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SPM > Cardiology > Flashcards

Cardiology Flashcards

1
Q

3 divisions of ACS

A

STEMI
- ST elevation of 1mm in 2 or more continguous leads
- ST elevation of 2mm in 2 or more chest leads
- ST depression in 2 or more leads V1-V4 (posterior stemi)
- new onset LBBB
NSTMI
- raised cardiac biomarkers
- ECG may show non-specific ischaemic changes like ST depression or T wave inversion
unstable angina
- non-specific ischaemic changes butbiomarkers normal

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2
Q

aetiology of atheromas qlaque

A
  • Fatty streaks start in childhood
  • Atheromatous plaques develop slowly throughout life
    o Endothelial damage means more permeable
    o LDLs become deposited in tunica intima and become oxidised
    o Migration of monocytes into tunica intima to become macrophages
    o Release cytokines that attract more monocytes and further damage endothelium
    o Take up oxidised LDLs and become foamy macrophages which release lipid contents -> plaque growth
    o Smooth muscle proliferation and hardening of plaque
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3
Q

classification of angina

A

class I-IV
I - no angina with ordinary physical activity. strenuous activity may cause symptoms
II - angina causes slight limitation on ordinary activity
III - angina causes marked limitaiton on ordinary activity
IV - angina occurs with any physical activity and may be present at rest

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4
Q

causes of stable angina

A

usually by coronary artery disease

less commonly by valve disease, hypertrophic obstructive cardiomyopathy or hypertensive heart disease

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5
Q

symptoms of stable angina

A

chest pressure or squeezing lasting several mins, which may radiate to one or both arms, neck or teeth
provoked by exercise or emtional stress

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6
Q

how does stable angina differ from unstable

A

pain from exertion lasts less than 10 minutes and is usually less
normal/unchanged ECG

angina is considered unstable if it occurs at rest, is new in onset and is severe (occurs with walking 1 flight of stairs, or similarly low level of exertion)

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7
Q

diamond classification for chest pain

A

1 sub-sternal discomfort of characteristic quality
2 provoked by exertion or stress
3 relieved by rest +/- nitrates within minutes

typical angina = all 3
atypical angina = 2/3
non-angina pain = none

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8
Q

INITIAL investigations for stable angina

A

take a history - age, male, presence of CV risk factors, history of CAD (e.g. previous MI) makes diagnosis more liekly

ECG - looking for changes that inficate ishcaemia or previous MI (i.e. that they already have CAD) such as pathological Q waves, LBBB, ST or T wave changes

then look at blood for things that could worsen workload of the heart e.g. FBC (anaemia), lipid profile (increased risk of CVD)

do U+E prior to starting meds and LFTs prior to starting statins

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9
Q

when to FURTHER investigate stable angina

A

after the inital clincal examination, must decide whether the probability of ischaemia is sufficient to warrent further testing

is done via age and sex and whether or not the pain is typical (via the Diamond criteria) - e..g increased age and a man is more likely angina

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10
Q

FURTHER investigations for stable angina depending on the CAD likliehood percentage

A
  • > 90% treat as known CAD – i.e. as known stable angina
  • 61–90% invasive angiography, or functional imaging if inappropriate (SPECT, stress echo, stree MIR)
  • 30–60% functional imaging (SPECT, stress echo, stress MRI)

• 10–29% CT calcium scoring (coronary artery calcification scanning)
If CT calcium score is 0 then angina is unlikely
1-400 then proceed to CT angiography
If >400 then invasive coronary angiography or functional imaging

• <10% reconsider diagnosis.

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11
Q

when is a stress exercise ECG useful for stable angina investigations

A

NICE – only done when there is diagnostic uncertainty in people with KNOWN CAD (e.g. previous MI or angioplasty) and NOT TO MAKE A PRIMARY DIAGNOSIS of CAD/stable angina

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12
Q

conservative management for stable angina

A

patient education

  • explain the factors that can provoke angina like exertion, emotional stress, exposure to cold or eating a large meal
  • advise to seek medical help if there is sudden worsening in the severity of their angina

conservative
- physical activity, smoking, alcohol, weight, stress, diet

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13
Q

medical management for stable angina

A

GTN spray for symptomatic relief - advise the person that if they experience chest pain they should stop what they are doing and rest. take the spray. then take a 2nd dose after 5 mins if still pain. call 999 if pain has not eased after 5 mins after the 2nd dose or earlier if pain is intensifying

a beta blocker or a CCB - If they cannot tolerate one or the other, then switch to the other one

low dose aspirin 75mg for secondary prevention

consider ACEi for people with stable angina and DM

offer a statin or HTN if needed

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14
Q

if a person with stable angina cannot tolerate or are contraindicated to beta blockers and CCBs then what should you consider monotherapy with

A

 Long-acting nitrate (e.g. isosorbide mononitrate)
 Nicorandil
 Ivabradine
 Ranolazine (consider seeking specialist advice when initiating ivabradine or ranolazine)

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15
Q

driving with angina

A
  • For those driving cars, driving must cease when symptoms occur at rest, with emotion or whilst driving
  • Driving may recommence when symptom control is achieved – do not need to inform DVLA
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16
Q

complications of stable angina

A
  • Stroke
  • MI
  • Unstable angina
  • Sudden cardiac death
  • Anxiety, depression, reduced QoL
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17
Q

prognosis of stable angina

A

With guideline-directed management, 58% of patients can expect to be free of angina within 1 year

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18
Q

when to offer a stain with stable angina

A

if cholesterol is >4mmol/L

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19
Q

3 different presentations of unstable angina

A

o exertional angina of new onset – even if relieved with rest and requiring a consistent amount of exertion to produce symptoms, angina is considered unstable when it first occurs
o exertional angina that was previously stable and now occurs with less physical exertion (occurs with walking 1 flight of stairs, or similarly low level of exertion)
o anginal symptoms at rest with no exertion

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20
Q

pathophysiology of unstable angina

A
  • the initiating lesion in CAD is a fissure in the vessel endothelial lining over an underlying cholesterol plaque
  • this results in a loss in the integrity of the plaque cap
  • leads to exposure of subendothelial matrix elements like collagen
  • this stimulates platelet activation and thrombus formation
  • release of TF directly activates the coagulation cascade and promotes formation of fibrin
    o If an occlusive thrombus forms, the patient may develop an acute ST segment elevation myocardial infarction
  • unless the affected myocardium is richly collateralised
  • If the thrombus formation is not occlusive, the patient may develop UA or non-specific ST changes on the ECG (ST depression or T-wave changes)
  • Myocardial supply and demand mismatch may cause ischaemia without significant CAD. These include:
    o Increased myocardial oxygen requirements such as fever, tachycardia, thyrotoxicosis
    o Reduced coronary blood flow: for example, hypotension
    o Reduced myocardial oxygen delivery such as anaemia or hypoxaemia
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21
Q

investigations for unstable angina

A

examination
ECG to rule out STEMI - may be normal or have T wave inversion or ST segment depression

troponins to rule out MI - measured at presentaiton then 3 hours after presentation

lipid profile, blood glucose, FBC

CXR - may show complications of ischaemia e.g. pulmonary oedema or explore alteraive diagnoses (pneumothorax or aortic aneursym)

echo - provides information about precipitating causes like AS or hypertrophic cardiomyopathy

coronary angiography = gold standard for assessing presence + severity of CAD

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22
Q

when to perform angiography on someone with CAD (unstable angina or NSTEMI)

A

work out risk of MI via TIMI score or GRACE score

o Urgent (<120 mins after presentation) if ongoing angina despite treatment and evolving ST changes, signs of cardiogenic shock or life-threatening arrythmias
 (with follow-on PCI if indicated)
• PCI vs CABG depends on coronary angiographic findings and comorbidities – discuss with interventional cardiologist if unsure
o High-risk patients for progression to MI or death require urgent coronary angiography (<24 hours)
 (with follow-on PCI if indicated)
o Patients with intermediate score should be referred to coronary angiography within <72 hours
 (with follow-on PCI if indicated)

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23
Q

conservative management of unstable angina / NSTEMI

A

patient education

admit to CCU and monitor closely

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24
Q

medical treatment of unstable angina/ NSTEMI

A 
aspirin 300mg 
oxygen if <90% or breathless 
nitrates 
morphine 5-10mg IV 
metoclompramide 10mg IV

perform a risk assessment to calculate a 6-month mortality rate (age, previous MI, BP, HR, ECG, bloods)

clopidogrel 300mg if >1.5% risk (continue the dual antiplatelet therapy for 12 months)
beta blocker if tachycardic or hyeprtension or LV function <40%
ACEi
statin

check serial ECGs and troponins

coronary angiography

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25
Q

what to do before discharge for unstable angina/NSTEMI

A

o assess Lv function - Assessment is recommended in all patients who have had an MI. Should be considered in all patients with unstable angina
o Continue fondaparinux (or LMWH or heparin) until discharge
o Offer information about cardiac rehabilitation
o Management of CV risk factors and lifestyle changes
o Arrangements for follow up

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26
Q

NSTEMI / unstable angina symptoms in men vs women

A
  • male
    o chest pressure/discomfort lasting at least several minutes
  • women
    o more commonly with middle/upper back pain
    o or may have upper abdominal pain (atypical presentation)
  • both can present with
    o sweating
    o dyspnoea
    o nausea
    o anxiety
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27
Q

troponins in NSTEMI

A

o >99th percentile of normal
o troponins rise 4-6 hours after onset of infarction, peak at 18-24 hours and may persist for 14 days or longer
o infarct size can be estimated from the troponin value measured at 72 hours

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28
Q

posterior MI on ECG

A

V1, V2, V3 : ST depression + wide R wave and high T wave in V2

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29
Q

lateral MI ECG

A

circumflex

I, aVL, V5, V6

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30
Q

pathphysiology of STEMI

A
  • STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque. This results in exposure of substances that promote platelet activation and aggregation, thrombin generation, and thrombus formation, causing interruption of blood flow. (type 1 MI)
  • can also occur due to imbalance in supply and demand (this would be type 2 MI – from teaching)
31
Q

STEMI diagnosis

A

A to E assessment
ECG - ST elevation or new LBBB
continuous cardiac monitoring is required due to high likelihood of cardiac arrythmias
troponins - but don’t have to wait for these to come back before starting intervention
coronary angiogram within 90 minutes

FBC, glucose, U+E and lipid profile should also be obtained

CXR post revascularisation
echo to asses LV function after reperfusion therapy

32
Q

other causes of ST segment elevation

A

high ST segment take off - a normal variant

acute pericarditis - not typical ‘coved’ appearance of acute MI - is concave upwards

LBBB - acute infarction can manifest as new LBBB - the problem is knowing whether the LBBB is new

33
Q

maganament STEMI

A

morphine - 5-10mg IV every 5-15mins until pain control is achieved
give antiemetic with the first dose of morphine; metoclopramide 10mg IV

oxygen if sats are below 95%

nitrate - GTN sublingual (NB in a complete occlusion is unlikely to help because needs a blood supply to work)

300mg aspirin orally

relocate - patient should be admitted to a unit with continuous cardiac monitoring and started on strict bed rest for first 12-24 hours

ticagrelor - 180mg loading dose

unfractionated heparin - 60 units/kg IV bolus initially followed by 12 units/kg/hour infusion during the PCI

PCI within 90minuts (radial or femoral artery + in majority of cases a stent will be inserted)

after the PCI:
ACE0, beta blocker, aspirin 75mg + 90mg BD ticagrelor, rehabilitation, statin

ABARS

34
Q

when is inotrope support or intra-aortic balloon pump used (IABP) in stemi

A

 patients with low CO states and cardiogenic shock may benefit from a dobutamine infusion (beta 1 agonist – increases contractility and CO)
 an IABP or a ventricular mechanical circulatory support device is recommended if pharmacological measures do not quickly improve the shocked state

35
Q

when is CABG done

A
  • If patient has more severe coronary artery disease like plaques in at least 3 of their vessels; triple vessel disease
36
Q

time cut off to perform PCI in STEMI

A

must have presented within 12 hours

if after this: can use PCI if there is continuing myocardial ischaemia

after this point - offer fibrinolysis (or if PCI cannot be delivered within 120 minutes)

37
Q

secondary prevention advice for someone that has had a MI

A
  • Stop smoking – options to aid this includes referral to NHS stop smoking service, drug treatment (bupropion or varenicline) and written supporting material
  • Cardioprotective diet
    o Minimize foods containing refined sugars, including fructose
    o <6g salt per day
    o Choosing wholegrain varieties
    o At least 2 portions of fish a week
    o Eating at least 4-5 portions per week of a mixture of unsalted nuts and seeds
    o At least 5 portions of fruits and vegetables a day
    o Total fat intake should be 30% or less of total energy intake, and saturated fat (which is mainly from animal sources) should be 7% or less
  • Exercise
    o Exercise at least 150 minutes per week of moderate-intensity aerobic activity (to the point of slight breathlessness)
    o Advise people to do muscle strengthening activities on 2 or more days a week that work all major muscle groups (legs, hips, back, abdomen, chest, shoulders and arms)
    o Encourage people who are unable to perform moderate intensity physical activity to exercise at their maximum safe capacity and increase the duration and intensity of activity as fitness improves
  • Keep alcohol within 14 units a week – if they do drink this much then spread it evenly over 3 days or more
  • Weight loss
38
Q

complications of STEMI

A

congestive HF due to myocardial damage + LV remodelling

ventricular arrythemias - VF is main killer for those with MI - have to continually monitor patient to avoid this

depression

recurrent ischaemia and infarction - caused by further plaque rupture and atherosclerosis progression

post infarction pericarditis (Dressler’s syndrome)

heart block

39
Q

cause of hypertrophic cardiomyopathy

A

genetic disease - caused by mutations in genes that encode components of the contractile apparatus
majority are autosomal dominant with variable penetrance - but 50% are sporadic

40
Q

what happens in hypertrophic cardiomyopathy

A

mutations lead to septal thickening - asymmetrical (septum more hypertrophied than the wall) - means less filling can occur
and they are stiffer so less compliant - again leading to less filling
this can lead to diastolic HF

the hypertrophied septum may lead to LV outflow obstruction - LV papillary muscle hypertrophy can furrther cause obstruction

hypertrophic obstructive cardiomyopathy occurs in around 25% - the obstruction is intermittent depending on for example HR (faster HR means shorter filling period)
When there is outflow obstruction – the smaller gap means faster blood flow through that outflow tract which pulls the mitral leaflet valve in further (venturi effect) – and this will cause a crescendo-decrescendo murmur (ejection systolic murmur)

41
Q

most common cause of sudden cardiac death in the young

A

hypertrophic cardiomyopathy

42
Q

presentation of hypertrophic cardiomyopathy

A

most people are asymptomatic and are detected by family screening of an affected person or by routine ECG

pre-syncope or syncope with exertion - either due to outflow tract obstruction or ventricular arrythemia
dyspnoea
angina
systolic ejection murmur
jerky carotid pulse due to rapid ejection and sudden obstruction to left ventricular outflow during systole
sudden death
bifid pulse
palpitations - enlarged heart muscle predisposes to arrythmias

43
Q

the systolic ejection murmur of hypertrophic cardiomyopathy

A

can be increased by manoevres that decrease afterload such as standing or Valsava maneovre (decreased blood entering the heart causes the LV to be smaller so the degree of obstruction increases)

and decreased by maneovres that increase afterload like squatting - this means the ventricle has more blood stretching it out so become less obstructed so murmur becomes less intense

44
Q

investigations for hypertrophic cardiomyopathy

A

ECG
- most common abnormality is in ST or T waves e.g. ST depression or T wave inversion
- deep Q waves
- left ventricular hypertrophy
- may see AF or WPW
CXR
- patients may have cardiomegaly secondary to LVH, or left atrial enlargement may be seen
echo- MR SAM ASH
- mitral regurg, systolic anteiror motion of the anterior mitral valve leaflet, asymmatric hypertrophy
exercise test and holter monitor to risk stratify

genetic testing of family members

45
Q

treatment of hypertrophic cardiomyopathy

A

asymptomatic at high risk of sudden death - ICD implantatino (e.g. if first degree relative died suddenly)
if not at high risk then observation + activity restriction

symptomatic with LV outflow tract obstruction:
negative inotropic and chronotropic agents + restriction from high-intensity activity (beta blockers - means heart has longer time to fill)

Amiodarone for arrythmias (AF, VT)
Anticoagulate for paroxysmal AF

46
Q

causes of dilated cardiomyopathy

A 
unknown cause
1/3 have a genetic component
sporadic
- ischaemia
- myocarditis 
- toxins - alcohol, chemo, metals
- autoimmune disorders - RA, SLE
- endocrine disorders
- neuromuscular 
- peripartum
47
Q

pathophsyiology of dilated cardiomyopathy

A

sarcomeres are added in series rather than in paralell

dilation –> decreased contractility –> LEVF

48
Q

symptoms of dilated cardiomyopathy

A

Clinical presentation is variable and can include stroke and other embolization effects, heart failure, cardiac arrhythmias, conduction defects and sudden cardiac death

Most cases will present as congestive heart failure - Dyspnoea, weakness, fatigue, oedema, raised JVP, pulmonary oedema…

49
Q

investigations for dilated cardiomyopathy

A 
-	Echo 
Marked dilation of the left ventricle
Reduced systolic and diastolic function 
look for mitral and tricuspid regurgitation
-	BNP 
Raised in heart failure  
-	ECG 
Will be abnormal (but non-specific) 
May see non-specific ST-segment and T wave changes. Sinus tachycardia, conduction abnormalities and arrhythmias (e.g. AF, VT…)
-	CXR 
Cardiomegaly, pulmonary oedema
-	Cardiac catheterisation 
Usually shows raised filling pressures 
-	Endomyocardial biopsies
Some patients are shown to have specific heart muscle disorders – e.g. myocarditis, amyloidosis, sarcoidosis or haemochromatosis
50
Q

2 types of hypertrophic cardiomyopathy

A

can be obstructive or non-obstructive. The non-obstructive type is often asymptomatic, although arrythmias and even sudden cardiac death can occur

51
Q

management of dilated cardiomyopathy

A

diuretics for symptomatic fluid overload
ACEi with reduced LVEF
digoxin for patients with inadequate response to ACEi and diuretics
spinoronlactone has also been shown to improve survival
nitrates for diastolic dysfunction + pulmonary congestion
wafarin for AF or history of PE
bi-ventricular pacing for Class III or IV HF
mitral annuloplasty or valve replacement
catheter ablation for recurrent ventricular tachy

left ventricular assist devices or trasplant

52
Q

pathophysiology of restrictive cardiomyopathy

A
  • Proliferation of connective tissue –> decreased elasticity of cardiac tissue –> walls are rigid –> abnormal diastolic filling due to decreased compliance
  • less compliant –> cant stretch –> less filling –> lower SV –> HF
53
Q

cariomyopathy and types of HF

A

hypertrophic - diastolic
dilated - systolic
restrictive - diastolic

54
Q

causes of restrictive cardiomyopathy

A

idiopathic
endomyocardial fibrosis - most commonly occurs in children and is thought to be caused by things like infection + nutritional deficiencies
infiltrative disease e.g. amyloid heart disease, haemochromatosis
sarcoidosis
scleroderma
radiation
Loffler endocarditis - eosinophils deposit in the heart tissue

55
Q

symptoms of restrictive cardiomyopathy

A

may be asymptomatic or have symptoms of HF

56
Q

gold standard investigation for restrictive cardiomyopathy

A

right ventricular biopsy via cardiac catheterisation

will demonstrate positivity for Congo red staining

57
Q

investigations for restrictive cardiomyopathy

A
  • Right ventricular biopsy via cardiac catheterization
  • ECG - may suggest a secondary cause for the cardiomyopathy and will often show low-amplitude QRS complex due to the restricted heart
  • CXR
  • Echo - Usually shows thickened ventricular walls, valves and atrial septum with small cavities
  • MRI - Is useful at distinguishing restrictive cardiomyopathy from constrictive pericarditis
  • Cardiac CT is sometimes undertaken
58
Q

management of restrictive cardiomyopathy

A
  • treat underlying cause if possible, e.g. treating the hemochromatosis
  • manage heart failure -diuretics, ACEi
  • All patients with restrictive cardiomyopathy and atrial fibrillation should be anticoagulated unless contra-indicated
  • beta blockers + CCBs - may be used for rate control in those with AF
  • ICD or pacemaker implantation may be indicated
  • Cardiac transplant - Especially in children – restrictive cardiomyopathy is primarily idiopathic and transplantation
59
Q

most common 2 causes of acute pericarditis

A

idiopathic

viral - most commonly due to coxsackie B virus and echovirus9

60
Q

causes of acute pericarditis

A

idiopathic
viral - most likely due to coxsackie B virus and echovirus
bacterial
post MI pericarditis - acute (early) or Dressler syndrome (late)

rarer causes

  • malignant pericarditis
  • uraemic pericarditis
  • autoimmune pericarditis
  • post radiation or post surgical
61
Q

early vs late post-MI pericarditis

A

early - occurs in about 20% of patients in the first few days following MI

late - Dressler’s syndrome - occurs 2-10 weeks post infarct in about 7% of patients. is an autoimmune condition where the body autoreacts against damaged myocardial tissue

62
Q

pathophysiology of pericarditis

A
  • the pericardium is well-innervated, and inflammation causes severe pain
  • the formation of a concomitant effusion is usually due to a response to the inflammation
63
Q

pericarditis - triad

A

chest pain
saddle shaped global ST segment elevations
pericardial friction rub

64
Q

symptoms of pericarditis

A

chest pain - sharp, pleuritic or aching (can mimic pain of ischaemia)
worse when lying down (differentiates it from PE or pnuemonia)
tripod position relieved pain

pericardial friction rub - high pitched or squeaky sound - best heard at left sternal edge with patient leaning forward

fever
myalgia

65
Q

investigations for pericarditis

A

ECG
- global upwardly saddle-shaped ST segment elevations with PR depressions in most leads
troponins
- elevated in some patients
FBC - elevated leukocyte count may suggest bacterial pericarditis
CRP
elevated creatinine
blood culture - when bacterial pericarditis is suspected then this is essential
CXR - usually normal unless a large pericardial effusion
echo - indicated when cardiac tamponade is suspected
pericardial fluid culture

66
Q

diagnostic criteria for pericarditis

A

typical chest pain
pericardial friction rub
widespread ST elevation
pericardial effusion

67
Q

management of pericarditis

A

VIRAL OR IDIOPATHIC
Bed rest
Anti-inflammatory medicines – ibuprofen or aspirin
If >14 days, can also give colchicine
If pain is still severe, steroids can be given
The pain and inflammation usually settle within a few weeks

OTHER CAUSES
Treat cause – e.g. anti-TB medicine for TB
Antibiotics for bacterial pericarditis

Tamponade or symptomatic effusion:
Pericardiocentesis

68
Q

causes of pericardial effusion

A

idiopathic - although it is generally assymed most cases are due to viral infection

iatrogenic after surgery

infection - viral, bacterial, tuberculous

metastatic malignancy

aortic dissection - will lead to blood rapidly filling the pericardium

direct penetrating injiry

immune mediated - SLE, Wegener’s granulomatosis, Dressler’d

69
Q

symptoms of pericardial effusion

A
  • Many small-to-moderate effusions formed over a long period of time will be relatively asymptomatic
  • Dyspnoea, chest pain
  • Light-headedness, syncope
  • Palpitations

softer heart sounds, obscured apex beat, low grade fecer

70
Q

Becks triad for cardiac tamponade

A

raised JVP
hypotension
muffled heart sounds

other: pulsus paradoxus (>10mmHg drop in systolic BP with inspiration)

71
Q

investigatoins for pericardial effusion

A

FBC - raised leukocytes
U+E - uraemic aetiology
blood culture- essential if bacterial pericarditits is suspected
ECG - may show raised ST segments
CXR - large globular or pear shaped heart + enlarge cardiac shadow
echo
cardiac CT or MRI - helpful is loculated pericardial effusions are suspected
pericardiocentesis - done when a tuberculous, malignant or purulent effusion is suspected
pericardial biopsy

72
Q

management of pericardial effusion

A

treat the cause e.g. cytotoxic drugs for malignancy
most resolve spontaneously
if they reaccumulate (e.g. due to malignancy) then may require pericardial fenestration
oxygen if circulation is compromised
fluids if hypovolaemic
pericardiocentesis for larger effusions
surgical approach is only recommended for very large effusions where repeated pericardiocentesis have failed

73
Q

management for cardiac tamponade

A
  • Oxygen
  • Volume expansion
  • Bed rest with leg elevation to improve venous return
  • Positive inotropic drugs e.g. dobutamine
  • if no haemorrhage, trauma, neoplasm, purulence:
    o 1st line is echo-guided pericardiocentesis
  • if haemopericardium, trauma, purulent effusion or neoplastic disease
    o 1st line is surgical drainage

SPM (9 decks)

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