Cardiology p1 Flashcards
(108 cards)
1
Q
SOCRATES for MI
A
S: Central / behind sternum O: sudden C: crushing, stabbing R: neck, shoulder, jaw A: sweatiness, SOB, nausea T: over mins E: increases with exercise, decreases with rest S: mild-severe
2
Q
SOCRATES for Aortic dissection
A
S: central O: sudden C: ripping R: back A: absent or delayed pulses, unequal upper limb BP, distal ischaemia, shock and neurological signs T: seconds E: S: mild-severe
3
Q
SOCRATES for pleural disease
A
S: localised to area of chest O: weeks C: sharp R: ?to shoulder A: coughing, pain in shoulder T: E: worse with breathing and coughing S: mild-severe
4
Q
SOCRATES for oesophageal disease
A
S: retrosternal O: after meals C: burning R: ? T: after meals E: worse lying down / food or bending over Better with antacids S: mild-severe
5
Q
SOCRATES for MSK disease
A
S: Local O: following trauma / causative event C: sharp / sore R: ? A: ? T: ? E: with certain movements S: mild-severe
6
Q
What conditions are included in ACS?
A
STEMI
NSTEMI
UA
7
Q
Describe the pathology of ACS
A
- atheromatous plaque formation in coronary arteries
- Fissuring/ulceration leads to platelet aggregation
- Localised thrombosis, vasoconstriction and distal thromboembolism
- Leads to ischaemia of myocardium
8
Q
What is diagnosis of ACS based on?
A
Cardiac markers - troponin
ECG - ST elevation
9
Q
Describe the history of a patient presenting with ACS?
A
Central crushing pain, usually >20 mins
not relieved by GTN
Radiates to left arm, neck and jaw
Associated with: SOB, nausea, fatigue, sweaty, palps
10
Q
What would be the examination findings of a patient presenting with ACS?
A
pulse, BP, O2 sats often normal
pale and clammy
tachycardia
11
Q
What investigations would you do for a patient with ACS?
what might you find?
A
ECG
Cardiac enzymes: trops (increased in first 4-8 hours, and max at 24 Hours)
FBC, U+E, LFT
glucose (decreases)
lipids (increased)
CXR
Transthoracic echo - helps in ddx of pericarditis, dissection or PE
12
Q
What is unstable angina?
A
Angina that occurs at rest
increased frequency
increased severity
13
Q
What is the cause of UA?
A
Fissuring of plaques - total vessel occlusion - progress to AMI
14
Q
How is MI diagnosed?
A
Increased trops
ECG- ST elevation = STEMI
No ST elevation = NSTEMI
15
Q
What are the three patterns of MI?
A
Regional MI (()%) Regional subendocardial infarction Circumferential subendocardial infarction (10%)
16
Q
What artery causes anterior MI?
A
Left anterior descending
17
Q
What are the ECG changes on an anterior MI?
A
V1-V4
18
Q
What artery causes inferior MI?
A
Right coronary
19
Q
What are the ECG changes on an inferior MI?
A
II, III, aVF
20
Q
What artery causes lateral changes?
A
left circumflex
21
Q
What are the ECG changes on lateral MI?
A
lead 1, aVL V5, V6
22
Q
What are the differences between STEMI and NSTEMI?
A
STEMI = full thickness whereas NSTEMI = partial thickness
no q waves, but can get ST depression and T-wave inversion
23
Q
What changes occur in 0-12 hours of MI?
A
Infarct not visible
Decreased oxidative enzymes
24
Q
What changes occur in 12-24 hours of MI?
A
Infarct = pale and blotchy
Intercellular oedema
25
What changes occur in 24-72 hours of MI?
Infarcted area excites acute inflammatory response
| dead area soft/yellow with neutrophil infiltration
26
What changes occur in 3-10 days of MI?
vascular granulation tissue in infarcted area
27
What changes occur in 10+ days of MI?
Collagen deposits become scar tissue
28
What is the management of ACS?
A-E + ECG and trops
```
MOANA:
M - morphine (5mg titrated up)
O - oxygen If sats <94%
A: anti-emetic - 10mg metoclopramide
N: nitrates - GTN spray or IV nitrates
A: Aspirin 300mg chewable
```
29
What is the management of STEMI?
CHECK local guidelines
PCI: gold standard treatment if available in timely fashion - i.e. under 2 hours -
praugrel + aspirin if not taking oral anticoagulant
Clopidogrel + aspirin if they are taking an oral anticoagulant
If you can't get PCI in 2 hours, THROMBOLYSIS:
ticagrelor. If ECG after 90 minutes shows this hasn't worked --> PCI
30
What is the management of NSTEMI?
```
BROMANCE:
Beta blocker
Reassurance
O2
Morphine 5mg
Aspirin 300mg
Nitrates
Clopidogrel 300mg
Enoxaparin - NOTE NOW FONDAPARINOUX
```
Assess using grace score.
Only give oxygen if sats below 95%
31
What is the GRACE score?
This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
>3% = PCI within 72 hours
<3%: Ticagrelor
32
What is the management if the grace score indicates high risk?
(>5-10% in 6 months, increased troponin or ST depression, diabetes)
Semi-elective PCI as inpatient
33
What is the management if the grace score = low risk?
Discharge with long term meds
| Outpatient stress test/angiography or elective PCI
34
What is the long term management of ACS?
```
48 hours bed rest
daily U+Es and cardiac enzymes
thromboprophylaxis (fondaparinoux)
Aspirin 75mg for life
Clopidogrel 75mg for 1 year
Bisoprolol
statin + ACEi
```
Oral nitrates
D/c on COBRAA
35
COBRAA?
```
5-7 days post discharge:
Clopidogrel (75mg) - N.B. now ticagrelor
Omega 3
Bisoprolol
Ramipril (2.5mg)
Atorvastatin (80mg)
Aspirin 75mg
```
36
What lifestyle advice immediately after MI?
Smoking cessation
No sex for 1 month
No air travel for 2 months
diet + exercise
37
What are the immediate complications of Acute MI?
Cardiac arrest - VF (most common cause of death)
VF
Bradyarrhythmia
38
What are the short term complications of MI?
Pulmonary oedema
Cardiogenic shock
Thromboembolism
VSD --> pan systolic murmur
Ruptured chordae tendinea --> Mitral regurg
Ruptured ventricle wall --> cardiac tamponade
39
How does pulmonary oedema occur following MI?
LH fails to pump
| Dilation of LV causes back pressure on pulmonary veins causing Extravasation of low protein fluid into the alveoli
40
How does cardiogenic shock occur following MI?
Decreased BP and decreased coronary flow = pump failure
41
What are the long term complications of MI?
Heart failure
Dressler's syndrome (immune mediated pericarditis)
Pericarditis
Ventricular aneurysm - Thrombus may form within the aneurysm increasing the risk of stroke
42
What is Dressler's syndrome?
Immune-mediated pericarditis
Sharp chest pian, increased lying down
43
What is the management of Dressler's?
high dose aspirin and NSAIDs - n.b. now aspirin and colchicine
44
What is angina caused by?
Narrowing of the coronary arteries reduces blood flow to the myocardium. During times of exercise, there is inefficient blood to meet the demands causing pain.
Therefore, exertional chest pain
45
What causes decreased perfusion in angina?
```
Atheroma
Embolus
Thrombosis
Inflammation of coronary arteries
Decreased BP
```
46
How does tissue demand increase in Angina?
Cardiac hypertrophy
| Increased CO
47
What is the cause of stable angina?
Decreased flow in atherosclerotic coronary arteries
48
Describe the Pathology of stable angina?
Arteriosclerosis: thickening and hardening of walls, decreased contractility and elasticity and decreased blood flow
Atheroma: thickening and hardening of walls so decreased tissue perfusion
49
How does atheroma formation occur?
Damage to endothelium
Entry of LDLs in the intima, macrophages form a fatty streak
Cytokines stimulated by macrophages: collagen deposition --> plaque
50
What are the risk factors for stable angina?
```
Increasing age
Males
FH
Smoking
Diet high in fat / low in fruit
obesity
increased BP
lipidaema
DM
```
51
How is diagnosis of angina done?
Clinical: mild ache - severe pain
Sweating/fear
increased with exercise, meals, cold, emotion
fades after rest
CT Coronary Angiography - Gold Standard diagnostic investigation. This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing
52
What ix would you do for ?angina?
```
Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)
```
53
What is the NICE tool for CAD?
```
clinical assessment of CAD:
>90% - stable angina treatment
61-70%: coronary angiography indicated
31-60: SPECT myocardial scan, exercise echo, stress MRI
10-30: CT calcium scoring
<10: investigate other cause
```
54
What are the indications for Stress ECG?
If resting ECG normal
ST depression >1mm shows ischaemia
+ve within 6 mins - angiography indicated
55
What is the first management of Angina?
Immediate: GTN N.B. nitrates are contraindicated in aortic stenosis
Long term: Beta-blocker / Calcium channel blocker (verapamil or diltiazem if mono therapy)
If disease not treated with one, add the other
(refractory disease - nicorandil)
Secondary prevention: Aspirin (75mg), atorvastatin, ACEi and they are already on beta blocker
56
What is given for secondary prevention of Angina?
Statin
Low dose aspirin
ACEi
57
How should the patient be counselled when starting a nitrate
sublingual GTN
Advise to sit down after spray
wait 5 mins and spray again
999 if still in pain after 10 mins - may be having an MI
Can use prophylactically
Nitrate free period if standard release isosorbide mononitrate
58
How do nitrates act?
```
Cause venorelaxation (decrease pre-load)
beware of venous pooling therefore dizziness on standing
```
Decreased aortic pressure
overall decreased O2 requirement of myocardium
coronary vasodilation - increased O2 delivery
59
How do b-blockers work?
work on b1 receptors to decrease HR and SV
60
What are the S/E of b-blockers
bronchoconstriction - don't use in asthma, COPD
cardiac depression / bradycardia
hypoglycaemia
fatigue
61
Give some examples of CCB
dihydropyridines: amlodipine or nifedipine
| rate limiting agents: verapamil/diltiazem
62
How do CCB work?
prevent SM contractions: decreased after load and CA vasodilation
Acton AVN to decrease HR
63
What are the S/E of CCB?
flushing
headache
ankle swelling
64
What are the procedural / surgical treatments for angina?
Percutaneous Coronary Intervention (PCI) with coronary angioplasty (dilating the blood vessel with a balloon and/or inserting a stent: catheter into brachial or femoral artery, feeding that up to the coronary arteries under xray guidance + contrast This can then be treated with balloon dilatation followed by insertion of a stent
PCTA
Co-prescribe aspirin and clopidogrel
CABG
65
What are the risks of angioplasty?
local dissection or CA or CA occlusion
1% mortality, 2% AMI
increased symptoms but no prognostic benefit
66
What are the indications for CABG?
Severe stenosis: symptom control for patients unsuitable for PCI
improved survival after MI
67
What are the employment and driving limitations following ACS?
2 months return to work
(not pilots/drivers, and heavy labour should seek lighter work)
Travel - avoid air travel for 2 months
sex - 1 month off
Driving: PCI - 1 week, and if not, 4 weeks
Angina - stop
68
What are the driving limitations for AAA?
notify DVLA if >6cm
| Disqualified if >6.5cm
69
What does the left circumflex artery supple?
Left atrium and left ventricle
70
What does the right coronary artery supply?
Right atrium and right ventricle
71
What does the left anterior descending artery supply?
left ventricle and inter ventricular septum
72
what does the left marginal artery supply?
left ventricle
73
What does the tricuspid valve separate
RA and RV
74
What does the mitral valve separate?
LA and LV
75
What does the left heart go to?
AORTA - BODY
76
What does the right heart go to?
pulmonary artery - lungs
77
What are the major branches of the aortic arch?
BCC: right CC and subclavian
Left common carotid
left subclavian
78
What is the management of blunt cardiac trauma?
CXR in resus
CT often needed
ECG
conservative
79
What is the management of Penetrating cardiac trauma?
complex ix and management
surgery
CXR
80
What is the presentation of cardiac tamponade?
Becks triad: hypotension
JVP increased
muffled heart sounds
CXR- rounded heart border
ECG: alternans QRS
Confirm with USS
Mx - pericardiocentesis and sternotomy and repair
81
What is myxoma? what are the signs?
```
Cardiac tumour
Signs - similar to infective endocarditis
MS
confirm on echo
mx = excision
```
82
What are the causes of constrictive pericarditis?
What are the signs?
Tx?
TB, RA, trauma
```
dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul's sign is positive
```
Excision of pericardium
83
What are the differences between cardiac tamponade and constrictive pericarditis?
JVP: Absent Y descent. X and Y present in constrictive pericarditis
pulsus paradox - present in cardiac tamponade, absent in constrictive pericarditis
Kussmaul sign: rare in cardiac tamponade but present in constrictive pericarditis
84
What is the pathophysiology of pulmonary oedema?
Increase in fluid in the alveolar wall
most common = LVF
increased pressure in alveolar capillaries and leakage of fluid
85
What is the presentation of pulmonary oedema?
dyspnoea
paroxysmal nocturnal SOB
orthopnoea
cough - frothy, blood stained sputum
ACUTE PRES: SOB, cough, anxiety, cheyne stokes breathing
86
What are the examination features of pulmonary oedema?
```
increased RR
increased HR and gallop rhythm
increased venous pressure
peripheral shut down
widespread crackles / wheeze
```
87
What investigations would you do for pulmonary oedema? What might you find?
ABG: T1RF or T2 due to impaired gas exchange
Bloods - FBC, U+E. glucose, D-dimer and CRP to rule out.
BNP
CXR: diffuse haziness/batwing oedema / Kerley B lines
ECG: tachycardia, arrhythmias
Echo
88
What are the causes of pulmonary oedema?
1. Increased capillary pressure: LVF, valve disease, arrhythmia, VSD, pulmonary venous obstruction, MI
fluid overload
2. Increased capillary permeability: ARDS, infection, DIC, toxins
3. Decreased plasma oncotic pressure: Renal/liver failure - hypoalbuminaemia
4. Lymph obstruction - tumour
5. Other: neuro/head injury / raised ICP
PE, altitude
89
What is the management of pulmonary oedema?
A-E
POUR SOD: Pour away fluids PLUS:
Sit upright
Oxygen
Diuretics - IV furosemide
```
If severe
IV diamorphine
IV furosemide
GTN spray 2 puffs
NIV
```
SBP >100: IV infusion of nitrate and CPAP if no improvement
DBP <100: treat as cardiogenic shock
alert ICU
90
What are the complications of ARDS?
Prolonged oedema --> pulmonary HTN which leads to irreversible structural changes to pulmonary arteries
Increased pressure to RV leads to RV hypertrophy leading to RHF and Cor Pulmonale
91
What is ARDS caused by?
Lungs responding to direct inhalation or blood-bourne insults.
Direct:
aspiration of gastric contents, smoke/toxins
pneumonia
near drowning
```
Indirect:
sepsis
trauma
pancreatitis
transfusion reaction
anaphylaxis
```
92
What is the pathophysiology of ARDS?
damage to type 2 pneumocystis - surfactant depletion and alveolar collapse
non-cardiogenic pulmonary oedema
93
What are the features of ARDS?
Decreased O2
absence of increased arterial pressure
CXR: bilateral ground glass appearace
decreased lung compliance
94
What is the management of ARDS?
```
Admit to ICU
100% O2
CPAP
IV nitrates
IV furosemide
Morphine and metoclopramide
Aminophylline if bronchospasm
```
95
What is open heart surgery?
| How is this different from closed heart surgery?
Any surgery requiring cardio-pulmonary bypass, whereas closed heart surgery does not require a bypass
96
What is the function of a cardiopulmonary bypass?
Takes over the function of the heart and lungs, allowing a motionless blood-free field for operation
97
What happens during a cardiopulmonary bypass?
Ascending aorta is clamped and cannulated and a venous Line inserted into the right atrium to drain venous blood
System involves a heat exchanger to regulate temperature, an oxygenator, an arterial pump and a filter
98
How is potential for ischaemic damage minimised in cardiopulmonary bypass?
(no coronary blood supply)
potential for ischaemic damage is minimised by arresting the heart in a high potassium solution and also cooling the myocardium to between 4 and 12 degrees
99
What are the main complications of a cardiopulmonary bypass?
Due to activation of the clotting cascade, within the bypass machine, with consumes clotting factors and platelets
This is prevented with high dose systemic heparin biro cannulation, reversed after this operation with protamine sulphate
Blood products may also be needed to reverse this
100
What is a median sternotomy?
Most common approach for operations on The heart and aortic arch - with any chamber or surface of the heart operable
101
When might an anterolateral thoracotomy be used?
Access to the right side of the heart
102
When might a Posterolateral thoracotomy be used?
Access to the distal aortic arch and descending thoracic aorta
103
When might a bilateral transverse thoracotomy be used?
Double lung transplants or heart-lung transplants
104
Which is better - CABG or PCI?
CABG provides better symptomatic relief and requires fewer late re-interventions than PCI
105
How is CABG performed?
Median sternotomy incision with CPB
Left internal mammary artery os the most common artery used as a conduit - harvested from the chest wall
Enlarges in response to demand, resistant to atheroma formation
106
Which vein was previously used for CABG?
Saphenous vein harvest - good secondary targets, however results are less good than IMA
107
What are the complications of CABG?
```
MI
bleeding
stroke
arrhythmias
tamponade
aortic dissection
respiratory / systemic complications
```
108
What are the two different types of valves?
Man made: ball in cage / bileaflet
durable BUT thrombogenic and require anti-coagulation with warfarin
Tissue valves: homographs / xenographs
Anticoagulation not required BUT more prone to degenerative failure
