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Phoebe's Cardio > Physiology > Flashcards

Physiology Flashcards

1
Q

Autorhythmicity

A

Hearts ability to beat rhythmically without a stimuli

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2
Q

Which node initiates heart beat

A

SA

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3
Q

Where is the SA node located

A

Upper right atrium, where SVC enters

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4
Q

Sinus rhythm

A

Heart controlled by SA node

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5
Q

How does cardiac excitation originate?

A
  1. SA node generates regular spontaneous pacemaker potentials
  2. Reaches threshold
  3. Action potential generated
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6
Q

Pacemaker potential

A

Due to:
Decrease in K+ efflux
Na and K + influx
Transient Ca ++ influx

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7
Q

Rising phase of action potential

A

Caused by:
Activation of long lasting Ca++ channels
Ca++ influx

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8
Q

Falling phase of depolarisation

A

Caused by:
Inactivation of Ca++ channels
Activation of K+ channels
K+ Efflux

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9
Q

How does cardiac excitation spread throughout the heart?

A
  1. SA node
  2. Passes to AV node by cell to cell conduction
  3. AV node allows delay to ensure atria are empty
  4. Passes down Bundle of His
  5. Into Purkinje Fibres
  6. Causes ventricles to contract
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10
Q

Only point of electrical contact between atria and ventricles

A

AV node

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11
Q

Where is the AV node

A

Vase of right atrium, at junction between atrium and vesicles

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12
Q

Phase 0

A

Fast Na+ influx

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13
Q

Phase 1

A

Closure of Na+ channels

Transient K+ efflux

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14
Q

Phase 2

A

Mainly Ca++ influx

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15
Q

Phase 3

A

Ca++ channels close

K+ efflux

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16
Q

Phase 4

A

Resting membrane potential

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17
Q

Ca++ influx stimulates

A

Systole

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18
Q

Bradycardia

A

HR <60

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19
Q

Tachycardia

A

HR >100

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20
Q

Neurotransmitter for heart

A

Acetylcholine acting through M2 receptors

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21
Q

Inhibitor for acetylcholine

A

Atropine - used in bradycardia to speed up heart

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22
Q

Stroke volume

A

Volume of blood ejected by each ventricle per heart beat

End diastolic - end systolic

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23
Q

Frank-Starling Law

A

The more the ventricle is filled with blood during diastole, the greater the volume of ejected blood will be during the resulting contraction

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24
Q

Starling law leads to increased …

A

SV in to the aorta

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25
Q

Afterload

A

Resistance to which the heart is pumping

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26
Q

Extra load

A

Load imposed after heart has contracted

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27
Q

Afterload increases

A

Heart unable to eject full SV
EDV decreased
Forced contraction due to Frank Starling mechanism

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28
Q

extrinsic neurotransmitter of stroke control

A

Noradrenaline
Increases force of contraction
Inotropic effect
Reduces duration of systole and diastole

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29
Q

Sympathetic nerve stimulation effect on Frank Starling Curve

A

Shift to left

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30
Q

Effect of parasympathetic nerves on ventricular contraction

A

Little innervation by vagus, little effect on SVC

Vagal stimulation influences rate not contraction here

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31
Q

Diastole

A

Heart ventricles relax and fill with blood

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32
Q

Systole

A

Heart ventricles contract and pump blood into aorta and pulmonary artery

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33
Q

Steps during cardiac cycle

A
  1. Passive filling
  2. Atrial contraction
  3. Isovolumetric ventricular contraction
    4 Ventricular ejection
  4. Isovolumetric ventricular relaxation
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34
Q

First heart sound (lub) caused by

A

shutting of AV valves (mitral and tricuspid) due to higher ventricular pressure than atrial
Systole begins

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35
Q

Second heart sound (dub) caused by

A

Pulmonary and aortic valves shutting as ventricle pressure lower than aortic/pulmonary
Diastole begins

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36
Q

Kortokoff sounds

A

Cuff placed > diastolic pressure and < systolic pressure

NO SOUND HEARD

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37
Q

Begin to release cuff

A

First sound heard

Systolic pressure

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38
Q

Release cuff until

A

Last sound heard
Diastolic pressure
5th Kortokoff sound

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39
Q

MAP

A

Diastolic + 1/3(systolic-diastolic)

= Diastolic + 1/3 Pulse pressure

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40
Q

Normal range of MAP

A

70-105

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41
Q

MAP needed to perfuse brain, kidneys etc

A

60

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42
Q

Baroreceptors preventing postural hypertension

A
  1. Person stands
  2. Venous return to heart decreases due to gravity
  3. MAP decreases
  4. Reduces firing rate in baroreceptors
  5. Vagal tone decreases, sympathetic tone increases
  6. Heart rate and stoke volume increase
  7. Systemic vascular resistance increases
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43
Q

Extracellular fluid

A

Plama volume + interstitial fluid volume

44
Q

If plasma volume falls

A

fluid shifts from interstitial compartment to plasma compartment

45
Q

2 Factors affecting extracellular fluid volume

A

Water excess or deficit

Na+ excess of deficit

46
Q

Hormones that regulate extracellular fluid volume

A

RAAS
NP’s
ADH

47
Q

Renin-Angiotensin-Aldosterone-System

A
  1. Renin released from kidneys, stimulating formation of Angiotensin 1 in blood from angiotensinogen
  2. Angiotensin 1 is converted to Angiotension 2 by angiotensin converting enzymes (ACE)
  3. Angiontensin 2 stimulates release of aldosterone
  4. Causes vasoconstriction
  5. Increases SVR
  6. Stimulates thirst and ADH release
  7. Aldosterone acts on kidneys to increase Na+ and H20 retention
  8. Increasing plasma volume and BP
48
Q

Where is aldosterone released from

A

Adrenal cortex

49
Q

Where is angiotensiongen produced

50
Q

Rate limiting step for RAAS

A

Renin secretion

51
Q

Renin secretion can be affected by

A

Renal artery hypotension
Stimulation of renal sympathetic nerves
Decreased Na+ in renal tubular fluid

52
Q

Natrieuretic Peptides

A

Peptide hormones synthesised by heart
Released in response to cardiac distension
Cause excretion of salt and water in kidneys, reducing blood volume and pressure

53
Q

Decrease renin release

A

Decrease BP

54
Q

Atrial Natriuretic Peptide

A

28 amino acid peptide synthesised and stored in atrial muscle cells
Released in response to cardiac distension

55
Q

Brain-type Natriuretic Peptide

A

32 amino acid peptide synthesised by heart ventricles, and brain

56
Q

where is ADH synthesised

A

hypothalamus

57
Q

where is ADH stored

A

posterior pituitary

58
Q

ADH release is stimulated by

A

increased plasma osmolality

59
Q

ADH

A

Increases reabsorption of water
Increase extracellular volume
Increase cardiac output and BP
Causes vasoconstriction

60
Q

Counter regulator to RAAS

61
Q

Resistance to blood flow is directly proportional to

A

Blood viscosity and length of blood vessel

62
Q

Resistance to blood flow is inversely proportional to

A

radius of blood vessel to the power of 4

63
Q

Adrenaline acting on alpha receptors causes

A

vasoconstriction

64
Q

Adrenaline acting on beta 2 receptors causes

A

vasodilatation

65
Q

Alpha receptors are present in

A

skin, gut, kidney arterioles

66
Q

Beta 2 receptors are present in

A

cardiac and skeletal muscle

67
Q

Angiotensin 2 causes

A

vasoconstriction

68
Q

Factors causing vasodilation

A 
Decreased pO2
Increased pCO2
Increased H+
Increased K+
Adenosine release
69
Q

Humoral agents causing vasodilatation

A

Histamine
Bradykinin
NO

70
Q

NO

A

Released due to release of Ca+ or chemical stimuli

Activates formation of cGMP

71
Q

cGMP

A

Secondary messenger for smooth muscle relaxation

72
Q

Humoral agents that cause vasoconstriction

A

Seratonin
Thromboxane A2
Leukotrines
Endothelin

73
Q

Increased venomotor tone

A

increases venous return, SV, MAP

74
Q

Increasing rate of breathing

A

increases venous return

75
Q

muscle activity increases

A

venous return to heart

76
Q

Acute CVS response to exercise

A
  1. Sympathetic nerve activity increases
  2. HR and SVR increases
  3. Sympathetic vasomotor nerves reduce flow to kidneys and gut (vasoconstriction)
  4. Blood flow to skeletal and cardiac muscles increase
  5. BP increase
77
Q

Effect of sympathetic stimulation on the heart

A

Increases rate by increasing firing rate of SA node
Decreases AV node delay
Increases force of contraction

78
Q

Shock

A

Abnormality of circulatory system resulting in inadequate tissue perfusion and oxygenation

79
Q

Stages in shock

A
  1. Shock
  2. Inadequate tissue perfusion
  3. Inadequate tissue oxidation
  4. Anaerobic metabolism
  5. Accumulation of metabolic waste products
  6. Cellular failure
80
Q

Hypovolaemic Shock cause by

A

Loss of blood

81
Q

Steps to hypovolaemic shock

A
  1. Loss of blood
  2. Decreased blood volume
  3. Deceased venous return
  4. Decreased end diastolic volume
  5. Decreased stroke volume
  6. Decreased CO and BP
  7. Inadequate tissue perfusion
82
Q

Cardiogenic shock is caused by

A

Decreased cardiac contractility

83
Q

Steps to cardiogenic shock

A
  1. Decreased cardiac contractility
  2. Decreased stroke volume
  3. Decreased CO and BP
  4. Inadequate tissue perfusion
84
Q

Causes of obstructive shock

A

Tension Pneumothorax

85
Q

Steps to obstructive shock

A
  1. Increased intrathoracic pressure
  2. Decreased venous return
  3. Decreased end diastolic volume
  4. Decreased stroke volume
  5. Decreased CO and BP
  6. Inadequate tissue perfusion
86
Q

Causes of neurogenic shock

A

Loss of sympathetic tone to blood vessels and heart

87
Q

Steps to neurogenic shock

A
  1. Loss of sympathetic tone to blood vessels and heart
  2. Massive venous and atrial dilation
  3. Decreased venous return
  4. Decreased SVR
  5. Decreased heart rate (UNLIKE OTHER SHOCKS)
  6. Decreased CO and BP
  7. Inadequate tissue perfusion
88
Q

Causes of vasoactive shock

A

Release of vasoactive mediators

89
Q

Steps to vasoactive shock

A
  1. Release of vasoactive mediators
  2. Massive venous and arterial dilation and increased capillary permeability
  3. Decreased venous return and decreased SVR
  4. Decreased CO and BP
  5. Inadequate tissue perfusion
90
Q

Treatment of shock

A 
ABCDE
High flow oxygen
Inatropes of cardio shock
Adrenaline in anaphylactic shock
Vasopressors in septic shock
91
Q

Elevated LDL and decreased HDL are associated with

A

Cardiovascular disase

92
Q

Lipoproteins

A

Microscopic spherical particle
Hydrophobic core
Hydrophilic coat with apoproteins

93
Q

Apoproteins

A

Recognised by receptors in liver and other tissues allowing lipoproteins to bind to cells

94
Q

4 classes of lipoproteins

A

HDL
LDL
VLDL
Chylomicrons

95
Q

Examples of HDL

A

apoA1, apoA2

96
Q

Examples of LDL

97
Q

Examples of VLDL

98
Q

Examples of chylomicrons

99
Q

ApoB containing lipoproteins

A

Deliver TAG’s to muscle for ATP biogenesis and adipocytes for storage

100
Q

Chylomicrons

A

Formed in intestinal cells
Transport dietary triglycerides
Exogenous pathway

101
Q

VLDL

A

Formed in liver cells
Transport TAG’s
Endogenous pathway

102
Q

Life cycle of ApoB

A

Assembly
Intravascular metabolism
Receptor mediated clearance

103
Q

Why is LDL bad cholesterol?

A

Causes atherosclerosis

104
Q

Why is HDL good cholesterol?

A

Removes excess cholesterol from cells by transporting it in plasma to liver so they can be eliminated

105
Q

Starling forces

A

favour filtration at arteriolar end, reabsorption at venular end

Phoebe's Cardio (22 decks)

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