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Physiology Flashcards

1
Q

Autorhythmicity

A

Heart is capable of beating rhythmically in the absence of external stimuli, or nervous stimuli

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2
Q

Specific location of the SA node

A

SA node is located in the upper right atrium close to where the Superior Vena Cava enters the right atrium

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3
Q

Spontaneous pacemaker potential

A

This gradual drift towards threshold. The cells in the SA node do not have a stable resting membrane potential. The spontaneous pacemaker potential takes the membrane potential to a threshold to generate an action potential in the SA nodal cells

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4
Q

Which ion channels are behind the spontaneous pacemaker potential ie. reaching threshold in pacemaker cells?

A

Decrease in K+ efflux superimposed on a slow Na+ influx (the funny current)

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5
Q

Which ion channels are responsible for the rising phase of the action potential in pacemaker cells?

A

Voltage-gated Ca++ channels resulting in Ca++ influx

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6
Q

Which ion channels are responsible for the falling phase of the action potential in pacemaker cells?

A

Activation of K+ channels resulting in K+ efflux (which had been decreased previously)

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7
Q

What is the pathway of the spread of excitation?

A

1) SA node 2) AV node and RA (via Bachmann’s bundle) 3) Bundle of His (R &L) 4) Purkinje fibres

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8
Q

How does the excitation spread between cardiac cells?

A

Via gap junctions

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9
Q

What is the only point of electrical contact between the atria and ventricles?

A

AV node

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10
Q

What important role does the AV node play?

A

Causes a delay in the spread of excitation to allow the ventricles time to fill. It does this as it is composed of slow conducting fibres

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11
Q

What is the resting membrane potential of ventricular cells?

A

-90 MV

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12
Q

Which ion channels are responsible for the rising phase (Phase 0) of action potentials in the ventricular cells?

A

Fast Na+ influx (reverses the membrane potential to +30mV)

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13
Q

Which ion channels are responsible for the initial falling phase (Phase 1) of action potentials in the ventricular cells?

A

Closure of Na+ channels and Transient K+ efflux

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14
Q

Which ion channels are responsible for the plateau phase (Phase 2) of action potentials in the ventricular cells?

A

Mainly Ca2+ influx though voltage gated Ca2+ channels

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15
Q

Which ion channels are responsible for the final falling phase (Phase 3) of action potentials in the ventricular cells?

A

Closure of Ca2+ channels and K+ efflux

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16
Q

Vagal tone of the heart

A

The vagus nerve (parasympathetic supply to the heart) exerts a continuous influence on the SA node under resting conditions (from 100 bpm to 70 bpm)

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17
Q

What effect does vagal stimulation have on the heart?

A

Negative chronotropic: Lowers intrinsic firing in the SA node (decreases slope of pacemaker potential to threshold) and prolongs the ventricular delay/plateau

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18
Q

Which neurotransmitter is responsible for the parasympathetic supply of the heart, and which receptors does it act on?

A

Acetylcholine through M2 receptors

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19
Q

How does atropine increase HR?

A

Acts as a competitive inhibitor of acetylcholine

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20
Q

Which areas does the parasympathetic system supply in the heart?

A

SA node and AV node

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21
Q

Which areas does the sympathetic system supply in the heart?

A

SA node, AV node and myocardium

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22
Q

**What effect does sympathetic stimulation have on the heart?

A

Increases HR (increases the slope of the pacemaker potential), decreases AV nodal delay AND increases the force of contraction

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23
Q

Which neurotransmitter is responsible for the sympathetic supply of the heart, and which receptors does it act on?

A

Noradrenaline acting through β1 adrenoceptors

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24
Q

All or None Law of the Heart

A

Gap junctions form low resistance communication pathways which ensures that each electrical excitation reaches all of the cardiac myocytes

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25
Q

What is the role of the desmosomes in the intercalated discs of the cardiac muscle?

A

Provide mechanical adhesion between adjacent cardiac cells. They ensure that the tension developed by one cell is transmitted to the next

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26
Q

What are the contractile units of the heart?

A

Sarcomeres of the myofibrils

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27
Q

Sliding filament theory

A

Muscle tension is produced by sliding of actin filaments on myosin filaments past each other to generate tension

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28
Q

What roles do ATP play in muscle contraction?

A

Needed for both contraction and relaxation. ATP is needed to energise the myosin head to actually form the cross bridge Also need ATP to help break down the crossbridge

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29
Q

What roles do Ca2+ play in muscle contraction?

A

Required to switch on cross bridge formation. Need it to form the Actin-myosin complex

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30
Q

How do action potentials cause ventricular systole?

A
  • Pacemaker cells of the SA node depolarise, which causes voltage-gated calcium channels to open.
  • Ca2+ moves into sarcoplasm which bind on to ryanodine receptors, this causes another flux of calcium to the sarcoplasm.
  • Ca2+ bind to troponin C, causing conformational change in the troponin-tropomyosin complex, and thus allowing myosin head binding sites on F-Actin to be exposed.
  • This transition allows cross bridge cycling to occur.
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31
Q

According to the sliding filament theory, how does contraction occur?

A
  • ATP binds to myosin head, causing it to change position and move up and out where it can bind to actin forming a cross-bridge.
  • Then when the ATP becomes ADP and unbinds the myosin moves down again causing a power stroke, pulling the filaments past each other.
  • The cross-bridge then dissociates and the cycle repeats
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32
Q

Why is the refractory period important in ventricular contraction?

A

Delay protects the heart from generating tetanic contractions (prolonged contraction)

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33
Q

Stroke volume

A

Volume of blood ejected by each ventricle per heartbeat (End diastolic volume - end systolic volume)

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34
Q

True or False: At rest, the cardiac fibres are at their optimum length for contraction

A

False, they aren’t, because they need room to get greater contraction in exercise etc

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35
Q

What brings around the changes in stroke volume?

A

Diastolic length of myocardial fibres which is determined by the volume of blood within the ventricle at the end of diastole/filling - preload

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36
Q

Preload

A

End diastolic volume - how much we load/stretch the heart with blood before it contracts

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37
Q

What is the main determinant of the preload?

A

Venous return

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38
Q

Starling’s Law

A

The greater the venous return, the greater the stretch and therefore the greater contractility and SV (The volume of blood leaving the ventricles should match the volume entering it)

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39
Q

Length-tension relationship

A

The changes in active tension caused by changes in preload are related to changes in the number of actin and myosin cross bridges formed, which depends on the sarcomere length (when tension (stretch) increases, length increases)

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40
Q

Length-dependent activation of the muscle fibre

A

Stretch also increases the affinity of troponin for Ca2+

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41
Q

Why doesnt cardiac muscle show a decrease in contraction when the stretch becomes too great and there is less overlap for cross bridges, like in skeletal muscle?

A

Because the greater stiffness of cardiac muscle normally prevents its sarcomeres from being stretched beyond its optimal length of 2.2 microns.

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42
Q

After load

A

The resistance into which the heart is pumping, which is imposed after heart contraction

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43
Q

What happens if there is a contuniusly raised after load e.g. hypertension?

A

Ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance

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44
Q

What part of the ANS is responsible for extrinsic control of stroke volume, and through what neurotransmitters?

A

Sympathetic system has a positive inotropic effect via noradrenaline

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45
Q

What effects does the sympathetic system have on the stroke volume?

A

Positive inotropic by increasing the force of contraction (increase peak ventricular pressure via cAMP) and also increases the rate of pressure change and also rate of ventricular relaxation

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46
Q

What is a normal healthy SV and CO?

A

70ml stroke volume and 5 litres a minute for CO

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47
Q

Cardiac cycle

A

Refers to all events that occur from the beginning of one heart beat to the beginning of the next

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48
Q

At a HR of 75 beats/min, what is the duration of ventricular diastole and systole?

A

Diastole = 0.5sec and systole 0.3sec (total duration of cardiac cycle is 0.8s)

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49
Q

What are the 5 events of the cardiac cycle?

A

1) Passive filling
2) Atrial contraction
3) Isovolumetric ventricular contraction
4) Ventricular ejection and repolarisation
5) Isovolumetric ventricular relaxation

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50
Q

What happens during the passive filling stage of cardiac cycle?

A

Pressure in atria and ventricles are close to zero so when AV valves open, blood flows into ventricles down pressure gradient (80% of filling is passive). Pressure in the sort is 80mmHg so aortic valve remains closed

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51
Q

What happens during the atrial contraction stage of cardiac cycle?

A

Atria contact, completing the final 20% of ventricular filling so the EDV of ~130ml

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52
Q

On the ECG, where does atrial depolarisation and then contraction occur?

A

Depolarisation = P wave, atrial contraction occurs between P wave and QRS

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53
Q

What happens during the isovolumetric ventricular contraction stage of cardiac cycle?

A

Ventricular contraction starts after the QRS and pressure rises, when it exceeds atrial pressure the AV valves close (first heart sound) indicating start of systole. The aortic valve is still closed however so the tension rises around a closed volume

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54
Q

What happens during the ventricular ejection stage of cardiac cycle?

A

When the ventricular pressure exceeds aorta/pulmonary artery pressure the aortic/pulmonary semilunar valve open and the stroke volume is ejected, leaving the end systolic volume (~60-70ml)

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55
Q

What happens during the ventricular repolarisation stage of cardiac cycle?

A

The T-wave in the ECG signals ventricular repolarisation. The ventricles relax and the ventricular pressure start to fall. When the ventricular pressure falls below aortic/pulmonary pressure: aortic/pulmonary valves shut - the second heart sound (dub) signalling the start of diastole

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56
Q

What happens during the isovolumetric ventricular relaxation stage of cardiac cycle?

A

Ventricle is again a closed box, as the AV valve is shut so the tension falls around a closed volume “Isovolumetric Relaxation”. When the ventricular pressure falls below atrial pressure, AV valves open, and the heart starts a new cycle

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57
Q

What signals the starts of systole?

A

S1

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58
Q

What signals the starts of diastole?

A

S2

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59
Q

Why doesnt the arterial pressure not fall to zero during diastole?

A

Aorta has a lot of elastic tissue, so when blood is ejected it stretches. Then when it relaxes, it recoils back and keeps driving the blood forward

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60
Q

Blood pressure

A

The outwards (hydrostatic) pressure exerted by the blood on blood vessel walls

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61
Q

What is the normal condition for blood flow throughout most of the circulatory system?

A

Laminar flow - characterized by concentric layers of blood moving in parallel down the length of a blood vessel

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62
Q

True or False: Laminar flow is audible through a stethoscope

A

False, normal blood flow is inaudible

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63
Q

When does blood flow stop in terms of taking BP?

A

When external pressure exceeds systolic pressure

64
Q

When does blood flow become turbulent and audible in terms of taking BP?

A

When the external pressure is between systolic and diastolic pressure

65
Q

When does blood flow become laminar and inaudible in terms of taking BP?

A

When the external pressure is below diastolic

66
Q

Fifth Korotkoff

A

Point at which the sound disappears - where diastolic pressure is recorded

67
Q

Where does the pressure gradient of the mean arterial pressure lie?

A

Between the aorta (start of systemic) and RA (end of pulmonary)

68
Q

Pressure gradient =

A

Mean arterial pressure (MAP) - central venous pressure (RA pressure)

69
Q

Mean arterial pressure

A

The average arterial blood pressure during a single cardiac cycle (including systole and diastole). Normally around 7-105mmHg

70
Q

Mean Arterial Pressure =

A

(2x diastolic pressure + systolic pressure) / 3 OR DBP + 1/3rd pulse pressyre

71
Q

What is the minimum MAP needed to perfuse the coronary arteries, brain, and kidneys?

A

60mmHg (needs to be high enough to perfuse organs but not too high as to cause damage to the blood vessels)

72
Q

What is the relationship of MAP with CO and TPR?

A

Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance

73
Q

Total peripheral resistance

A

Is the sum of resistance of all peripheral vasculature in the systemic circulation

74
Q

Where are the 2 groups of baroreceptors, what do they do and where do they singal?

A

Aortic arch and carotid sinus. They measure blood pressure by degree of stretch and then signal to medulla via CN IX and CN X

75
Q

What is responsible for the sympathetic tone in the heart and where?

A

Sympathetic fibres releasing noradrenaline onto beta-receptors - vasomotor tone. Fibres in the atria SA and AV node, and also in the ventricles

76
Q

What is responsible for the parasympathetic tone in the heart and where?

A

Parasympathetic fibres via acetylcholine. Fibres only in the atria, so can’t affect contractility

77
Q

True or False: Baroreceptors are responsible for blood pressure at all time durations

A

False, only short term

78
Q

What happens when a normal person suddenly stands up from lying down?

A

1) Venous return to the heart decreases due to gravity
2) Mean arterial pressure transiently decreases which reduced firing of baroreceptors
3) Vagal tone to the heart decreases, sympathetic tone increases
4) Sympathetic constrictor tone increases as well as HR and SV, increasing TPR
5) This increases the venous return to the heart

79
Q

What causes postural hypotension?

A

Results from failure of Baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position

80
Q

What happens to baroreceptors if high BP is sustained?

A

Firing decreases and they re-set, only firing again if there is an acute change in MAP

81
Q

True or False: decreased BP causes decreased baroreceptor discharge

A

True

82
Q

What makes up the total body fluid?

A

Intracellular fluid (2/3rd) + Extracellular Fluid (1/3rd)

83
Q

What is extracellular fluid volume and what makes it up?

A

This is the fluid which bathes the cells and acts as the go- between the blood and body cells. Plasma Volume (PV) + Interstitial Fluid Volume (IFV).

84
Q

What are the 2 main factors affecting the ECF?

A

Water excess/deficit and Na+ excess/deficit

85
Q

What happens if the plasma volume falls?

A

Compensatory mechanisms shifts fluid from the interstitial compartment to the plasma compartment (part of the ECF) which would increase CO

86
Q

Which hormones regulate the extracellular fluid volume?

A

• Renin-Angiotensin- Aldosterone System hormones: Renin, Angiotensin and Aldosterone • Atrial Natriuretic Peptide - ANP • Antidiuretic Hormone (Vasopressin) - ADH

87
Q

Describe the RAAS system

A
    1. Renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced by the liver)
    1. Angiotensin I is converted to angiotensin II by Angiotensin converting enzyme - ACE (produced by pulmonary vascular endothelium)
    1. Angiotensin II:
      * stimulates the release of Aldosterone from the adrenal cortex
      * Causes systemic vasoconstriction which increases TPR
      * Also stimulates thirst and ADH release
    1. Aldosterone (a steroid hormone) acts on the kidneys to increase sodium and water retention – increases plasma volume
88
Q

Where is renin released from?

A

Juxtaglomerular apparatus in the kidney

89
Q

What is Anti-diuretic hormone?

A

Peptide hormone derived from a pre-hormone precursor synthesised by the hypothalamus and stored in the posterior pituitary

90
Q

What stimulates the secretion of ADH?

A

Secretion stimulated by (1) reduced extracellular fluid volume or (2) increased extracellular fluid osmolarity (main stimulus)

91
Q

What is the action of ADH?

A

ADH acts in the kidney tubules to increase the reabsorption of water (conserve water) - i.e. causing the production concentrate urine (antidiuresis). This would increase extracellular and plasma volume and hence cardiac output and blood pressure. It also vasoconstrictor blood vessels to increase TPR and BP

92
Q

What is the action of Atrial Natriuretic Peptide (ANP) systemm?

A

Causes excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure. Acts as a vasodilator - decreases blood pressure. Essentially acts as a counter-regulatory mechanism for the RAAS

93
Q

Which systems and hormones promote reabsorption of water?

A

RAAS and ADH

94
Q

Which systems and hormones promote excretion of water?

A

ANP

95
Q

What are the main sites of TPR?

A

Arterioles

96
Q

What is resistance of blood flow proportional to and inversely proportional to?

A

Proportional to blood viscosity and length of blood vessel; and inversely proportional to radius of blood vessel to the power of 4 (meaning a small change in radius has a large effect on resistance): R ∝ η.L/r4

97
Q

Which receptors does adrenaline act on to cause vasoconstriction and vasodilation?

A

Adrenaline acting on α receptors causes vasoconstriction predominant in skin, gut and kidneys , and acting on β receptors in cardiac and skeletal muscles causes vasodilation

98
Q

True or False: Intrinsic control of vascular smooth muscles can over-ride extrinsic control

A

True, they include local chemical and physical factors

99
Q

What are examples of local metabolites that can cause relaxation of arteriolar smooth muscle?

A

• Decreased local PO2 • Increased local PCO2 • Increased local [H+] (decreased pH) • Increased extra-cellular [K+] • Increased osmolality of ECF • Adenosine release (from ATP)

100
Q

What are examples of local humeral agents that can cause relaxation of arteriolar smooth muscle?

A

• Histamine • Bradykinin • Nitric Oxide (NO

101
Q

What are examples of local humeral agents that can cause constriction of arteriolar smooth muscle?

A

• Serotonin • Thromboxane A2 • Leukotrienes • Endothelin

102
Q

What are examples of physical factors that can affect arteriolar smooth muscle?

A

Temperature, myogenic response to stretch and shear stress

103
Q

Which 4 factors influence venous return?

A

1) Increased sympathetic venomotor tone 2) Increased skeletal muscle pump from large veins in between muscles 3) Increased blood volume 4) Increases respiratory pump

104
Q

Metabolic hyperaemia

A

Increase in blood flow that occurs when tissue is active eg. exercise

105
Q

What are some of the chronic CVS responses to regular exercise?

A
  • Reduces BP
  • Reduction in sympathetic tone and noradrenaline levels
  • Increased parasympathetic tone to the heart
  • Cardiac remodelling
  • Reduction in plasma renin levels
  • Improved endothelial function: vasodilators vasoconstrictors
  • Arterial stiffening
106
Q

Shock

A

An abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

107
Q

What is the pathway of shock to cellular failure?

A

1) Shock
2) Inadequate tissue perfusion
3) Inadequate tissue oxygenation
4) Anaerobic metabolism
5) Accumulation of metabolic waste products
6) Cellular failure

108
Q

What is the pathway of hypovolaemic shock to inadequate tissue perfusion?

A

1) Loss of blood volume
2) Decreased venous return
3) Decreased EDV
4) Decreased SV
5) Decreases CO and BP
6) Inadequate tissue perfusion

109
Q

Cariogenic shock

A

Sustained hypotension caused by decreased cardiac contractility

110
Q

What is the pathway of caridogenic shock to inadequate tissue perfusion?

A

1) Decreased cardiac contractility
2) Decreased SV
3) Decreased CO and BP
4) Inadequate tissue perfusion

111
Q

Obstructive shock

A

Occurs with tension pneumothorax, the intrathroacic pressure/transmural pressure is important for lung inflation, but also the venous return as the negative pressure gradient is needed to draw blood from the rest of the body into the venous system in the RA of the heart, since the MAP is generally low in the venous system

112
Q

What is the pathway of obstructive shock to inadequate tissue perfusion?

A

1) Increased intrathoracic pressure
2) Decreased venous return and EDV
3) Decreased SV, CO and BP
4) Inadequate tissue perfusion

113
Q

Neurogenic shock

A

Occurs with damage to spinal cord

114
Q

What is the pathway of neurogenic shock to inadequate tissue perfusion?

A

1) Loss of sympathetic tone
2) Massive venous and arterial vasodilation
3) Decreased venous retune and TPR
4) Decreased CO and BP
5) Inadequate tissue perfusion

115
Q

Vasoactive shock

A

Septic shock - which is a body-wide inflammatory response to infection, leads to dangerously low blood pressure

116
Q

What is the pathway of vasoactive shock to inadequate tissue perfusion?

A

1) Release of vasoactive mediators
2) Massive venous and arterial vasodilation and capillary permeability
3) Decreased venous return and TPR
4) Decreased CO and BP
5) Inadequate tissue perfusion

117
Q

What is the management of shock?

A
  • 1) ABCDE
  • 2) High flow oxygen
  • 3) Specific management:
    • Volume replacement if hypovolaemic
    • Inotropes for cariogenic
    • Chest drain for tension pneumo
    • Adrenaline for anaphylactic
    • Vasopressors for septic shock
118
Q

Up until what proportion of blood volume loss, can compensatory mechanisms maintain blood pressure?

A

>30%

119
Q

What are the signs of hypovolaemic shock?

A

Tachycardia, higher resp rate and decrease in BP and pulse pressure

120
Q

Pulse pressure

A

Difference between systolic and diastolic pressure (usually around 40mmHg)

121
Q

What are 3 main special adaptation of coronary circulations?

A

High capillary density, high basal blood flow and high oxygen extraction

122
Q

What intrinsic mechanisms act on coronary blood flow?

A

↓ Po2, metabolic hyperaemia and adenosine (product of breakdown from ATP) are all potent vasodilators

123
Q

Why is left coronary blood flow almost 0 during isovolumetric ventricular contractions?

A

Because the muscle constricts the arteries (doesn’t affect right coronary flow)

124
Q

Auto regulation of cerebral blood flow

A

Guards against changes in cerebral blood flow if mean arterial blood pressure changes within a range (~ 60 - 160mmHg)

125
Q

True or False: ↑ PCO2 causes cerebral vasoconstriction

A

False, increased PCO2 causes vasodilation

126
Q

Cerebral Perfusion Pressure =

A

Mean Arterial Pressure (MAP) - ICP

127
Q

What is special about the pulmonary circulation?

A
  • Dual supply from RA and also bronchial circulation.
  • Pulmonary capillary pressure is low (~ 8-11 mmHg) compared to systemic capillary pressure (~ 17-25 mmHg)
  • Absorptive forces exceed filtration forces - protects against pulmonary oedema
  • Hypoxia causes vasoconstriction of pulmonary arterioles.
    • Completely opposite to effect of hypoxia on systemic arterioles, to help divert blood from poorly ventilated areas of lung to well ventilated ones.
128
Q

Net filtration pressure (NFP) is proportional to..

A

Forces favouring filtration - forces opposing filtration

129
Q

Filtration co-efficient (Kf)

A

How permeable the capillaries are

130
Q

Which forces favour filtration (movement of fluid out of capillaries)?

A

Pc - capillary hydrostatic pressure

πi - Interstitial fluid osmotic pressure

131
Q

Which forces oppose filtration (movement of fluid into capillaries)?

A

πc - Capillary osmotic pressure

Pi - Interstitial fluid hydrostatic pressure

132
Q

True or False: Starling forces favour filtration at arteriolar end, reabsorption at venular end

A

True

133
Q

Oedema

A

Accumulation of fluid in interstitial space

134
Q

Why does pulmonary oedema cause breathlessness?

A

Diffusion distance increases as it has to pass through the fluid, so gas exchange is compromised. Compliance is also reduced as the fluid means that it is harder to stretch.

135
Q

What are the causes of oedema?

A

1) Raised capillary pressure (from arterial dilation or raised venous pressure)
2) Reduced plasma osmotic pressure
3) Lymphatic insufficiency
4) Changes in capillary permeability

136
Q

What causes pulmonary oedema in LHF?

A

Increased distribution of blood into the pulmonary circulation due to increased hydrostatic pressure, backing up from the systemic circulation

137
Q

What are the normal ranges for blood pressure?

A

108-132/75-83 mmHg

138
Q

What are the normal values for total cholesterol?

A

5 mmol/L or less

139
Q

What are the normal values for HDL cholesterol?

A

4 mmol/L or less

140
Q

What are the normal values for blood glucose?

A

4.0-5.9 mmol/L before a meal and under 7.8 mmol/L after

141
Q

What does a molar rash indicate?

A

Mitral stenosis

142
Q

What angle should a patient be sitting at for a precordial and chest exam?

A

45 degrees

143
Q

What do parasternal heaves indicate?

A

Right ventricular hypertrophy

144
Q

What grade of murmur is palpable?

A

Grade 4

145
Q

Which murmur radiates to the carotids?

A

Aortic stenosis

146
Q

Which murmur radiates to the axilla?

A

Mitral regurgitation

147
Q

What is a normal BMI range?

A

18-25 kg2/m

148
Q

Why is smoking a risk factor for heart disease?

A
  • Damages the lining of your arteries, leading to atherosclerosis.
  • The carbon monoxide in tobacco smoke reduces the amount of oxygen in your blood - meaning your heart has to pump harder to meet body’s oxygen demand
  • The nicotine in cigarettes stimulates your body to produce adrenaline, which makes your heart beat faster and raises your blood pressure, making your heart work harder.
  • Your blood is more likely to clot, increases the risk of having a heart attack or stroke.
149
Q

What are the branches of the left coronary arteries?

A

LAD and circumflex

150
Q

What are the branches of the right coronary arteries?

A

Posterior and marginal branches

151
Q

What are the vessels that supply the tunica adventitia of the vessels?

A

Vaso vasorum

152
Q

What system is used to grade murmurs?

A

Levine’s scale

153
Q

Where do you place the chest leads for an ECG?

A
  • V1 – 4th intercostal space – right sternal edge
  • V2 – 4th intercostal space – left sternal edge
  • V4 – 5th intercostal space – mid clavicular line
  • V3 – midway between V2 & V4
  • V5 – anterior axillary line – same horizontal level as V4
  • V6 – mid-axillary – same horizontal level as V4
154
Q

Where do you place the limb leads for an ECG?

A
  • RED – Right arm – ulnar styloid process at the wrist
  • YELLOW – Left arm – ulnar styloid process at the wrist
  • GREEN – Left leg – at the ankle – medial / lateral malleolus
  • BLACK – Right leg – at the ankle – medial / lateral malleolus

“Ride Your Green Bike”

155
Q
A

RW Cardiovascular (14 decks)

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