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Cardio > Cardio W1 > Flashcards

Cardio W1 Flashcards

1
Q

muscarinic receptors of the heart and what acts on them

A

M2 receptors, acetylcholine

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2
Q

inotropic

A

force

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3
Q

chronotropic

A

HR

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4
Q

Frank Starling

A

as EDV increases, the SV increases

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5
Q

beta receptors on the heart and what acts on them

A

B1 receptors, noradrenaline

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6
Q

what does the PR interval indicate

A

AV node delay

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7
Q

what are striation of cardiac muscle caused by

A

contractile fibres

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8
Q

four phases of action potential generation in pacemaker cells

A 
phase 0: Na+ channels open 
phase 1: Na+ close, transient K+ efflux
phase 2: Ca++ open (L-type channels)
phase 3: K+ efflux
phase 4: resting potential
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9
Q

what is the A band

A

myosin only

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10
Q

what is the I band

A

between myosin

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11
Q

what is the H zone

A

between actin

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12
Q

What is happening when muscle is relaxed

A

no cross bridge because the actin binding site is blocked by the troponin- tropomyosin complex

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13
Q

what is happening when muscle contracts

A

Ca++ binds to troponin and pulls the troponin-tropomyosin complex away to expose binding site and cross bridge forms

actin-myosin cross bridge forms, power stroke pulls actin inwards during contraction

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14
Q

time of pacemaker cell AP vs Ventricular muscle AP

A

250ms, 800ms

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15
Q

what happens to calcium after AP has passed

A

Ca++ influx ceases and Ca++ goes back into SR by Ca++ATPase (relaxation)

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16
Q

what effects the stroke volume?

A

preload, afterload, myocardial contractility

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17
Q

Effect of sympathetic stimulation on frank starling curve and shift?

A

greater contractility, so for every EVD, there is a greater SV
Frank starling curve shifts to the left

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18
Q

How to record BP using kortkoff sounds

A

record systolic BP when you hear the 1st heart sound, then record diastolic BP when the heart sounds disappear

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19
Q

Normal HR

A

60-100BPM

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20
Q

normal systemic BP

A

90/60mmHg to 120/80mmHg

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21
Q

Definition of hypertension

A

average clinical BP of 140/90mmHg or above and a daytime average of 135/85mmHg or above

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22
Q

What is MABP

A

average arterial BP during a single cardiac cycle involving contraction and relaxation of the heart

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23
Q

How to calculate MABP

A

(2D+S)/3 or DBP+ (PP/3)

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24
Q

Normal range for MABP

A

70-105mmHg

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25
Q

what systems regulate BP in long term and their effect on BP

A

RAAS (increase)
Naturetic peptides
ADH

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26
Q

Describe whole RAAS

A

fall in BP-kidney releases renin- renin causes conversion of angiotensinogen (liver) to angiotensin 1. angiotensin 1 is converted to angiotensin II by ACE (lung vascular endothelium). Angiotensin II causes vasoconstriction, vascular muscle hypertrophy, increased thirst, increased ADH and aldosterone release (adrenal cortex). Aldosterone increased plasma volume and increased BP, water and sodium reabsorption form the kidneys.

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27
Q

what is the rate limiting step in RAAS

A

renin release

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28
Q

what releases renin

A

granular cells

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29
Q

what monitors tubular Na+ in kidney tubules

A

macula densa

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30
Q

Physiological closing of S2

A

pulmonary valve closes before the aortic valve

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31
Q

contents of juxtaglomerular apparatus and their function

A

granular cells (renin release) and macula densa (monitors Na+ in kidney tubules)

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32
Q

Three stimuluses of renin release

A
  1. Reduced renal BP due to reduced overall BP
  2. Decreased Na+ in kidney tubules
  3. Stimulation of renal sympathetic nerves
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33
Q

Function of Naturetic peptides and all its actions

A

To reduced BP by excretion of salt and water is response to cardiac distension or neurohormonal stimuli

also reduce renin release and act as vasodilators

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34
Q

Two types of naturetic peptide

A

ANP 28 AA (atria)

BNP 32AA (ventricles)

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35
Q

Name and describe the 4 types of shock

A

Hypovolaemic (non/haemorrhagic)
Obstructive (TPX, PE, tamponade)
Cardiogenic (eg MI)
Distributive (neurogenic- spinal cord injury, vasoactive-septic or anaphylactic shock)

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36
Q

until what point can body compensate for loss in blood volume

A

until loss of >30% blood volume

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37
Q

Amount of exercise adults should do weekly

A

150 minutes/week moderate exercise or 75 minutes per week of intense exercise

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38
Q

Amount of exercise children should do weekly

A

1h per day for 5 days a week

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39
Q

X ray features of heart failure

A 
Alveolar oedema
B lines
Cardiomegaly
Diversion of vessels (upper zone vessel enlargement)
Effusion
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40
Q

Events during cardiac cycle

A
  1. Passive Filling (80%)
  2. Atrial Contraction
  3. Isovolumetric ventricular contraction
  4. Ventricular Ejection
  5. Isovolumetric ventricular diastole
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41
Q

What is the average EDV

A

130ml

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42
Q

What causes the closure of AV valves

A

when ventricular pressure is greater than atrial pressure

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43
Q

when do aortic and pulmonary valve open

A

when ventricular pressure exceeds pressure in vessels

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44
Q

Average stroke volume

A

70ml

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45
Q

4 areas of cardiac auscultation

A

aortic- 2nd int space, right parasternal edge
pulmonary- 2nd, left parasternal edge
tricuspid- 4th int space, left parasternal edge
mitral- 5th int space, left midclavicular line

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46
Q

When does JVP occur and which waves are normal and abnormal

A

occurs after atrial contraction
a and c wave= normal
v wave= abnormal

a= atrial contraction
c= bulging of tricuspid into atria in ventricular contraction
v= rise in atrial pressure during atrial filling
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47
Q

Where is most blood in the body

A

peripheral veins

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48
Q

Diameter of arterioles

A

30-200 micrometers

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49
Q

Diameter in capillaries

A

4-8 micrometers

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50
Q

what are pericytes

A

connective tissue with contractile properties, outside of capillaries

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51
Q

describe the 3 types of capillaries

A

continuous- no gaps- skin, muscle, nerves, lungs, connective tissue

fenestrated- 50 nanometer pores- gut mucosa, kidney glomeruli, endocrine glands

discontinuous/sinusoidal- large gaps- spleen, bone marrow

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52
Q

Diameter of PCV

A

10-30 micrometers

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53
Q

When do PVC become venules

A

acquire intermittent smooth muscle and 50 micrometers diameter

54
Q

what are valves

A

inward expansions of the tunica intima in veins

55
Q

what is on the outer layer of the heart

A

mesothelium

56
Q

core of heart valves

A

dense irregular connective tissue- the lamina fibrosa which is continuous with the fibrous skeleton of the heart

57
Q

blood supply of the heart valves

A

valves have no blood vessels

58
Q

Diameter of pacemaker cells and compare to contractile cells

A

4-8 micrometers

smaller than contractile cells

59
Q

Appearance of pacemaker cells

A

small, pale

60
Q

Location and Appearance of Purjunke fibres

A

subendothelial layer

larger than cardiac cells, clear area in the centre and pink in margins- myosin and actin at the periphery

61
Q

Equation for resistance to blood flow

A

R=nL/r4

62
Q

What regulates blood pressure in arterioles in the short term

A

Baroreceptor reflex

63
Q

Nervous innervation of arterioles

A

Sympathetic- a1 adrenoceptors- noradrenaline
(vasomotor tone)

no parasympathetic innervation (except penis and clitoris)

64
Q

Effect of adrenaline on alpha and beta receptors

A

alpha- vasoconstriction (skin, gut, kidneys)

B2- vasodilation (cardiac and skeletal muscle)

65
Q

Effect of angiotensin II and ADH on vascular smooth muscle

A

vasoconstriction

66
Q

can extrinsic control of VSM over ride intrinsic control?

A

No

intrinsic factors can over ride extrinsic factors

67
Q

How in NO produced in vascular endothelial cells

A

L-arginine via NO synthase

68
Q

why may NO be released

A

increased BP or chemical signalling

69
Q

Chemicals that cause vasoconstriction of blood vessels

A

Serotonin, Thromboxane A2, Endothelin, Leukotrienes

70
Q

Factors which increase venous return

A

blood volume
venomotor tone
respiratory pump
skeletal muscle pump

71
Q

Effect of exercise on frank-Starling curve

A

Contractility of heart increases- FS curve shifts to the left

72
Q

Describe depolarisation and repolarisation

A

Depolarisation is becoming more positive

Repolarisation is becoming more negative

73
Q

What does an ECG provide information on?

A

Rate, Rhythm, Chamber size, axis

main test for MI and ischaemia

74
Q

Contents of 12 lead ECG

A

3 limb leads ( L1, L2, L3)
3 augmented voltage lead (aVL, aVR, AVF)
6 chest leads (V1-6)

75
Q

Horizontal leads

A

chest leads V1-V6

76
Q

Vertical leads

A

AVL, AVR, AVF, L1, L2, L3

77
Q

Which lead is used as the rhythm strip

A

Lead II

78
Q

Normal Duration of P wave

A

less than 0.12s (120ms), 0.08-0.1s

79
Q

what is an S wave

A

downward deflection after R wave

80
Q

what is a q wave

A

downward deflection before R wave

81
Q

What is a R wave

A

Upward deflection that does not have to come after Q wave

82
Q

Normal duration of QRS complex

A

less than 0.1s (less than 100ms)

83
Q

Why is the Twave an upward deflection

A

repolarisation moving away from seeing electrode

84
Q

Normal duration of PR interval

A

0.12-0.2ms

85
Q

Normal duration of QT interval

A

0.44s men, 0.46s in women

86
Q

what are precordial leads

A

chest leads

87
Q

what are unipolar leads and bipolar leads

A

augmented voltage leads, limb leads

88
Q

Lateral leads

A

Lead I and AVL

89
Q

Inferior leads

A

aVF, LII and LIII

90
Q

what does each chest lead ‘look at’

A

V1-V2- IV septum
V3-V4- anterior heart
V5-V6- lateral (left)

91
Q

positions of each chest lead

A

V1 4th int space right parasternal
V2 4th int space left parasternal
V3 between V2 and V4
V4 5th int space, midclavicular line (left)
V5 same horizontal level as v4, anterior axillary line
V6 same horizontal level as V4, midaxillary line

92
Q

Duration of one small ECG square

A

0.04s

93
Q

Speed of ECG paper

A

25mm/s

94
Q

Calculating HR with normal rhythm

A

300/no of small squares in R-R interval

95
Q

Calculating HR with abnormal rhythm

A

no of QRS complex in 30 small squares

96
Q

What is normal sinus rhythm

A

Normal sinus rhythm is characterized by P waves that are upright in leads I and II of the ECG
but inverted in the cavity leads AVR and V1

97
Q

What can a normal ECG now exclude

A

MI
Intermittent rhythm disturbances (24h/7day ECG)
Stable angina

98
Q

What investigation for stable angina

A

Exercise ECG- look for ST changes before/ after exercise (usually not shown at rest)

99
Q

what is TLC

A

the real or apparent loss of consciousness with loss of awareness, loss of motor control, loss of responsiveness and amnesia for a short duration

100
Q

what is syncope

A

TLC due to cerebral hypoperfusion which is short and rapid and results in spontaneous recovery

101
Q

Types of syncope

A

Reflex syncope, Orthostatic hypoperfusion, cardiac syncope

102
Q

Reflex syncope

A

when there is a fall in HR (cardioinhibition) or vasopressin which causes reduced CO due to neural reflexes via vagal stimulation

103
Q

Types of reflex syncope

A

vasovagal reflex syncope
situational reflex syncope
carotid sinus reflex syncope

104
Q

Postural hypotension defintion

A

when there in a change in BP within 3 minutes of standing from lying down by
20mmHg SBP with/without symptoms
10mmHg DBP with symptoms

105
Q

Causes of cardiac syncope

A
  • Arrhythmia (bradycardia or tachycardia)
  • Acute MI
  • Structural cardiac disease (aortic stenosis, hypertrophic cardiomyopathy)
  • Other (PE, Tamponade, TPX)
106
Q

Action of ivabradine and its use

A

Blocks HCN channels (reduced Na+ Influx/funny current) used in angina to reduce HR

107
Q

What is calcium induced calcium release

A

when intracellular calcium acting on ryanodine II receptors causes Ca2+ influx from the SR

108
Q

Two methods of calcium efflux

A

to extracellular space via Na+/Ca2+ exchanger 1 (NCXR)

to SR via Ca2+ATPase (SERCA)

109
Q

Influence of PKA on relaxation

A

PKA phosphorylates phospholamban, increasing Ca2+ATPase activity therefore increased relaxation

110
Q

Action of PDE

A

converts cAMP to 5AMP (inactive)

111
Q

Name the catecholamines and describe their selectivity

A

Dobutamine (B1)
Adrenaline (b over a)
NA (a OVER B)

112
Q

What is dobutamine used in

A

acute HF, but will cause early death if used in chromic HF

113
Q

Uses of BB

A

Angina (1st line), HF (Carvedilol, start low, go slow), Hypertension, arrhythmia

114
Q

What is atropine + its effect

A

Atropine is a non-selective muscarinic antagonist- increases HR

115
Q

use of atropine

A

used in Bradycardia and ACh poisoning

116
Q

What type of drug is digoxin, its action, and what is it used to treat

A 
Inotropic drug (cardiac glycoside) which increases heart contractility 
Na/K ATPase blockade increases Ca2+ influx from SR

used IV in acute HF, oral in chronic HF, HF with AF

117
Q

side effects of digoxin

A

blurred yellow vision
effect of digoxin is increased in hypokalaemia
oscillatory after potentials (Ca2+ overload)
Arrhythmia
heart block (excessive AV depression)
N+V+D
Gynaecomastia

118
Q

Contraction of VSM

A

calcium combines with calmodulin to make calcium-calmodulin complex, which activates MLCK.
MLCK phosphorylates MLC- contraction

119
Q

Relaxation of VSM

A

MLC phosphatase will dephosphorylate MLC-relaxation

120
Q

what activates MLC phosphatase

A

PKG

121
Q

Action of organic nitrates

A

metabolism of ON to NO causes relaxation of smooth muscle. reduced preload and afterload. Redirects blood to areas of ischaemia. venodilation at low doses, arterial dilation at higher doses.

122
Q

Types of ON and what they are used in

A

Isosorbide mononitrate- short term relief (spray/patch)
tablet in stable angina, IV in unstable

Glyceryl trinitrate- prophylaxis (need 8 hour nitrate free period)

used in all types of ANGINA

123
Q

Side effects of ON

A

Hypotension, headaches, dizziness/syncope, Methaemoglobin (cyanide poisoning treatment), reflex tachycardia (px with BB)

124
Q

types of CCB and what they are used in

A

Verapamil- heart (dysrhythmia)
amlodipine (vascular- used in hypertension)
diltiazem (heart and vascular)

also used in angina

125
Q

Side effects of CCB

A

ankle oedema, flushing, hypotension

126
Q

what is bradykinin

A

potent vasodilator inhibited by ACE

127
Q

SE of ACEI

A

dry cough, angioneurotic oedema, hypotension, hyperkalaemia (less aldosterone)

128
Q

who is ACEI contraindicated in? who are they good for?

A

Pregnant/child-bearing age women and bilateral renal stenosis

diabetic neuropathy

129
Q

what are ACEI/ARB used in?

A

Hypertension (1st line for under 55 non-African/Caribbean, diabetic neuropathy)
Cardiac Failure
Post-MI

130
Q

Use of nicorandil
type of drug
SE

A

used in refractory angina (NO activity)
K channel opener
mouth ulcer

131
Q

Use of alpha antagonists

SE

A

Hypertension with prostatic hypertrophy

postural hypotension

132
Q

Describe types of diuretics and side effects

A

Thiazide diuretics- mild- hypertension
loop diuretics- stronger-HF- hypocalcemia

Hypokalaemia and Hyponatremia
Gout, hyperglycaemia therefore diabetes, impotence

Cardio (2 decks)

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