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Cardiovascular for finals > High yield Exam cram > Flashcards

High yield Exam cram Flashcards

1
Q

What is preload?

A

how full the ventricle is when it starts to contract

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2
Q

What is after load?

A

how much force is required to push the blood out of the heart

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3
Q

How is cardiac output calculated?

A

Heart rate x stroke volume

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4
Q

How is stroke volume calculated?

A

End diastolic volume – end systolic volume

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5
Q

How is ejection fraction calculated?

A
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6
Q

How is mean arterial pressure calculated?

A
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7
Q

Name the parasympathetic neurotransmitters and receptors

A

Acetylcholine
Muscarinic receptors

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8
Q

Name the sympathetic neurotransmitter and receptor

A

Adrenaline
Beta 1 receptors

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9
Q

What happens to blood vessels when alpha receptors are targed with antagonists (blockers)

A

Vasoconstriction

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10
Q

Where are the pacemaker cells of the heart located and what is their function

A

SA Node
Set the heart rate (depolarise and set off an action potential which is then carried throughout the heart)

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11
Q

Briefly explain the stages of the cardiac cycle

A

0- depolarisation, sodium influx

1- peak depolarisation, efflux of potassium and chloride

2- Platau phase, Calcium influx, potassium efflux

3- repolarisation, efflux of potassium

4- return to base potential maintained by influx and efflux of potassium

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12
Q

What should the paper speed be for an ECG?

A

25mm/s

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13
Q

How many seconds is one large square on an ECG?

A

0.2s

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14
Q

How many seconds is one small square on an ECG?

A

0.04s

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15
Q

What should a normal P-R interval be (in seconds and in squares!)

A

0.12-0.2 (3-5 small squares)

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16
Q

What should a normal QRS be (in seconds and in squares!)

A

<0.12s (<3 small squares)

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17
Q

What should a normal QT interval be (in seconds and in squares!)

A

<0.42s at 60BPM (<10.5 small squares)

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18
Q

How can the heart rate be calculated from an ECG?

A

count how many QRS complexes in 30 big boxes then x10 for BPM (30 big squares = 6 seconds!)

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19
Q

What does ARIBAR stand for?

A

Any electrical activity?
Rate?
Irregular or regular rhythm?

Broad QRS complexes?
Any P waves?
Relationship between P wave and QRS

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20
Q

What are the 4 classes of cardiac drugs?

A

Class I: membrane stabilising drugs (e.g. lidocaine, flecainide)

Class II: beta-blockers

Class III: amiodarone; sotalol (also Class II)

Class IV: calcium-channel blockers (includes verapamil but not dihydropyridines)

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21
Q

What type of drug are aspirin, tiagcrelor and clopidogrel?

A

Anti-platelet

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22
Q

What is the MOA of aspirin?

A

COX inhibitor

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23
Q

What is the MOA of ticagrelor and clopidogrel?

A

P2Y12 ADP receptor antagonist

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24
Q

Name some anticoagulant drugs

A

Prasugrel
Fondiparinux
Heparin
Warfarin
DOACs (-ban)

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25
Q

What is the MOA of prasugrel and fondiparinux?

A

P2Y12 inhibitors

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26
Q

What is the MOA of LMW heparin?

A

Activates antithrombin III. Forms a complex that inhibits factor Xa

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27
Q

What is the MOA of unfractioned/standard heparin?

A

Activates antithrombin III. Forms a complex that inhibits thrombin, factors Xa, IXa, Xia and XIIa

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28
Q

What is the MOA of warfarin?

A

Vit K antagonist

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29
Q

What is the roe of vitamin K in the coagulation cascade?

A

co-factor in the production of clotting factors II, VII, IX and X (1972)

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30
Q

What is the MOA of apixiban?

A

Direct Factor Xa inhibitor

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31
Q

What is the MOA of dabigatran?

A

Prevents activation of fibrinogen into fibrin

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32
Q

What conditions are B blockers contraindicated in?

A

asthma
peripheral vascular disease
raynauds
heart block
HF

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33
Q

Name some central and peripherally acting calcium channel blockers

A

Central - diltazem/ verapamil
Peripheral - Amlodipine/ felodipine

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34
Q

Describe how the effects of central and peripheral CCB’s are different

A

Central - rate limiting
Peripheral - lower BP by causing vasodilation

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35
Q

What is the function of ivabradine and how does it achieve this function?

A

Rate limitation - blocks potassium channels in the sinoatrial node

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36
Q

What is the MOA of statins?

A

inhibit 3H3MG CoA reductase in the liver which stops production of cholesterol

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37
Q

What is the MOA of ACE inhibitors?

A

Prevents ACE from cleaving angiotensin I into angiotensin II

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38
Q

What type of drug is spironolactone?

A

Aldosterone Antagonist (potassium sparing diuretics)

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39
Q

What is the MOA of nicorandil?

A

Potassium channel agonist

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40
Q

What is the MOA of furusomide?

A

inhibit the Na+/K+/2Cl- co-transporter

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41
Q

What kind of drugs are losartan & candesartan?

A

Angiotensin receptor blockers

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42
Q

How does adenosine work?

A

binds to adenosine (A1 & A2) receptors in the AV node which slows/ blocks conduction through the AV node

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43
Q

How does amiodarone work?

A

increase action potential duration by blocking potassium channels and prolonging the repolarisation of myocytes

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44
Q

What is INR?

A

a measure of how long blood takes to clot

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45
Q

What does an INR of 2 mean?

A

blood takes twice as long as normal to clot

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46
Q

What scoring system can be used to assess the risk of bleeding in patients on warfarin?

A

HASBLED

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47
Q

When should warfarin levels be assessed?

A

12 hours after last dose

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48
Q

What should your INR be if you are NOT on warfarin?

A

<1.1

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49
Q

What is the therapeutic range for warfarin?

A

2-3

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50
Q

What is the target INR if you have had a VTE?

A

2.5

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51
Q

What should the target INR be if you have had multiple VTE?

A

3.5

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52
Q

What is the target INR in AF?

A

2.5

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53
Q

What is the target INR if you have a mechanical heart valve?

A

2.5-3.5

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54
Q

What should doctors do if INR is between 5-8 and the patient is not bleeding?

A

withhold 1-2 doses
reduce subsequent maintenance dose

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55
Q

What should doctors do if INR is 5-8 and the patient is bleeding?

A

Stop warfarin
give vit K 1-3mg IV
restart vit K when INR <5

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56
Q

What should doctors do if INR >8 and the patient is not bleeding?

A

stop warfarin
vit K 1-5mg oral
repeat dose of vit K if INR is still too high within 24 hours
restart warfarin when INR<5

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57
Q

What should doctors do if INR >8 and the patient is having minor bleeding?

A

Stop warfarin
1-3mg vit K IV
repeat dose of vit K if INR is still too high within 24 hours

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58
Q

What should doctors do if the warfaranised patient is having major bleeding?

A

stop warfarin
5mg vit K IV
Prothrombin complex or FFP

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59
Q

which valves are in the Left side of the heart?

A

Mitral valve -> Aortic valve

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60
Q

which valves are in the right side of the heart?

A

Tricuspid -> pulmonary

61
Q

How many leaflets do each of the heart valves have?

A

All heart valves have 3x leaflets except mitral (2x)

62
Q

Describe the murmur of mitral stenosis

A

Mid to late diastolic, loud S1 & split S2, rumbling, low pulse volume

63
Q

Describe the murmur of aortic regurgitation

A

Early diastolic, high pitched, blowing

64
Q

Describe the murmur of mitral regurgitation

A

Holosystolic, Soft S1 & split S2, high pitched, blowing

65
Q

Describe the murmur of aortic stenosis

A

Ejection systolic, soft S2 & S4, slow rising

66
Q

Which pathology would give a collapsing pulse

A

PDA
Aortic regur

67
Q

Which pathologies give an ejection systolic murmur

A

Tetrology of fallot
HOCM
pulmonary stenosis
Aortic stenosis

68
Q

Which pathology gives a loud S2

A

Pulmonary hypertension

69
Q

What is heard in L ventricular failure?

A

S3

70
Q

What is heard in a L->R shunt?

A

Loud S1

71
Q

What pathology gives a continuous murmur?

A

Septal defects

72
Q

What is rheumatic heart disease?

A

a result of body’s overreaction to a group A beta-haemolytic streptococcal infection.

73
Q

What histological finding is indicative of rheumatic heart disease?

A

Aschoff bodies

74
Q

What valvular pathology does rheumatic heart disease cause?

A

Mitral stenosis (the only cause of this is rheumatic heart disease!)

75
Q

Describe first degree heart block

A

Prolonged PR interval

76
Q

How is first degree heart block managed?

A

No treatment required

77
Q

Describe Second degree heart block, Mobitz I (Wenckebach)

A

PR intervals progressively elongate until a QRS is dropped

78
Q

How is second degree heart block, Mobitz I (Wenckebach) managed?

A

No treatment required

79
Q

Describe Second degree heart block, Mobitz II

A

PR intervals are consistent but some complexes are dropped

80
Q

How is Second degree heart block, Mobitz II managed?

A

Pacemaker if symptomatic

81
Q

Describe third degree heart block

A

No correlation between P and QRS

82
Q

How is third degree heart block managed?

A

Pacemaker

83
Q

How is VF managed?

A

Shock
CPR
Adrenaline 1mg & Amiodarone 300mg

84
Q

How is pulseless VT managed?

A

Shock
CPR
Adrenaline 1mg & Amiodarone 300mg

85
Q

How is pulsed VT managed?

A

Unstable
- synchronised cardioversion 1st line
- Amiodarone + synchronised cardioversion 2nd line

Stable
- Amiodarone 1st line
- Cardioversion 2nd line

86
Q

How is Atrial flutter managed?

A

Direct-current (DC) cardioversion.

Antiarrhythmic drugs/nodal rate control agents.

Rapid atrial pacing to terminate atrial flutter.

Ablation of the abnormal circuit

87
Q

How is SVT managed?

A

vagal manoeuvres/ carotid sinus massage and adenosine can be given to terminate an episode.

88
Q

How is Wolf-parkinson-white identified on an ECG?

A

Delta wave (upstroke of QRS- nike tick!)

89
Q

How is wolf Parkinson white managed?

A

Vagal manoeuvres
Adenosine to revert to sinus rhythm

90
Q

How is torsades de pointes managed?

A

Vagal manoeuvres
IV magnesium sulphate, beta blocker, and atrial pacing

91
Q

How is a LBBB identified on an ECG?

A

V1 WilliaM V6

92
Q

How is RBBB identified on an ECG?

A

V1 MorroW V6

93
Q

What scoring system should be used to assess whether a patient with atrial fibrillation should be anticoagulated or not

A

CHADSVASC

94
Q

What would a CHADSVASC of 0, 1 and 2 mean for coagulation?

A

0= no treatment

1= anticoagulate males (not females scoring 1)

> 2 = anticoagulated

95
Q

What are the 4H’s and 4T’s of cardiac arrest (reversible causes)

A

Hypoxia
Hypovolaemia
Hypo- / hyperkalaemia / metabolic
Hypothermia

Thrombosis - coronary or pulmonary
Tamponade - cardiac
Toxins
Tension pneumothorax

96
Q

What type of STEMI occurs when there is a block in the right coronary artery? Give the corresponding ECG leads and the areas of the heart supplied by this artery

A

Inferior STEMI (Leads II, III and aVF)

This branch supplies right atrium & ventricle, Inferior aspect of left ventricle and posterior septal area

97
Q

What type of STEMI occurs when there is a block in the Left Circumflex Artery? Give the corresponding ECG leads and the areas of the heart supplied by this artery

A

Lateral STEMI (Leads I, aVL, V5-6)

This branch supplies left atrium and posterior aspect of left ventricle

98
Q

What type of STEMI occurs when there is a block in the Left anterior descending artery? Give the corresponding ECG leads and the areas of the heart supplied by this artery

A

Anterior STEMI (Leads V1-4)
This branch supplies anterior aspect of left ventricle and anterior aspect of septum

99
Q

List the primary prevention methods for Acute coronary syndrome

A

Diet – total fat <30% calories

Exercise – 150 mins moderate intensity per week or 75 mins high intensity.

Statin- If QRISK >10%. Atorvastatin 20mg. Give regardless of QRISK if diabetic or CKD.

100
Q

What is the acute treatment of stable angina?

A

GTN – Immediate relief

B Blocker/CCB – long term relief

101
Q

What is the secondary prevention for stable angina?

A

A-Antiplatelet (aspirin/ Clopidogrel/ ticagrelor)
A-Atorvastatin 80mg
A-Atenolol
A-ACE Inhibitor

102
Q

What is the acute management of unstable angina?

A

Give MONA
Morphine, oxygen, nitrates, aspirin 300mg

Same day assessment

103
Q

What is the acute treatment of STEMI?

A

Give MONA
Morphine, oxygen, nitrates, aspirin 300mg

Then..

PCI if within 12 hours of symptom onset and within 2 hours of presenting. Give Prasugrel.

OR

Thrombolysis if within 12 hours of symptoms but PCI not available within 2 hours

104
Q

What is the acute treatment of NSTEMI?

A

B – basis for decision = GRACE
* Low risk ≤3% - give ticagrelor
* High risk ≥3% - PCI immediately if unstable or within 72 hours if stable. Give prasugrel or tiacagrelor,
A – Aspirin 300mg
T – Ticagrelor 180mg (clop if bleed risk, prasugrel if going for angio)
M - morphine
A – antithrombin (fondaparinux – don’t give if going for angio!)
N – Nitrate

105
Q

What is the secondary prevention of unstable angina, STEMI and NSTEMI?

A

A-Antiplatelet (Clopidogrel/ ticagrelor) for 12 months
A-Atorvastatin 80mg
A-Atenolol
A-ACE Inhibitor
A-Aspirin 75mg indefinitely
A-Aldosterone antagonist for those with heart failure

106
Q

How can unstable angina be differentiated from NSTEMI?

A

NSTEMI- raised trops
Unstable angina - normal trops

107
Q

What is meant by primary and secondary prevention?

A

Primary = before disease has occurred
Secondary = After disease has occurred

108
Q

Which type of patients would benefit from a CABG?

A

> 70% stenosis of left main stem artery

significant proximal three-vessel coronary artery disease

two vessel coronary artery disease that includes significant stenosis of proximal left anterior descending coronary artery and who have an ejection fraction < 50%.

109
Q

Name 4 Post MI complications that occur within 0-3 days of MI

A

Arrhythmia
Cardiogenic shock
Pericarditis
Stoke

110
Q

What is a late complication of MI (>2 weeks after)

A

Left ventricular aneurism

111
Q

How does the body sense blood pressure?

A

using sinuses in the aortic arch and carotid arteries (carotid baroreceptor)

112
Q

What controls
A) Short term blood pressure
B) Long term blood pressure
???

A

The arterial baroreflex = short term control

kidneys via renin-angiotensin-aldosterone system = Long term control

113
Q

List the stages of hypertension and the correlating clinic and ambulatory blood pressures

A
114
Q

List the clinic and ambulatory blood pressure targets for patients <80 and patients >80

A
115
Q

List the causes of secondary hypertension

A

R – Renal disease
O – Obesity
P – Pregnancy
E – Endocrine
D – Drugs (alcohol, NSAIDs)

116
Q

How is hypertension managed?

A

ACE (-pril) – If <55 or diabetic
CCB (-pine) If >55 or African-carribean
Combination
Indapamide
ARB (e.g. candesartan)

117
Q

How is resistant hypertension managed?

A

K+ > 4.5 = thiazide like diuretic
K+ < 4.5 =spironolactone

118
Q

What is the definition of orthostatic hypertension?

A

blood pressure decrease of 20 mmHg systolic and/or a diastolic pressure of 10 mmHg within three minutes of standing.

119
Q

How is heart failure diagnosed?

A
  • Pro-BNP
  • ECHO then MUGA scan for left ventricular dysfunction
120
Q

How does Pro-BNP help guide urgency of investigation?

A

400-2000 = echo within 6 weeks
>2000 = echo within 2 weeks

121
Q

Describe the stages of heart failure and the associated ventricular function

A
122
Q

How is heart failure managed?

A

ABAL

A- ACE inhibitors
B- Beta blockers
A- Aldosterone receptor blockers
L- Loop diuretic

123
Q

What is infective endocarditis?

A

Infection of the endocardium (innermost layer of the heart)

124
Q

Which valve is most commonly affected in infective endocarditis?

A

Mitral

125
Q

How does infective endocarditis look on an ECG?

A

Prolonged PR interval

126
Q

What is the criteria used in infective endocarditis?

A

Modified dukes

127
Q

What is the overall most common cause of infective endocarditis and the most common cause seen in IVDUs

A

S. Aureus

128
Q

What is the most common cause of infective endocarditis in developing countries and in those with poor dental hygiene?

A

Strep viridian’s

129
Q

What is the most common cause of infective endocarditis seen with indwelling lines or within 2 months of prosthetic valve surgery?

A

Strep epidermidis

130
Q

What is the most common cause of infective endocarditis in those with colorectal cancer?

A

Strep Bovis

131
Q

What is the most common non-infective cause of endocarditis?

A

SLE

132
Q

what is the initial blind therapy for infective endocarditis?

A

Amoxicillin

133
Q

What antibiotic should be given in endocarditis if the patient has staph and a natural valve

A

Fluclox

134
Q

What antibiotic should be given in endocarditis if the patient has staph and a prosthetic valve?

A

fluclox, ripampicin + gent

135
Q

What antibiotic should be given in endocarditis if the patient has strep?

A

Benzylpenicillin

136
Q

What is the difference between a true aneurism and a false aneurism?

A

True = involves all 3 layers
False= involves 1 or 2 layers

137
Q

Describe the Stanford classification of aneurisms

A
138
Q

Describe the DeBakey classification of aneurysms

A
139
Q

How does a forward aneurism tear present?

A
140
Q

How does a backward aneurism tear present?

A
141
Q

What findings can be seen on CT

A
  • Mediastinal widening
  • False lumen can be seen on CT
142
Q

Describe the management of an aortic aneurism

A
143
Q

Which classification system can be used to classify peripheral limb disease?

A

Fontaine Classification

144
Q

Describe the stages of the Fontaine classification

A
145
Q

What is the first line investigation in limb ischaemia?

A

duplex scan

146
Q

Describe the difference between arterial and venous ulcers in terms of appearance, location and treatment

A
147
Q

How long should a provoked DVT be treated for?

A

3 months

148
Q

How long should an unprovoked DVT/ DVT in malignant picture be treated for?

A

6 months

Cardiovascular for finals (1 decks)

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