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Medicine block > Cardiology medicine block > Flashcards

Cardiology medicine block Flashcards

1
Q

What is the triad of presenting signs in ACS?

A
  1. ECG changes
  2. Raised troponin
  3. Cardiac chest pain
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2
Q

Define these terms in relation to the triad of ACS presenting symptoms:

  • STEMI
  • NSTEMI
  • Unstable angina
A

STEMI - ST elevation, raised troponin, cardiac chest pain
NSTEMI - ST depression, T wave inversion or normal ECG, raised troponin, cardiac chest pain
Unstable angina - ST depression, T wave inversion or normal ECG, cardiac chest pain, normal troponin

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3
Q

How is troponin used in diagnosis of ACS?

A

hs-Tnl = high sensitivity troponin test. Also measure CK in STEMI pt.
Male >34 ng/L
Female >16 ng/L
These indicate a high likelihood of myocardial necrosis.

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4
Q

When else can troponin be increased?

A
  • Advanced renal failure
  • Large PE
  • Aortic dissection/stenosis
  • HCM
  • Stroke
  • Sepsis
  • Malignancy
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5
Q

Draw the different ECG changes in ACS and label

A

Answers on iPad

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6
Q

What is the initial and medical management of a STEMI?

A
  • IV access, high flow O2, pain relief - morphine + antiemetic
  • Prasugrel = 300mg load and then 75mg OD rest of life - this is for pt going to have PCI, <75, >60 kg
  • If pt doesn’t fit ^ criteria = clopidogrel 600mg load, 75 OD 12 months or ticagrelor 180mg load, 90mg BD 12 months
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7
Q

What is the interventional management of STEMI?

A

PCI - percutaneous coronary intervention. Is a non surgical way of opening and stenting obstructed coronary arteries.

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8
Q

What is the preventative management of STEMI?

A

Will need to reduce CVS RF:

  • Medication = statin to reduce cholesterol, bisoprolol, ACEi/ARB to prevent further muscle damage
  • Control BP and DM
  • Stop smoking
  • Need a CVS RF screen - FBC, HbA1c, lipids, random glucose
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9
Q

What is the management of NSTEMI/unstable angina?

A
  • Pain relief - morphine + antiemetic
  • Aspirin 300mg load, 75mg OD
  • LMWH - enoxaparin if no immediate PCI planned
  • Repeat ECG and risk assessment
  • Grace >3% = PCI w/i 72 hours and ticagrelor
  • Grace <3% = fibrinolysis eg. ticagrelor
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10
Q

What are the clinical features of stable angina?

A

Chest discomfort on exercise that is relieved by rest. Can get radiating symptoms such as tight throat and arm heaviness. Sometimes hard to distinguish it between GORD and pulm/MSK disease.

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11
Q

What are some specific qs to ask in stable angina hx? What are you looking for on examination?

A

Hx - T+R, RF, exercise tolerance

Exam - BMI, BP, evidence of PVD, hyperlipidaemia, carotid bruits, murmurs esp aortic stenosis

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12
Q

What are the Ix into stable angina?

A
  • ECG
  • FBC
  • Full lipid profile
  • Glucose and HbA1c
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13
Q

What drug treatments are all pt w stable angina given?

A
  • Aspiring 75mg OD or clopidogrel if can’t tolerate
  • GTN
  • Statin and ACEi
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14
Q

What are some additional drug treatments that are offered to treat stable angina?

A
  • B blockers for symptomatic relief and rate limitation
  • Non dihydropyridine CCB eg. diltiazem also for rate limitation
  • Ivabradine also for rate limitation
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15
Q

What are some non cardiac causes of chest pain?

A
  • Costochondritis
  • PE
  • Pneumonia
  • Pneumothorax
  • Gastro oesophageal
  • Psychosomatic
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16
Q

What are the stages of hypertension?

A

Stage 1 - 140/90 mmHg, ABPM 135/85 mmHg
Stage 2 - 160/100 mmHg, ABPM 150/95 mmHg
Severe hypertension - 180 mmHg or 110 mmHg

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17
Q

What are some specific qs to ask in a hypertension hx?

A

Sx - headaches, visual changes

RF - PMH TIA, stroke, DM, angina, syncope, FH HTN, coronary artery disease, renal disease

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18
Q

What are some sx associated w hypertension that may suggest of specific cause of hypertension?

A

Sweat, palpitations, anxiety = pheochromocytoma

Muscle weakness and tetany, increased Na+ and reduced K+ = hyperaldosteronism

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19
Q

What signs are you looking for on exam of someone w hypertension?

A
  • Signs of Cushing’s and PVD
  • Radio femoral delay
  • Renal bruits
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20
Q

What are the Ix into hypertension?

A
  • Urine dip for albumin and haematuria
  • Bloods - glucose, U&Es, eGFR, lipid profile
  • Fundoscopy - hypertension related retinopathy
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21
Q

When should treatment for hypertension be offered?

A
  • Stage 1 HTN if target organ damage, CVS disease, DM or renal impairment
  • Stage 2 HTN for anyone else
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22
Q

What are the target BPs?

A
  • Low/mod risk <140 mmHg
  • Stroke, DM, IHD, CKD = <130/80 mmHg
  • All pt diastolic <90 mmHg but <85 if DM
  • CKD and overt proteinuria <130 mmHg
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23
Q

What is the conservative treatment of HTN?

A
  • Weight loss and increase exercise
  • Mod salt intake
  • Stop smoking
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24
Q

What is the pharmacological treatment of HTN?

A

Under 55s = ACEi/ARB or above 55 or black = CCB.
Additionally:
+CCB then +thiazide like diuretic

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25
Q

How do you treat resistant HTN?

A

ACEi/ARB +CCB +thiazide like diuretic +a/b blocker +another diuretic

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26
Q

What are the hypertensive emergencies and their presentations?

A

= increase in BP that if sustained will cause end organ damage.
Presentation - high BP + pulm oedema, AKI, MI, encephalopathy

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27
Q

What are the signs of end organ damage?

A
  • Encephalopathy
  • LV failure
  • Aortic dissection
  • Unstable angina
  • Renal failure
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28
Q

What is the treatment of hypertensive emergencies?

A

Reduce diastolic BP to 100mmHg in 5-12 hours.

  • Sodium nitroprusside
  • Labetalol
  • GTN
  • Esmolol - acts in 1 min and lasts 10-20 mins, give loading dose then start infusion
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29
Q

What is hypertensive urgency and how does it present?

A

Severe increase in BP that will cause damage in days.

Present - increase BP w/o critical illness but often retinal changes, diastolic >130 mmHg

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30
Q

What is the treatment of hypertensive urgency?

A

Reduce BP to 100 mmHg diastolic over 48-72 hours:
nifedipine and amlodipine for 3 days then amlodipine forever.
Pt normally tolerate ACEi and CCB combination.

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31
Q

What are the symptoms of phaechromocytoma?

A

Most common sign - hypertension. Triad:

  1. Sweating
  2. Tachycardia
  3. Headaches
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32
Q

What are the Ix into phaechromocytoma?

A
  • CT/MRI for adrenal tumour

- Urine levels of metanephrines and catecholamines

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33
Q

What is the treatment of phaechromocytoma?

A
  • Resection of tmour

- a blocker before op to control HTN then add on B blocker

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34
Q

What is primary aldosteronism and how is it diagnosed?

A

Increased aldosterone = high Na+ low K+.

Aldosterone:renin ratio, renin low and aldosterone high.

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35
Q

What are the clinical features of Cushing’s disease?

A
  • Abdo obesity and thin legs and arms
  • Purple striae and easy bruising
  • Muscle weakness
  • High cortisol
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36
Q

What are the Ix for a diagnosis of Cushing’s?

A
  • 24 hour urine cortisol excretion (is increased)
  • Low dexamethosone suppression test
  • Hyperglycaemic
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37
Q

What are the causes of heart failure?

A
  • IHD, cardiomyopathy
  • Hypertension
  • Afib
  • Valvular heart disease
  • Chronic lung disease
  • Previous cancer and chemo drugs
  • HIV
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38
Q

What are the presentations of heart failure?

A
  • ~ 50% have HFrEF
  • Can have clinical features of HF w HFNEF
  • Fluid overload, renal impairment
  • Increased NHproBNP
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39
Q

What are the Ix into HF?

A
  • Bloods - eGFR, FBC, LFTs, TFTs, BNP, ferritin/transferrin
  • CXR
  • MRI heart
  • Echocardiography, most important Ix
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40
Q

What are the signs of heart failure on CXR?

A
  • Cardiomegaly
  • Pleural effusion + alveolar oedema
  • Perihilar shadowing = batwing distribution
  • Air bronchograms
  • Increased width vascular pedicle
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41
Q

What are the signs of heart failure on an echo?

A
  • Dilated and poorly contracting LV
  • Reduced diameter, stiff LV
  • Vascular heart disease
  • Pericardial disease
  • Atrial myxoma - tumour in atrium
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42
Q

What is the conservative management of heart failure?

A
  • Stop smoking and reduce alcohol
  • Salt restriction
  • Fluid restriction, esp if hyponatraemia
  • Weight monitoring for early identification of fluid accumulation
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43
Q

What is the pharmacological management of heart failure?

A
  1. Diuretics, sx management eg. furosemide, can get low K+ so spironolactone or ACEi can balance
  2. ACEi/ARB, if HTN, increases survival, vasodilators if can’t tolerate eg. hydralazine
  3. ARNI, if HFrEF
  4. B blockers, ivabradine if can’t tolerate
  5. Nitrates, reduce preload, pulm oedema and SOB
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44
Q

What is ARNI?

A

Angiotensin receptor neprilysin inhibitor = valsartan + sacubitril

45
Q

What is device therapy in heart failure?

A

If pharmacological management fails:

  • CRT - cardiac resynchronisation therapy if LBBB (broad QRS), narrows QRS
  • ICD - implanted cardiac defib which reconverts VT/VF to avoid sudden cardiac death
46
Q

What are the symptoms of aortic stenosis?

A
  • Angina, HF, syncope
  • Reduced exercise tolerance
  • Dyspnoea on exertion
47
Q

What are the causes of aortic stenosis?

A
  • Increasing age and calcification
  • Congenital bicuspid valve
  • CKD
  • Rheumatic fever
48
Q

How do you diagnose valvular heart disease?

A

Echocardiography

49
Q

What are the indications for surgery in valvular heart disease? What are the surgical options?

A

Indications - severe disease and sx, or severe disease, asymptomatic and LV dysfunc or abnormal exercise tolerance
Options - aortic valve repair or transcatheter aortic valve implant

50
Q

What is the aortic stenosis murmur?

A

Best heard in 2nd ICS, right sternal border, is harsh and noisy here. Ejection systolic crescendo decrescendo murmur. Associated w delayed peripheral pulses. Radiates to carotid arteries in neck.

51
Q

What are the sx of aortic regurgitation?

A

Dyspnoea on exertion and reduced exercise tolerance.

Asymptomatic for many years until LV dilation and eventual HF.

52
Q

What are the causes of aortic regurgitation?

A
  • Calcific degeneration
  • Rheumatic fever
  • Marfan’s
  • Idiopathic dilation
  • Congenital bicuspid valve
  • Infective endocarditis
53
Q

What is the aortic regurgitation murmur?

A

Early diastolic blowing murmur. Best heard left sternal border, 3rd/4th ICS. Associated w collapsing pulse and De Musset’s sign.

54
Q

What is De Musset’s sign?

A

Head bobbing

55
Q

What is the pharmacological treatment of aortic regurgitation?

A

ACEi reduces rate of LV dilation by reducing afterload.

56
Q

What are the causes of mitral regurgitation? What is the pharmacological management?

A

Causes - infective endocarditis, rheumatic fever, mitral valve prolapse, IHD
Drug - diuretics by reducing afterload so reducing LV dilation

57
Q

What are the RF of infective endocarditis?

A
  • Mitral valve prolapse
  • Prostheses
  • Rheumatic fever,
  • Valvular disease
  • Congenital heart disease
  • IVDU
58
Q

What are the causative organisms of IE?

A
  • Viridans group of streptococci
  • Staph aureus
  • Enterococci
  • Fungi in immunosuppressed
59
Q

When should you suspect IE? What are the sx?

A

Suspect - unexplained fever, bacteraemia and systemic illness, new murmur
Sx - fever, night sweats, malaise, valve insufficiency

60
Q

What are the initial Ix into IE?

A
  • ECG, CXR
  • Bloods - CRP, FBC, LFTs, U&E
  • Urine dip
61
Q

What are the diagnostic Ix into IE?

A
  • Echo - TOE, transoesophageal echo most sensitive

- Blood cultures - need 3-6 from diff areas, if pt stable delay abx until results come back

62
Q

What are the major diagnostic criteria of IE?

A
  • Positive cultures
  • Endocardial involvement
  • Positive echo = vegetation and abscess
  • New valve regurg
  • Dehiscence prostheses
63
Q

What are the minor diagnostic criteria of IE?

A
  • IVDU
  • Anatomical abnormality
  • > 38 degrees pyrexia
  • Suggestive echo and cultures
  • Vasculitis/embolic phenomenom
64
Q

What is the management of IE?

A

Abx therapy:
- Streptococci - benzylpenicillin/vancomycin + low dose gentamicin
- Enterococci - amoxicillin/vancomycin + low dose gentamicin
- Staphylococci - flucloxacillin/vancomycin + gentamicin
Surgery.

65
Q

How do you check the response to IE treatment?

A
  • ECG
  • Echo - assess abscess and vegetation size
  • Bloods
66
Q

What is considered to be bradycardia?

A

HR <60 BPM but can also be relative or absolute.

  • Absolute - <40 BPM
  • Relative - HR too slow for haemodynamic state of pt eg. BP <90 mmHg, <40 bpm, poor perfusion and urine output
67
Q

What are the different classifications of bradycardia?

A
  • Sinus node dysfunc bradycardia

- AV node block

68
Q

What are the causes of bradycardia?

A
  • Node dysfunction
  • Medications
  • Hypothyroidism
  • Hypothermia
69
Q

What are the different types of AVN dysfunction?

A
  • First degree AVN block
  • Second degree AV block, Mobitz type 1
  • Second degree AV block, Mobitz type 2
  • Complete AV block/third degree
70
Q

Describe first degree AV block

A

PR interval >0.2 secs. No specific treatment indicated, if dizzy or syncope then consider cardiac monitoring..

71
Q

Describe second degree AV block, Mobitz type 1

A

Progressive lenghtening of PR interval then failure of atrial impulse to conduct V. Often occurs after inf MI.

72
Q

Describe second degree AV block, Mobitz type 2

A

Constant PR interval followed by sudden drop of QRS, more serious than Mobitz type 1.

73
Q

Describe complete AV block

A

No conduction from atria to ventricles so no relationship between P waves and QRS.

74
Q

What are the causes of complete AV block?

A
  • Digoxin toxicity
  • Follow after inf STEMI + resolve
  • Severe hyperkalaemia
75
Q

How do you treat complete AV block?

A

Urgent transcutaneous pacing required w/i 24 hours
- Stop digoxin and verapamil (can both cause heart block)

76
Q

What complications does Afib increase the risk of?

A
  • Cardioembolic stroke
  • Cardiac instability
  • Risk of death
  • ACS, heart failure
77
Q

How do you diagnose Afib?

A
  • Manual pulse checks
  • Assess sx - breathless, palpitations, syncope, chest pain, hx of stroke
  • ECG to confirm irreg pulse caused by Afib
78
Q

Describe Afib on an ECG

A

No visible P waves

79
Q

What are the Ix into Afib?

A
  • 24hr cardiac monitor

- Echo

80
Q

What is the management of Afib?

A
  • Anticoag to prevent stroke - informed by CHAD-VASC score, offer if score of 2+, DOACs
  • Rate control
  • Rhythm control
81
Q

What are the rate control drugs in Afib?

A

Slow conduction at AVN to reduce V conduction + HR:

  • B blocker
  • Digoxin
  • Diltiazem/verapamil if LVEF >40%
82
Q

What is a reduced ejection fraction?

A

<40%

83
Q

What are the first line treatments for supraventricular tachy?

A

Vagal manoeuvres - breath holding and Valsalva (pt blow hard into syringe). These slow conduction at AVN and can interrupt re entrant circuit.
Carotid massage - massage carotid sinus on non dominant side

84
Q

What are the risks of carotid massage?

A

Auscultate for bruits before attempt due to risk of stroke from emboli.
Don’t perform on both sides.

85
Q

What are bruits?

A

Blowing vascular sounds resembling heart murmurs over partially occluded blood vessels.

86
Q

What are AVNRT and AVRT?

A

AVNRT - AVN re entry tachy
AVRT - atrio ventricular re entry tachycardia
Not sure how these are different

87
Q

What is upper lobe diversion?

A

Pulm venous diversion - increased LA pressure and early sign of pulm oedema.
On CXR = dilation of upper lobe pulm veins

88
Q

What is the medical management of SVT?

A
  • Adenosine - blocks AVN conduction, if tachy due to AVNRT/AVRT, short acting and short t1/2
  • CCB
  • Flecainide IV but not if MI
89
Q

What are the SE and risks of adenosine use?

A
  • Chest pain, flushes and hypotension
  • Avoid in pt w asthma/COPD as adenosine causes bronchoconstriction
  • Administer w crash trolley next to pt = risk significant brady
90
Q

Describe ventricular tachycardia

A

Rapid broad complex tachy shortly after a STEMI is classically VT.

91
Q

What is the medical management of VT?

A
  • B blockers
  • Amiodarone
  • Lidocaine
  • Cardioversion if haemodynamically unstable
92
Q

What are the causes of Afib?

A
  • IHD
  • Valvular heart disease, especially mitral valve disease
  • Thyrotoxicosis
    + HTN, coronary artery disease, PE, pneumonia, substance misuse
  • Sleep apnoea is a RF
93
Q

What is the mitral regurgitation murmur? Where is it best heard?

A

Holosystolic/pansystolic murmur, whoosh w HS1

Best heard over the apex of the heart, 5th ICS, MCL.

94
Q

What is the mitral stenosis murmur?

A

Loud S1 and early diastolic opening snap then low pitched rumbling diastolic murmur.

95
Q

What is the main cause of mitral stenosis?

A

Rheumatic fever

96
Q

What are the clinical signs of mitral stenosis?

A
  • Mitral facies - pink/purple cheeks

- Jugular vein distension

97
Q

What are the clinical signs of mitral regurgitation?

A
  • Peripheral oedema

- Haemopytsis

98
Q

What are the differentials for chest pain?

A

Cardiac - STEMI/NSTEMI, angina, pericarditis, aortic dissection
Resp - pneumonia, PE, pneumothorax
Other - GORD, gallstones, neuropathy, cellulitis, MSK pain

99
Q

What are the differentials for SOB?

A

Cardiac - HF, SVC obstruction, valvular heart disease, anaemia
Resp - pneumothorax, PE, pneumonia, COVID, asthma/COPD
Other - anaphylaxis, anxiety attack, nephrotic syndrome (swell and SOB), DKA causes hyperventilation if met acidosis

100
Q

What are the top 3 causes of heart failure?

A
  1. IHD
  2. HTN
  3. Valvular heart disease, aortic stenosis most common
101
Q

What are the differentials for palpitations?

A

Arrhythmia - tachycardia, Afib, ectopics, Aflutter
Hyperthyroidism
Anxiety
Drug use - SSRIs, MDMA, cocaine

102
Q

Narrow complex tachycardia vs wide complex tachycardia

A

Narrow - V depolarised by His Purkinje system so tachy originates in A
Wide - V not depolarised normally, tachy originates in V

103
Q

What are the differentials for syncope?

A

Cardiac syncope - no warning and complete recovery immediately
Vasovagal syncope - get nausea, vagal stim of GI = vom
Epileptic shock
Addisons - postural hypotension
Hypoglycaemia

104
Q

What is palpitation that wakes a pt up at night and then they have to wee classic of?

A

Arrhythmia - Afib caused by parasympathetics (active at night) causes palpitation at night.
Then arrhythmia causes release of ANP which makes pt wee = ANP suppresses Na+ reabsorption at collecting duct = naturesis and diuresis.

105
Q

What is decompensated vs compensated HF?

A

Decompensated - structural/func change to heart reducing ejection of blood, symptomatic = wheeze, cough, oedema, reduced exercise tolerance, fatigue
Compensated - asymptomatic

106
Q

How do you assess fluid status?

A
  • Dry mucous membranes
  • Reduced urine output
  • Hypotension
  • Reduced cap refil time
  • Tachycardia
107
Q

What are some findings on fundoscopy?

A
  • Cotton wool spots - pre proliferative diabetic retinopathy
  • Neovasculisation - proliferative diabetic retinopathy
  • Retinal haemorrhages - hypertension
  • Optic disc swelling - hypertension
  • Papilloedema - raised ICP
  • Optic nerve atrophy - pale optic disc
  • Cherry red spot - due to central artery occlusion
  • Roth spot - IE
108
Q

What can affect BNP levels?

A

Being on Ramipril can give a falsely low result

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