Brainscape's Knowledge GenomeTM

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


See full index

Cardiovascular > Revision > Flashcards

Revision Flashcards

1
Q

Medical Management of NSTEMI

A 
Antiplatelets
Anticoagulation
Tirofiban
Nitrates
B-Blockers (Ca2+ if contraindicated)
ACEI
Statins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pericarditis and Dressler’s

A

ECHO

NSAIDs or steroids (severe)

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

Signs of cardiac temponade

A 
Low CO
Pulsus paradoxus
Raised JVP
Muffled heart sounds
Diagnose with ECHO and the pericardial aspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

LV aneurysm

A

Persistent ST elevation

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

Wenckenbach’s phenomenon

A

Mobitz Type I heart block

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

Post-MI AF/flutter

A

Treat with digoxin +/- B-Blocker

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

In PVC or non-sustained VT

A

Avoid AADs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Positive Electrode

A

Recording electrode (LA, LL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PE on ECG

A

S1 Q3 T3
Deep S waves
Pathological Q waves
T wave inversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hypothermia on ECG

A

Bradycardic with J wave

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

ECG changes in hyperkalaemia

A

Tall tented T waves
Later = decreased height of p waves, increased PR
Even later = widening of QRS, merging of QRS and t wave

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

QT interval

A

0.36-0.44 seconds

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

Manifestation of aldosteronism

A

Low K+

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

Flushing and Palpitations

A

Phaechromocytoma

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

Young female with high BP

A

Fibromuscular dysplasia affecting the renal arteries (will see a corkscrew effect)

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

Anti-Anginal drug treatment

A

1st. B-Blocker OR Ca2+ blocker
2nd. B-Blocker + Ca2+ blocker
3rd.
Long acting nitrate
Ivabradine
Ranolazine
Nicorandil

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

Side Effects of Ca2+ channel blockers

A 
Dihydropyridines 
Calf swelling, gingival hypertrophy, reflex tachycardia
Rate Limiting 
eg. verapamil, diltiazem
Complete heart block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Side Effects of Nicorandil

A

Blue vision

Mouth Ulcers

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

Metabolic effect of B-Blockers

A

Hypoglycaemia (B2 adrenoceptors in liver)

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

3 CVS effects of adrenaline

A

Positive ino/chronotrope- (B1)
Redistribution of blood flow to heart (A1)
Coronary artery dilation (B2)

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

Determining axis of heart

A

Look at Lead I and aVF

  • I up and aVF down = left axis deviation
  • I down and aVF up = right axis deviation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Criteria for diagnosing left ventricular hypertrophy

A

S wave depth in V1

Talles R wave height in V5/6 >35mm

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

Digoxin Toxicity on ECG

A

Slows HR
Reverse tick on T wave
Shortened QT
Flattened, biphasic or inverted T waves

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

Signs of constrictive pericarditis

A 
Raised JVP
JVP rises paradoxically with inspiration
Quiet heart sounds
Diastolic pericardial knock
CXR - small heart and pericardial calcification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute endocarditis

A

Sepsis
Cardiac failure
(caused by organisms such as staph. aureus

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

What might aortic root abscess lead to …

A

Prolongation of PR, then complete AV block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Antibiotic treatment of endocarditis if penicillin allergic

A

Vancomycin

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

Staph aureus (endocarditis)

A

Flucloxacillin

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

Prosthetic valve (endocarditis)

A

Vancomycin, Gentamicin, Rifampicin

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

MRSA (endocarditis)

A

Vancomycin, Gentamicin, Rifampicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Strep. viridans (endocarditis)

A

Benzylpenicillin + Gentamicin

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

Enterococcus (endocarditis)

A

Amoxicillin/Vancomycin + Gentamicin

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

Staph. epidermis (endocarditis)

A

Gentamicin, Vancomycin, Rifampicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Signs, Symptoms and Causes of Myocarditis

A 
Signs = arrhythmia, cardiac failure
Symptoms = breathlessness, fever, chest pain, palpitations
Causes = enteroviruses e.g. echovirus, influenza A
Diagnosis = throat swab or stool swab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Brugada Syndrome

A

Polymorphic VT/VF preceded by AF in young person with a structurally normal heart
ST elevation + RBBB in V1-V3 which is intermittent and can be induced
Sodium channel mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Long QT syndrome

A

Polymorphic VT (TdP) triggered by adrenergic stimuli with long QT, syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Catecholaminergic polymorphic VT

A

Bidirectional/polymorphic VT triggered by stress or activity (normal resting ECG)
Treat: ICD, B-Blockers, Flecainide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hypertrophic cardiomyopathic

A

Sarcomeric genes, thickened septum, obstruction to outflow, heart failure, angina, AF at young age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment of hypertrophic cardiomyopathic

A

As for heart failure

ICD (implantable cardioversion defibrillator)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Suspect dilated cardiomyopathy…

A

Lamin A/C mutation
First degree AV block
Neuromuscular symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Arrhythmogenic RV cardiomyopathy

A

fibrofatty replacement of cardiomyocytes

Family history of sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Improving survival in transposition the great vessels

A

Balloon atrial septostomy to increase the size of the patent foramen ovale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pre-ductal saturation

Pos-ductal

A

Right Hand

Left Foot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Mitral regurgitation (symptomatic with LVEF <30%)

A

ACEI
B-Blocker
Loop Diuretic
Intra-aortic ballon counterpulsation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

CXR with straight left heart border

A

Mitral stenosis (increased pulmonary vasculature)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Murmur which results in very low diastolic blood pressure

A

Aortic regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Valve replacement in aortic regurgitation

A

not TAVI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Non-shockable rhythms

A

Asystole

PEA (pulseless electrical activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Management of asystole

A

Cannot defibrillate, must use adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Temperature management if unconscious after ROSC (return of spontaneous circulation) post-arrest

A

32-36oC for 12-24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Commonest cause of polymorphic VT

A

Ischaemia

52
Q

Treatment of fast AF in heart failure

A

Digoxin

DC shock

53
Q

Key investigation in suspected heart failure

A

ECHO - indicates the cause, and if any LV dysfunction

54
Q

Drugs to avoid in chronic heart failure

A

NSAIDs (cause fluid retention)

Verapamil (negative inotrope)

55
Q

Treatment of heart failure

A 
B-Blockers, ACEIs
Diuretics (furosemide)
Spironolactone if still symptomatic
Digoxin
Ivabradine (if HR remains fast)
Vasodilators (important in black people with HF)
56
Q

What can be used to diagnose heart failure/why?

A

Plasma BNP

Reflects the myocyte stretch

57
Q

Imaging in stroke

A
  1. CT

2. MRI

58
Q

Treatment of ischaemic stroke

A

Patient presents within 3-4.5 hours = 1. Ateplase 2. Aspirin after 24 hours
Patient presents after 4.5 hours = Aspirin

59
Q

Secondary prevention of stroke

A

Aspirin + dipyridamole/clopidogrel
Statins
Anti-coagulants in AF
Anti-hypertensives

60
Q

VTE and anti-coagulation

A
  1. LMWH for 5 days/ until INR >2 for 24 hours
  2. Warfarin for 3 months
  3. Re-assess
    Cancer patient: LMWH
    Drug User: Rivaroxaban
61
Q

Pre-test probability scoring systems in PE

A

Wells (>3 high risk) or Geneva (>10 is high risk)

62
Q

Investigation in chronic venous disease

A

Duplex ultrasound

63
Q

Management of claudication

A
  1. Exercise (30-45 mins/week)
  2. Symptom relief with cilostazol (PDE inhibitor)
  3. CV drugs to reduce the CV risk
  4. Revascularisation (angioplasty + stent, bypass)
64
Q

Tension

A

(pressure x radius) / thickness

65
Q

CABG is the main treatment

A

3 vessel disease

Left main stem CA disease

66
Q

Marked hypertension

A

190/95 in aortic dissection

67
Q

Gold standard for investigating CHD

A

Angioplasty

68
Q

Platelet granules

A 
alpha = vWF, factor V. PDGF, fibrinogen, anti-heparin
dense = ADP, 5-HT
69
Q

Spirinolactone only suitable if

A

K+ < 4.5 mmol/L

70
Q

Higher dose thiazide therapy

A

Stage 4 hypertension if K+> 4.5 mmol/L

71
Q

Hypertension in young fertile females

A

BCD

72
Q

Stage 1 Hypertension

A

Clinic: 140/90

Home/Ambulatory: 135/85

73
Q

Stage 2 Hypertension

A

Clinic: 160/100

Home/Ambulatory: 150/95

74
Q

Severe Hypertension

A

Clinic: >180/>110

75
Q

Phaeochromocytoma

A

Tumour of the adrenal medulla

76
Q

Eruptive xanthomas

A

Due to abrupt rise in serum triglyceride = small red/yellow papules on buttox/thighs

77
Q

Adverse effects of heparin and LMWH

A

Haemorrhage, Osteoporosis, Hypoaldosteronism, Hypersensitivity

78
Q

Treatment of the adverse effects of LMWH

A

Protamine sulphate

79
Q

LMWH

A

Inhibits Factor Xa
Subcutaneous
1st order kinetics
Renal excretion

80
Q

Treatment of fibrinolytic-induced haemorrhage

A

Tranexamic Acid

81
Q

Role of GP IIb IIIa

A

To bind fibrinogen resulting in soft plug formation

82
Q

Activation of chylomicrons and VLDL

A

Transfer of apoCII from HDL

83
Q

How does adenosine work?

A

Activates ACh sensitive K+ channels (GIRK) causing hyperpolarisation which supresses impulse conduction

84
Q

Purkinje Fibre Cells

A

Larger than normal cardiac muscle cells
Glycogen but no T-tubules
Sparse actin and myosin filaments
Allow for inferior to superior conduction

85
Q

Extracellular Fluid

A

3/4 interstitial

1/4 plasma

86
Q

NFP

A

i.e

Forces pulling water out - Forces drawing water in

87
Q

Factors causing oedema

A

Decreased plasma osmotic pressure (low protein)
Increased capillary pressure
Lymphatic insufficiency
Changes in capillary permeability

88
Q

Atrial Contraction

A

Occurs between the P wave and QRS complex

89
Q

Isovolumetric Contraction

A

Tension rises around a closed volume, causing a steep increase in ventricular pressure

90
Q

Consequences of hypovolaemic shock

A 
Pulse rate increases
Resp rate increases
Blood pressure falls
Pulse pressure falls (esp. SBP)
Urine output decreases
Mental status deteriorates
91
Q

Anatomical and Functional Assessment of the heart gold standard

A

Cardiac MRI

92
Q

What valvular abnormality is aortic coarctation associated with?

A

Bicuspid aortic valve

93
Q

Hypertrophic Cardiomypoathy Presentation

A

Young Patient
Arrhythmia
Family History of SCD

94
Q

Opening snap

A

Mitral Stenosis

95
Q

Ejection click

A

Congenital pulmonary of aortic stenosis
OR
Mechanical aortic valve

96
Q

Mid-systolic click

A

Mitral valve prolapse

97
Q

Causes of 3rd Heart Sound

A

LVF
Mitral regurgitation
Physiological in athletes/young children

98
Q

4th Heart Sound

A

At apex with bell, due to atrial contraction causing rapid flow into a stiff ventricle

99
Q

Decreased LV compliance

A

Myocardial ischaemia
Hypertension
Aortic Stenosis
(send for ECHO)

100
Q

Appearance of tetralogy of Fallot on CXR

A

Boot shaped heart

101
Q

Describe what the transverse pericardial sinus is and the surgical significance

A

‘Space’ posterior to the ascending aorta and pulmonary trunk
Used to identify and isolate the great vessels in cardiopulmonary bypass

102
Q

What does AF in patients with Wolff-Parkinson-White Syndrome result in?

A 
Ventricular Fibrillation (broader QRS)
Sudden Cardiac Death
103
Q

Cause of Atrial Flutter

A

Macro-re-entrant circuit only in the right atrium

104
Q

Treatment of Atrial Flutter (1st Line)

A

Ablation

105
Q

Associations with early after depolarisations

A

Ca2+ overload: associated with catecholamines, digoxin and heart failure

106
Q

What happens in complete heart block?

A

Purkinje Fibres become the ventricular pacemaker

= slow firing and so bradycardia

107
Q

Drugs used to treat SVT and mechanism

A 
Adenosine = activates A1 receptors, open GIRK channels and hyperpolarising AVN to briefly supress conduction
Digoxin = slows conduction and prolongs refractory period (AVN, Bundle of His)
Verapamil = slows conduction and prolongs refractory period
108
Q

Type IB ant-arrhythmic drug

A

Lignocaine

109
Q

Uses of Lignocaine

A

Ventricular Arrhythmias following MI (largely affect ischaemic zones)

110
Q

Type Ia Effect on AP

A

Lengthens the AP by decreasing AP upstroke gradient and prolonging repolarisation

111
Q

Type Ib Effect on AP

A

Shortens repolarisation preventing premature beats

112
Q

Type Ic Effect on AP

A

No effect on repolarisation/duration of AP, but depresses conduction

113
Q

‘Events’ which may lead to the development of TdP

A

Hypokalaemia
Renal Impairment
Prolongation of AP

114
Q

Why do ectopic beats lead to light headedness?

A

Transient change in arterial pressure

115
Q

Where is renin released from?

A

Juxtaglomerular apparatus in the kidney (granular cells)

116
Q

Stimulants of renin release

A

Renal artery hypotension
Stimulation of renal sympathetic nerves
Decreased sodium concentration in tubular fluid

117
Q

What initially brings about changes in stroke volume?

A

Changes in the diastolic length of myocardial fibres

118
Q

What is radial-radial delay a sign of?

A

Subclavian steal syndrome (stenosis/occlusion of the subclavian artery)

119
Q

What is long term control of MAP achieved by?

A

Changes in blood volume

120
Q

What is ANP released in response to ?

A

Atrial distension in hypovolaemic states

121
Q

What does ANP cause?

A

Salt and water excretion
Vasodilation
Decreased renin release

122
Q

Where are osmoreceptors located?

What is their function?

A

Near the hypothalamus

To recognise an increase in plasma osmolarity > trigger ADH release

123
Q

Function of ADH

A

Regulate extracellular fluid volume and osmolarity

124
Q

Function of RAAS

A

Long term regulation of MAP

125
Q

Aldosterone

A

To regulate the total body Na+ and ECFV in the long term

Cardiovascular (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions