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Phase 2a medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is acute coronary syndrome?

A

Umbrella term that describes ST elevation MI, unstable angina, non-ST elevation MI
All have same pathology - plaque rupture leads to thrombosis and inflammation
Rarely due to emboli, coronary spasm and necrosis

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2
Q

What is an ST elevation MI?

A 
Complete occlusion of a major coronary artery previously affected by atherosclerosis
Full thickness damage of heart muscle
Pathological Q waves some time after MI
ST segment is elevated
Tall T waves
May be new LBBB in larger MIs
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3
Q

What is unstable angina?

A

Angina of recent onset
Cardiac chest pain with crescendo pattern
Deterioration in previously stable angina with symptoms frequently occurring at rest
Angina of increasing frequency or severity, occurs on minimal exertion or even at rest

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4
Q

What is a non-ST elevation MI?

A

Occurs by developing a complete occlusion of a minor vessel or partial occlusion of a major artery previously affected by atherosclerosis
Retrospective diagnosis made on troponin results
Partial thickness damage of heart muscle
Non-Q wave infarction - ST depression and/or T wave inversion
Thrombus occluding vessel, rise in serum troponin or creatinine kinase

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5
Q

What are the 5 types of MI?

A

Type 1 - spontaneous MI with ischaemia due to a primary coronary event
Type 2 - MI secondary to ischaemia due to increase O2 demand or decreased supply such as coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension
Type 3,4,5 - MI due to sudden cardiac death, relatd to PCI and related to CABG respectively

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6
Q

Name 5 factors that could increase your risk of having an ACS

A 
Age
Male
Family history of IHD - MI in first degree relative below 55
Smoking
Hypertension
DM
Hyperlipidaemia
Obesity, sedentary lifestyle
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7
Q

Name 5 causes of ACS

A

Atheroma/stenosis of coronary arteries impairing blood flow
Valvular disease
Aortic stenosis
Arrhythmia
Anaemia - loss O2 transported to heart muscles

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8
Q

What occurs to the heart during an ACS attack?

A

Death of cardiac myocytes due to myocardial ischaemia
Rupture or erosion of fibrous cap of coronary artery plaque
Leads to platelet aggregation and adhesion, localised thrombus formation, vasoconstriction, and distal thrombus embolisation
Thrombus formation -> fibrotic plaque -> atherosclerotic plaque -> plaque rupture/fissure and thrombosis -> MI or ischaemic stroke or critical leg ischaemia or sudden CVS death
Unstable angina - partial occlusion, plaque has necrotic centre and ulcerated cap
MI - plaque has necrotic core but thrombus results in total occlusion

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9
Q

How does unstable angina present?

A

Chest pain, new onset, at rest with crescendo pattern
Breathlessness
Pleuritic chest pain
Indigestion
Recent destabilisation of pre-existing angina with moderate or severe limitations of daily
exercise
Troponin normal, normal/undetermined ECG

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10
Q

How does MI present?

A 
Acute central chest pain lasting more than 20 minutes associated with sweating, nausea, dyspnoea, fatigue, SOB, palpitations
May present w/o chest pain in elderly or diabetics
Distress/anxiety
Pallor
Increased pulse and reduced BP
Reduced 4th heart sound
Signs of HF - increased JVP
Tachy/bradycardic
Peripheral oedema
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11
Q

What could be a differential diagnosis of ACS?

A 
Stable angina
Pericarditis
Myocarditis
Aortic dissection
Pulmonary embolism
Pleurisy 
Oesophageal reflux/spasm
Rib fracture, chest trauma, costochondritis
GORD
Anxiety/panic attack
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12
Q

How is ACS treated?

A 
Pain relief - GTN spray (angina), IV opioid 
Anti-emetics
Oxygen - if hypoxic
Antiplatelets - aspirin, P2Y12 inhibitors, glycoprotein IIb/IIIa agonists
Beta-blockers
Statins
ACE inhibitors
Coronary revascularisation
Risk factor modifications
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13
Q

How does ischaemia present on an ECG?

A

ST depression and T wave flattening

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14
Q

What investigations would you do on a patient with suspected unstable angina?

A

FBC - anaemia aggravates it
Cardiac enzymes - excludes infarction
ECG - when pain shows ST depression
Coronary angiography

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15
Q

What is a myocardial infarction?

A

Plaque rupture leads to clot formation that occludes one of the coronary arteries causing myocardial cell death and inflammation

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16
Q

What are the symptoms of an MI?

A 
Acute central chest pain radiating to jaw or shoulder
Lasting > 20 mins
Nausea
SOB
Plapitations
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17
Q

What are the signs of an MI?

A

Clammy and pale
4th heart sounds
Pansystolic murmur
May later develop peripheral oedema

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18
Q

How would you manage an acute MI?

A

12 lead ECG
O2 if stats < 94%
IV access for bloods and enzymes
Brief history = RFs pulse, BP, JVP, murmurs, signs of congestive cardiac failure
300mg aspirin PO
Morphine 5-10mg IV and an anti-emetic
Refer for PCI or thrombolysis ASAP as long as not contraindicated
B-blocker IV and ACE-I if evidence of HF and patient normotensive

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19
Q

What management would you put in place for a patient who had had an acute MI?

A

Aspirin 75mg OD, reduces risk of repetition
B-blocker - long term, if contraindicated then verapamil
ACE-I if in HF
Statin - reduced cholesterol post-MI beneficial
Address modificable risk factors
Return to work after 2 months
Encorage exercise and no air travel for 2 months

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20
Q

What is an acute myocardial infarction?

A

Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial ischaemia due to complete occlusion of artery by thrombosis

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21
Q

How common are MIs?

A

5/1000 per annum in UK of STEMI
STEMI most common medical emergency
Worse prognosis in elderly and those with left ventricular failure
Early mortality - 30% outside hospital, 15% in
Late mortality - 5-10% first year, 2-5% annually after

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22
Q

What are the 2 types of MI?

A

STEMI - complete occlusion of major coronary artery previously affected by atherosclerosis
NSTEMI - complete occlusion on minor or partial occlusion of major coronary artery

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23
Q

Name 5 risk factors for development of an MI

A 
Increasing age
Male
History of premature coronary heart disease
Premature menopause
Diabetes
Smoking
Hypertension
Hyperlipidaemia
Obesity and sedentary lifestyle
Family history of IHD - MI in first degree relative below 55
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24
Q

What pathology occurs in a STEMI?

A

Sub-endocardial myocardium initially affected but continued ischaemia, infarct zone extends through sub-endocardial myocardium, producing a transmural Q wave MI
Early reperfusion may salvage regions of myocardium - reducing future mortality and morbidity

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25
Q

How does an NSTEMI present on an ECG?

A

Diagnosis made retrospectively after troponin results
ST depression and T wave inversion
Troponin I or T increased
Myoglobin released

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26
Q

Name 5 complications of an acute MI?

A

Sudden death - due to ventricular fibrillation
Arrhythmias - electrical instability following infarction
Pericarditis - transmural infarct resulting in inflammation of pericardium in STEMI
Cardiac rupture
Ventricular aneurysm - due to stretching of newly formed collagenous scar tissue

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27
Q

What is angina?

A

Chest pain or discomfort as a result of reversible myocardial ischaemia
Usually implies narrowing of one or more of the coronary arteries
Tends to be exacerbated on exertion and relieved by rest

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28
Q

How common is angina?

A

More common in men
1.7% deaths per year
7% CV events per year

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29
Q

What are the different types of angina?

A

Stable angina - induced by effort, relieved by rest
Unstable angina - crescendo angina, angina of recent onset (less than 24h) or deterioration in previously stable angina with symptoms frequently occurring at rest, occurs on minimal exertion or even at rest
Prinzmetal’s angina - caused by coronary artery spasm (rare)

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30
Q

Give 5 risk factors for developing angina

A 
Smoking 
Sedentary lifestyle
Obesity
Hypertension
DM
Family history
Genetics
Age
Hypercholesterolaemia
Depression/anxiety
Stress - high demand/low control
Hostile, competitive behaviour
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31
Q

Give 5 possible causes of angina

A

Atheroma/stenosis of coronary arteries impairing blood flow (most common)
Valvular disease
Aortic stenosis
Arrythmia
Anaemia - less O2 transported to heart muscle

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32
Q

What occurs during angina?

A

Mismatch between blood supply and metabolic demand
Ischaemic metabolites including adenosine stimulate nerve endings producing pain
Athersclerosis
Plaque continues to encroach upon lumen - increased risk of haemorrhage or exposure to tissue HLA-DR antigens which might stimulate T cell accumulation
Drives inflammation reaction against part of plaque contents
Complications develop including ulceration, fissuring, calcifcation and aneurysm change

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33
Q

How does Ohm’s law link to angina?

A

Adaptation
As plaque progresses to 50% vascular lumen size, vessel can no longer compensate by re-modelling and becomes narrowed
Drives variable cell turnover within plaque with new matrix surfaces and degradation of matrix
May progress to unstable plaque

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34
Q

How does stable angina present?

A

Central chest tightness and heaviness
Provoked by exertion, especially after meal or in the cold weather or by anger or excitement
Relieved at rest or by GTN spray
Pain may radiate to one or both arms, neck, jaw or teeth
Dyspnoea, nausea, sweatiness, faintness, palpitations, syncope

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35
Q

How is stable angina diagnosed?

A

12 lead ECG - often normal, possible ST depression, flat/inverted T waves, look for signs of past MI
Treadmill test - ECG whilst patient running uphill on treadmill, monitor time can exercise for, ST depression, sign of late ischaemia, many patients unsuitable
CT scan calcium storing - CT heart if atherosclerosis in arteries calcium will light up white, significant Ca indicates angina
SPECT/myoview - radiolabelled tracer injected into patient, taken up into coronary arteries as good blood supply, areas of little blood supply will not light up, no light after exercise indicative of myocardial ischaemia
Cardiac catheterisation
Bloods - anaemia
CXR - heart size, pulmonary vessels
Angiogram - shows luminal narrowing

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36
Q

Name 5 differential diagnoses of angina

A 
Pericarditis/myocarditis
PE
Chest infection
Dissection of aorta
GORD
Costochondritis
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37
Q

How is stable angina treated?

A

Reassure
Modify modifiable risk factors
Treat underlying conditons
Drugs - aspirin, statins, b-blockers, GTN spray, CCB, ivabradine
Revascularisation - stents, only when patient not stable on drugs
CABG, PCTA

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38
Q

What is a coronary artery bypass graft?

A 
Bypass surgeries
Internal mammary artery for left side
Saphenous vein for right side
Good prognosis but longer recovery
Not for frail
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39
Q

What is PCTA?

A

Stenting or ballooning the narrowing, risk of restenosis or thrombosis, less invasive

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40
Q

What is atherosclerosis?

A

Deposition of fatty deposits within inner walls of arteries
Causes hardening of arteries
Formation of focal elevated lesions in intima of large and medium sized arteries such as coronary arteries
Fatty streaks present from around 10 years of age

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41
Q

What coronary arteries are most commonly occluded by atherosclerosis?

A

LAD, circumflex and right coronary

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42
Q

Name 5 risk factors for developing atherosclerosis?

A 
Age - tends to be over 50s, progressive, chronic disease
Tobacco smoking - free radicals damage endothelium
High serum cholesterol
Obesity - metabolic syndrome, increase systemic lipids
Diabetes
FHx
Hypertension - shearing forces
Sex
Race
Sedentary lifestyle
Alcohol consumption
Stress
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43
Q

What is that pathophysiology of atherosclerosis?

A

Formed of lipid, necrotic core, connective tissue, fibrous cap
Injury to epithelial cells leading to endothelial dysfunction
Activation of endothelial cells - signals sent to circulating leukocytes which accumulate and migrate into vessel wall - monocytes and T helper cells
Inflammation
LDL deposited in intima, accumulates in arterial wall, undergoes oxidation and glycation
Monocytes -> macrophages that then phagocytose LDLs and become foam cells
Foam cells promote migration of SMC from media to intima and SMC proliferation
Increase SMC proliferation leads to more collagen synthesis
Foam cells die releasing contents driving growth of plaque
Growth of plaque increases pressure causing plaque to rupture leading to coagulation cascade in blood vessel leading to thrombosis

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44
Q

Name 5 conditions atherosclerosis can cause

A

MI
Angina - stable and unstable
Stroke
Gangrene

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45
Q

How is atherosclerosis treated?

A 
Percutaneous coronary artery intervention (PCI)
Toxal, sirolimus
Aspirin - COX-1 inhibitor
Clopidogrel/ticargrelor
Statins
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46
Q

How is an atherosclerotic plaque composed?

A

Central lipid core
Cap of fibrous tissue
Covered by arterial endothelium
Cap - made of collagen (produced by SMCs), inflammatory cells reside here (macrophages, T lymphocytes, mast cells)

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47
Q

What are foam cells?

A

Macrophages that have phagocytosed oxidised lipoproteins, also release chemokines to attract more macrophages, release IGF1 (growth factor) causing SMC to migrate to intima and to proliferation, proinflammatory cytokines, DNA

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48
Q

Why is diabetes a risk factor for atherosclerosis?

A

Increased free radicals which increases oxidation of LDLs

Less NO so less relaxation of blood vessels

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49
Q

What primary prevention methods could you use to prevent atherosclerosis?

A

Lifestyle changes

  • Decrease alcohol intake
  • Improve diet - less fats, salt and sugar
  • Increase amount of physical activity
  • Stop smoking
  • Try to lose some weight
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50
Q

What secondary prevention methods could you used to prevent the progression of atherosclerosis?

A 
Statin treatment
Aspirin
Anti-hypertensives
Help with nicotine replacement therapies to help stop smoking
Lifestyle advice
Diabetic clinic and refer to dietician
GTN spray
Gym voucher
Weight loss groups
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51
Q

What is heart failure?

A

Inability of heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolising tissues despite the normal or increased cardiac filling pressures
Impairment of heart contractility - LV systolic dysfunction most common
State where heart unable to pump enough blood to satisfy the needs of metabolising tissues
Symptomatic condition where breathlessness, fluid retention and fatiuge are associated with a cardiac abnormality that reduces CO

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52
Q

What is heart failure with diastolic function?

A

Heart requires energy to relax, problem with not relaxing (hypertension)
Preserved ejection fraction

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53
Q

What is ischaemic HF?

A

Reduced blood supply to heart

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54
Q

What is valvular HF?

A

Damage or defect in one of four valves

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55
Q

What is myopathic HF?

A

Disease of heart muscle, makes it harder to pump blood around body

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56
Q

What is hypertensive HF?

A

Due to overworking of heart

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57
Q

What is cor pulmonale?

A

High BP in pulmonary arteries leading to right sided HF

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58
Q

How common is HF?

A 
Common 2-20%
2% NHS expenditure
Disabiling
Deadly
80% HF death within 5 years
Treatable
Median age 80
Majority chronic
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59
Q

What are the different types of HF?

A

Actute HF = acute decompensated CHF
- Generally under 70, male, LV ejection fraction < 40%
Acute heart failure - 71-76, equally male and female, 50% LVEF > 40%
Chronic HF

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60
Q

What is the NYHA classification?

A

New York Heart Association classificaiton
Class I - high risk of developing HF
Class II - slight limitation (mild HF)
Class III - marked limitation (moderate HF)
Class IV - inability to carry out any physical activity without discomfort (severe HF)

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61
Q

What are the stages of HF?

A

A - high risk of developing HF
B - asymptomatic HF
C - symptomatic HF
D - end-stage HF

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62
Q

Name 5 causes of HF

A 
Hypertension
Alcohol excess
Cardiomyopathy
Endocardial
Pericardial
MI
Obesity
Superimposed infection
AF and arrhythmias
Excess alcohol
Endocrine
NSAIDs
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63
Q

Name 5 risk factors for developing HF

A 
Hypertension
Cardiomyopathy
Hypertension
Coronary artery disease
Heart attack
Diabetes
Certain medications - NSAIDs
Congenital heart defects
Valvular heart disease
Viruses
Alcohol, smoking
Obesity
Irregular heart beats
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64
Q

What are the symptoms of HF?

A 
SOB
Fatigue
Ankle swelling
Non-specific symptoms
Cold peripheries
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65
Q

What are the signs of HF?

A

Acute - pleural oedema
Chronic - ankle oedema and abdominal ascites
Crackles and tachycardia non-specific but sensitive
Murmurs

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66
Q

How is HF diagnosed?

A

CXR/blood tests - FBC, LFTs, U&Es, BNP, TFTs, B-type natriuretic peptide (raised in HF)
Cardiac enzymes - creatinine kinase, troponin I and T
ECG
Echo (TTE) - done within 48 hours
Myocardial perfusion imaging
Raised NTproBNP - 72% chance of having HF
CXR

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67
Q

Name 5 differential diagnoses of HF

A 
COPD
PE
Pneumothorax
Anaphylaxis
Asthma
Pneumonia
Foreign body obstruction
ACS
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68
Q

How is HF treated?

A

Loop diuretics - to treat severe oedema, symptomatic treatment of congestion
ACE-I
Aldosterone antagonist
B-blockers
ARB (angiotensin II receptor blockers) - instead of ACEI if contraindicated
Calcium glycoside
Surgery - mitral/aortic valve repair/replacement
Defibrillator
Palliative care
1st line - ACEI, low dose, slow uptitration
2nd line - aldsoterone antagonist
Digoxin/ivabradine
Lifestyle - education, obesity control, diet, smoking cessation, cardiac rehab

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69
Q

Give 5 complications of HF

A 
Renal dysfunction
Rhythm disturbances
Systemic thromboembolism
DVT and PE
LBBB and bradycardia
Hepatic dysfunction
Neurological and psychological complications
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70
Q

How is CO calculated?

A

CO = HR x SV

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71
Q

What is the difference between systolic HF and diastolic HF?

A 
Sytolic
- Failure to contract
- EF < 40%
- IHD, MI, CM
Diastolic
- Inability to relax and fill
- EF > 50%
- Constritive pericarditis, cardiac tamponade (accumulation of fluid in pericardial space), hypertension
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72
Q

What is the difference between low output HF and high output HF?

A

Low
- Decreased CO, fails to increase with exertion
- Could be due to pump failure, excessive pre-load, chronic increased afterload
High
- Anaemia
- Pregnancy
- Hyperthyroidism

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73
Q

What occurs during HF?

A

Once heart begins to fail compensatory changes occur

As HF progresses, these compensatory changes become overwhelmed (pathological)

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74
Q

What compensatory changes occur in HF?

A

Sympathetic stimulation - increases afterload by causing peripheral vasoconstriction
RAAS - salt and water retention, increases afterload and preload (increases volume and vasoconstriction)
Cardiac changes - ventricular dilatation, myocyte hypertrophy
Increased preload

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75
Q

What are the symptoms of left-sided heart failure?

A

Exertional dyspnoea
Fatigue
Paroxysmal noturnal dyspnoea
Nocturnal cough - pink, frothy sputum

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76
Q

What are the signs of left-sided heart failure?

A 
Cardiomegaly (displaced apex beat)
3rd and 4th heart sounds
Crepitations in lung bases
Weight loss
Reduced BP
Tachycardia
Cool peripheries
Heart murmur
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77
Q

What are the symptoms of right sided HF?

A

Peripheral oedema
Ascites
Nausea
Anorexia

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78
Q

What are the signs of right sided HF?

A 
Raised JVP
Hepatomegaly
Pitting oedema
Ascites
Weight gain (fluid)
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79
Q

What can cause right sided HF?

A

LV failure
Pulmonary stenosis
Lung disease (cor pulmonale)

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80
Q

What can be seen on a CXR in HF?

A 
ABCDE
Alveolar oedema
Kerley B lines (interstital oedema)
Cardiomegaly
Dilated prominent upper lobe vessels
Pleural Effusion
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81
Q

How do you treat acute HF?

A 
100% oxygen
Nitrates - GTN (dilate vessels)
IV opiates
IV furosemide (to reduce fluid overload)
Inotropic drug - to increase contractility of dilated vessels
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82
Q

How do you treat chronic HF?

A

ACEI/ARB (valsartan)
B-blockers
CCB and other vasodilators
Diuretics and digoxin (furosemide)

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83
Q

What is the difference between primary and secondary hypertension?

A

Primary - high BP that doesn’t have a secondary cause
Secondary - high BP that does have a secondary cause eg kidney disease, adrenal disease, thyroid problems, obstructive sleep apnoea, high aldosterone
Most cases primary

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84
Q

What is the epidemiology of hypertension?

A 
Often symptomless - requires screening
Major risk factor in CVD
Remains under diagnosed, under treated and poorly controlled
Prevalence in those older than 35
More common in men
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85
Q

What is stage 1 hypertension?

A

More than or equal to 140/90mmHg clinic BP
Daytime ABPM greater than or equal to 135/85mmHg
Don’t need to treat unless increased risk of CVS events due to diabetes/end-organ damage (stroke, TIA, MI) or high QRISK
30-40% increased risk of death per 10mmHg
5 year lower life expectancy on average if untreated

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86
Q

What is stage 2 hypertension?

A

More than or equal to 160/100mmHg clinic BP

Daytime averge ABPM greater than or equal to 150/95mmHg

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87
Q

What is stage 3 hypertension?

A

Clinic systolic BP greater than or equal to 180mmHg and/or diastolic greater than or equal to 110mmHg
Start immediate anti-hypertensive drug treatment

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88
Q

What are the possible causes of essential/primary hypertension?

A 
Primary cause unknown
Multifactorial involving
Genetic susceptibility
Excessive sympathetic nervous system activity
Abnormalities of Na/K membrane transport
High salt intake
Abnormalities in RAAS
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89
Q

What are the potential causes of secondary hypertension?

A

Renal disease
Pregnancy
Endocrine causes - Cushing’s (corticosteroids), Conn’s (aldosterone), phaemochromocytoma (catecholamines - vasoconstriction, increased cardiac contractility, increased in HR)
Coarctation of aorta
Drugs - corticosteroids, cyclosporin, erythropoietin, contraceptive pill, SSRIs, NSAIDs, immunosuppressives, cold cures
Alcohol, amphetamines, ecstasy, cocaine

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90
Q

Name 5 risk factors for developing hypertension

A 
FHx
Age
Race - more common in Afro-Caribbean population
Overweight/obese
Sedentary lifestyle
Smoking
Too much salt
Alcohol
Diabetes
Stress
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91
Q

What vascular changes occur in hypertension?

A

Accelerates atherosclerosis due to shearing forces exerted on vessel walls
Thickening of media of muscular arteries
Smaller arteries and arterioles typically affected
Results in endothelial cell dysfunction associated with impaired NO mediated dilatation and enhance secretion of vasoconstrictors including endothelins and prostaglandins

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92
Q

What is hypertension a major risk factor for?

A

IHD
Intracerebral haemorrhage
Renal disease (cause and result) - kidney size often redued, small vessels show intimal thickening and medial hypertrophy, numbers of sclerotic glomeruli increased

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93
Q

What is malignant hypertension?

A

Markedly raised diastolic pressure, usually over 120mmHg and progressive renal disease
Rare
Renal vascular changes prominent and usually evidence of acute haemorrhage and papilloedema
Can occur in previously fit individuals, often black males in 30s-40s

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94
Q

How does malignant hypertension present?

A

Proteinuria - if affecting kidneys

Haemorrhages/papilloedema (swelling of optic nerve) - worse prognosis than cancer

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95
Q

How is malignant hypertension diagnosed?

A

Look for end-organ damage
Urinalysis - albumin-creatinine ratio, protein, haematuria
Blood tests - serum creatinine, eGFR, fasting glucose, cholesterol
Fundoscopy/ophthalmoscopy
ECG - LV hypertrophy, past MI
Echo - LV hypertrophy
24h ABPM

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96
Q

How is hypertension treated?

A 
Treatment goal 140/90mmHg
Change diet - high consumption of fruit/veg and low fat
Regular physical exercise
Reduce alcohol intake
Reduce salt intake
Lose weight if obese
Stop smoking - increases CVS risk
ACD pathway
Lifelong treatment
Check BP every 6 months
Withhold certain drugs in pregnancy
Withhold during surgery
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97
Q

What is the ACD pathway?

A

For treating hypertension in under 55s or non-Afro-Caribbeans
ACE-I eg ramipril (or ARB if ACE-I contraindicated)
CCB
Diuretics
Beta-blockers if combination of all 3 don’t work
Also consider addition of spironolactone, high dose thiazide-like diuretic, alpha-blocker

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98
Q

How do you treat hypertension in over 55s and Afro-Caribbeans?

A

CCB 1st line

Add ACEI/ARB after CCB not working

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99
Q

What are the potential complications of hypertension?

A 
Stroke
MI
HF
Angina
T2DM
Vascular dementia
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100
Q

What are the two types of aortic aneurysm?

A

Abdominal aortic aneurysm - aortic diameter exceeding 3cm

Thoracic abdominal diameter

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101
Q

When is AAA more common?

A

More commonly occurs below renal arteries
Incidence increases with age
More common in men
5% of population over 60

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102
Q

When is TAA more common?

A

Ascending thoraco-abdominal aneurysms occur more commonly in patients with Marfan’s or hypertension
Descending/arch TAAs secondary to atherosclerosis

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103
Q

Name 5 risk factors for developing AAA?

A 
Severe atherosclerotic damage
FHx
Smoking
Male
Increasing age
Hypertension
COPD
Trauma
Hyperlipidaemia
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104
Q

Name 5 risk factors for developing TAA

A 
Strong genetic link - autosomal dominant trait
Certain connective tissue disorders - Marfan's, Ehler's-danlos, Loeys-dietz
Mycotic aneurysm endocarditis
Aortic dissection
Weight lifting, cocaine, amphetamine use - rise in BP
Hypertension
Increasing age
Smoking
Bicuspid/unicuspid aortic valves
Atherosclerosis
COPD
Renal failure
Previous aortic aneurysm repair
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105
Q

Why does an AAA occur?

A

Degradation of elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and SMC loss
Dilatation affects all 3 layers of vascular tunic
Doesn’t then pseudoaneurysm

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106
Q

Why does TAA occur?

A

Inflammation, proteolysis and reduced survival of SMCs in aortic wall
Once aorta reaches crucial diameter, loses all distensibility so rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture

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107
Q

How does an unruptured AAA present?

A

Often asymptomatic
Picked up via routine examination
Pain in abdomen, back, loin or groin
Pulsatile abdominal swelling

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108
Q

How does a ruputred AAA present?

A 
More likely if hypertension, female, smoker, strong FHx
Intermittent/continuous abdominal pain (radiating to back, iliac fossa/groin)
Pulsatile abdominal swelling
Collapse
Hypotension
Tachycardia
Profound anaemia
Sudden death
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109
Q

How does a TAA present?

A 
Most asymptomatic
Diagnosed incidentally
Pain in chest/neck/upper back/mid-back/epigastrium
Aortic regurgitation
Fever if infective cause
Symptoms due to compression of local strucutures
Acute pain
Collapse, shock, sudden death
Cardiac tamponade
Haemoptysis
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110
Q

Give 5 differential diagnoses of AAA

A 
GI bleed
Ischaemic bowel
MSK pain
Perforated GI ulcer
Pyelonephritis
Appendicitis
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111
Q

Give 4 differential diagnoses of TAA

A

Thoracic back pain
Arterial ischaemia
Collapse
MI

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112
Q

How is an AAA diagnosed?

A

Abdominal ultrasound - can assess aorta to degree of 3mm

CT an MRI angiography scans

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113
Q

How is TAA diagnosed?

A

CT/MRI
Aortography - assess position of key branches relative to aneurysm
Transoesophageal echo
Ultrasound

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114
Q

How is an AAA treated?

A

Small aneurysms below 5.5cm generally monitored
Treat underlying causes
Modify risk factors
Smoking cessation
Vigorous BP control
Lowering of lipids in blood
Surgery - if larger than 5.5cm and expanding yearly and symptomatic - open surgical repair/endovascular repair

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115
Q

How is a TAA treated?

A 
Immediate urgent surgery required for ruptured
Symptomatic - surgery regardless of size
Regular CT/MRI monitoring every 6 months
Rigorous BP control with B-blockers
Smoking cessation
Treat underlying cause
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116
Q

What is an aortic dissection?

A

Tear in aorta causing inner and middle layer of aortic wall to separate

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117
Q

How common is aortic dissection?

A

Medical emergency that can lead to death
Affects more men than women
Most common between 50-70, rare below 40
Very rare in children

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118
Q

How is aortic dissection classified?

A

Classified by timing of diagnosis from origin of symptoms
Acute - less than 2 wks
Subacute - 2-8 wks
Chronic - more than 8 wks

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119
Q

What are the potential causes of aortic dissection?

A

Inherited
Degenerative eg cystic medial disease (degenerative disease of aortic wall)
Atherosclerotic
Inflammatory eg giant cell arteritis
Trauma eg shearing stresses in RTA
Connective tissue disorders eg Marfan’s and Ehlers-Danlos

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120
Q

What occurs when an aortic dissection happens?

A

Begins with tear in intima
Blood under pressure then penetrates the diseased medial layer and flows between the layers of the aorta, forcing the layers apart resulting in dissection
Blood forms a haematoma separating the intima from the adventitia and creating a false lumen
False lumen extends for a variable distance in either direction - anterograde/retrograde

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121
Q

Where is an aortic dissection most likely to happen?

A

Within 2-3cm of aortic valve

Distal to left subclavian artery in descending aorta

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122
Q

How does an aortic dissection present?

A

Sudden onset of severe and central chest pain radiating to back and down arms - mimics an MI
Pain often described as tearing in nature - may be migratory
Hypertension
Pain maximal from time of onset - unlike MI where pain gains in intensity
Shock
Neurological symptoms secondary to loss of blood supply to spinal cord
Aortic regurgitation, coronary ischaemia and cardiac tamponade
Distal extension may produce acute kidney failure, acute lower limb ischaemia or visceral ischaemia
Peripheral pulses may be absent

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123
Q

Name 5 differential diagnoses for aortic dissection

A

ACS, MI, aortic regurgitation without dissection, MSK pain, pericarditis, cholecystitis, atherosclerotic embolism

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124
Q

How is aortic dissection diagnosed?

A

CXR - widened mediastinum

Urgent CT, transoesophageal echo or MRI will confirm diagnosis

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125
Q

How is aortic dissection treated?

A 
If hypertension - urgent anti-hypertensive medication to reduce BP to less than 120mmHg - IV B-blockers or vasodilators
Analgesia - morphine
Surgery to replace aortic arch
Endovascular intervention with stents
Long term follow up with CT or MRI
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126
Q

What is aortic stenosis?

A

Narrowing of aortic valve resulting in obstruction of left ventricular stroke volume leading to symptoms of chest pain, breathlessness, syncope and fatigue
Normal aortic valve 3-4cm2
Symptoms occur when valve area 1/4 of normal

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127
Q

What is aortic regurgitation?

A

Leakage of blood into LV from aorta during diastole due to ineffective coaptation of aortic cusps
Can be associated with aortic stenosis

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128
Q

What is the classification of aortic stenosis?

A

Supravalvular
Subvalvular
Valvular - most common

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129
Q

What are the main causes of aortic stenosis?

A

Calcific aortic valvular - essentially calcification of aortic valve resulting in stenosis
Calcification of congenital bicuspid aortic valve
Rheumatic heart disease

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130
Q

What are the main causes of aortic regurgitation?

A

Rheumatic fever
Congenital bicuspid aortic valve
IE

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131
Q

What are the risk factors that could lead to aortic stenosis?

A

Congenital bicuspid aortic valve

Male

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132
Q

What are the risk factors that could lead to aortic regurgitation?

A

Marfan’s and Ehlers-Danlos syndrome
SLE
Aortic dilatation
IE or aortic dissection

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133
Q

What occurs during aortic stenosis?

A

Narrowing obstructed LV emptying and pressure gradient develops between LV and aorta resulting in increased afterload
Increased LV pressure and compensatory LV hypertrophy
Results in relative ischaemia of LV myocardium and consequent angina, arrhythmias and LV failure
Obstruction to LV emptying relatively more severe on exercise
When compensatory mechanisms exhausted LV function rapidly declines

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134
Q

What occurs during aortic regurgitation?

A

Reflux of blood from aorta through aortic valve into LV during diastole
LV dilation and hypertrophy to maintain total volume of blood ejected from LV
Progressive dilation leads to HF
Diastolic pressure falls due to regurgitation so coronary perfusion decreases
Large LV size mechanically less efficient, demand for O2 greater and cardiac ischaemia develops
Combined pressure and volume overload

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135
Q

How does aortic stenosis present?

A 
Syncope
Angina
HF
Dyspnoea on exertion due to HF
Sudden death
Slow rising carotid pulse and decreased pulse amplitude
Heart sounds - soft/absent S2, prominent S4 due to LV hypertrophy, ejection systolic murmur (crescendo-decresendo)
Pulsus tardus - late
Pulsus parvus - weak
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136
Q

How does aortic regurgitation present?

A 
Asymptomatic for years
Exertional dyspnoea
Orthopnoea - dyspnoea 
lying down
Paroxysmal nocturnal dyspnoea
Palpitations
Angina
Syncope
Wide pulse pressure
Apex beat displaced laterally
Early diastolic murmur at L sternal border
Systolic ejection murmur
Collapsing water hammer pulse
Quincke's sign - capillary pulsation in nail beds
De Musset's sign - head nodding with heart beat
Pistol shot femoral - sharp bang heard
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137
Q

What could be a differential diagnosis for aortic stenosis?

A

Aortic regurgitation

Subacute bacterial endocarditis

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138
Q

What could be a differential diagnosis for aortic regurgitation?

A

HF
IE
Mitral regurgitation

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139
Q

How is aortic stenosis diagnosed?

A

Echo - LV size and function, doppler derived gradient and valve area, diagnostic
ECG - LV hypertrophy, LA delay, LV strain pattern due to pressure overload - depressed ST segments and T wave inversion in leads orientated towards LV
CXR - LV hypertrophy, calcified aortic valve

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140
Q

How is aortic regurgitation diagnosed?

A

Echo - evaluation of aortic valve and aortic root, measurement of LV dimensions and function, cornerstone decision making and follow up evaluation
CXR - enlarged cardiac silhouette and aortic root enlargement
ECG - LV hypertrophy due to volume overload, tall R waves and deeply inverted T waves in left-sided chest leads, deep S waves in R side leads

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141
Q

How is aortic stenosis treated?

A

Rigorous dental hygiene, IE prophylaxis in dental procedures
Limited role for medication as mechanical problem
Vasodilators contraindicated in severe as may trigger hypotension and syncope
Surgical aortic valve replacement definitive treatment - any patients with severe, decreasing EF, undergoing CABG with moderate/severe
Transcatheter aortic valve implantation (TAVI) - if not fit for surgery

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142
Q

How is aortic regurgitation treated?

A

Vasodilators such as ACEi improve stroke volume and reduce regurgitation but only if symptomatic
Serial echos to monitor progression
Surgery for valve replacement before LV dysfunction

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143
Q

What is atrial fibrillation?

A

Choatic irregular atrial rhythm at 300-600bpm, AV node responds intermittently, hence irregular ventricular rate
Mechanically ineffective

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144
Q

How common is AF?

A

Most common sustained cardiac arrhythmia
Males more than females
5-15% patients over 75
Paroxysmal (self-terminating) or persistent

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145
Q

How is AF classified?

A

Acute - onset within previous 48h
Paroxysmal - stops spontaneously within 7 days
Recurrent - 2 or more episodes
Persistent - continuous for more than 7 days and not self-terminating
Permanent

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146
Q

What can cause AF?

A 
Idiopathic
Any condition resulting in raised arterial pressure, increased muscle mass, atrial fibrosis or inflammation and infiltration of atrium
Hypertension
HF
Coronary artery disease
Valvular heart disease especially mitral stenosis
Cardiac surgery
Cardiomyopathy
Rheumatic heart disease
Acute excess alcohol intoxication
Thyrotoxicosis
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147
Q

Name 5 risk factors for developing AF

A 
Older than 60
Diabetes
Hypertension
Coronary artery disease
Prior MI
Structural heart disease
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148
Q

What occurs during atrial fibrillation?

A

Continuous rapid activation of atria by multiple re-entry waves 300-600/min
Rapidly depolarising automatic foci, located within pulmonary veins
Atria respond electrically at this rate, no coordinated mechanical action, only proportion of impulses conducted to ventricles due to refractory period of AVN
Ventricular response depends on rate and regularity of atrial activity, entry to AV node, balance between sympathetic and parasympathetic tone
CO drops 10-20% as ventricles not primed reliably by atria
Higher risk of thrombotic events, blood pools and remains still and clots
HR - 120-180bpm

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149
Q

How does AF present?

A 
Asymptomatic
Palpitations
Dyspnoea or chest pains
Fatigue
HF
No P waves
Rapid and irregular QRS rhythm
Apical pulse rate greater than radial rate
1st heart sound variable intensity 
Irregularly irregular pulse
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150
Q

How is AF diagnosed?

A

ECG - absent P waves, irregular and rapid QRS complex

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151
Q

What could be a differential diagnosis of AF?

A

Atrial flutter

Supraventricular tachyarrhythmias

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152
Q

How if AF treated?

A

Acute management - when due to acute precipitating event, cardioversion (conversion to sinus rhythm electrically or pharamcologically), ventricular rate control with drugs that block AV node eg CCB, B-blocker, digoxin, anti-arrhythmic
Long term and stable patient management
- Rate control - AV nodal slowing agents plus oral coagulation - B-blockers/CCB/digoxin
- Rhyhtm control - for younger, symptomatic and physically activate patients, cardioversion and amiodarone, anti-coagulation
Calculate stroke risk - 5x risk of stroke (embolism due to thrombus formed in atrium)

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153
Q

What is the target INR with treatment with warfarin?

A

2-3

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154
Q

What is atrial flutter?

A

Organised atrial rhythm with an atrial rate typically between 250-350bpm

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155
Q

How common is atrial flutter?

A

Often associated with atrial fibrillation and frequently require similar initial therapeutic approach
Paroxysmal or persistent
Much less common than atrial fibrillation

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156
Q

Name 5 things that can cause atrial flutter

A 
Idiopathic
Coronary heart disease
Obesity
Hypertension
HF
COPD
Pericarditis
Acute excess alcohol intoxication
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157
Q

What is a risk factor for developing atrial flutter?

A

Atrial fibrillation

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158
Q

What occurs during atrial flutter?

A

Continuous rapid activation of atria by multiple re-entry wavelets
Rapidly repolarising automatic foci, located within pulmonary veins
Atria respond electrically at this rate, no co-ordinated mechanical action, only proportion on impulses conducted to ventricles
Ventricular response depends on rate and regularity of atrial activity, entry to AV node, balance between sympathetic and parasympathetic tone
CO drops 10-20% as ventricles not primed reliably by atria
Higher risk of thrombotic events, blood pools and remains still and clots

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159
Q

How does atrial flutter present?

A 
Palpitations
Breathlessness
Chest pain
Dizziness
Syncope
Fatigue
Atrial rate - 300bpm
Ventricular rate - 150bpm
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160
Q

How is atrial flutter diagnosed?

A

ECG - definitive
Regular saw-tooth like atrial flutter waves between QRS complexes due to continuous atrial depolarisation
F waves may be unmasked by slowing AV conduction by carotid sinus massage or IV adenosine

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161
Q

What could be a differential diagnosis of atrial flutter?

A

Atrial fibrillation

Supraventricular tachyarrhythmias

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162
Q

How is atrial flutter treated?

A

Electrical cardioversion but anti-coagulated before
Catheter ablation - create conduction block
IV amiodarone to restore sinus rhythm and use beta-blocker to suppress further arrhythmias

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163
Q

How is atrial flutter different to atrial fibrillation?

A

Atrial flutter - atria beat regularly but more often

Atrial fibrillation - atria beat irregularly and faster

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164
Q

What is a cardiac arrhythmia?

A

Abnormality of cardiac rhythm

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165
Q

Give 5 complications of cardiac arrhythmias

A 
Sudden death
Syncope
HF
Chest pain
Dizziness
Palpitations
Asymptomatic
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166
Q

What is bradycardia?

A

Heart rate slow < 60 bpm during day and < 50 bpm at night
Usually asymptomatic unless heart very slow
Normal in athletes due to increased vagal tone and thus parasympathetic activity

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167
Q

What is tachycardia?

A

Heart rate fast > 100 bpm

More symptomatic when arrythmia fast and sustained

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168
Q

How can tachycardias be further classified?

A

Supraventricular tachycardia - arise from atrium or AV junction
Ventricular tachycardia - arise from ventricles

169
Q

What can cause bradycardia?

A

Extrinsic (treat underlying cause) - drug therapy BB digoxin, hypothyroidism, hypothermia, raised intracranial pressure
Intrinsic (treat with atropine or temporary pacing in acute cases) - acute ischaemia, infarction of SAN, sick sinus syndrome

170
Q

What is long QT syndrome?

A

ECG where ventricular repolarisation (QT interval) is greatly prolonged

171
Q

What can cause long QT syndrome?

A

Congenital - Jervell-Lange-Nielsen syndrome (autosomal recessive mutation in cardiac potassium and sodium-channel genes), Romano-Ward syndrome (autosomal dominant)
Acquired - hypokalaemia, hypocalcaemia, drugs (amiodarone, tricyclic antidepressants), bradycardia, acute MI, diabetes

172
Q

How does long QT syndrome present?

A

Syncope
Palpitations
Polymorphic ventricular tachycardia usually terminates spontaneously but may degenerate to ventricular fibrillation

173
Q

How do you treat long QT syndrome?

A

Treat underlying cause

If acquires give IV isoprenaline (contraindicated for congenital)

174
Q

What is mitral stenosis?

A

Obstruction of left ventricle inflow that prevents proper filling during diastole
Normal valve area = 4-6cm2
Symptoms begin at less than 2cm2

175
Q

What is mitral regurgitation?

A

Backflow of blood from LV to LA during sytole

Mild physiological MR seen in 80% normal individuals

176
Q

What can cause mitral stenosis?

A

Rheumatic heart disease secondary to rheumatic fever (infection with group A beta-haemolytic streptococcus), inflammation leads to commisural fusion and reduction in mitral valve orifice area causing charateristic pattern seen on echo
Progresses to valve thickening, cusp fusion, calcium deposition, severely narrowed valve orifice and progressive immobility of valve cusps
Prevalence and incidence decreasing due to a reduction of rheumatic heart disease
Also - IE, mitral annular clacification, congenital

177
Q

What can cause mitral regurgitation?

A

Abnormalities of valve leaflets, chordae tendinae, papillary muscles/LV
Mitral valve prolapse
Ischaemic mitral valve
Rheumatic heart disease
IE
Papillary muscle dysfunction/rupture, dilated cardiomyopathy

178
Q

Name 2 risk factors for developing mitral valve stenosis

A

History of rheumatic fever

Untreated strep infection

179
Q

Name 5 risk factors for developing mitral regurgitation

A 
Female
Lower BMI
Advanced age
Renal dysfunction
Prior MI
180
Q

What happens to the heart in mitral stenosis?

A

Thickening and immobility of valve leads to obstruction of blood flow from LA to LV
LA pressure increases = LA hypertrophy and dilatation
Pulmonary venous, arterial and right heart pressure increases
Increase in pulmonary capillary pressure = pulmonary oedema
Partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction
Pulmonary hypertension leads to RV hypertrophy, dilatation and failure with subsequent tricuspid regurgitation

181
Q

What happens to the heart in mitral regurgitation?

A

Regurgitation into LA = LA dilatation but little increase in LA pressure in longstanding regurgitation
Pure volume overload due to leakage of blood into LA during sytole
LA enlargement, LV hypertrophy to maintain CO and increases contractility
Progressive LA dilatation and RV dysfunction due to pulmonary hypertension
Progressive LV volume overload leads to dilatation and progressive HF

182
Q

How does mitral stenosis present?

A

No symptoms until 2cm2
Progressive dyspnoea due to LA dilatation (pulmonary congestion) worse with exercise, fever, tachycardia, pregnancy
Haemoptysis - rupture of bronchial vessels due to increases pulmonary pressure
RHF - pulmonary hypertension, weakness, fatigue, abdominal and lower limb swelling
AF - LA dilatation = palpitations
Systemic emboli (AF)
Mitral facies - bilateral, cyanotic or dusky pink discolouration over upper cheeks due to vasoconstriction in response to lowered CO
Heart sounds - diastolic murmur, lower opening S1 snap, tapping non-displaced apex beat
Chest pain
Low volume pulse

183
Q

How does mitral regurgitation present?

A

Auscultation - soft S1 and pan systolic murmur at apex radiating to axilla, prominent S3, displaced hyperdynamic apex
Exertional dyspnoea - pulmonary venous hypertension
Fatigue and lethargy - reduced CO
Increased SV felt as palpitation
RHF symptoms and eventually congestive HF

184
Q

How is mitral stenosis diagnosed?

A

CXR - LA enlargement, pulmonary oedema/congestion, calcified mitral valve
ECG - AF, LA enlargement
Echo - assess mobility, gradient and area

185
Q

How is mitral regurgitation diagnosed?

A

ECG - LA englargement, AF, LV hypertrophy
CXR - LA enlargement, central pulmonary artery enlargement, LV enlargement
Echo - estimation of LA and V size and function, valve structure assessment, transoesophageal

186
Q

How is mitral stenosis treated?

A 
Mechanical problem
B-blocker control HR (if in AF) and prolongue disatole for improved diastolic filling
Diuretics for fluid overload
Anticoagulate - warfarin
Percutaneous mitral balloon valvotomy
Mitral valve replacement
187
Q

How is mitral regurgitation treated?

A 
Vasodilators - ACEI
HR control for AF - BBs, CCB, digoxin
Anticoagulation for AF and flutter
Diuretics for fluid over load
Serial echo
- Mild 2-3 years
- Moderate 1-2 years
- Severe 6-12 months
Surgery for any symptomatic patient at rest or exercise for repair
If asymptomatic EF less than 60%, new onset AF
188
Q

What is pericarditis?

A

Inflammatory pericardial syndrome with/without effusion

189
Q

What can cause pericarditis?

A

Viral (most) - enterovirus, herpesvirus, adenovirus, parvovirus B19, EBV, mumps, coxsackie B
Bacterial - mycobacterium TB, pneumonia, rheumatic fever, staph, strep
Autoimmune - Sjorgren’s, RA, scleroderma, systemic vasculitis
Neoplastic - secondary metastatic tumours, lymphoma
Metabolic - uraemia, myoxedema
Traumatic and iatrogenic - early onset (rare - direct/indirect injury), delayed onset (pericardial injury syndromes, iatrogenic trauma)
Other - amyloidosis, aortic dissecion, pulmonary arterial hypertension, chronic HF, post-MI

190
Q

How does a major pericarditis present?

A 
Fever > 38
Subacute onset
Large pericardial effusion
Cardiac tamponade
Lack of response to aspirin/NSAIDs after at least 1 wk therapy
191
Q

What can cause a minor pericarditis?

A

Myopericarditis
Immunosuppression
Trauma
Oral anticoagulation therapy

192
Q

How does pericarditis present?

A

Chest pain - severe, sharp pleuritic pain, rapid onset, left anterior chest/epigastrium, radiates to arm, relieved by sitting forwards
Dyspnoea, cough, hiccups
Viral prodrome, antecedent fever
Skin rash, joint pain, eye Sx, weight loss

193
Q

How is pericarditis diagnosed?

A 
Pericardial rub
Sinus tachycardia
Tachypnoea
Fever
Signs of effusion
Beck's triad - hypotension, elevated jugualr veins, distant muffled heart sounds
ECG
Bloods - FBC, CRP, cardiac enzyme
CXR
Echo
194
Q

Name 5 differential diagnoses of pericarditis

A 
Pneumonia
Pleurisy
PE
Chostocondritis
GORD
Myocardial ischaemia/infarction
Aortic dissection
Pneumothorax
Pancreatitis
Peritonitis
Herpes zoster - shingles
ECG pericarditis
Blood tests
195
Q

How is pericarditis treated?

A

Sedentary activity until resolution of symptoms and ESR/CRP - mainly for athletes 3 months
NSAID (ibuprofen 600mg TDS 2 wks) or aspirin (750-1000mg BD 2wk) large dose for pain and inflammation
Colchicine (0.5mg BD 3 wk) limited by nausea and diarrhoea, reduces recurrence
Corticosteroids for symptomatic relief
Manage complications

196
Q

What does a saddle-shaped ST and PR depression suggest?

A

Pericarditis

197
Q

What do tall tented T waves and pathological Q waves suggest?

A

Hyperkalaemia

198
Q

What does ST depression suggest?

A

Stable angina

199
Q

What do absent P waves suggest?

A

Atrial fibrillation

200
Q

What does an early diastolic heart murmur suggest?

A

Mitral stenosis

201
Q

What does and early-systolic click suggest?

A

Mechanical heart valve

202
Q

What does an ejection systolic crescendo-decrescendo murmur suggest?

A

Unstable angina

203
Q

What does an end-diastolic heart murmur suggest?

A

Aortic stenosis

204
Q

What does a pansystolic murmur suggest?

A

Mitral regurgitation

205
Q

What is peripheral vascular disease?

A

Partial blockage of leg or peripheral vessels vy an atherosclerotic plaque and/or resulting thrombus in insufficient perfusion of lower limb resulting in lower limb ischaemia
Commonly caused by atherosclerosis and usually affects aorta-iliac and infra-inguinal arteries

206
Q

What is acute lower limb ischaemia?

A

May occur because of embolic or thrombotic disease

Rapid decrease in lower limb blood flow due to acute occlusion of peripheral artery

207
Q

What is thrombotic disease?

A

Chronic atherosclerotic stenosis in patient who has previously reported symptoms of claudication

208
Q

In whom is peripheral vascular disease more common?

A

Men

209
Q

Name 5 risk factors for developing peripheral vascular disease

A 
Smoking
Hypertension
Diabetes
Hypercholesterolaemia
Physical inactivity
Obesity
210
Q

What occurs in chronic lower limb ischaemia?

A

Always due to atherosclerosis of arteries distal to aortic arch
Symptoms of ischaemia

211
Q

What occurs in mild ischaemia?

A

Stress induced by physiological malfunction
Exercise induced angina
Intermitted claudication - cramping pain induced by exercise
Pain as a result of lactic acid produciton
Leg pulses often absent
Pain distal to site of atheroma

212
Q

What occurs in moderate ischaemia?

A

Structural and functional breakdown
Ischaemic cardiac failure
Critical limb ischaemia
Vascular dementia

213
Q

What occurs in severe ischaemia?

A

Infarction

Gangrene

214
Q

How does thrombotic disease present?

A 
6Ps
Pain
Pallor
Perishingly cold
Pulselessness
Paralysis
Paraesthesia
The more Ps, the more sudden and complete the ischaemia
215
Q

Name 3 differential diagnoses for PVD?

A

Osteoarthritis of hip/knee due to knee pain at rest
Peripheral neuropathy - paraesthesia
Arteritis

216
Q

How do you diagnose PVD?

A

Exclude arteritis - ESR/CRP raised in arteritis
FBC - Hb to exclude anaemia/polycythaemia
ECG - cardiac ischaemia
Ankle/brachial pressure index 0.5-0.9 = intermittent claudication, less than 0.5 = critical leg ischaemia
Colour duplex ultrasound
MRICT

217
Q

How do you treat PVD?

A

Risk factor modification - smoking cessation. antiplatelets ect
Revascularisation for critical ischaemia
Bypass procedure
Amputation for severe

218
Q

How do you treat acute ischaemia?

A

Surgical emergency - revascularisation within 4-6hrs to save limb

219
Q

What is intermittent claudication?

A

Ischaemic pain
Tissue not dying just suffering
Moderate/mild exercise, O2 debt resulting in lactic acid - pain

220
Q

What is critical ischaemia?

A

Tissue dying and suffering at rest
Blood supply inadequate to allow basal metabolism
No reserve available for increased demand
Resting pain - typically nocturnal
Gangrene/infection risk

221
Q

Give 2 signs/symptoms of critical ischaemia

A

Severe nocturnal pain in all toes of left foot only relieved by hanging foot over edge of bed (gravity for perfusion)
Non-healing painful ulcer on big toe with no trauma

222
Q

Give 3 signs/symptoms of acute ischaemia

A

Acute MI
Loss of use of R side of body
Fast, irregular pulse

223
Q

What is shock?

A

Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised hypoxia and/or an inability of cells to utilise oxygen
Low BP systolic < 90mmHg

224
Q

What can cause hypovolaemic shock?

A

Low blood volume

225
Q

What can cause cardiogenic shock?

A

Heart not pumping

226
Q

What can cause distributive shock?

A

Septic shock
Anaphylactic shock
Neurogenic shock

227
Q

What can cause anaemic shock?

A

Not enough O2 carring capacity

228
Q

What can cause cytotoxic shock?

A

Cell poisoned

229
Q

What is ‘Tennis score’?

A

Score for staging of hypovolaemic shock
Class 1 - 15% blood loss, pulse below 100bpm, normal BP, PP normal, resp rate 14-20, slightly anxious
Class 2 - 15-30% blood loos, pulse greater than 100bpm (tachycardic), BP normal (autonomic response), PP decreased, resp rate 20-30, mildly anxious
Class 3 - 30-40% blood loss, pulse above 120bpm, resp rate 30-40, PP decreased, confused

230
Q

What occurs in hypovolaemic shock?

A

Secondary to haemorrhagic shock
Loss of blood due to GI bleed, trauma, peri/post operative, splenic rupture
Loss of fluid - dehydration, burns, pancreatitis

231
Q

What can cause cardiogenic shock?

A 
Cardiac tamponade - limits CO
PE - flow of blood to lungs blocked
Acute MI
Fluid overload
Myocarditis - inflammation of muscle
232
Q

What occurs in septic shock?

A

Shock when infection becomes out of control
Disruptive shock
Systemic inflammatory response associated with infection
Sepsis complicated by persistent hypotension that is unresponsive to fluid resuscitation
Acute vasodilation from inflammatory cytokines

233
Q

What occurs in anaphylactic shock?

A

Release of IgE due to allergic response
Intense allergic reaction
Massive release of histamine and other vasoactive mediators causing haemodynamic collapse
Accompanied by breathlessness and wheeze due to bronchospasm

234
Q

What happens in the heart during shock?

A

Reduction in ventricular filling leading to a fall in BP and SV reducing hypotension
Reduced stimulation of baroreceptors in aortic arch and carotid sinuses resulting in increases sympathetic activity with release of noradrenaline and adrenaline
Vasoconstriction and increased myocardial contractility and HR to help restore BP and CO
Reduction of perfusion of renal cortex stimulating juxtaglomerular apparatus to release renin
Vasopressin released in response to decreased blood volume - aquaporin 2 channels increased water retention
Cortisol - fluid retention
Glucagon - raised blood sugar levels

235
Q

How does shock present?

A 
Skin pale, cold, sweaty and vasoconstricted
Pulse weak and rapid
PP reduced 
Reduced urine output
Confusion, weakness, collapse, coma
236
Q

How does hypovolaemic shock present?

A 
Skin cold, pale, clammy, slate grey
Drowsiness and confusion - inadequate tissue perfusion
Increased sympathetic tone
Tachycardia - narrow PP, weak pulse
Sweating
BP maintained but later hypotension
237
Q

How does cardiogenic shock present?

A

Signs of heart failure
Raised JVP
Gallop rhythm
Basal crackles and pulmonary oedema

238
Q

How does septic shock present?

A 
Pyrexia and rigors
Nausea and vomiting
Vasodilation with warm peripheries
Bounding pulse
Temp > 38 or < 36
Tachycardia > 90bpm
RR > 20 breaths/min
WBC > 12 x10^9/L or < 4x10^9/L
239
Q

How does anaphylactic shock present?

A 
Signs of profound vasodilation
Warm peripheries
Low BP
Tachycardia
Bronchospasm
Pulmonary oedema
240
Q

How is shock diagnosed?

A

Capillary refill time

More than 3 seconds to refill after 5 seconds compression = bad

241
Q

How is shock treated?

A

ABC
B - 100% O2 and correct immediately if life threatening problems such as congestive HF, bronchospasm, tension pneumothorax
C - establish IV access, fluids and blood if acute blood loss, ensure haemostasis
In septic shock - take blood cultures before antibiotics

242
Q

What is a potential complication from shock? And where might be most affected?

A

Organ failure after recovery

Kidneys, lungs, heart, brain

243
Q

What can cause neurogenic shock?

A

Spinal cord injury
Epidural
Spinal anaesthesia

244
Q

What is the difference between sepsis, severe sepsis, septic shock and septicaemia?

A

Sepsis - life-threatening response to organisms that can lead to tissue damage, organ failure and death
Severe sepsis - sepsis with sepsis-induced organ-dysfunction or tissue hypoperfusion
Septic shock - when sepsis leads to a dangerously low BP and abnormalities in cellular metabolism
Septicaemia - blood poisoning

245
Q

What is tachycardia?

A

HR > 100bpm

Physiological response to exercise and excitement

246
Q

What is AVNRT?

A

AV-nodal re-entrant tachycardia
More common in women
Strikes without obvious provocation
Attack may stop spontaneously or continue indefinitely

247
Q

What is AVRT?

A

Atrioventricular re-entrant tachycardia

248
Q

What is supraventricular tachycardia?

A

Arises from atria/atrioventricular junction
AVNRT and AVRT paroxysmal SVTs
Presents between 12-30
Young patients with no/little structural heart disease
AV node essential component

249
Q

What is ventricular tachycardia?

A

Pulse of more than 100bpm with at least 3 irregular heartbeats in a row
Found in patients with structurally normal hearts - benign condition
May lead to cardiomyopathy if untreated
Inadequate filling of ventricles due to rapid ventricular beating and less time for filling
Reduced CO and decrease in amount of oxygenated blood circulating

250
Q

What is sustained ventricular tachycardia?

A

Ventricular tachycardia for longer than 30 seconds

251
Q

Name 5 risk factors for AVNRT

A 
Exertion
Emotional stress
Coffee
Tea
Alcohol
252
Q

What is the pathophysiology of AVNRT?

A

Short refractory period and slow conduction or long refractory period with fast conduction (more common)
Atrial impulse occurs early slow pathway toakes over in propagating atrial impulses to ventricles
Once propagates fast pathway finished refractory period and transmits pulses again
Repeats - re-entrant loop at AV, sends signals through AV node at faster rate tan normal pacemaker so tachycardia
Atria contract slowly in first cycle then fast in next

253
Q

What is the pathophysiology of AVRT?

A

Atrial activation after ventricle activation
Prone to AF
Wolff-Parkinson-White syndrome
Premature beat from SAN -> AVN accessory pathway in refractory period, so travels down IV septum via purkinje cells until meets accessory pathway
Out of refractory period conducts impulse back to atria - re-entry circuit leading to tachycardia

254
Q

What is the pathophysiology of Wolff-Parkinson-White syndrome?

A

Normal AV conduction but with accessory pathway
SAN depolarises impulse travels to AVN via atria as well as accessory pathway
Accessory pathway - quick conduction, abnormal depolarisation of ventricles
Pre-excitation ECG - short PR interval, wide QRS

255
Q

How does AVNRT present?

A

Rapid regular palpitations with abrupt onset and sudden termination
Chest pain and breathlessness
Neck pulsations - atrial conductions against closed AV valves
Polyuria

256
Q

How does AVRT present?

A

Palpitations
Severe dizziness
Dyspnoea
Syncope

257
Q

How does VT present?

A

Breathlessness - lack of lung perfusion
Chest pain - lack of heart perfusion
Palpitations
Light headed or dizzy - lack of brain perfusion

258
Q

How does SVT present?

A 
Dizziness
Syncope
Hypotension
Cardiac arrest
Pulse rate between 120-220 bpm
259
Q

How is AVNRT diagnosed?

A

ECG - QRS complexes typical BBB, P waves either not visible or seen immediately before or after QRS complex due to simultaneous atrial or ventricular activation

260
Q

How is AVRT diagnosed?

A

ECG - short PR, wide QRS

261
Q

How is SVT diagnosed?

A

ECG - rapid ventricular rhythm, broad abnormal QRS complex greater than 0.14 seconds

262
Q

How are AVNRT and AVRT treated?

A

Emergency cardioversion if haemodynamically unstable
Vagal manoeuvres if stable
- Breath holding
- Carotid massage
- Valsalva manoeurvre
IV adenosine
Surgery - catheter ablation of accessory pathway in AVRT and modification of slow pathway AVNRT

263
Q

How is VT treated?

A

B-blockers to slow sinus rate

264
Q

How is SVT treated?

A

Haemodynamically unstable - emergency cardioversion

Stable - IV beta-blocker, IV amiodarone

265
Q

What can also cause tachycardia?

A 
Anaemia
Fever
HF
Thyrotoxicosis
Acute PE
Hypovolaemia
Atropine
266
Q

What is a supraventricular tachycardia?

A

Any tachycardia that arises from atrium/atroventricular junction
4 main types - AF, atrial flutter, AVNRT and AVRT

267
Q

What is tetralogy of Fallot?

A

Most common form of congenital heart disease

Cyanotic cardiac disorder with highest survival to adulthood

268
Q

What occurs in tetralogy of Fallot?

A

Large, maligned ventricular septal defect
Overriding aorta
RV outflow obstruction
RV hypertrophy
Stenosis of RV outflow (pulmonary stenosis) leads to RV being at higher pressure than left
Blue blood passes from RV to LV
Patients are blue

269
Q

How does tetralogy of Fallot present?

A 
Central cyanosis
Low birth weight and growth
Dyspnoea on exertion
Delayed puberty
Systolic ejection murmurs
Toddler's may squat
270
Q

How is tetralogy of Fallot diagnosed?

A

CXR - boot shaped heart

271
Q

How it tetralogy of Fallot treated?

A

Full surgical treatment during first 2 yrs of life due to progressive cardiac debility and cerebral thrombosis risk
Often get pulmonary valve regurgitation in adulthood and require redo surgery

272
Q

What is ventricular ectopic?

A

Premature ventricular contraction
Most common post-MI arrhythmia
Can also occur in healthy patients

273
Q

What is a risk factors for developing a ventricular ectopic?

A

MI

274
Q

What occurs during a ventricular ectopic?

A

Extra/missed/heavy beats
LV dysfunction if ectopics are frequent
Broad and bizzare QRS as arise from abnormal site in ventricular myocardium
Complete compensatory pause as AV node or ventricle is refractory resulting in missed beat
Can provoke ventricular fibrillation

275
Q

How does a ventricular ectopic present?

A

Uncomfortable especially when frequent
Pulse irregular owing to premature beats
Usually asymptomatic
Can feel faint/dizzy

276
Q

How is a ventricular ectopic diagnosed?

A

ECG - widened QRS complex

277
Q

How is ventricular ectopic treated?

A

Reassure patient

Give beta-blockers if symptomatic - to slow down sinus rate

278
Q

What is an atrial-septal defect?

A

Abnormal connection between two atria

Patent foramen ovale

279
Q

How common is atrial-septal defects?

A

Often first diagnosed in adulthood
1/3 congenital heart disease
More common in women

280
Q

What occurs in the heart in an atrial septal defect/

A

Slightly higher pressure in LA than RA
L -> R shunt
NOT blue
Increased flow from R heart to lungs
If untreated - R heart overload and dilation, R ventricle dilates to accommodate increased pulmonary flow
- RV hypertrophy
- Pulmonary hypertension - Eisenmenger’s reaction
- Increases risk of IE
As heart compliance falls with age, the shunt increases
Can lead to heart failure and shortness of breath by 40

281
Q

How does an atrial-septal defect present?

A 
Dyspnoea
Exercise intolerance
Atrial arrhythmias from RA dilation
Pulmonary flow murmur
Fixed split second heart sound
282
Q

How in an atrial-septal defect diagnosed?

A

CXR - large pulmonary arteries, large heart
ECG - right BBB due to RV hypertrophy
ECHO - hypertrophy, dilation of right side of heart and pulmonary arteries

283
Q

How is an atrial-septal defect treated?

A

Surgical closure

Percutaneous (keyhole)

284
Q

What is the difference between primum ASD and secundum ASD?

A

Primum - earlier presentation, may involve AV vales

Secundum - may be asymptomatic until adulthood

285
Q

What is Eisenmenger’s complex?

A

Shunt reversed due to development of pulmonary hypertension -> cyanosis and organ damage

286
Q

What is an atrio-ventricular septal defect?

A

Hole in very centre of heart
Includes - ventricular septum, atrial septum, mitral and tricuspid valves
Can be complete or partial
Associated with Down’s syndrome

287
Q

What occurs in the heart in atrio-ventricular septal defect?

A

Instead of 2 separate atrio-ventricular valves, just on big malformed one which usually leaks

288
Q

How does a complete atrio-ventricular septal defect present?

A

Breathlessness as neonate
Poor weight gain and feeding
Torrential pulmonary flow - Eisenmenger’s resulting in cyanosis over time

289
Q

How does a partial atrio-ventricular defect present?

A

Can present late in adulthood

Presents similar to a ventricular/atrial defect - dyspnoea, tachycardia, exercise intolerance

290
Q

How is an atrio-ventricular defect treated?

A

Pulmonary artery banding if large defect in infancy - band reduces blood flow to lungs reducing pulmonary hypertension and Eisenmenger’s syndrome
Surgical repair challenging
Partial defect left alone if no R heart dilatation

291
Q

What is a bicuspid aortic valve?

A

2 cusps aortic valve

Can go undetected, can be severely stenotic in infancy or childhood

292
Q

How common is a bicuspid aortic valve?

A

Most common form of cogenital heart disease
More common in males
Degenerate quicker than normal valves
Regurgitant earlier than normal valves
Associated with coarctation and dilation of ascending aorta
May eventually develop aortic stenosis - requires replacement - IE

293
Q

What should patients with a bicuspid aortic valve avoid? Why?

A

Intense exercise may accelerate complications

Yearly ECHO on affected patients

294
Q

What does a bicuspid aortic valve lead to?

A

Aortic stenosis +/- aortic regurgitation

Can also pre-dispose individual to IE, aortic dilation, aortic dissection

295
Q

How is a bicuspid aortic valve treated?

A

Treat surgically with a valve replacement

296
Q

What is coarctation of the aorta?

A

Narrowing of aorta at or just distal to, to insertion of ductus arteriosis

297
Q

In whom is coarctation of the aorta more common in?

A

Men

298
Q

What happens in the heart with coarctation of the aorta?

A

Net narrowing of aorta just after arch, with excessive blood flow being diverted through carotid and subclavian vessels into systemic vascular shunts to supply to rest of the body
Stronger perfusion to upper body compared to lower
Associated with Turner’s syndrome
Resultant decreased renal perfusion, leads to systemic hypertension that persists even after surgical correction

299
Q

What can coarctation of aorta lead to?

A

Berry aneurysms and patent ductus arteriosis

Increased risk of IE

300
Q

How does coarctation of the aorta present?

A

Often asymptomatic for years
Right arm hypertension
Bruits over scapulae and back from collateral vessels
Murmur
Headahces and nose bleeds
Hypertension in upper limbs
Discreptant blood pressure in upper and lower body
Long term - hypertension - early coronary artery disease, early strokes, sub-arachnoid haemorrhage
Radio-femoral delay

301
Q

How is coarctation of the aorta diagnosed?

A

CXR - dilated aorta indented at site of coarctation
ECG - LV hypertrophy
CT - accurately demonstrate coarctation and quantify flow

302
Q

How is coarctation of the aorta treated?

A

Surgery
Balloon dilatation and stening
Risk of aneurysm and at site of repair

303
Q

What is the difference between severe and mild coarctation of aorta?

A

Severe - block aorta, collapse with heart failure

Mild - raised BP, systolic murmur (best heart over left scapula (scapula briut)

304
Q

What is infective endocarditis?

A

Infection of endocardium or vascular endothelium of heart

Subacute bacterial endocarditis

305
Q

Who is more at risk of IE?

A

Valves with congenital or acquired defects
R sided IE more common with IV drug users
Normal valves with virulent organisms such as streptococcus pneumoniae or S aureus
Prosthetic valves or pacemakers

306
Q

Who is more at risk of IE?

A 
More common in developing countries
Disease of - elderly, those with prosthetic valves, young IV drug user, young with congenital heart disease
More common in men
Those with poor dental hygiene
Dental treatment
IV cannula
Skin and soft tissue infection
Cardiac surgery
Pacemaker
307
Q

What pathogens cause IE?

A

S aureus
P aeruginosa
S viridans

308
Q

What is the pathophysiology of infective endocarditis?

A

Consequence of 2 factors - presence of organisms in bloodstream and abnormal cardiac endothelium facilitating adherence and growth
Poor dental hygiene - bacteria from dental plaques get into blood, IVDU, soft tissue infections
Damage endocardium promotes platelets and fibrin deposition allowing organism to adhere and grow, leading to infected vegetation
Aortic and mitral valve most affected - IV drug users exception where R
Virulent organisms destory valve they are on resulting in regurgitation and worsening heart failure

309
Q

How does infective endocarditis present?

A

New valve lesion/regurgitant murmur
Embolic events unknown origin
Sepsis of unknown origin
Haematuria, glomerulonephritis, suspected renal infarction
Fever plus risk factor
Headache, fever, malaise, confusion, night sweats
Finger clubbing
S aureus - high fever, feel ill rapidly
Valve dysfunction
Splinter haemorrhages on nail beds of fingers
Embolic skin lesions
Osler nodes - tender nodules in digits
Janeaway lesions - haemorrhages and nodules on fingers
Roth spots - retinal haemorrhages with white or clear centres seen on fundoscopy
Petechiae

310
Q

How is IE diagnosed?

A

Dukes criteria
Blood cultures - 3 from different sites over 24 hrs, take before antibiotics started
If not staph - penicillin - benzylpenicillin and gentamycin
If staph - vancomycin and rifampicin
Treat complications
Surgery - remove valve and replace with prosthetic one - if infection can’t be cured, remove infected devices, remove large vegetations before they embolise
Good oral health for prevention

311
Q

What is patent arteriosus?

A

Where ductus arteriosus fails to close after birth

312
Q

What happens to the heart with a patent ductus arteriosus?

A

Ductus arteriosis persistent communication between the proximal left pulmonary artery and descending aorta
Foeatal pulmonary vascular resistance high and right heart pressure exceeded that of left - flow from right to left atrium through foramen ovale and pulmonary artery to aorta via ductus arteriosus
Some premature babies and cases of maternal rubella ductus arteriosus doesn’t close
Remains open then there is abnormal left-to-right sunt and eventually means that lung circulation overload with pulmonary hypertension and right-side cardiac failure subsequently
Increases risk of IE

313
Q

How does patent ductus arteriosus present?

A

Continuous machinery murmurs
Bounding pulse
Large then large heart and breathlessness
Eisenmenger’s syndrome with differential cyanosis that is clubbed with blue toes but pink and not clubbed fingers
Tachycardia

314
Q

How is patent ductus arteriosus diagnosed?

A

CXR - large shunt in aorta and pulmonary arterial system may be prominent
ECG - demonstrate left arterial abnormality and LV hypertrophy
ECHO - dilated LA and LV

315
Q

How is patent ductus arteriosus treated?

A

Can be surgically or percutaneously
Low risk complications
Venous approach may require and AV loop
Indometacin can be given to stimulate duct closure

316
Q

What is the symptoms of peripheral arterial disease?

A

Cramping pain in calves, thighs and buttocks relieved by rest

317
Q

What are the signs of peripheral arterial disease?

A

Absent pulses
Punched out ulcers
Postural colour change (Bueger’s test)
6Ps - pain, pallor, pulselessness, paraesthesis, paralysis, perishingly cold

318
Q

What investigations do you need to do in peripheral arterial disease?

A

Exclude DM, arteritis, anaemia, renal disease, lipids
ABPI - normal is 1-1.2, PAD is 0.5-0.9
Colour duples USS - quick and non-ivasive, can show vessels and blood flow within them
MRI/CT angiography - to identify stneoses and quality of vessels
Blood tests - raised CK-MM, shows muscle damage

319
Q

How do you manage peripheral arterial disease?

A

Risk factors modification - quit smoking, treat HTN, lower cholesterol, improve DM control, lower fat diet
Medications - antiplatelets, clopidogrel is recommended as 1st line
Exercise programmes - reduce claudication by improving blood flow
PTA or surgery if severely stenosed

320
Q

How common is structural/congenital heart defects?

A

1% of all lives births have some form of cardiac defect
Vary from all minor to incompatable with life ex-utero
Overall male predominance
Atrial septal defect and patent dutus arteriosus occur more commonly females

321
Q

Name 5 risk factors for having a structural/congenital heart disease

A 
Affected sibling
Maternal prenatal rubella infection - persistent ductus arteriosus and pulmonary valvular and arterial stenosis
Maternal alcohol misuse
Single genes
Drugs
Diabetes of mother
Genetic abnormalities
322
Q

When do you get finger clubbing?

A

Prolonged cyanosis

323
Q

What is a ventricular septal defect?

A

Abnormal connection between 2 ventricles
Many close spontaneously during childhood
20% of congenital heart defects

324
Q

What occurs in the heart with a ventricular septal defect?

A

Higher pressure in LV then RV
L to R shunt - not blue
Increased blood through lungs

325
Q

How do large ventricular septal defects present?

A 
Pulmonary hypertension
Eisenmenger's complex
Cyanosis
Small, breathless, skinny baby
Increased resp rate
Tachycardia
326
Q

How do small ventricular septal defects present?

A

Large systolic murmur
Thrill (buzzing sensation)
Well grown

327
Q

What do large ventricular septal defects look and sound like?

What do small ventricular septal defects look and sound like?

A

Large defects - CXR (big heart), murmurs vary in intensity (pansystolic), cause more problems in infancy

Small defects - normal HR, normal size, asymptomatic, increase IE risk, louder murmur/thrill

328
Q

How are ventricular septal defects treated?

A

Medical initially since many will spontaneously close
Surgical closure
If small - no intervention required
Prophylactic antibiotics
Moderately size lesion - furosemide, ACEi

329
Q

What is pulmonary stenosis?

A

Narrowing of outflow of RV

Can be valvular, subvalvular or supravalvular

330
Q

How does severe pulmonary stenosis present?

A 
RV failure as neonate
Collapse 
Poor pulmonary blood flow
RV hypertrophy
Tricuspid regurgitation
331
Q

How do you treat pulmonary stenosis?

A

Balloon valvoplasty - place catheter with balloon with balloon through femoral vein then inflate balloon at stenosis to crush it - can result in regurgitation
Open valvotomy
Shunt - to bypass blockage

332
Q

What is cardiomyopathy?

A

Group of diseases of myocardium that affects the mechanical or electrical function of the heart

333
Q

What are the different types of cardiomyopathy?

A

Hypertrophic
Dialted
Restricted
Arrhythmogenic right ventricular

334
Q

What is hypertrophic cardiomyopathy?

A

Ventricular hypertrophy/thickening of muscle
Quite common, second most common cardiomyopathy
1/500
Autosomal dominant - familial
May present at any age
Most common cause of sudden cardiac death in the young

335
Q

What is dilated cardiomyopathy?

A

Dilated left ventricle which contracts poorly/has thin muscle
Most common cardiomyopathy
Autosomal dominant
Can be caused by ischaemia, alcohol, thyroid disorder, familial/genetic

336
Q

What is restricted cardiomyopathy?

A

Rare

Caused by amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis

337
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium
Familial form autosomal dominant but can be recessive

338
Q

What can increase your risk of having a cardiomyopathy?

A

Family history

339
Q

What occurs in hypertrophic cardiomyopathy?

A

Sarcomeric protein gene mutations eg troponin T and B-myosin
All in absence of hypertension and valvular disease
Hypertrophic, non-compliant ventricle impair diastolic filling resulting in reduced stroke volume and thus cardiac output
Thick powerful heart is disarray of cardiac myocytes so conduction affected

340
Q

What occurs in dilated cardiomyopathy?

A

Caused by cytoskeletal gene mutations
Left ventricle or right ventricle or all 4 chamber dilatation and thus dysfunction
Poorly generated contractilve force leads to progressive dilatation of heart with some diffuse interstitial fibrosis

341
Q

What occurs in restrictive cardiomyopathy?

A

Normal or decreased volume of both ventricles with bilateral enlargement, normal wall thickness, normal cardiac valves and impaired ventricular filling
Restrictive physiology
Poor dilation of heart restricts its ability to take on blood and pass it to the rest of the body
Rigid myocardium restrict diastolic ventricular filling

342
Q

What occurs in arrhythmogenic RV cardiomyopathy?

A

Desmosome gene mutation
RV replaced by fat and fibrous tissue
Muscle dies and replaced by fat as part of inflammatory process

343
Q

How does hypertrophic cardiomyopathy present?

A 
Hypertrophy of myocardium
Sudden death
Chest pain, angina, dyspnoea, dizziness, palpitations, syncope
LV outflow obstruction
Cardiac arrhythmia
Ejection systolic murmur
Jerky carotid pulse
344
Q

How does dilated cardiomyopathy present?

A 
SOB and fatigue
Heart failure
Arrhythmias
Thromboembolism
Sudden death
Increased JVP
345
Q

How does restricted cardiomyopathy present?

A 
Dyspnoea
Fatigue
Embolic symptoms
Elevated JVP with diastolic collapse and elevation of venous pressure with inspiration
Hepatic enlargement
Ascites
Dependent oedema
3rd and 4th heart sounds
346
Q

How does arrhythmogenic cardiomyopathy present?

A

Cardiac cells held less together
Arrhythmia most common
Syncope
R heart failure

347
Q

How is hypertrophic cardiomyopathy diagnosed?

A

ECG - abnormal, LV hypertrophy sings, progressive T wave inversion, deep Q waves
Echo - ventricular hypertrophy, small left ventricle cavity
Genetic analysis

348
Q

How is dilated cardiomyopathy diagnosed?

A

CXR - cardiac enlargement
ECG - tachycardia, arrythmia, non-specific T wave changes
Echo - dilated vessels

349
Q

How is restrictives cardiomyopathy diagnosed?

A

CXR, ECHO, ECG - abnormal but non-specific

Cardiac catheterisation helps diagnose restrictive cardiomyopathy

350
Q

How is arrhythmogenic cardiomyopathy diagnosed?

A

ECG - usually normal by may show T wave inversion
ECHO - could be normal, advanced disease show right ventricular dilation
Genetic testing

351
Q

How is hypertrophic cardiomyopathy treated?

A

Amiodarone - anti-arrythmatic medication
CCB
B-blocker

352
Q

How is dilated cardiomyopathy treated?

A

HF and AF treated in normal way

353
Q

How is restricted cardiomyopathy treated?

A

No specific treatment with poor prognosis
Patients die within a year
Cardiac transplantation

354
Q

How is arrhythmogenic cardiomyopathy treated?

A

B-blockers
Amiodarone for symptomatic arrhythmias
Occasionally cardiac transplant indicated

355
Q

What is heart block?

A

Block in either AV node/HIS bundle results in AV block

Block in lower conduction system produces bundle branch block

356
Q

What can cause heart block?

A

Coronary artery disease
Cardiomyopathy
Fibrosis of conducting tissues in elderly

357
Q

What are the different types of AV block?

A

First degree
Second degree - type 1 and 2
Third degree

358
Q

What is first degree AV block?

A

‘If the R is far from the P then you have first degree’
Prolongation in PR interval greater than 0.22 seconds
Every atrial depolarisation followed by conduction to ventricles but with delay
Asymptomatic so no treatment

359
Q

What can cause first degree heart block?

A

Hypokalaemia, myocarditis, inferior MI, AVN blocking drugs eg b-blockers, CCB, digoxin

360
Q

What is second degree heart block?

A

‘Longer longer longer drops, then you have a Wenkebach’ (Mobitz I
‘If some Ps don’t get through, then you have a Mobitz II’
When some P waves conduct, others don’t

361
Q

What is a Mobitz I heart block?

A

PR interval before blocked P wave longer than after blocked P wave
Light headedness, dizziness, syncope
Doesn’t require a pacemaker unless poorly tolerated
Progressive PR interval prolongation until beat dropped, P wave fails to conduct then cycle restarts

362
Q

What can cause a Mobitz I heart block?

A

AVN blocking drugs

Inferior MI

363
Q

What is a Mobitz II heart block?

A

PR interval constant and QRS interval dropped
Failure of conduction through His-Purkinje system
SOB, postural hypotension, chest pain
High risk of developing sudden complete AV block and pacemaker should be inserted

364
Q

What can cause a Mobitz II heart block?

A 
Anterior MI
Mitral valve surgery
SLE
Lyme disease
Rheumatic fever
365
Q

What is a third degree heart block?

A

‘Ps and Qs don’t agree, the you have a third degree’
Complete AV block
Spontaneous escpae rhythm originated below block keeps ventricles going
P waves completely independent of QRS

366
Q

What can cause third degree heart block?

A

Structural heart disease, IHD, hypertension, endocarditis, Lyme disease

367
Q

How is third degree heart block treated?

A

IV atropine or permanent pacemaker insertion

368
Q

What is bundle branch block?

A

Usually asymptomatic

Slightly widening of QRS complex - incomplete BBB

369
Q

What is RBBB?

A

R bundle no longer conducts, ventricles don’t get impulses at same time
QRS M wave in V1, W in V5 and V6 (MaRRoW)

370
Q

What can cause RBBB>

A

PE, IHD, A/VSD

371
Q

What is LBBB?

A

Late activation of LV
Deep S wave leads I and V6, tall late R in V1
WiLLiaM - QRS in V1 and 2, M in V4-6

372
Q

What can cause LBBB?

A

IHD, aortic valve disease

373
Q

What are ACEI used for?

A

Hypertension, heart failure, diabetic nephropathy

374
Q

Name 3 examples of ACEi’s

A 
Ramipril
Enalapril
Perindopril
Liniopril
Trandolapril
375
Q

What are the main adverse effects of ACEI’s?

A

Related to angiotensin II formation - hypotension, acute renal failure (release more renin causing BP to drop further), hyperkalaemia, teratogenic effects in pregnancy (angiotensin II important for baby development)
Related to increased kinin production - dry chronic cough (ACE also breaks down bradykinin so inhibited = more bradykinin), rash, anaphylactiod reaction

376
Q

How do ACEi’s work?

A

Block action of ACE enzyme in lungs preventing conversion of angiotensin I to angiotensin II

377
Q

What does angiotensin II do?

A

Potent vasocontrictor
Stimulates aldosterone release
Increases peripheral resistance

378
Q

What does aldosterone do?

A

Increases Na+
Therefore water retention
Increased blood volume and BP

379
Q

What are ARBs used for?

A

Hypertension
Diabetic neuropathy
heart failure (when ACEI contraindicated)

380
Q

How do ARBs work?

A

Block AT-1 receptor that angiotensin II works at preventing the action of angiotensin II

381
Q

Name 3 examples of ARBs

A 
Candesartan
Losartan
Valsartan
irbesartan
Telmisartan
382
Q

What are the main adverse effects of ARBs?

A 
Symptomatic hypotension
Hyperkalaemia
Potential renal dysfunction
Rash
Angio-oedema
Contraindicated in pregnancy
Generally well tolerated
383
Q

What are CCBs used for?

A

Hypertension, IHD eg angina and arrhythmia

384
Q

Which CCBs have an effect on electrial conductivity?

A

Diltiazem and verapamil

385
Q

Name 3 examples of CCBs

A 
Amlodipine
Diltiazem
Verapamil
Nifedipine
Felodipine
Lacidipine
386
Q

How do L-type CCBs work?

A

Block calcium ion channels
Dihydropyridine - nifedipine, amlodipine, felodipine, lacidipine preferentially affect vascular smooth muscle, peripheral arterial vasodilators
Phenylalkylamines - verapamil main effect on heart, reduced HR and force of heart contraction
Benzothiozepines - diltiazem, intermediate heart/peripheral vascular effects

387
Q

What are the main adverse effects of CCBS?

A

Due to peripheral vasodilation - flushing, headache, oedema, palpitations (decreased BP so body tried to correct by increasing HR)
Due to -vely chronotropic effects - bradycardia, atrioventricular block, postural hypotension
Due to -vely inotrophic effects - worsening of cardiac failure
Verapamil causes constipation

388
Q

How to beta-adrenoceptor blockers work?

A

Block beta-adrenoceptors causing slowing down of heart rate

389
Q

What are b-blockers used for?

A

IHD - angina, heart failure, arrythmia, hypertension

390
Q

Name 3 examples of B-blockers

A 
Bisoprolol
Carbvedilol
Propranolol
Metoprolol
Atenolol
Nadolol
391
Q

Which B-blockers are more B-1 selective?

A

Metoprolol

Bisoprolol

392
Q

Which B-blocker is in the middle in terms of selectivity?

A

Atenolol

393
Q

Which B blocker is non-selective?

A

Propranolol
Nadolol
Carvedilol

394
Q

Why do you need to be careful with B-blocker selectivity?

A

Seletive B1 in asthma since non-selective used will also block B-2 resulting in airway constriction and thus worsening of asthma

395
Q

What are the main adverse effects of B-blockers?

A 
Fatigue
Headache
Sleep disturbance/nightmares
Bradycardia
Hypotension
Cold peripheries
Erectile dysfunction
Bronchospasm
Worsening of asthma/COPD by bronchospasm
PVD - claudication or raynauds
HF is given standard dose acutely - give in small doses and increase slowly
396
Q

What are diuretics indicated for?

A

Hypertension and heart failure

397
Q

What are the different classes of diuretics and give an example for each?

A

Thiazides - cause Na+ and thus water loss in urine, act on distal tubule, less potent - bendroflumethiazide, hydrochlorothiazide, chlorothalidone
Lopp diuretics - act on loop of Henle, more potent, furosemide (blocks Na/K/2Cl transporter), bumetanide
Potassium-sparing diuretics - spironolactone, eplerenone
Aldosterone antagonists

398
Q

What are the main adverse effects of diuretics?

A 
Hypovolaemia (mainly loop)
Hypotension (mainly loop)
Hypokalaemia
Hyponatraemia
Hypomagnesaemia
Hypocalcaemia
Hyperuricaemia - gout
Erectile dysfunction (thiazides)
Impaired glucose tolerance (thiazides)
399
Q

Name an alpha-1 adrenoceptor blocker

A

Doxazosin

400
Q

Name a centrally acting anti-hypertensive

A

Moxonidine

Methyldopa - can be used in pregnancy

401
Q

Name a direct renin inhibitor

A

Aliskiren

402
Q

What are the cardiac natriuretic peptides?

A

ANP - atria

BNP - brain natriuretic peptide - ventricle

403
Q

When are the natriuretic peptides released?

A

When stretching of atrial or ventricular muscle cells
Raised atrial or ventricular pressures
Volume overload

404
Q

What are the main effects of the natriuretic peptides?

A

Increased renal excretion of sodium and water
Relax vascular smooth muscle
Increase vascular permeability
Inhibit action/release of aldosterone, angiotensin II, endothelin and ADH
In HF raised natriuetic peptdes in serum blood

405
Q

How do nitrates work?

A

Arterial and venous dilators
Reduce pre-load and afterload
Lower BP

406
Q

What are nitrates used for?

A

IHD (angina) and HF

407
Q

Give 3 examples of nitrates

A

Isosorbide mononitrate (long acting)
GTN (glyceryl trinitrate) spray - commonly gives headache, potent vasodilator
GTN infusion

408
Q

What are the main potential side effects of nitrates?

A

Headache
GTN spray syncope
Potential tolerance to drug

409
Q

How are antiarrhythmic drugs classified?

A

Vaughan Williams classification
Classes 1 and 3 - rhythm control
Classes 2 and 4 - rate control

410
Q

What are class I antiarrhythmic drugs?

A

Sodium channel blockers - flecainide

411
Q

What are class II antiarrhythmic drugs?

A

B-blockers

412
Q

What are class III antiarrhythmic drugs?

A

Prolong action potential

Amiodarone, sotalol

413
Q

What are class IV antiarrhythmic drugs?

A

CCBs - verapamil, diltiazem, amlodipine

414
Q

How does digoxin work?

A

Cardiac glycoside
Inhibits Na/K pump - found everywhere
Main effect on heart - bradycardia (increased vagal tone), increased ectopic activity, increased force of contraction by increased intracellular Ca2+
Slowing AV conduction
Narrow therapeutic range otherwise side effects

415
Q

What are the potential side effects of digoxin?

A

Nausea, vomiting, diarrhoea, confusion

416
Q

When is digoxin used?

A

AF to reduce ventricular rate response

Severe HF as positive inotropic

417
Q

How does amiodarone work?

A

Blocks potassium rectifier current that are responsible for repolarisation of heart

418
Q

What are the potential adverse effects of amiodarone?

A 
QT prolongation
Polymorphic ventricular tachycardia
Interstitial pneumonitis
Abnormal liver function
Hyperthyroidism/hypothyroidism
Sun sensitivity
Slate grey skin discolouration
Optic neuropathy
Multiple drug interacton
Large volume of distribution

Phase 2a medicine (13 decks)

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