Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals Revision > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the management for Unstable Angina?

A

GTN/Opiates to manage pain
Optimise medication: 75mg aspirin, 12m ticagrelor/clopi, ACE-i, B-blocker, Statin

Routine OP angiogram + echo
? revascularisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the management for NSTEMI?

A 
B-A-T-M-A-N
B-blocker
Aspirin 300mg
Ticagrelor
Morphine if in severe pain
Anticoagulate: Fondaparinux
Nitrate

Then long-term cardioprotection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the management for a STEMI?

A 
Morphine if in pain
Oxygen if sats low
Nitrate
Aspirin 300mg 
Fondaparinux treatment dose.

PCI if <2 hours.
Thrombolysis if >2hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Complications of MI

A 
DARTH VADER
Death
Arrhythmia
Ruptured ventricle
Tamponade 
Heart Failure
Valve disease
Aneurysm of ventricle
Dresler Syndrome
Embolism
Regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Dresler Syndrome?

A

Post- MI inflammatory immune response
Causes pericarditis 2-3w post-MI
Sx: Pleuritic CP, low grade fever and pericardial rib.
Can cause pericardial effusion or tamponade

Rx: NSAIDs +/- steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the GRACE score?

A

Scoring system for people post-STEMI to assess risk of death or repeat MI in 10 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the ACS secondary prevention medications?

A 
6 As:
Aspirin 75mg
Another antiplatelet for 12m
ACE-i
Atenolol or other B-blocker
Atorvastatin
Aldosterone antagonist in HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of chronic heart failure?

A
  1. Hypertension
  2. Myocardial ischaemia
  3. Valve disease
  4. Arrhythmias
  5. Connective tissue disorders
  6. Renal failure and subsequent chronic overload
  7. Increased pulmonary vascular resistance- cor pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What investigations should you do if you suspect CCF?

A
  1. Bloods:
    FBC (anaemia), U&E (renal failure/pre-meds), LFT (meds), BNP, Troponin, Glucose, TFT
  2. ECG
  3. Imagine: Echo (diagnostic) + CXR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the medical management of CCF?

A
  1. Diuretic therapy: furosemide 40mg OD
  2. ACE-I and B-blocker
  3. Spironolactone
  4. Aspirin and statin

DIGOXIN- first line if concurrent AF, second line after the above in HF without AF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the causes of ACUTE heart failure?

A

Fluid overload (iatrogenic often)
Sepsis
Post-MI
Arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How would you approach a patient presenting with acute HF?

A

A-E assessment

  • > expect tachycardia, tachypnoea, low sats, basal creps, S3 sound
  • > O2 supplementation, IV access, attach to monitoring

ECG, ABG, Bloods at bedside
CXR + Echo when available

1- Stop any IV fluids, sit upright
2-Diuretic therapy e.g. IV furosemide 40mg STAT
3- O2 supplementation
4- If still unstable: CPAP, inotropic medication, intubation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the symptoms and signs of cardiac tamponade?

A

Symptoms:
Chest pain, shortness of breath, fatigue, syncope/pre-syncope

Signs:
Muffled heart sounds, low BP, raised JVP on inspiration
Pulsus paradoxus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is pulsus paradoxus?

A

Decrease in BP on inspiration, classic sign of cardiac tamponade, tension pneumothorax, severe pericarditis

Get patient to breathe in and hold it - record BP, repeat with expiration and look for a difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How would you approach a patient with suspected cardiac tamponade?

A

A-E assessment
Attach to continuous monitoring, O2 if needed and get IV access
Bloods: FBC, troponin, BNP, group and save, ABG, U&E, LFT
ECG
USS/Echo is diagnostic

Once confirmed, call cardiothoracics urgently for pericardiocentesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the main causes of hypertension?

A

R-O-P-E

Renal: CKD, renal artery stenosis, hypoperfusion
Obesity
Pregnany-induced / pre-eclampsia
Endocrine: Conn’s/primary hyperaldosteronism, pheochromocytoma, Cushing’s, hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the stages of hypertension?

A

Stage 1: >140/90 in clinic or >135/85 at home
Stage 2:>160/100 in clinic or >150/90 at home
Stage 3:>180 systolic or >110 diastolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is hypertension diagnosed?

A

Take 3 BP readings in clinic and use the lowest.

If high, 24 hr ambulatory tape / home readings to rule out white coat HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What investigations are indicated in those diagnosed with hypertension?

A

Rule out end organ damage:

  • Bloods: HbA1c, U&E, lipids
  • Urine dip + albumin:creatinine ratio
  • ECG
  • Fundoscopy

Should calculate QRISK to help dictate management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is QRISK?

A

A score which calculates the risk of CVD/ a cardiac event occurring in the next 10 years.

QRISK > 10: prescribe statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When should medical management be used in hypertension?

A
  • All those with S2 hypertension and above (>160/100)

- Those with S1 hypertension + other CV comorbidities/end-organ damage or QRISK >10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the treatment algorithm for hypertension?

A
  1. ACE-inhibitor / ARB
    - > If >55 or afro-caribbean, CCB first
  2. ACE-i + CCB
    - > if AC, ARB + CCB
  3. ACE-i + CCB + Thiazide diuretic
  4. If K+ <4.5 add spironolactone, if K+ >4.5 add a/b-blocker

Target BP: <140/90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is malignant hypertension?

A

Severely elevated BP (S3) with new/sudden-onset target organ damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the symptoms of malignant hypertension?

A 
Headache
Shortness of breath
Palpitations
Anxiety
Epistaxis

In severe cases, can present with encephalopathy as a result of cerebral oedema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you manage malignant hypertension?

A

Test for end-organ damage

IV labetalol / nicardipine
-> need to control slowly to prevent cardiac/cerebral ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the main causes of AF?

A

S-M-I-T-H

Sepsis
Mitral valve dysfunction
Ischaemic heart disease
Thyrotoxicosis
Hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the signs and symptoms of AF?

A

Symptoms:
May be asymptomatic
Breathlessness, palpitations, chest pain, tiredness, syncope
May present with symptoms of thrombotic complication: PE, MI, stroke

Signs: irregularly irregular pulse, may be tachycardic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How would you manage AF?

A

Rate control, rhythm control, anticoagulation.

In new-onset (<48hr), unstable or reversible cause: DC cardioversion = first line
If >48 hrs, needs 3w anticoagulation first.

Rate control: B-blocker - > calcium channel blocker - > digoxin if inactive

Rhythm control: cardioversion = 1st line or medical: flecainide or amiodarone

Anticoagulate: CHADSVASC + HASBLED score
DOAC = 1st line, warfarin 2nd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How would you manage paroxysmal symptomatic AF?

A

Flecanide pill-in-pocket therapy

Anticoagulation based on chadsvasc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the risk factors for infective endocarditis?

A 
Systemic infection
Indwelling lines
Prosthetic valves / joints / grafts
Unsterile injections- IVDU, piercings, tattoos
Immunosuppression
Poor dentition
Acquired valve disease e.g. rheumatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the most common causative organisms and affected valves in infective endocarditis?

A

Organisms:
S. aureus in acute disease
Viridans streptococci in subacute disease

Valves:
Mitral valve most common in general public
Tricuspid valve most common in IVDUs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the symptoms associated with infective endocarditis?

A

General:
Fever, malaise, fatigue, night sweats, tachycardia, shortness of breath, weight loss

Specific:
Pleuritic chest pain, cough, arthralgia, myalgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the signs on examination associated with infective endocarditis?

A

Splinter haemorrhages, Janeway lesions, Osler nodes and palmar erythema

Poor dentition, petechiae

New murmur - usually mitral regurgitation

Signs of HF and arrhythmias

Signs of infective emboli

34
Q

How is infective endocarditis diagnosed?

A

Duke’s criteria:
> 2 major criteria
> 1 major + 3 minor criteria
> 5 minor criteria

Major: findings on blood cultures (>2 sets, 12hr apart) or on echocardiogram

Minor: RFs, fever, vascular abnormality, immune phenomena (infection markers etc)

ECG should also be done to assess for complications

35
Q

How is infective endocarditis managed?

A
  1. Infectious Diseases team input
  2. SEPSIS 6 if septic
  3. 2-6w IV antibiotics depending on cause
    - > empirical and narrow down to sensitive
  4. Surgical valve replacement / repair depending on echo findings

Supportive treatment: fluids, O2 etc

36
Q

What is the difference between post-MI pericarditis and Dresler syndrome?

A

Post-MI occurs 1-3 days after an infarction, Dresler syndrome occurs weeks-months after.

37
Q

What are the causes of pericarditis?

A

Infective:
Coxsackie B virus = most common
Staph / strep / fungal
Toxoplasmosis

Non-infective:
Post-MI / Dresler syndrome
Rheumatological / inflammatory causes
Uraemia
Radiotherapy
Post-operative
38
Q

What are the symptoms of pericarditis?

A

Sharp, pleuritic chest pain - retrosternal, may radiate to neck/shoulders, improves on leaning forward
Low-grade fever
Tachypnoea, Dyspnoea
Non-productive cough

39
Q

What are the signs associated with pericarditis?

A

Pericardial rub on auscultation- heard loudest at L sternal border with patient sat leaning forward
Tachycardia, tachypnoea
Quiet heart sounds
Low-grade fever
May have signs of HF/ fluid overload if patient has constrictive disease

40
Q

What investigations should you do in patients with suspected pericarditis?
What would you expect to find?

A 
Bloods:
FBC- may have raised WCC (leukocytes)
U&E- rule out uraemia 
Cultures if infective symptoms
CRP/ESR- raised
Troponin: may be raised
CK: may be raised
BNP/D-dimer as exclusive tests

ECG: widespread saddle-shaped STE, PR depression, may have ST depression in avR and V1.

TTE: may have pericardial effusion, rule out tamponade

41
Q

What is the management for pericarditis?

A
  1. Supportive treatment, often self-limiting
  2. NSAIDs +/- colchicine
  3. If severe, associated with inflammatory syndromes or uraemia -> prednisolone
  4. Surgical: pericardiectomy in constrictive disease
42
Q

What is the inheritance pattern of HOCM?

A

Autosomal dominant

43
Q

What are the symptoms associated with HOCM?

A

Often asymptomatic until sudden cardiac arrest
May have exertion dyspnoea, angina, dizziness, syncope and palpitations
ES murmur on auscultation
Biphasic pulse

44
Q

What are the diagnostic criteria for HOCM?

A

Non-dilated LV hypertrophy (>15mm) with no other disease which may explain it

45
Q

What investigations should be done in HOCM?

A

ECG: LVH, deep Q waves, may have giant inverted T waves in precordial leads
May have non-specific ST/T wave changes, P wave changes or LBBB
Associated with VT, AF and atrial flutter in more acute disease

TTE: Wall thickness, outflow abnormality, asymmetrically thickened septum

Genetic testing and family screening

Ambulatory ECG

46
Q

What are the management options for HOCM?

A

Lifestyle change and counselling

B-blockers and/or calcium channel blockers in symptomatic - usually verapamil or diltiazem

ICD implantation

47
Q

In what condition would you hear a third heart sound?

A

Heart Failure

48
Q

What is the most common heart murmur?

A

Aortic Stenosis

49
Q

What are the most common causes of mitral stenosis?

A

Rheumatic fever

Infective endocarditis

50
Q

What would you expect to find on auscultation in somebody with mitral stenosis?

A

Mid-diastolic murmur - low pitched

Loudest at apex on expiration

51
Q

What would you expect to find on auscultation in somebody with mitral regurgitation?

A

Pan-systolic, high pitched murmur
May radiate to the L axilla
May be associated with S3
Loudest at the apex and on expiration

52
Q

What conditions are associated with mitral regurgitation?

A 
Marfan's
Ehlers Danlos syndrome
Endocarditis and rheumatic heard disease
IHD
Age
53
Q

What would you expect to find on auscultation in somebody with aortic stenosis?

A

Ejection systolic murmur, high pitched, loudest on inspiration
May radiate to carotids

Causes slow-rising pule and narrow pulse pressure

54
Q

What is the target INR for those with prosthetic heart valves?

A

2.5-3.5

55
Q

What are the major complications of valve replacements?

A

Thrombus formation
Infective endocarditis
Haemolysis and anaemia
Bleeding as a result of warfarin

56
Q

What is an alternative treatment to valve replacement in aortic stenosis?

A

Transcatheter aortic valve implantation

57
Q

What are the shockable and non-shockable arrest rhythms?

A

Shockable: VT, VF

Non-shockable: PEA, asystole

58
Q

How do you tell a ventricular tachycardia apart from a supra ventricular?

A 
Ventricular = broad complex
SV = narrow complex
59
Q

How do you manage atrial flutter?

A
  1. Medical
    Rate control: B-blocker or cardioversion if new
    Anti-coagulate based on CHASVASC
  2. Treat any underlying reversible cause
  3. Radiofrequency ablation of re-entrant rhythms
60
Q

How would you manage a patient with SVT?

A
  1. Continuous ECG monitoring
  2. Valsalva manoeuvre + carotid sinus massage
  3. Adenosine or verapamil
  4. DC cardioversion - must be synchronised, otherwise can degrade into VF
60
Q

How would you manage a patient with SVT?

A
  1. Continuous ECG monitoring
  2. Valsalva manoeuvre + carotid sinus massage
  3. Adenosine or verapamil
    6mg -> 12mg -> 12 mg adenosine via large proximal cannula
  4. DC cardioversion - must be synchronised, otherwise can degrade into VF

Long term: rate control with B-blockers / CCB / Amiodarone, or radio-frequency ablation

61
Q

What are the features of WPW on ECG and how is it managed?

A
  1. Short PR interval
  2. Broad QRS
  3. Delta wave- slurred upstroke on QRS

Management: radio-frequency ablation of abnormal rhythm

62
Q

What is the difference between VT and Torsades de Pointes?

A

VT is monomorphic broad complex tachycardia

TdP is polymorphic broach complex tachycardia - appearance of twisting around the baseline

63
Q

What are the causes of Torsades de pointes?

A 
Prolonged QT interval:
1. Medication:
   Macrolide antibiotics (erythromycin), Lithium, antipsychotics, citalopram, amiodarone
  1. Electrolyte imbalance:
    HYPO - kalaemia, magnesaemia, calcaemia
  2. Other:
    Hypothermia, myocardial ischaemia, raised ICP
64
Q

How would you manage somebody with Torsades de Pointes?

A
  1. Stop any causative medication and correct any electrolyte abnormality
  2. IV magnesium + infusion = first line to stabilise myocardium
  3. In case of VF/arrest -> defibrillation
65
Q

How would you manage a patient with unstable bradycardia?

A
  1. A-E and cardiac monitoring
  2. Atropine IV 500mcg + repeat up to 6 doses
  3. Other inotropes e.g. noradrenaline
  4. Transcutaneous pacing using defib

In long term= implantable cardiac pacemaker

66
Q

How would you manage VT in: pulseless, unstable and stable patients?

A
  1. Pulseless:
    Defibrillate, CPR, intubate and get access
    IV adrenaline, amiodarone
    Rule out 4Hs and 4Ts
  2. Unstable
    IV amiodarone 5mg/kg, O2
    DC cardioversion, sotalol
    External pacing
  3. Stable:
    O2, IV amiodarone or sotalol
    Cardioversion with sedation
    External pacing

Any cardioversion should be synchronised, as depending on the focus of the abnormal rhythm the shock can cause degeneration into VF.

67
Q

What are the different causes of VF?

A
  1. Cardiac
    Myocardial infarction, myopathy, Torsades de Pointes, Channelopathies, Aortic stenosis / dissection,
    tamponade, myocarditis, blunt trauma
  2. Respiratory
    Tension pneumothorax, PE, pulmonary hypertension, apnoea, bronchospasm, aspiration
  3. Other
    Sepsis, Seizure, Stroke
68
Q

What are the 4Hs and 4Ts to rule out in non-shockable arrests?

A

Hypoxia
Hypovolaemia
Hyper / hypokalaemia
Hyper / hypothermia

Toxicity
Tension pneumothorax
Tamponade
Thromboembolism- PE/MI

69
Q

How would you manage somebody in VF?

A
  1. Initiate CPR and attack pads to see if shockable
  2. Shocks initiated every 2 minutes with good compressions in between
  3. Establish airway and access (2 large bore cannula if possible)
  4. IV Adrenaline 1mg every 3-5 mins (1ml 1:10,000)
  5. IV amiodarone if confirmed VF
70
Q

How do sodium levels affect ECG traces?

A

They don’t.

71
Q

What are the causes of hyperkalaemia?

A

Renal failure, acidosis, DKA, haemolysis
Addisons, insufficient steroid substitution, insulin deficiency
K+ substitution, K+ sparing diuretics, ACE-I, ARB, Digoxin toxicity

72
Q

What are the signs

A
72
Q

What are the signs of hyperkalaemia on ECG?

A

Tall, tented T waves
Broad QRS
Flat P waves

Sine wave formation in severe

73
Q

What are the causes of hypokalaemia?

A

Diarrhoea, vomiting, alcoholism, malnutrition

Hyperaldosteronism, glucose infusion, diuretics, adrenergic agonists, steroids, insulin

74
Q

What are the signs of hypokalaemia on ECG?

A

Wide, flat T waves (even T wave inversion in severe)
ST depression
Increased P wave amplitude and PR interval length
U waves
Prolonged QT - predisposes to TdP

75
Q

What are the signs of Hypercalcaemia on ECG?

A

Short QT
Prolonged QRS
Bradycardia

76
Q

What are the signs of hypocalcaemia on ECG?

A

Long QT

Shortened QRS

77
Q

Which is more dangerous cardiologically, hyper or hypomangnesaemia?

A

HYPOmagnesaemia - can lead to SVT, hence first line treatment is IV magnesium

78
Q

If a patient suffers complete heart block following an MI, which vessel is most likely affected?

A

Right coronary

Finals Revision (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions