be left or right ventricular failure
  • acute or chronic HF
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34
Q

Causes of LHF

A
  • coronary artery disease
  • arrhythmias
  • MI
  • cardiomyopathy
  • congenital heart defects
  • valvular heart disease
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35
Q

Causes of RHF

A
  • COPD
  • pulmonary HTN
  • right ventricular infarct
  • cor pulmonale
  • progression of LHF
  • PE
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36
Q

Causes of systolic HF

A
  • IHD
  • MI
  • cardiomyopathy
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37
Q

Causes of diastolic HF

A
  • aortic stenosis
  • chronic HTN
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38
Q

Pathophysiology of HF

A
  1. myocardium fails
  2. decreased volume of blood ejected, increased preload
  3. increased ventricular load causes hypertrophy of myocardium
  4. increase in muscle growth to compensate and pump more blood out
  5. increased myocardial demand for oxygen
  6. myocardium becomes ischaemic → patchy fibrosis → stiffness and reduced contractibility
  7. decreased contractibility = increased workload and amount of blood remaining
  8. more force needed to maintain cardiac output
  9. cells become tired → pathological
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39
Q

How does HF activate RAAS

A
  • increased afterload and preload
  • increased cardiac work
  • damage to myocytes
  • decreased cardiac output
  • activates RAAS and adrenergic pathway
  • Na+ and water retention
  • increased HR and contraction force
  • cardiotoxicity
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40
Q

Common clinical presentation of HF

A
  • SOB
  • fatigue
  • peripheral oedema
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41
Q

Symptoms of LHF

A
  • exertional dyspnoea
  • orthopnoea
  • nocturnal cough
  • wheeze
  • nocturia
  • cold peripheries
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42
Q

Symptoms of RHF

A
  • peripheral oedema
  • ascites
  • facial engorgement
  • epistaxis
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43
Q

Signs of HF

A
  • tachycardia
  • elevated JVP
  • cardiomegaly
  • 3rd/4th heart sounds
  • displaced apex beat
  • bi-basal crackles
  • pleural/peripheral effusion
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44
Q

Investigations for HF

A
  • ECG → may indicate cause
  • BNP
  • chest xray
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45
Q

What is BNP

A
  • brain natriuretic peptide
  • marker of HF
  • released when myocardial walls are under stress
  • levels correlated to ventricular wall stress and HF severity
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46
Q

Chest xray findings in HF

A

ABCDE

  • alveolar oedema
  • B Kerley lines
  • cardiomegaly
  • dilated upper lobe vessels of lungs
  • effusions (pleural)
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47
Q

Treatment of HF

A
  • lifestyle changes
  • diuretics reduce preload and pressure on ventricles → loop/thiazide/aldosterone antagonist
  • ACEi for LV systolic dysfunction
  • beta blocker and spironolactone to decrease mortality
  • digoxin for symptom relief
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48
Q

What is cor pulmonale?

A

right sided HF caused by chronic pulmonary arterial HTN

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49
Q

Causes of cor pulmonale

A
  • chronic lung disease
  • pulmonary vascular disorders
  • neuromuscular and skeletal diseases
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50
Q

Signs and symptoms of cor pulmonale

A
  • cyanosis
  • tachycardia
  • raised JVP
  • RV heave
  • pan systolic murmur
  • hepatomegaly
  • oedema
  • dyspnoea
  • fatigue
  • syncope
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51
Q

Investigations for cor pulmonale

A
  • ABG → hypoxia +/- hypercapnia
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52
Q

Management of cor pulmonale

A
  • treat underlying cause
  • oxygen
  • same treatment as HF
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53
Q

Pathophysiology of PVD

A
  • commonly atherosclerosis → claudication of vessels
  • other causes of claudication = aortic coarctation, temporal arteritis, Burger’s
  • end stage PVD = critical limb ischaemia
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54
Q

Risk factors of PVD

A
  • hyperlipidaemia
  • history of CAD
  • age >40
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55
Q

What are the signs of critical limb ischaemia

A

6 Ps

  • pain
  • paresthesia
  • pulselessness
  • pallor
  • paralysis
  • poikilothermia = perishingly cold
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56
Q

Presentation of PVD

A
  • pain in lower limbs on excercise, relieved on rest = intermittent claudication
  • severe = unremitting pain in foot
  • legs may be pale, bold, loss of hair, skin changes
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57
Q

Investigation for PVD

A
  • ankle brachial pressure index ≤0.90
  • ABPI = doppler ultrasonography
  • should be 1
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58
Q

Treatment for PVD

A

control risk factors - lifestyle changes

antiplatelet therapy

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59
Q

Treatment for critical limb ischaemia

A

as stated plus:

  • revascularisation eg stenting, angioplasty, bypassing
  • amputation if unsuitable
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60
Q

What is pericarditis?

A

inflammation of the pericardium +/- effusion

2 types

  • fibrinous = dry
  • effusive → purulent serous/haemorrhagic
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61
Q

Causes of acute pericarditis

A
  • infection
  • autoimmune → RA, sjogren’s, SLE
  • secondary metastatic tumours
  • traumatic and iatrogenic
  • post cardiac injury
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62
Q

What infections can cause acute pericarditis?

A
  • enteroviruses
  • adenoviruses
  • mycobacterium TB
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63
Q

Pathophysiology of pericarditis

A
  1. inflammation
  2. narrowing of pericardial space and scarring
  3. if untreated, build up of exudate and adhesions in pericardial space → pericardial effusion
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64
Q

Symptoms of pericarditis

A
  • severe chest pain
  • dyspnoea
  • cough
  • hiccups
  • fever
  • myalgia
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65
Q

Signs of pericarditis

A
  • pericardial rub on auscultation
  • tachycardia
  • peripheral oedema
  • increased JVP
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66
Q

Investigations for pericarditis

A

ECG = DIAGNOSTIC

  • saddle shaped ST elevation
  • diffuse ST elevation in all leads
  • PR depression

chest xray → effusion may cause cardiomegaly

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67
Q

What is chest pain like in pericarditis

A
  • sharp, pleuritic, rapid onset
  • worse when laying flat, relieved sitting forwards
  • radiates to trapezius ridge
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68
Q

Treatment for pericarditis

A
  • reduce physical activity until symptoms resole
  • NSAIDs with gastric protection → ibuprofen/aspirin
  • colchicine 3 months
  • treat cause
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69
Q

What is infective endocarditis

A
  • an infection of the endocardium or vascular endothelium of the heart
  • fever and new murmur = infective endocarditis until proven otherwise
70
Q

What microorganisms cause infective endocarditis

A
  • staph aureus
  • streptococcus viridans
  • strep bovis
  • enterococci
  • coxiella burnetii
71
Q

Risk factors for infective endocarditis

A
  • IVDU
  • immunocompromised
  • people with prosthetic valves
  • aortic/mitral valve disease
  • poor dental hygiene
  • pacemakers
  • IV cannula
72
Q

Pathophysiology of infective endocarditis

A
  • abnormal cardiac endothelium and organisms in bloodstream
  • adherence and growth of organisms
  • infective endocarditis
  • LHS of heart = most common side effected
  • RHS affected in IVDU
73
Q

Symptoms of endocarditis

A
  • fever
  • rigors
  • night sweats
  • malaise
  • weight loss
74
Q

Signs of endocarditis

A
  • anaemia
  • splenomegaly
  • clubbing
  • new murmurs
  • sepsis
  • embolic events
75
Q

Typical presentation of endocarditis

A
  • embolic skin lesions
  • petechiae
  • splinter haemorrhages
  • osler nodes
  • janeway lesions
  • roth spots
76
Q

Investigations for endocarditis

A
  • Duke criteria
  • echo
  • ECG → long PR interval, regular

transoesophageal echo = more sensitive, uncomfortable, better at diagnosing

77
Q

Treatment for endocarditis

A
  • antibiotics
  • treat any complications
  • surgery
78
Q

What surgery can be used to treat endocarditis?

A
  • replace valve if infection cannot be treated with Abs
  • remove/replace infected devices
  • remove large vegetations at risk of embolising
79
Q

Prevention of endocarditis

A
  • good oral health
  • no IV drug use
  • educate surgery patients on symptoms
80
Q

What is pericardial effusion

A
  • occurs if pericarditis is untreated
  • buildup of exudate in pericardial space
  • puts pressure on cardiac myocytes → cardiac dysfunction
81
Q

Signs of pericardial effusion

A
  • bronchial breathing at left base
  • muffled heart sounds
82
Q

Treatment for pericardial effusion

A
  • treat the cause
  • pericardiocentesis

complication = cardiac tamponade

83
Q

What is cardiac tamponade

A
  • life threatening
  • accumulation of fluid in pericardial space
  • compression of heart chambers
  • decreased venous return and filling of heart
  • reduces cardiac output
84
Q

Symptoms and signs of cardiac tamponade

A
  • Beck’s triad
  • pulsus paradoxus = large decrease in stroke volume
85
Q

What is Beck’s triad?

A
  • falling BP
  • rising JVP
  • muffled heart sounds
86
Q

Investigations for cardiac tamponade

A

GOLD STANDARD = echo

87
Q

Treatment for cardiac tamponade

A

pericardiocentesis

88
Q

Murmur in mitral stenosis

A
  • mid-diastolic murmur with opening snap
89
Q

Symptoms of mitral stenosis

A
  • haemoptysis due to pulmonary oedema
  • palpitations AF
90
Q

Signs of mitral stenosis

A
  • malar flush
  • tapping apex beat
  • low volume pulse
  • loud S1
91
Q

Causes of mitral stenosis

A
  • rheumatic heart disease
  • IE
92
Q

Murmur in mitral regurgitation

A

pansystolic high pitched whistling murmur

93
Q

Symptoms of mitral regurgitation

A
  • palpitations
  • exertional dyspnoea
  • fatigue
  • weakness
94
Q

Signs of mitral regurgitation

A
  • AF
  • displaced, thrusting apex
  • soft/absent S1
95
Q

Causes of mitral regurgitation

A
  • idiopathic
  • IHD
  • rheumatic heart disease
  • EDS, Marfans
96
Q

Complication of mitral regurgitation

A

congestive HF

97
Q

Murmur in aortic stenosis

A

ejection systolic murmur

98
Q

Symptoms of aortic stenosis

A

triad of

  • syncope
  • angina
  • dyspnoea
99
Q

Signs of aortic stenosis

A
  • sustained heaving apex
  • slow rising pulse
  • narrow pulse pressure
  • soft S2 if severe
100
Q

Causes of aortic stenosis

A
  • idiopathic
  • rheumatic heart disease

AS = most common valve defect

101
Q

Murmur in aortic regurgitation

A
  • early diastolic murmur
  • Austin flint murmur at apex
102
Q

Symptoms of aortic regurgitation

A
  • palpitation
  • angina
  • dyspnoea
103
Q

Signs of aortic regurgitation

A
  • water hammer pulse
  • wide pulse pressure
  • displaced apex
  • Corrigan’s pulse → collapsing
104
Q

Causes of aortic regurgitation

A
  • idiopathic
  • EDS, Marfans
105
Q

Treatment for valve defects

A
  • treat symptoms
  • replace defective valve
106
Q

What is VTE?

A
  • venous thromboembolism
  • blood clots develop in circulation
  • due to stagnation of blood and hyper-cogulable states
107
Q

What is a DVT?

A
  • deep vein thrombosis
  • thrombus that develops in the venous circulation
108
Q

What is a PE?

A
  • pulmonary embolism
  • once thrombus develops, it can travel → embolise
  • deep veins → through RHS of heart → lungs → PE
109
Q

What is a complication of VTE?

A
  • if patient has a hole in heart, clot can pass through LHS of heart into systemic circulation
  • causes large stroke
110
Q

Risk factors for VTE

A
  • immobility, long haul travel
  • recent surgery
  • pregnancy
  • hormone therapy with oestrogen → pill, HRT
  • malignancy
  • polycythaemia
  • SLE
  • thrombophilia → antiphospholipid syndrome
111
Q

VTE prophylaxis

A
  • hospital admission → risk assessment for VTE
  • LMW heparin if high risk

contraindicated if active bleeding or existing coagulants

112
Q

Presentation of DVT

A
  • unilateral
  • calf/leg swelling
  • dilated superficial veins
  • calf tenderness
  • oedema
  • colour changes in leg
113
Q

What is a Wells score?

A

predicts risk of patients with symptoms having a DVT/PE

114
Q

Diagnosis of VTE

A

D-dimer

DIAGNOSTIC FOR DVT = doppler US leg

GOLD STANDaRD FOR PE = CT pulmonary angiogram
- V/P scan if contraindicated

115
Q

Initial management of VTE

A
  • anticoagulation
  • catheter directed thrombolysis
116
Q

Long-term anticoagulation in VTE

A

DOAC, warfarin, LMW heparin

  • 3 months if cause reversible
  • 3-6 months if active cancer
117
Q

What is an aneurysm?

A

weakening of vessel wall followed by dilation due to increased wall stress

118
Q

What is the most common vessel aneurysm?

A

abdominal aortic aneurysm

119
Q

Pathophysiology of aortic aneurysm

A
  1. inflammation and degeneration of smooth muscle cells
  2. loss of structural integrity of aortic wall
  3. vessel widens
  4. mechanical stress acts on weakened wall tissue
  5. can lead to dilation or rupture
120
Q

Complication of dilated aneurysm

A

peripheral thromboembolism

121
Q

Risk factors of aortic aneurysm

A
  • SMOKING
  • family history
  • connective tissue disorders
  • age
  • atherosclerosis
  • male
122
Q

Presentation of AAAs

A
  • most are asymptomatic
  • commonly found below renal arteries → infrarenal
  • if big, pulsatile mass on palpation, bruit on auscultation
  • lower back/abdominal pain if expanding rapidly
123
Q

Diagnosis of aortic aneurysms

A
  1. ultrasonography
124
Q

Management of aortic aneurysms

A

symptomatic → repair

asymptomatic
- surveillance
- if diameter >5.5cm (m) or >5cm (f) → repair

125
Q

Complications of aortic aneurysms

A
  • rupture of AAA
  • thromboembolism
  • fistula formation
126
Q

Presentation of ruptured AAA

A
  • acute onset of severe, tearing abdominal pain with radiation back, flank, groin
  • painful pulsatile mass
  • hypovolaemic shock
  • syncope
  • nausea, vomiting
127
Q

Diagnosis of ruptured AAA

A

clinical to save time

128
Q

Treatment of ruptured AAA

A
  • urgent surgery → endovascular aneurysmal repair
  • maintain haemodynamic stability
129
Q

What is an aortic dissection?

A
  • tear in the intimal layer of aorta
  • leads to collection of blood between intima and medial layers
  • mainly in ascending aorta
130
Q

Pathophysiology of aortic dissection

A
  • tear in intimal layer
  • blood passes through media propagating distally or proximally
  • false lumen
  • can occlude flow through branches of aorta
  • ischaemia of affected regions
130
Q

Pathophysiology of aortic dissection

A
  • tear in intimal layer
  • blood passes through media propagating distally or proximally
  • false lumen
  • can occlude flow through branches of aorta
  • ischaemia of affected regions
131
Q

Risk factors of aortic dissection

A

male
- 40-60
- HTN → most common
- trauma
- vasculitis
- cocaine use
- connective tissue disorders in younger adults

132
Q

Clinical features of aortic dissection

A
  • sudden and severe tearing pain in chest radiating to back
  • hypotension
  • asymmetrical BP
  • syncope
133
Q

Diagnosis of aortic dissection

A
  • ECG
  • chest xray
  • CT
134
Q

Management of aortic dissection

A
  • maintain haemodynamic stability
  • opioid analgesia
  • endovascular stent-graft repair
  • antihypertensives post surgery
135
Q

How do you maintain haemodynamic stability?

A
  • fluid resuscitation
  • ionotropes
  • noradrenaline
136
Q

What is atrial fibrillation?

A
  • chaotic irregular rhythm
  • irregular ventricular rate

ECG
- no P waves
- irregularly irregular QRS

137
Q

Causes of a fib

A
  • idiopathic
  • HTN
  • HF
  • coronary artery disease
  • valvlular heart disease
  • cardiac surgery
  • cardiomyopathy
  • rheumatic heat disease
138
Q

Pathophysiology of a fib

A
  • continuous rapid activation of atria
  • no organised mechanical action
  • 300-600bpm
139
Q

Risk factors for a fib

A
  • 60+
  • diabetes
  • high BP
  • past MI
  • structural heat disease
140
Q

Presentation of a fib

A
  • asymptomatic
  • palpitations
  • dyspnoea
  • chest pain
  • fatigue
  • apical pulse>radial
141
Q

Treatment of a fib

A

cardioversion

  • LMW heparin
  • shock with defib
142
Q

What is atrial flutter?

A
  • organised atrial rhythm
  • rate of 250-250bpm

ECG → saw tooth pattern = DIAGNOSTIC

143
Q

Causes of atrial flutter

A
  • idiopathic
  • coronary heart disease
  • obesity
  • HTN
  • HF
  • COPD
  • pericarditis
144
Q

Risk factors of atrial flutter

A

atrial fibrillation

145
Q

Presentation of atrial flutter

A
  • palpitations
  • breathlessness
  • chest pain
  • dizziness
  • syncope
  • fatigue
146
Q

Treatment of atrial flutter

A
  • cardioversion
  • catheter ablation → creates conduction block
  • IV amiodarone → restore sinus rhythm
147
Q

What is bundle branch block?

A
  • block in conduction of one of the bundle branches
  • ventricles don’t receive impulses at the same time
148
Q

ECG changes in right BBB

A
  • MaRRoW
  • wide QRS

DIAGNOSTIC

149
Q

Causes of right BBB

A
  • PE
  • IHD
  • atrial ventricular septal defect
150
Q

Causes of right BBB

A
  • PE
  • IHD
  • atrial ventricular septal defect
151
Q

Pathophysiology of right BBB

A
  • right bundle doesn’t conduct
  • impulse spread from LV to RV
  • late activation of RV
152
Q

Presentation of right BBB

A
  • asymptomatic
  • syncope/presyncope
153
Q

Treatment of right BBB

A
  • pacemaker
  • cardiac resynchronisation therapy
  • reduce BP
154
Q

ECG changes in left BBB

A
  • WiLLiaM
  • wide QTS and notched top
  • T wave inversion in lateral leads

DIAGNOSTIC

155
Q

Causes of left BBB

A
  • IHD
  • aortic valve disease
156
Q

Pathophysiology of left BBB

A
  • left bundle doesn’t conduct
  • impulse spreads from RV to LV
  • late activation of LV
157
Q

Presentation of left BBB

A

same as right BBB

158
Q

Treatment of left BBB

A

same as right BBB

159
Q

What is heart block?

A

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

160
Q

What are the different types of heart block?

A

1st degree

2nd degree

  • Mobitz I
  • Mobitz II

3rd degree

161
Q

1st degree heart block

A
  • PR interval >200ms
  • asymptomatic
162
Q

ECG changes 2nd degree Mobitz I

A
  • progressive lengthening of PR interval
  • one non-conducted P wave
  • next PR interval is shorter
163
Q

Presentation of 2nd degree Mobitz I

A
  • light headedness
  • dizziness
  • syncope
164
Q

ECG changes in 2nd degree Mobitz II

A
  • SOB
  • postural hypotension
  • chest pain
165
Q

ECG changes in 3rd degree heart block

A
  • P waves and QRS at different rates → dissociation
  • abnormally shaped QRS
166
Q

Presentation of 3rd degree heart block

A
  • dizziness
  • blackouts
167
Q

Treatment for 3rd degree heart block

A
  • permanent pacemaker
  • IV atropine
168
Q

Causes of heart block

A
  • athletes
  • sick sinus rhythm
  • MI
  • drugs
  • congenital
  • aortic valve calcification
  • cardiac surgery/trauma
169
Q

Treatment for heart block

A
  • cardioversion
  • catheter ablation
  • IV amiodarone

Phase 2a Green Conditions (10 decks)

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