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The cardiovascular system > Physiology > Flashcards

Physiology Flashcards

1
Q

Where in the heart does excitation normally originate?

A

pacemaker cells in the SA node

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2
Q

Where is the SA node located?

A

In the upper right atrium close to where the superior vena cava enters the right atrium

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3
Q

A heart controlled by the SA node is said to be in ….?

A

Sinus Rhythm

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4
Q

Cells in the SA node have a stable resting potential T/F?

A

False

they have no resting potential

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5
Q

How does cardiac excitation normally originate?

A
  • cells in the SA node generate regular spontaneous pacemaker potentials
  • which takes the membrane potential to a threshold
  • over time the threshold is reached and an AP is generated
  • resulting in the generation of regular spontaneous APs
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6
Q

What causes the pacemaker potential?

A
  • Decrease in K+ efflux
  • NA+ influx (funny current)
  • transient Ca++ influx
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7
Q

What happens to the pacemaker AP when the threshold is reached?

A
  • depolarisation
  • caused by the activation of long lasting (L-type Ca++ channels)
  • which results in Ca++ influx
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8
Q

What causes the depolarisation phase of the pacemaker AP?

A
  • inactivation of L-type Ca++ channels

- activation of K+ channels resulting in K+ efflux

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9
Q

How does cardiac excitation spread across the heart?

A
  • cell to cell current flow via gap junctions
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10
Q

Where is the AV node located?

A

At the base of the right atrium; just above the auction of the atria and ventricles

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11
Q

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

A

The AV node

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12
Q

Describe the characteristics of AV node cells

A
  • small in diameter

- slow conduction velocity

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13
Q

Why is conduction to the AV node delayed?

A
  • allows atrial systole to precede ventricular systole
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14
Q

How is excitation spread to the ventricles?

A
  • through the bundle of His and the network of purkinje fibres
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15
Q

What is the resting membrane potential of atrial and ventricular myocytes?

A
  • 90 mV
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16
Q

What happens in phase 0 of a myocyte AP

A
  • fast NA+ influx

- leading to depolarisation (+20mV)

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17
Q

What happens in phase 1 of the myocyte AP?

A
  • closure of Na+ channels and transient K+ efflux
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18
Q

What happens in phase 2 of the myocyte AP?

A
  • mainly Ca++ influx

- plateau phase

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19
Q

What happens in phase 3 of the myocyte AP?

A
  • closure of Ca++ channels and K+ efflux

- repolarisation

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20
Q

What happens in phase 4 of the myocyte AP?

A

return to resting membrane potential

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21
Q

sympathetic stimulation ……… HR

A

Increases

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22
Q

parasympathetic stimulation ………. HR

A

Decreases

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23
Q

Describe parasympathetic innervation of the heart?

A
  • vagus nerve exerts a continuous influence on the SA node under resting conditions
  • vagal tone dominates under normal resting conditions, slowing HR
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24
Q

What is normal resting HR?

A

60-100 bpm

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25
Q

Parasympathetic stimulation ……. AV node delay

A

increases

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26
Q

What is the NT for the parasympathetic supply of the heart?

A
  • acetylcholine acting through M2 receptors
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27
Q

sympathetic stimulation ….. AV node delay?

A

decreases

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28
Q

Which parts of the heart are supple by cardiac sympathetic nerves?

A
  • SA node
  • AV node
  • myocardium
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29
Q

What is the NT for the sympathetic supply of the heart?

A
  • noradrenaline acting through beta1 adrenoceptors
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30
Q

What does the P wave on an ECG represent?

A

atrial depolarisation

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31
Q

What does the QRS complex on an ECG represent?

A
  • ventricular depolarisation
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32
Q

what does the T wave represent?

A
  • ventricular repolarisation
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33
Q

What does the PR interval represent?

A
  • AV node delay
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34
Q

What does the ST segment represent?

A

ventricular systole

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35
Q

What does the TP interval represent?

A

diastole

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36
Q

What is the role of desmosomes in the heart?

A

provide mechanical adhesion between adjacent cardiac cells

insure that the tension developed by one cell is transmitted to the next

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37
Q

What are myofibrils?

A

contractile units of muscle

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38
Q

Actin is the ….. filament and causes the ….. appearance in myofibrils and fibres

A

thin/light

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39
Q

Myosin is the ….. and causes the ……. appearance

A

thick/dark

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40
Q

how are actin and myosin arranged in each myofibril?

A

into sarcomeres

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41
Q

How is muscle tension produced?

A

by sliding of actin filaments on myosin filaments

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42
Q

force generation is ATP independent T/F?

A

F, it depends upon an ATP dependent interaction between thick an thin filaments

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43
Q

What molecule is required to switch on cross bridge formation?

A

Ca2+ binding to troponin

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44
Q

Where is the Ca2+ released from?

A

The sarcoplasmic reticulum

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45
Q

In cardiac muscle what is the release of Ca2+ dependent on?

A

the presence of extra cellular Ca2+

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46
Q

What happens to the Ca2+ when the AP has passed?

A

the influx ceases and Ca2+ is re-sequestered in SR by Ca2+ ATPase and the heart muscle relaxes

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47
Q

What is the importance of the long cardiac refractory period?

A

prevents tetanic contraction

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48
Q

Why is it not possible to produce another AP during the refractory period of the ventricular AP?

A
  • during the plateau phase the Na+ channels are in a closed state
  • during the descending phase the K+ channels are open and the membrane cannot be depolarised
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49
Q

What is stroke volume and how is it calculated?

A
  • the volume of blood ejected by each ventricle per heart beat
  • SV = end diastolic volume (EDV) - End systolic volume (ESV)
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50
Q

What is the end diastolic volume (EDV)

A

the volume of blood within each ventricle at the end of diastole

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51
Q

how is EDV determined?

A

it is determined by the venous return to the heart

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52
Q

What causes changes in stroke volume?

A

diastolic length/diastolic stretch of muscle fibres

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53
Q

What does starlings law of the heart state?

A

the more the ventricle is filled with blood during diastole (EDV) the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume)

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54
Q

How can the affinity of Ca2+ for troponin be increased?

A

by stretching the muscle

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55
Q

What is after load?

A

the resistance into which the heart is pumping

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56
Q

the ventricular muscle is supplied by ………. nerve fibres and the NT is ……

A

sympathetic/noradrenaline

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57
Q

What is the positive inotropic effect

A

stimulation of sympathetic nerves increases the force of contraction

58
Q

describe the effect of sympathetic stimulation of ventricular contraction?

A
  • force of contraction increases (greater Ca2+ influx)
  • cAMP mediated
  • peak ventricular pressure rises
  • rate of pressure change during systole increases
  • thus reducing the duration of systole
  • rate of ventricular relaxation increases
  • reducing the duration of diastole
59
Q

How does sympathetic nerve stimulation effect the frank starling curve?

A

shifts to the left

60
Q

What is cardiac output, how is it calculated and what is the average for a resting adult ?

A
  • the volume of blood pumped by each ventricle per minute
  • CO = SV x HR
  • 5L per minute
61
Q

What is diastole?

A
  • the heart ventricles are relaxed and filled with blood
62
Q

What is systole?

A
  • the heart ventricles contract and pump blood into the aorta and pulmonary artery
63
Q

What events occur during the cardiac cycle?

A
  1. passive filling
  2. atrial contraction
  3. Isovolumetric ventricular contraction
  4. ventricular ejection
  5. Isovolumetric ventricular relaxation
64
Q

Describe passive filling?

A

AV valves open so venous return flows into ventricles

65
Q

Describe Atrial contraction?

A
  • the P wave in the ECG signals depolarisation and the atria contracts between the P wave ad QRS complex
  • atrial contraction complete the END diastolic volume
66
Q

describe Isovolumetric ventricular contraction

A
  • ventricular pressure rises\
  • when ventricular pressure exceeds atrial pressure the AV valves shut
  • producing first heart sound
  • ventricular pressure rises very steeply
67
Q

describe ventricular ejection?

A

when ventricular pressure exceeds aorta/pulmonary pressure aortic/pulmonary valves open

  • Stroke volume is ejected
  • aortic pressure rises
  • ventricular pressure starts to fall
  • aortic/pulmonary valves close and second heart sound is produced
68
Q

describe isovolumetric ventricular relaxation

A

the tension falls around a closed volume

when the ventricular pressure fallows below atrial pressure the AV valves open and a new cycle begins

69
Q

When do the first and second heart sounds take place?

A

1st: during isovolumetric ventricular contraction
2nd: during ventricular ejection

70
Q

What causes the first heart sound?

A
  • closure of mitral and tricuspid valves
71
Q

What causes the second heart sound?

A

closure of aortic and pulmonary valves

72
Q

The first heart sound signals the beginning of ……… and the second heart sound signals the beginning of ………

A

systole/ diastole

73
Q

What is BP?

A

The outward hydrostatic pressure exerted by the blood on the blood vessel walls

74
Q

what is systolic arterial BP?

A

the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts

75
Q

What is diastolic arterial BP?

A

the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes

76
Q

What is hypertension?

A

clinic BP of 140/90 mmHg or higher

day time average of 135/85 mmHg or higher

77
Q

what is pulse pressure and what is it normally?

A

the difference between systolic and diastolic blood pressures
- normally between 30-50mmHg

78
Q

When does the blood flow in an artery become turbulent?

A

when the pressure exerted on the artery is between systolic and diastolic

79
Q

laminar flow is audible through a stethoscope T/F?

A

false

turbulent flow

80
Q

When is diastolic pressure recorded?

A

at the 5th Korotkoff sound

81
Q

What is the main driver of the flow around the systemic circulation?

A
  • a pressure gradient between the aorta and the right atrium
  • pressure gradient = MAP - central venous pressure (CVP)
82
Q

What is MAP and how is it calculated?

A
  • The average arterial BP during a single cardiac cycle which involves contraction and relaxation of the heart
  • ((2xdiastolic) + systolic)/3
  • normally between 70-105 mmHg
  • MAP = SV x HR x SVR
83
Q

What is cardiac output and how is it calculated?

A
  • the volume of blood pumped by each ventricle of the heart per minute
  • CO = SV x HR
84
Q

What are the major resistance vessels?

A

the arterioles

85
Q

Where are the baroreceptors mainly found?

A

in the aortic arch and the bifurcation of the carotid artery

86
Q

What is postural hypotension?

A

The failure of baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position

87
Q

How is postural hypotension indicated?

A
  • positive result indicted by a drop within 3 minutes of standing from lying position
  • systolic drop of at least 20mmHg
  • diastolic drop of at least 0 mmHg
88
Q

What are the 2 main factors that affect extracellular fluid volume

A
  1. water excess or deficit

2. Na+ excess or deficit

89
Q

What are the hormones that regulate extracellular fluid volume?

A
  1. The Renin-Angiotensin Aldosterone system RAAS
  2. Natriuretic peptides
  3. Antidiuretic Hormone ADH
90
Q

Describe the Renin Angiotensin aldosterone system

A
  • renin is released from kidneys and stimulates formation of angiotensin I in the blood from angiotensinogen
  • Angiotensin I is converted to angiotensin II by angiotensin converting enzyme ACE
  • angiotensin II stimulates the release of aldosterone from the adrenal cortex - causes systemic vasoconstriction
  • aldosterone acts on the kidneys to increases sodium and water retention - increasing plasma vol
91
Q

What causes renin to be released from the juxtaglomerular apparatus in the kidneys?

A
  1. renal artery hypotension (caused by systemic hypotension)
  2. stimulation of renal sympathetic nerves
  3. decreased Na+ in renal tubular fluid - sensed by macula dense
92
Q

What are natriuretic peptides and how do they work?

A
  • peptide hormones synthesised by the heart
  • released in response to cardiac distension or neurohormonal stimuli
  • cause exertion of salt and water - reducing blood vol and BP
  • decrease renin release
  • act as vasodilators
93
Q

Describe atrial natriuretic peptide?

A
  • 28 amino acid synthesised and stored by atrial muscle cells
  • released in response to atrial distension
94
Q

describe brain type natriuretic peptide?

A
  • 32 amino acid peptide synthesised by heart ventricles and brain
  • can be measured in patients with suspected HF
95
Q

How is BNP formed?

A
  • ## first synthesised as prepro-BNP which is then cleaved to pro-BNP
96
Q

Describe ADH?

A
  • synthesised by the hypothalamus and stored in the posterior pituitary
97
Q

What is secretion of ADH stimulated by?

A
  1. reduced extracellular fluid volume

2. increased extracellular osmolarity (main stimulus)

98
Q

What does ADH do?

A
  • acts in the kidney tubules to increase the reabsorbtion of water
  • increases extracellular and plasma volume and hence cardiac output and BP
  • causes vasoconstriction - increases BP
99
Q

resistance to blood flow is directly proportional to …….. and ………… It is inversely proportional to …………

A

blood viscosity
length of blood vessel
radius of blood vessel

100
Q

The vascular smooth muscles are supplied by …….. nerve fibres. The NT is ……. acting on …….. receptors

A

sympathetic
noradrenaline
alpha

101
Q

What is the vasomotor tone and what causes it?

A

The vascular smooth muscles are partially constricted at rest.
It is caused by tonic discharge of sympathetic nerves and continuous release of noradrenaline

102
Q

increased …….. discharge will ………. vasomotor tone leading to …………

A

sympathetic
increased
vasoconstriction

103
Q

adrenaline acting on alpha receptors causes vasoconstriction T/F

A

True

adrenaline acting on B2 receptors causes vasodilation

104
Q

Where are alpha receptors mainly found?

A

in the skin, gut and kidney arterioles

105
Q

Where are B2 receptors mainly found?

A

cardiac and skeletal muscle arterioles

106
Q

name 2 hormones other than adrenaline that cause vasoconstriction?

A 
angiotensin II 
antidiuretic hormone (ADH)
107
Q

describe some factors that cause relaxation of arteriolar smooth muscle resulting in vasodilation and metabolic hyperaemia?

A
  • decreased local PO2
  • increased local PCO2
  • increased local [H+]
  • increased extracellular [K+] (decreased pH)
  • increased osmolarity
  • adenosine release
108
Q

name some humoral agents which result in vasodilation?

A
  • histamine
  • bradykinin
  • nitric Oxide
109
Q

How is NO produced?

A
  • continuously produced by vascular epithelium from the amino acid L-arginine through enzymatic action of NOS
110
Q

How does NO cause smooth muscle relaxation?

A

diffuses from the vascular endothelium into adjacent smooth muscle cells where it activates the formation of cGMP that serves as a 2nd messenger for smooth muscle relaxation

111
Q

Give examples of humeral agents that cause vasoconstriction?

A

serotonin
thromboxane A
Leukotrienes
endothelin

112
Q

give examples of physical things that cause vasoconstriction?

A
  • cold temperatures

- myogenic response to stretch (MAP increases)

113
Q

give examples of physical things that cause vasodilation

A
  • warm temperatures
  • myogenic response to stretch (MAP falls)
  • sheer stress
114
Q

What are the factors that influence venous return to the heart?

A
  • increased venomotor tone
  • increased skeletal muscle ‘pump’
  • increased blood volume
  • increased respiratory ‘pump’
  • increased atrial pressure
115
Q

What does increased venomotor tone cause?

A

increased venous return, stroke volume and MAP

116
Q

How can the respiratory pump be used to increase venous return?

A

By increased rate and depth of breathing

117
Q

how can the skeletal muscle pump be used to increase venous return?

A

By increasing muscle activity

118
Q

What is shock?

A

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

119
Q

adequate tissue perfusion depends on ……………. and ……………….?

A

adequate BP and adequate CO

120
Q

Describe the mechanism of hypovolaemic shock?

A

loss of blood vol > decreased blood vol > decreased venous return > decreased EDV > decreased SV > decreased CO and BP > inadequate tissue perfusion

121
Q

What is cariogenic shock?

A

sustained hypotension causes by decreased cardiac contractility

122
Q

describe the mechanism of cariogenic shock?

A

decreased cardiac contractility > decreased SV > decreased CO and BP > inadequate tissue perfusion

123
Q

Give an example of something that may cause obstructive shock?

A

tension pneumothorax

124
Q

describe the mechanism of obstructive shock?

A

inc intrathoracic pressure > dec venous return > dec EDV > dec SV > dec CO and BP > dec tissue perfusion

125
Q

describe the mechanism of neurogenic shock?

A

loss of sympathetic tone to blood vessels and heart > massive venous + arterial vasodilation - effect on HR > dec venous return and SVR, dec HR > dec CO and BP > inadequate tissue perfusion

126
Q

What causes neurogenic shock

A

injury to the spinal cord

127
Q

Describe vasoactive shock?

A

release of vasoactive mediators > massive venous and arterial vasodilation - inc capillary permeability > dec venous return and SVR > dec CO and BP > inadequate tissue perfusion

128
Q

outline the treatment of shock?

A
  • ABCDE
  • high flow oxygen
  • vol replacement (not cardiogenic)
  • immediate chest drain for pneumothorax
  • adrenaline for anaphylactic shock
  • vasopressors for septic shock
  • treat cause
129
Q

Why would volume replacement not be appropriate in cardiogenic shock?

A
  • the heart muscle is damaged therefore increasing blood volume will make the heart work harder and cause further damage
130
Q

other than haemorrhage what else can cause hypovolaemic shock?

A
  • vomiting
  • diarrhoea
  • excessive sweating
131
Q

compensatory mechanisms can maintain BP until ….. is lost

A

> 30%

132
Q

Define transient loss of consciousness

A

A state of real or apparent loss of consciousness with loss of awareness, characterised by amnesia for the period of unconsciousness, loss of motor control, loss of responsiveness and a short duration

133
Q

name some of conditions that can result in TLOC?

A
  • head trauma
  • syncope
  • epileptic seizures
  • TLOC mimics
  • other causes
134
Q

define syncope?

A

transient loss of consciousness due to cerebral hypoperfusion, characterised by rapid onset, short duration and spontaneous complete recovery

135
Q

Describe a reflex syncope?

A
  • all syncopes in which neural reflects modify heart rate and or vascular tone hence predisposing to a fall in MAP of sufficient severity to affect cerebral perfusion causing a transient period of cerebral hypo perfusion resulting in syncope or near syncope
136
Q

Describe the vasovagal reflex syncope?

A
  • most common type of syncope
  • faint triggered by emotional distress
  • associated with a typical prodrome
  • main risk is injury when falling
  • treatment: education, reassurance, avoidance of triggers, adequate hydration
137
Q

describe the situational reflex syncope?

A
  • faint during or immediately after a specific trigger eh cough, micturition
  • treat the cause
138
Q

describe the carotid sinus reflex syncope?

A
  • triggered by mechanical manipulation of the neck, shaving, tight collar
  • more common in elderly especially males
  • may occur after head and neck surgery or radiation
139
Q

Describe the cardiac syncope?

A
  • caused by a cardiac event resulting in sudden drop in CO

- can be caused by: arrhythmias, acute MI, structural cardiac disease, other cardio disease

140
Q

describe the features that suggest a cardiac syncope/

A
  • during exertion or when supine
  • presence of structural cardiac abnormality or coronary heart disease
  • family history of sudden death at young age
  • sudden onset palpitations followed by syncope
  • findings on ECG suggestive of arrhythmic syncope

The cardiovascular system (6 decks)

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