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2a > Cardio > Flashcards

Cardio Flashcards

1
Q

What is Angina?

A

Mismatch of oxygen demand and supply to heart muscle. Leas to chest pain or discomfort due to reversible ischaemia. Exacerbated by exertion.

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2
Q

What are some types of angina?

A

Stable angina – the most common type, pain on exertion

Prinzmetal’s angina/Variant angina (coronary artery spasm) – shut down of arteries means increased resistance and decreased flow

Microvascular angina (Syndrome X) – increase in downstream resistance but main arteries are okay

Crescendo angina – occurs at rest with minimal exertion

Decubitus angina – caused by lying flat

Unstable angina – chest pain at rest, can occur at any time. Difficult to distinguish from MI, need to be treated in hospital

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3
Q

Most common cause of stable angina?

A

Ischaemic heart disease. Narrowing of coronary arteries due to atherosclerosis.

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4
Q

Environmental factors exacerbating angina?

A
  • Cold weather
  • Heavy meals
  • Emotional stress
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5
Q

Medical conditions that exacerbate angina due to reduced blood supply?

A
  • Anaemia
  • Hypoxaemia
  • Polycythaemia
  • Hypothermia
  • Hypovolaemia (shock)
  • Hypervolaemia
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6
Q

Medical conditions that exacerbate angina due to increased blood demand?

A
  • Hypertension
  • Tachyarrhythmia
  • Valvular heart disease
  • Hyperthyroidism
  • Hypertrophic cardiomyopathy
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7
Q

Risk factors for angina?

A
  • Increasing age
  • Cigarette smoking
  • Fam Hx
  • Diabetes Mellitus
  • Hyperlipidaemia
  • Hypertension
  • Kidney disease
  • Obesity
  • Physical inactivity
  • Stress
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8
Q

Clinical features of angina?

A
  • Crushing central chest pain
  • May radiate to arms, neck and jaw
  • May have SOB
  • Provoked by physical exertion
  • Relieved by rest or GTN spray
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9
Q

Investigations for angina?

A
  • 12 lead ECG
  • Exercise testing w/ ECG
  • Myoview scan - looks at perfusion on exercise
  • Stress echo - USS when given inotropic drug
  • CT scan calcium scoring
  • Coronary angiography
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10
Q

Management of angina?

A
  • Lifestyle: smoking cessation, w loss, diet, exercise
  • GTN spray for sx relief
  • Statins
  • Aspirin
  • BB’s - negatively inotropic and chronotropic so reduce O2 demand
  • ACE-i
  • K+ channel openers
  • Ivabradine
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11
Q

Surgical management of angina?

A
  • Percutaneous coronary intervention - including stenting and balloon dilatation
  • CABG
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12
Q

Effects of beta blockers on heart?

A
  • Decrease HR
  • Decrease LV contractilitity
  • Decrease cardiac output
  • Decrease oxygen demand
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13
Q

Main s/e of beta blockers?

A
  • Tiredness, nightmares
  • Bradycardia
  • Cold hands and feet
  • Erectile dysfunction – always ask because patients may not volunteer this information
  • Depression
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14
Q

C/i for beta blockers?-

A
  • Asthma
  • Prinzmetals angina
  • Severe heart block
  • Excessive bradycardia
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15
Q

Effects of nitrates?

A
  • Predominantly venodilators
  • Decrease venous return by increasing venous capacity
  • Decreaes preload due to less venous return
  • Decreases afterload by causing arterial dilatation
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16
Q

S/e of nitrates?

A
  • Headaches
  • Dizziness
  • Light headedness
  • Nausea
  • Flushing
  • Burning and tingling under the tongue (GTN)
  • Low BP
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17
Q

Effects of CCB’s?

A
  • Decreases blood pressure
  • Decreases afterload
  • Decreases cardiac oxygen demand
  • Coronary artery dilation
  • Negatively chronotropic so decreases HR
  • Negatively inotropic so decreases LV contraction –decreases cardiac workload
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18
Q

S/e of CCBs?

A

Arterial dilatation which causes:

  • Hot flushes
  • Postural hypotension
  • Swollen ankles
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19
Q

3 classes of ACS?

A

1) STEMI - Q wave infarction
2) NTSTEMI - Non Q wave infarction, ST depression/T wave inversion
3) Unstable angina - no ecg changes

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20
Q

How to diagnose each ACS?

A

STEMI : ECG features at presentation

NSTEMI: Retrospective diagnosis made after troponin results available.

Unstable angina: Use pattern of the pain. No significant troponin rise.

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21
Q

What are the types of MI?

A

Type 1 – spontaneous MI with ischaemia due to a primary coronary event (e.g. plaque erosion/rupture)

Type 2 – MI secondary to ischaemia due to increased oxygen demand or decreased supply (e.g. coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension, hypotension)

Type 3, 4, 5 – Diagnosis of MI in sudden cardiac death, after PC and after CABG respectively

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22
Q

Causes of ACS?

A
  • Rupture of an atherosclerotic plaque and consequential arterial thrombosis (MOST COMMON)
  • Coronary vasopsasm w/o plaque rupture
  • Drug abuse (amphetamines, cocaine)
  • Dissection of coronary artery due to CTD (eg marfans)
  • Thoracic aortic dissection
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23
Q

Risk factors for ACS?

A
  • Male gender
  • Increased age
  • Renal failure
  • LVSD
  • Elevated NT-proBNP level
  • Fam Hx
  • Smoking, diabetes, htn, hyperlipidaemia
  • Obesity + Physical inactivity
  • Premature menopause
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24
Q

Signs and symptoms of ACS?

A
  • Unremitting cardiac chest pain
  • Usually severe but may be mild or absent in a silent MI (be aware that less pain does not mean it’s a ‘better’ MI)
  • Occurs at rest
  • New onset angina with limitation of ADL’s
  • Associated with: Sweating, SOB, nausea and/or vomiting, dyspnoea, fatigue and palpitations
  • 1/3 occur in bed at night
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25
Q

Investigations for ACS?

A
  • 12 lead ECG
  • Vital signs
  • Biochemical markers: Cardiac troponin, Creatine Kinase MB, Myoglobin
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26
Q

Immediate management of ACS?

A
  • 2222/999

- MONA: Morphine, oxygen, nitrates, aspirin 300mg STAT

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27
Q

Hospital management of ACS?

A
  • Oxygen therapy if hypoxic
  • Pain relief - nitrates, narcotics
  • Aspirin
  • Clopidogrel - P2Y12 inhibitor
  • Fondaparinux
  • Consider: Beta-blockers and other anti-anginals
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28
Q

What are P2Y12 inhbitors?

A

Antiplatelets used in combo with aspirin.

Clopidogrel, Prasugrel, Ticagrelor.

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29
Q

Complications of MI?

A
  • Heart failure
  • Rupture of wall of infarcted ventricle
  • Rupture of interventricular septum
  • Mitral regurg
  • Arrhytmias
  • Heart block
  • Pericarditis
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30
Q

What is Dressler syndrome?

A
  • May develop weeks or months after MI
  • A secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium
  • It consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion
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31
Q

What is heart failure?

A

The inability of the heart to deliver sufficient perfusion to the body.

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32
Q

Difference between systolic and diastolic HF?

A 
Systolic  = HF and ventricles not contracting
Diastolic = HF and the ventricles not relaxing (ejection fraction the same but cardiac output reduced due to reduced diastolic ventricular filling)
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33
Q

Causes of Heart failure?

A
  • Myocardial dysfunction from IHD or Prev MI ( MOST COMMON)
  • Hypertension
  • Alcohol excess
  • Cardiomyopathies
  • Valve defects leading to ventricular hypertrophy
  • Endocarditis
  • Pericardial causes
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34
Q

Symptoms of heart failure?

A

3 cardinal symptoms: SoB, Fatigue, Ankle swelling

2 specific symptoms: Orthopnoea, Paroxysmal nocturnal dyspnoea

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35
Q

Signs of heart failure?

A
  • Peripheral/pitting oedema
  • Diffuse crackles at both lung bases
  • Tachycardia
  • Raised JVP
  • S3 on auscultation
  • Displaced apex beat (due to LV hypertrophy)
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36
Q

Investigations for heart failure?

A
  • Hx and Exam
  • CXR
  • Blood tests - including BNP
  • 12 lead
  • Echocardiography for valve assessment
  • Myocardial perfusion imaging
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37
Q

X-Ray signs for heart failure?

A 
A - Alveolar oedema
B - Kerley B lines
C - Cardiomegaly (PA XR only)
D - Upper lobe diversion of blood vessels
E - Pleural effusion
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38
Q

Management of ACUTE heart failure?

A
  • Stablise using A –> E
  • High flow O2
  • Loop diuretics: IV Furosemide or IV Bumetanide
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39
Q

Lifestyle advice for heart failure?

A
  • Smoking cessation
  • Low salt intake
  • Low sat fat intake
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40
Q

Management of CHRONIC HF without preserved ejection fraction? (EF<35%)

A
  • ANY STAGE: Furosemide for sx relief
    1) Beta blocker + ACEi/ARB
    2) BB + ACEi + Spironolactone
    3) Hydralazine + Nitrate
    4) Sacubitril valsartan

If resistant can add: Digoxin, Ivabradine, Amiodarone

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41
Q

Management of CHRONIC HF with preserved ejection fraction? (EF>35%)

A

Just give furosemide for symptomatic relief.

No need for ACEi or BB>

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42
Q

Which medications actually improve prognosis in HF?

A
  • ACE-i
  • BB
  • ARBs
  • Aldosterone antagonists
  • Hydralazine and nitrates
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43
Q

How do beta blockers work in HF?

A
  • Beta blockers oppose sympathetic stimulation
  • They prevent heart rate and contractility increasing
  • This means there will be no increased oxygen demand for the heart
  • Should be started early when the patient is stable
  • NOT affected by ethnicity in the same way as some other cardiac medications
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44
Q

Surgical options for heart failure?

A
  • Valve replacement: TAVI or open surgery if caused by valve defect
  • Transplantation - Last resort, no donors
  • Resynchronisation and defibrillatiors - can improve sx and mortality
  • Palliative care - HF kills more than cancer.
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45
Q

What is Tricuspid regurgitation? (RARE)

A
  • Usually functional and secondary to dilatiation of the RV in severe RVF
  • Can also be caused by RHD, IE or carcinoid syndrome
  • On exam: Pansystolic murmur, elevated JVP, liver enlarged, oedeema
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46
Q

What is pulmonary regurgitation? (RARE)

A
  • Results from pulm htn and dilatation of the valve ring

- Early diastolic murmur on auscultation

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47
Q

What is pulmonary stenosis?

A

Narrowing of outflow of RV into lungs. Usually congential eg ToF

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48
Q

Signs and symptoms of pulmonary stenosis?

A
  • Right ventricular failure as neonate
  • Collapse
  • SOB due to poor pulm bloodflow
  • RV hypertrophy
  • Tricuspid regurgitation - too much blood in RV
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49
Q

Diagnosis and management of pulmonary stenosis?

A
  • ECHO
  • Balloon valvuloplasty
  • Open valvotomy
  • Open trans-annular patch
  • Shunt to bypass blockage
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50
Q

What is mitral regurgitation?

A
  • Backflow of blood from the left ventricle to the left atrium during ventricular systole
  • Mild (physiological) seen in 80%
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51
Q

What are causes of mitral regurgitation?

A

1) Myxomatous degeneration: Weakening of connective tissue. Causes MV prolapse. Seen in Ehler-Danlos and Marfans.
2) Ischaemic MR: Complication of coronary heart disease
3) Rheumatic heart disease
4) Infective endocarditis
5) Age related changes

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52
Q

Symptoms of mitral regurgitation?

A
  • Exertional dyspnoea

- HF sx: may coincide with increased haemodynamic burden eg. preg, infection, af. Get SOB, fatigue, ankle swell

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53
Q

Auscultatory signs of MR?

A
  • Soft S1
  • Pansystolic murmur heard loudest at apex
  • Radiates to axilla
  • S3 sound - chronic HF, LA overload
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54
Q

Investigations for MR?

A
  • ECHO is gold standard
  • 12 lead may show LV enlargement, AF and LVH
  • CXR - LA enlarged, central pulm artery enlargement
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55
Q

Medications for MR?

A
  • Vasodilators such as ACE-i - to reduce preload
  • Rate control for any associated AF w/ BB, CCB, digoxin
  • Anticoagulation in AF and atrial flutter
  • Diuretics for fluid overload
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56
Q

Surgery indications for MR?

A

Any symptoms at rest of on exercise (repair if feasible)

Asymptomatic but EF < 60%

Asymptomatic but new onset AF

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57
Q

What is mitral stenosis?

A
  • Obstruction of LV inflow that prevents proper filling during diastole
  • Normal area of MV 4-6cm2, sx begin at below 2cm2
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58
Q

Causes of mitral stenosis?

A
  • Rheumatic heart disease (most common, but falling)
  • Infective endocarditits
  • Mitral annular calcification (age related)
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59
Q

Symptoms of mitral stenosis?

A
  • Shortness of breath - due to pulm congestion
  • Haemoptysis - in later stages
  • Other sx in advanced: Increased JVP, hepatomegaly, peripheral oedema
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60
Q

Physical signs of Mitral Stenosis?

A
  • Mild diastolic murmur heard at mitral area
  • Heard best when pt on left side and breathing out
  • Malar flush in face
  • S1 opening snap loud
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61
Q

Investigations for mitral stenosis?

A
  • ECG: may show AF and LA enlargement (P mitrale)
  • CXR: LA enlargement and pulm congestion
  • ECHO: GOLD STANDARD. Assess for mv mobiliy, gradient and area,
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62
Q

Difference between P mitrale and P pulmonale?

A

P mitrale = bifid P wave, seen with LEFT atrial hypertrophy (i.e. in mitral stenosis)

P pulmonale = a tall, narrow, peaked P wave, seen with any process that causes RIGHT atrial hypertrophy, such as tricuspid regurgitation and pulmonary hypertension.

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63
Q

Treatment of Mitral regurgitation?

A
  • Medications: Sx impriove w/ BB, CCB, digoxin to control rate and prolong diastole. Diuretics for fluid overload.
  • Surgery: Percutaneous mitral valloon valvotomy -> any symptomatic patient
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64
Q

What is Aortic Regurgitation?

A

Defined as backflow/leakage of blood from the aorta in the into the LV during diastole due to ineffective closure of the aortic cusps

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65
Q

Causes of aortic regurg?

A
  • Bicupsid aortic valve
  • Rheumatic damage
  • Degenerative/age related
  • Infective endocarditis
  • Chronic regurgitration can occur due to arthritdities: Reiters syndrome, ank spond, rheum arthritis
  • CTD -> marfans, osteogenesis imperfecta
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66
Q

Risk factors for aortic regurgitatiion?

A
  • Age

- Genetic predispostion with bicuspid aortic valve

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67
Q

Symptoms of aortic regurgitation?

A
  • Dyspnoea inc: Orthopnea, PND

- Palpitations

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68
Q

Investigations for AR?

A
  • CXR: Enlarged cardiac silhoutte and aortic root enlargement
  • ECHO: Diagnositc in valve problems
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69
Q

Murmur heard in aortic regurgitation?

A
  • End diastolic murmur

- Heard loudest at left sternal edge

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70
Q

Management of aortic regurg?

A

Medical - vasodilators (ACEi)

Surgery - definitive tx, if there is sx at rest or exercise or if EF goes below 50%

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71
Q

Clinical signs of aortic regurg on exam?

A

Quincke’s – nail bed capillary pulsation

Collapsing pulse (aka waterhammer pulse, occurs due to hyperdynamic circulation)

Wide pulse pressure

Corrigan’s sign – pulsatile JVP/neck pulsation

De Mussett’s sign – head nodding

Duroziez’s sign – murmur on femoral artery compression

Traube’s – ‘pistol shot’ sound over femorals

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72
Q

What is aortic stenosis?

A

An increase in afterload due to stiffening of the aorta

The most common and most important valve disease

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73
Q

Criteria for aortic stenosis?

A
  • Valve area <1cm
  • Ejection fraction <40
  • Mean valve gradient >40mmHg
  • Symptomatic: Angina, syncope, breathlessness
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74
Q

Causes of aortic stenosis?

A
  • Commonest cause: Age related calcification
  • Congenital aortic stenosis
  • Congenital biscuspid valve
  • Rheumatic heart disease
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75
Q

Symptoms of aortic stenosis?

A

1) Syncope
2) Angina
3) Dyspnoea

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76
Q

Physical signs of aortic stenosis?

A
  • Slow rising pulse (pulsus tardus)
  • Decreased pulse amplitude
  • Heart sounds - soft/absent second heart sound, S4 gallop due to LVH
  • Ejection systolic murmur
  • Radiates to the carotids
  • Narrow pulse pressure
  • Thrill
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77
Q

Management of aortic stenosis?

A

Medical tx limited, as mechanical problem

Surgical replacement:
- TAVI (Transcutaneous Aortic Valve Implantation) or Balloon Valvuloplasty or Surgical valve replacementr

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78
Q

What are surgery indications for aortic stenosis?

A

Indications for surgery – any SYMPTOMATIC patient with severe AS, any patient with decreasing ejection fraction

If asymptomatic- medical management and surveillance and dental prophylaxis

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79
Q

What needs to be done for all valvular disease?

A

Infective endocarditis prophylaxis with abx and good dental hygeine

Serial ECHO’s

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80
Q

Main risks of valve replacement surgery?

A
  • Bleeding
  • VTE/Stroke
  • Haemolysis due to mechanical valve
  • IE
  • LV dysfunction
  • Valve prolapse/leak
  • AF
  • Bradyarrhytmia requiring PPM insertion
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81
Q

Which murmurs are heard loudest on held inspiration?

A

Tricuspid and pulmonary (right sided valves, before the lungs)

Ask them to HOLD on maximal inspiration

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82
Q

Which murmurs are heard loudest on held expiration?

A

Mitral and aortic (left valves, after the lungs)

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83
Q

Murmur that radiates to carotids?

A

Aortic Stenosis

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84
Q

Murmur radiates to the axilla?

A

Mitral regurgitation

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85
Q

Different types of heart valves?

A 
Mechanical = better for younger patients, lasts 20-25 years,
Tissue = better for older patients with higher bleeding risk, lasts 10 years
Mechanical = lifelong warfarin, 
Tissue = no warfarin
Mechanical = will ‘click’ as heart sounds, 
Tissue = heart sounds normal
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86
Q

What is dilated cardiomyopathy?

A

Dilated heart leading to systolic (+/- diastolic ) dysfunction
All 4 chambers affected but more LV than RV

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87
Q

Causes of dilated cardiomyoptahy?

A
  • Alcohol – may improve with thiamine
  • Postpartum
  • Hypertension
  • Inherited (1/3 of DCM patients, autosomal dominant defects mainly)
  • Infectious - coxsacki B
  • Endocrine – hyperthyroidism
  • Infiltrative – Haemachromatosis, sarcoidosis
  • Neuromuscular – Duchenne’s
  • Nutritional deficiencies
  • Drugs e.g. Doxorubicin
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88
Q

Features of DCM

A
  • Arrhytmias
  • Emboli
  • Mitral regurg
  • HF symptoms
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89
Q

Management of DCM?

A

Lifestyle measures – weight loss, exercise, smoking cessation, limit alcohol intake, avoid excess salt and saturated fats

Heart failure medications – ACEi, ARB, B-Blockers, Diuretics, Digoxin, Aspirin/warfarin

Devices – LVAD, pacemaker, ICDs

Heart transplant

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90
Q

What is Takotsubo cardiomyopathy?

A
  • Non-ischaemic cardiomyopathy
    AKA ‘broken heart syndrome’ and ‘Takotsubo apical ballooning syndrome’
  • Associated with a transient, apical ballooning of the myocardium – resembles an ‘octopus pot’
  • May be triggered by stress (i.e. bad news about a relatives death etc.)
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91
Q

Features of takotsubo cardiomyopathy?

A
  • Chest pain
  • Features of heart failure – SOB, fatigue, ankle swelling
  • ST elevation
  • Normal coronary angiogram

Supportive therapy only

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92
Q

What is arrhythmogenic RV cardiomyopathy?

A
  • Form of inherited cardiovascular disease which may present with syncope or sudden cardiac death in young people after hypertrophic cardiomyopathy
  • Inherited in an autosomal dominant pattern with variable expression
  • RV myocardium is replaced by fatty and fibrofatty tissue
  • 50% patients have mutation of one of the several genes which encode components of desmasome
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93
Q

Symptoms of arrhythmogenic RV cardiomyopathy?

A
  • Palpitations
  • Syncope
  • Sudden cardiac death
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94
Q

ECG signs on arrhythmogenic RV cardiomopathy?

A
  • Abmormalities in v1-v3
  • Typically T wave inversion
  • Epsilon wave in about 50%
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95
Q

ECHO and MRI changes in arrhythmogenic RV cardiomopathy?

A

Echo changes - Often subtle in the early stages. May show enlarged, hypokinetic RV with a thin free wall

MRI – shows fibrofatty tissue

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96
Q

Management of arrhythmogenic RV cardiomyopathy managed?

A
  • Drugs - solatolol
  • Catheter ablation to prevent VT
  • ICD
97
Q

What is Naxos disease?

A

Autosomal recessive variant of arrhythmogenic cardiomyopathy.

Triad of : ARVC, Palmoplantar kerartosis, Woolly hair

98
Q

What is hypertrophic obstructive cardiomyopathy? (HOCM)

A
  • Autosomal dominant
  • Disorder of muscle tissue caused by defects in the genes encoding contractile proteins
  • Most common defect = mutation in the gene encoding B-myosin heavy chain protein
  • Prevalance - 1 in 500
99
Q

Features of HOCM?

A
  • Often asymptomatic
  • Dyspnoea, angina, syncope,
  • Sudden death – most commonly due to ventricular arrhythmias
  • Arrhythmias and heart failure
  • Jerky pulse, large ’a’ waves, double apex beat
  • Ejection systolic murmur – increases with Valsalva manouever and decreases on squatting
100
Q

What are the associations with HOCM?

A

Freidrich’s ataxia – will also have features of weakness, poor coordination and hearing impairment

Wolff-Parkinson White syndrome – presents with palpitations, dizziness and a high heart rate

101
Q

ECHO features of HOCM?

A

MR SAM ASH:
Mitral regurgitation (MR)
Systolic anterior motion (SAM) of the anterior mitral valve leaflet
Asymmetric hypertrophy (ASH)

102
Q

ECG features of HOCM?

A
  • LVH
  • Progressive T wave inversion
  • Deep Q waves
  • Atrial fibrillation may occasionally be seen
103
Q

Classic causes of restricive cardiomyopathy?

A
  • Amyloidosis
  • Post-radiotherapy
  • Loefflers endocarditis
104
Q

What is coarctation of the aorta?

A

Congenital narrowing of the descending aorta at the site of insertion of the ductus arteriosus

105
Q

Clinical signs of coarctation?

A
  • Differential hypertension (higher BP in arms than legs)
  • Buzzes over scapulae and back from collateral vessels
  • Murmur: systolic murmur that is loudest below the left scapula
  • Radio-femoral delay

Notching on inferior border of ribs on x-ray.

106
Q

Presentation in neonates:

A
  • If severe: presents in first 3 weeks of life with poor feeding, lethargy, tachypnoea or congestive cardiac failure and shock
  • Pulses may be reduced in amplitude and delayed in the limbs
  • BP higher in upper limbs than lower limbs
  • Differential cyanosis: upper body pink, lower body cyanotic
  • Murmur: typically systolic in left infraclavicular area
107
Q

Presentation in later life:

A
  • Usually asymptomatic: diagnosis usually made on examination – prompted often by presence of murmur or hypertension
  • Can cause headache, nosebleeds and leg cramps – particularly with exercise
  • Lower limb muscle weakness, cold feet or neurological leg symptoms
  • BP higher in upper limbs than lower
  • Systolic or continuous murmur usually heard in the left infraclavicular area under the left scapula
108
Q

Associations with Coarctation?

A
  • Turners syndrome
  • Bicuspid aortic valve
  • berry aneurysms
  • Neurofibromatosis
109
Q

management of coarctation?

A
  • Surgical: end to end repair – remove the narrowed part of the aorta and join the 2 ends together once the narrow part has been removed
  • Prostaglandin E1 used to open the ductus arteriosus and achieve improved haemodynamic stability (surgery is the definitive treatment but prostaglandins used in the interim when patients present acutely)
  • Diuretics and inotropes
  • ACEi and ARAs alongside beta blockers
  • Surgery
  • Balloon angioplasty
110
Q

What is a patent ductus arteriosus?

A
  • Ductus arteriosus is a foetal shunt that connects pulmonary artery to aorta, bypassing lungs
  • Failure of it to close
  • Due to fact the BP is higher in aorta than pulm artery after birth, blood shunts backwards from aorta to pulm artery
  • results in increased blood flow through lungs
111
Q

What can persistent PDA lead to?

A

Eisenmengers syndrome.

If the PDA remains untreated and the extent of damage to the pulmonary vasculature increases so much that it causes pulmonary hypertension and therefore reverses the direction of the shunt

Before this point, PDA is acyanotic, but if it reaches this point it can become cyanotic

112
Q

ECG of Eisenmengers?

CXR of Eisenmengers?

A

Right ventricular hypertrophy

Cardiomegaly and pulmonary engorgement

113
Q

Risk factors for PDA?

A
  • Premature babies
  • Born at high altitude
  • Maternal rubella in first trimester
114
Q

Features of PDA?

A
  • Left subclavicular thrill
  • Continuous machinery murmur
  • Large volume, bounding, collapsing pulse
  • Wide pulse pressure
  • Heaving apex beat
115
Q

How is PDA managed?

A

Indomethacin closes the connection in the majority of cases

if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair

116
Q

What are the four features of Tetralogy of Fallot?

A

1) Large VSD
2) Overriding Aorta
3) Pulmonary stenosis
4) Right ventricular hypertrophy

Cyanotic. Right to left shunt.

117
Q

Risk factors for ToF

A
  • Viral illness during pregnancy
  • Alcoholism during pregnancy
  • Poor nutrition during pregnancy
  • Mother >40
  • Parent with ToF
  • Presence of Downs or DiGeorge
118
Q

Symptoms of ToF?

A
  • Cyanosis “attacks”
  • SOB and tachpnoea - particularly during exercise
  • Syncope
  • FtT/Poor weight gain
  • Tiring easily during play
  • irritability and prolonged crying
  • Clubbing of fingers and toes
  • Audible heart murmur
119
Q

ToF: CXR and ECG signs?

A

CXR: Boot shaped heart

ECG0=: RVH

120
Q

Management of ToF?

A
  • Surgical repair, good prognosis.
121
Q

What are symptoms of VSD?

A

Small: Asymptomatic

Large:

  • Small breathless skinny baby
  • Increased resp rate
  • Tachycardia
  • Big heart on CXR
  • Murmur
  • FtT
122
Q

Signs of VSD?

A
  • Pan-systolic murmur
  • Louder in small defects.
  • Heard in tricuspid region
123
Q

Complications of VSD?

A
  • Aortic regurgitation
  • Infective endocarditis
  • Eisenmengers complex
  • Right heart failure
  • Pulm htn
124
Q

Features of Atrial septal defects?

A
  • Ejection systolic murmuer
  • Fixed split S2
  • Embolism can cause strokes
125
Q

X-ray signs for ASD?

A

CXR: Big pulm artery, big heart

ECHO to diagnose

126
Q

Main risk factor for AVSD?

A

Downs Syndrome

127
Q

Features of AVSD?

A
  • Breathlessness as neonate
  • Poor weight gain
  • Poor feeding
  • Forceful pulmonary blood flow
128
Q

What is DVT?

What is PE?

A

DVT= Clots in the deep veins within the knee and groin

PE= Clots in the pumonary arteries

129
Q

Risk factors for DVT/PE?

A
  • Increasing age
  • Surgery, immobility, leg fracture
  • Active cancer
  • OC pill / HRT / PRegnancy (oestrogen increased)
  • Long haul flights
  • Inherited thrombophilia
130
Q

DVT signs and symtpoms?

A

Symptoms: Pain and swelling in leg, ususally calf, unilateral

Signs: Tenderness, swelling, warmth, discolouration

131
Q

Symptoms of PE?

A
  • Breathlessness
  • Pleuritic chest pain
  • Dyspnoea
  • Haemoptysis
  • Tachycardia/Tachypnoea
  • May have s/s of DVT
132
Q

Signs of PE?

A
  • Tachycardia
  • Tachypnoea
  • Pleural rub on auscultation
  • Signs of precipitating cause
133
Q

How to investigate DVT/PE?

A
  • Wells score
  • D-Dimer
  • USS compression test
  • Gold standard for PE: CTPA
  • Can do V/Q scan
134
Q

Components of Wells score?

A
  • Active cancer
  • Recent immobilisation of lower extremities
  • Bedridden for >3days or major surgery within 12 weeks
  • Entire leg swollen
  • Localised tenderness along deep venous system
  • Calf swelling >3cm
  • Pitting oedema in symptomatic leg
  • Superficial non-varicose collateral veins
  • Prev DVT
  • ALTERNATIVE DX LIKELY (-2)
135
Q

ECG features in PE?

A

S1, Q3, T3 – 20% of patients only

  • Large S wave in lead 1
  • Large Q wav in lead 3
  • Inverted T was in lead 3
  • Right bundle branch block
  • Right axis deviation
  • Sinus tachycardia
136
Q

Two ways to prevent DVT/PE?

A
  • LMWH on admission following assessment

- TED stockings

137
Q

Treatment of DVT/PE?

A
  • LMWH or Fondaparinux when diagnosed
  • Vit K antagonist (eg Warfarin) within 24hrs
  • LMWH continue for at least 5 days or until INR above 2
  • Warfarin for at least 3 months
138
Q

Treatment of massive PE in which there is circulatory failure?

A

Thrombolysis

139
Q

Difference between arterial and venous thrombus?

A

Arterial - platelet rich, tx with antiplatelets.

Venous - fibrin rich, tx with anticoagulation

140
Q

What is infective endocarditis?

A

Infection of the heart valves or other endocardial lined structures within the heart.

141
Q

Risk factors for IE?

A
  • Prev episode
  • Hx of rheumatic fever
  • Prosthetic valves or other devices (ICD, PPM)
  • Congenital heart defects
  • IVDU
142
Q

Causative organisms for IE?

A
  • Staph Aureus (esp in acute and IVDU)
  • Coagulase negative staph eg. S. Epidermidis (colonise lines)
  • Streptococcus Viridans (mouth and dental)
  • Streptococcus Bovis (ass w/ colorectal cancer)

Non-infective cause: Malignancy, SLE

143
Q

Causes of IE that will be culture negative?

A
  • Prior antibiotic therapy
  • Coxiella burnetii
  • Bartonella
  • Brucella
  • HACEK:Haemophilus, Actinobacillus,
    Cardiobacterium, Eikenella, Kingella)
144
Q

Features of IE?

A
  • FEVER + NEW MURMUR = IE until proven otherwise
  • Septic signs: Fever, rigors, night sweaets, malaise, weight loss, anaemia, splenomegaly, clubbing
  • Cardiac signs: Any new murmur or change in existing
145
Q

Investigations for IE?

A
  • Blood cultures - from 3 sites at 3 times
  • ECG - long PR interval
  • ECHO - shows vegetations (TOE best)
146
Q

Diagnostic criteria for IE?

A

Duke Criteria

Diagnosis made if:

  • Pathological criteria positive
  • 2 major criteria
  • 1 major and 3 minor
  • 5 minor
147
Q

What are pathological criteria in Dukes?

A
  • Positive histology or microbiology of pathological material
  • Obtained at autopsy or cardiac surgery
148
Q

Major criteria in Dukes?

A

Positive blood culture

  • typical organism found in 2 sep cultures
  • persistently +ve cultures

Evidence of endocardial involvement

  • positive ECHO
  • New valvular regurg
149
Q

Minor criteria in Dukes?

A
  • Predisposing heart condition or IVDU
  • Microbiological evidence doesn’t meet major criteria
  • Fever >38
  • Vascular phenomena (see slide)
  • Immunological phenomena (see slide)
150
Q

What are vascular phenomena of IE?

A
  • Major emboli
  • Splenomegaly
  • Clubbing
  • Splinter haemorrhages
  • janeway lesions
  • Petechiae
  • Purpura
151
Q

What are immunological phenomena of IE?

A
  • Glomerulonephritis
  • Oslers nods
  • Roth spots
152
Q

IE management?

A
  • Early liaison with cardiologist and microbiolgy. Abx treatment based on cultures.
  • Treat complications - arrhythmia, HF, heart block
  • Surgery - drain infection or replace valve
153
Q

What are some secondary causes of hypertension?

A

Endocrine disorder: Pheochromacytoma, Cushing’s syndrome, hyperthyroidism, Conn’s syndrome, CAH, Acromegaly, Liddle’s syndrome, primary hyperaldosteronism

Kidney disease: Polycystic kidneys, glomerulonephritis, renal artery stenosis, pyelonephritis

Other: Genetic, coarctation, NSAIDs, COCP, Glucocorticoids, Obesity

Pregnancy: Pre-eclampsia

154
Q

First line management for hypertension (not drugs)?

A
  • Lifestyle modification
  • W loss
  • Diet and exercise, less salt
  • Reduced alcohol
  • Smok cessation
155
Q

First line medical therapy for htn?

A

If <55: ACE-i (or ARB if not tolerated)

If >55 or Black: CCB or Thiazide

156
Q

Step up treatment of hypertension?

A

2nd line: ACE-i + CCB or ACE-i + Thiazide

3rd line: ACE-i + CCB + Thiazide

4th line: Add further diuretic or alpha blocker or beta blocker

157
Q

Gold standard for HTN diagnosis?

A

Ambulatory 24hr blood pressure monitoring

158
Q

Investigating end-organ damage associated with hypertension?

A

Fundoscopy - to check for hypertensive retinopathy
Urine dipstick - to check for renal disease, either as a cause or consequence of hypertension
ECG - to check for left ventricular hypertrophy or ischaemic heart disease

159
Q

Intrinsic causes of sinus bradycardia?

A
  • Acute ischaemia and infarction of sinus node

- Chronic degenerative changes such as fibrosis of atrium and sinus node (sick sinus) in elderly

160
Q

Extrinsic causes of sinus bradycardia?

A
  • Drug therapy ( BB, digitalis, digoxin)
  • Hypothyroidism
  • Hypothermia
  • Cholestatic jaundice
  • Raised ICP
161
Q

Causes of heart block?

A
  • Coronary artery disease
  • Cardiomyopathy
  • Fibrosis of conducting tissue - esp elderly
162
Q

3 types of AV/Heart block?

A

First degree AV block:
- Long PR interval

Second degree AV block:

  • Mobitz type 1 (Wencheback) : Progressively prolonged PR, followed by dropped QRS
  • Mobitz type 2 - Long PR, dropped QRS

Third degree/complete heart block
- No association whatsoever between P waves and QRS complexes

163
Q

ECG of RBBB?

A
  • Secondary R wave in V1
  • Slurred S waves in V5 and V6

MaRRoW

  • M shape in V1
  • W in V6
164
Q

Causes of RBBB?

A
  • PE
  • RVH
  • IHD
  • Congenital heart disease (ASD, VSD, ToF)
165
Q

ECG of LBBB?

A
  • Secondary R wave in the LV leads (v4-V6)
  • Deep slurred S waves in V1 and V2
  • Wide QRS

WiLLiaM

  • W shape in V1
  • M in V6
166
Q

Where do supraventricular tachycardias arise from?

A

Atrium or atrioventricular junction

167
Q

Causes of sinus tachycardia?

A
  • Physiological response in exercise/excitement
  • Fever
  • Anaemia
  • Heart Failure
  • Thyrotoxicosis
  • Acute PE
  • Hypovolaemia
  • Drugs
168
Q

What are atrioventricular junction tachycardias?

A

Tachycardia arises as a result of re-entry circuits in which there are 2 separate pathways for impulse conduction

169
Q

3 types of regular narrow complex tachycardias?

A

1) Atrioventricular nodal re-entry (AVNRT)
2) Atrioventricular re-entry (AVRT)
3) Focal atrial tachycardia (FAT)

170
Q

What is AVNRT?

A
  • Commonest SVT
  • DUe to presence of ring or conducting pathway
  • Allows re-entry circuit and an impulse to produce continuos tachycardia
171
Q

Symptoms of AVNRT?

A
  • heart racing - palpitations
  • Ass chest pain and breathlessness
  • Neck pulsation
172
Q

ECG for AVNRT?

A
  • P waves - not seen or seen immediately before or after QRS complex
  • QRS - Normal shape
  • Narrow complex
173
Q

Acute management of AVNRT?

A
  • Vagal manoeuvers eg Valsalva
  • Adenosine
  • Electrical cardioversion
174
Q

Prevention of AVNRT?

A
  • Beta blockers
  • CCB
  • Fleicainide
  • Catheter ablation
175
Q

What is atrioventricular re-entry tachycardia? (AVRT)

A
  • Due to presence of an accessory pathway that connects the atria and ventricles
176
Q

Causes of AVRT?

A
  • Acessory pathways which are remnant muscle strands between atria and ventricles.
  • Wolff Parkinson-White syndrome is best known AVRT
177
Q

What is Wolff Parkinson-White syndrome

A
  • Congenital accessory conducting pathway between the atria and ventricles
  • Leading to an atrioventricular re-entry tachycardia (AVRT)
  • As the accessory pathway does not slow conduction, AF can degenerate rapidly to VF
178
Q

ECG changes of WPW syndrome?

A
  • Short PR interval
  • Wide QRS complexes with a slurred upstroke ‘Delta Wave’
  • Left axis deviation in right sided pathway
  • Right axis deviation in left sided pathway
179
Q

Associations of WPW?

A
  • HCM
  • Mitral valve prolapse
  • Ebsteins anomaly
  • Thyrotoxicosis
  • Secundum ASD
180
Q

WPW management?

A

Definitive: Radiofrequency ablation of acessory pathway
Medical: Sotalol, amiodarone, flecainide

181
Q

What is atrial fibrillation?

A
  • Atrial activity is chaotic and mechanically ineffective
  • The AV node conducts a proportion of the atrial impulses to produce an irregular ventricular response –> giving rise to an irregularly irregular pulse
182
Q

Signs and symptoms of AF?

A

Symptoms: Palpitations, dyspnoea, chest pain, fatigue

Signs: Irregularly irregular pulse

183
Q

Investigations for AF?

A

ECG:
Irregularly irregular R-R interval
Absent P waves
Tachycardia

184
Q

Medications for rate control in AF?

A
  • Beta blocker or a rate-limitng CCB
185
Q

Medications used to maitain sinus rhytm in AF?

A
  • Sotalol
  • Amiodarone
  • Flecainide
186
Q

Assess patients stroke risk in AF?

A

CHADS2VASC

Congestive HF 1
HTN 1
Age >75 2
Diabetes 1
Prev stroke or TIA 2
Vascular disaese (IHD, PVD) 1
Age >65 1
Sex category female 1
187
Q

What risk score used before anticoagulation prescribed in AF?

A

HASBLED

H Hypertension uncontrolled, sys BP >160
A Abnormal renal or liver function
S Stroke
B Bleeding hx
L Labile INR
E Elderly >65
D Drugs predisposing to bleeding or Alcohol >8/week
188
Q

What is atrial flutter?

A

A form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves

189
Q

ECG on atrial flutter?

A
  • Sawtooth appearance
190
Q

Symptoms of atrial flutteR?

A
  • Palpitations
  • Breathlessness
  • Chest pain
191
Q

Management of atrial flutter/

A

Similar to AF.
Rate and rhythm control.
Stroke prophylaxis

192
Q

Atrial ectopic beats?

A

These are caused by premature discharge of an ectopic atrial focus (i.e. a node that’s in the wrong place in the atrium)

Can occur in bursts:
Couplets/triplets
Bigeminy/trigeminy

On ECG – produces an early and abnormal P wave, usually followed by a normal QRS complex

Treatment not usually needed, unless they cause symptomatic palpitations or provoke more significant arrhythmias – in which case B-blockers may be effective

193
Q

What is ventricular tachycardia?

A

Broad complex tachycardia originating from a ventricular ectopic focus

Has the potential to precipitate ventricular fibrillation and hence requires urgent treatment

2 main types of VT:
Monomorphic VT– most commonly caused by myocardial infarction
Polymorphic VT – e.g. torsades de pointes which is precipitated by prolongation of the QT interval

194
Q

Causes of prolonged QT interval?

A 
Congenital: 
 - Jervell-Lange-Nielsen syndrome
 - Romano-Ward syndrome
Drugs:
 - Amiodarone, sotalol,
 - TCAs, fluoxetine
 - Chloroquine
 - Terfenadine
 - Erythromycin
Other:
 - Hypocalcaemia, hypokalaemia, hypomagnesia
 - Acute MI
 - Myocarditis
 - Hypothermia
 - SAH
195
Q

What is VF and how is it managed?

A
  • Very rapid and irregular ventricular activation but no mechanical effect
  • 0 cardiac output
  • Pt is pulseless and unconscious, no resp.
  • Tx: DEFIB
196
Q

Symptoms and signs of acute pericarditis?

A

Symptoms:

  • Chest pain, may be pleuritic.
  • Non-produc cough, dyspnoea, flu like sx

Signs:

  • Pericardial rub
  • Tachypnoea
  • tachycardia
197
Q

Causes of acute pericarditis?

A
  • Viral infections (coxsackie B and echovirus commonly)
  • TB
  • Uraemia
  • Trauma
  • Post MI (including dresslers)
  • CTD
  • Hypothyroidism
  • Malignancy
198
Q

What is Dresslers?

A
  • Pericarditis occurring secondary to Mi or pericardial damage
  • At least 2 weeks after MI
  • This makes it DIFFERENt to normal post MI pericarditis (which occurs in first few days)
  • Raises ESR massively
199
Q

ECG changes for pericarditis?

A
  • Widespread saddle shaped ST elevation across all leads

- PR depression - specific

200
Q

Treatment of pericarditis?

A
  • Tx of underlying
  • Bed rest
  • Oral NSAIDS (not in first few days after MI)
  • Corticosteroids
201
Q

Complications of pericarditis?

A
  • Chronic pericarditis
    This can thick and become…
  • Restricrtive/ constricitve pericarditis
202
Q

Features of constrictive pericarditis?

A
  • Dyspnoea
  • RHF - elevated JVP, ascites, oedema, hepatomegaly
  • Pericardial knock - loud S3
  • Kussmauls sign positive
  • CXR shows pericardial calcification
203
Q

Treatment of constrictive pericarditis?

A
  • Complete resection of pericadium

- Risky procedure tho dude

204
Q

What is pericardial effusion?

A
  • Collection of fluid within the pericardial sac

- Can put pressure on ventricles, causing cardiac tamponade

205
Q

Clinical features of pericardial effusion/tamponade?

A
  • Heart sounds soft and distant
  • Apex beat obscured
  • Friction rub
  • Ewarts sign
  • Kussmauls sign
  • Friedrichs sign
  • Pulsus paradoxus
206
Q

Investigations for tamponade/pericardial effusion?

A
  • ECG –low voltage QRS complexes
  • CXR –will show anenlarged heart(globular or pear shaped), with precise outlines. The pulmonary veins willnot be distended.
  • Echo –this is the most useful test, as it is able to directly detect the tamponade
  • MRI –maybe do one of these if you suspect haemopericardium
  • Pericardiocentesis –this is indicated when you suspect an infection is the cause (e.g. TB, malignancy)
  • Pericardial biopsy –this can be done if you still suspect TB, despite a negative pericardiocentesis
  • Blood cultures / antibody screen –to look for the underlying cause
207
Q

Treatment of effusion/tamponade?

A
  • Tx of underlying cause
  • Tamponade = pericardiocentesis and chest drain
  • If keeps coming back, could be malignancy
208
Q

What is aneurysm?

A

An artery that has a localised dilation with a permanent diamater of 1.5x that of the particular artert

209
Q

Difference between true and pseduoaneurysms?

A

True = the wall of the artery forms the wall of the aneurysm (most common in order - abdominal aorta, popliteal, femoral and thoracic aorta)

False/pseudo = other surrounding tissues form the wall of the aneurysm (most common in femoral artery following puncture – inadequate pressure once the puncture tool removed, blood can spill out and form a haematoma)

210
Q

Risk factors for AAA?

A

Same rf as atheromatous disease.

  • Htn
  • Smoking
  • Age
  • Diabetes
  • Obesity
  • High LDL
  • Sedentary lifestyle
  • Genetic factors
211
Q

Specific causal factors for AAA?

A
  • Coarc of aorta
  • Marfans and other CTDs
  • Prev aortic surgery
  • Pregnancy
  • Trauma
  • Age
  • Male
212
Q

Features of AAA?

A
  • Symptomless - often indicdental imaging finding, ususally AXR
  • Mean age 65
213
Q

Complications of AAA?

A
  • IVC obstruction
  • Impaired blood flow to lower limbs
  • Thrombosis and embolism
  • Main risk = Dissection and rupture
214
Q

AAA management?

A

NICE guidelines: Aortic aneurysm of >5.5cm in diameter should be treated.

If below, risk of surgery > than dissection risk.

215
Q

What is ruptured AAA?

A

Where the wall of the aorta completely fails and blood escapes freely into the abdominal cavity

Different from dissection, but dissection often leads to rupture

216
Q

What is aortic dissection?

A

Where blood escapes through the innermost layer of the wall of the artery and prises apart the media, making a new lumen

Sometimes this lumen is absorbed back into the main lumen, creating a ‘double barrelled aorta’

This may be stable, but may rupture. If it’s close to the valve (TAA) – may compromise valve function

The dissection sometimes tracks all the way back to the pericardium, causing haemopericardium

217
Q

Classification of aortic dissection?

A

Type A: 2/3 of cases, ascending aorta and descending aorta

Type B: Descending aorta only, distal to left subclavian origin

218
Q

Symptoms of aortic dissection?

A
  • Pain - sudden 10/10, tearing, radiates to back
  • Collapse
  • Expansile mass in abdo
  • Shocl
  • Hypotension
  • tachycardia
  • Anaemia
  • Sudden death
  • Other sx: teste pain, renal colic sx, diveriticulitis sx, non specific back pain
219
Q

Symptoms of AAA rupture?

A
  • Epigastric pain radiating to back
  • Pain may also be present in - groin, iliac fossae, tasticles
  • Can be constant or intermittent

Dont dismiss it as renal colic

220
Q

3 main patterns of peripheral arterial disease?

A

1) Intermittent claudication
2) Critical limb ischaemia
3) Acute limb-threatening ischaemia

221
Q

Features of intermittend claudication?

A
  • Aching or burning in leg muscles following walking
  • Pt can walk for predictable distance before sx start
  • Usually relieve within minutes
  • Not at rest
222
Q

How to assess intermittent claudication?

A
  • Check the femoral, popliteal, posterior tibialis and dorsalis pedis pulses
  • Check ankle brachial pressure index (ABPI)
  • Duplex ultrasound is the first line investigation
  • Magnetic resonance angiography (MRA) should be performed prior to any intervention
223
Q

Features of critical limb ischaemia?

A

1 or more of:

  • Rest pain in foot for >2weeks
  • Ulceration
  • Gangrene

Pt reports hanging legs out of bed to ease pain.
ABPI <0.5 suggests critical limb ischaemia

224
Q

Features of acute limb-threatening ischaemia?

A
  • Pale
  • Pulseless
  • Painful
  • Paralysed
  • Paraesthesia
  • Perishingly cold
225
Q

Other features of PVD?

A
  • Arterial ulcers (punched out)
  • Gangrene
  • Reduced/absent peripheral pulses
  • Skin atrophy - in chronic disease
  • Hair loss - in chronic disease
  • Cyanosis
  • Excessive sweating
  • Erectile dysfunction
226
Q

PVD syndrome causing erectile dysfunction?

A

Leriche Syndrome.

The result of distal aortic disease.
Other features: Buttock pain and pale cold legs.

227
Q

Management of PAD?

A 
Lifestyle
 - Smok cessation
 - Exercise
 - Diet and w loss
 - Avoid cold weather
 - Inspect feet
Treating comorbidities
 - HTN
 - DM
 - Obesity
All patients should be placed on statin, atorvastatin 80mg.
Clopidogrel first line.
228
Q

Treatment of severe PAD/critical limb ischaemia?

A
  • Angioplasty
  • Stenting
  • Bypass surgery
  • Amputation
229
Q

What is shock?

A

Circulatory failure, tissue hypo-perfusion, energy deficit, accumulation of metabolites.

230
Q

5 classifications of shock?

A

1) Septic
2) Haemorrhagic
3) Neurogenic
4) Cardiogenic
5) Anaphylactic

231
Q

What is septic shock?

A
  • Low BP despite massive efforts to resuscitate
  • Infective source + SIRS (3T w/ white sugar)
  • Evidence of organ dysfunction (confusion, ARDS, hypovolaemia, AKI, liver dysfunction)
232
Q

Management of septic shock?

A
  • Prompt admin of antibiotics to cover likely pathogens + search for source
  • haemodynamic stabilisation
  • Modulation of septic response - eg tight glycaemic control
233
Q

What is haemorrhagic shock?

A
  • Inadequate tissue perfusion due to loss of blood volume

- Class depends on volume lost

234
Q

Possible causes of shock in trauma pt’s?

A
  • Trauma > Haemorrhage most likely
  • Tension pneumothorax
  • Spinal cord injury
  • Myocardial contusion
  • Cardiac tamponade
235
Q

What is neurogenic shock?

A
  • Occurs following spinal cord transection, usually at high level
  • Resultiung in interruption of the autonomic nervous system
  • Result is either decreased sympathetic tone or increased parasympathetic tone
  • The effect of which
    • -> decrease in peripheral vascular resistance due to marked vasodilation
    • -> decreased preload and decreased CO
    • -> decreased tissue perfusion AKA SHOCK

Use peripheral vasoconstrictors to return tone to normal

236
Q

Cardiogenic shock?

A

In medical patients - main cause is IHD
In trauma – myocardial trauma or contusion

Treatment – supportive
Transthoracic echo should be used to determine evidence of pericardial fluid or direct myocardial injury

237
Q

What is anaphylaxis?

A

A severe, life-threatening, generalised or systemic hypersensitivity reaction

238
Q

Features of anaphylaxis?

A
  • Sudden onset with rapid progression of sx
  • Airway: Swelling, hoarseness, stridor, obstruction
  • Breathing: SOb, wheeze, confusion due to hypoxia, cyanosis, resp arrest
  • Circulatory: shock (pale/clammy), tachycardia, hypotensive, low consciousness, cardiac arrest
  • Skin: Flushing, urticaria, angioedema
239
Q

Treatment of anaphylactic shock?

A
  • IM adrenaline
  • Can be repeated every 5 mins

Dosage:

  • 1:1000 adrenaline
  • Adult and children >12: 500mcg
  • Children 6-12 300mcg
  • Children <6 150mcg

2a (7 decks)

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