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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
Afterload
Resistance to which the heart is pumping
26
Extra load
Load imposed after heart has contracted
27
Afterload increases
Heart unable to eject full SV EDV decreased Forced contraction due to Frank Starling mechanism
28
extrinsic neurotransmitter of stroke control
Noradrenaline Increases force of contraction Inotropic effect Reduces duration of systole and diastole
29
Sympathetic nerve stimulation effect on Frank Starling Curve
Shift to left
30
Effect of parasympathetic nerves on ventricular contraction
Little innervation by vagus, little effect on SVC | Vagal stimulation influences rate not contraction here
31
Diastole
Heart ventricles relax and fill with blood
32
Systole
Heart ventricles contract and pump blood into aorta and pulmonary artery
33
Steps during cardiac cycle
1. Passive filling 2. Atrial contraction 3. Isovolumetric ventricular contraction 4 Ventricular ejection 5. Isovolumetric ventricular relaxation
34
First heart sound (lub) caused by
shutting of AV valves (mitral and tricuspid) due to higher ventricular pressure than atrial Systole begins
35
Second heart sound (dub) caused by
Pulmonary and aortic valves shutting as ventricle pressure lower than aortic/pulmonary Diastole begins
36
Kortokoff sounds
Cuff placed > diastolic pressure and < systolic pressure | NO SOUND HEARD
37
Begin to release cuff
First sound heard | Systolic pressure
38
Release cuff until
Last sound heard Diastolic pressure 5th Kortokoff sound
39
MAP
Diastolic + 1/3(systolic-diastolic) | = Diastolic + 1/3 Pulse pressure
40
Normal range of MAP
70-105
41
MAP needed to perfuse brain, kidneys etc
60
42
Baroreceptors preventing postural hypertension
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
43
Extracellular fluid
Plama volume + interstitial fluid volume
44
If plasma volume falls
fluid shifts from interstitial compartment to plasma compartment
45
2 Factors affecting extracellular fluid volume
Water excess or deficit | Na+ excess of deficit
46
Hormones that regulate extracellular fluid volume
RAAS NP's ADH
47
Renin-Angiotensin-Aldosterone-System
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
Where is aldosterone released from
Adrenal cortex
49
Where is angiotensiongen produced
Liver
50
Rate limiting step for RAAS
Renin secretion
51
Renin secretion can be affected by
Renal artery hypotension Stimulation of renal sympathetic nerves Decreased Na+ in renal tubular fluid
52
Natrieuretic Peptides
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
Decrease renin release
Decrease BP
54
Atrial Natriuretic Peptide
28 amino acid peptide synthesised and stored in atrial muscle cells Released in response to cardiac distension
55
Brain-type Natriuretic Peptide
32 amino acid peptide synthesised by heart ventricles, and brain
56
where is ADH synthesised
hypothalamus
57
where is ADH stored
posterior pituitary
58
ADH release is stimulated by
increased plasma osmolality
59
ADH
Increases reabsorption of water Increase extracellular volume Increase cardiac output and BP Causes vasoconstriction
60
Counter regulator to RAAS
NP's
61
Resistance to blood flow is directly proportional to
Blood viscosity and length of blood vessel
62
Resistance to blood flow is inversely proportional to
radius of blood vessel to the power of 4
63
Adrenaline acting on alpha receptors causes
vasoconstriction
64
Adrenaline acting on beta 2 receptors causes
vasodilatation
65
Alpha receptors are present in
skin, gut, kidney arterioles
66
Beta 2 receptors are present in
cardiac and skeletal muscle
67
Angiotensin 2 causes
vasoconstriction
68
Factors causing vasodilation
``` Decreased pO2 Increased pCO2 Increased H+ Increased K+ Adenosine release ```
69
Humoral agents causing vasodilatation
Histamine Bradykinin NO
70
NO
Released due to release of Ca+ or chemical stimuli | Activates formation of cGMP
71
cGMP
Secondary messenger for smooth muscle relaxation
72
Humoral agents that cause vasoconstriction
Seratonin Thromboxane A2 Leukotrines Endothelin
73
Increased venomotor tone
increases venous return, SV, MAP
74
Increasing rate of breathing
increases venous return
75
muscle activity increases
venous return to heart
76
Acute CVS response to exercise
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
Effect of sympathetic stimulation on the heart
Increases rate by increasing firing rate of SA node Decreases AV node delay Increases force of contraction
78
Shock
Abnormality of circulatory system resulting in inadequate tissue perfusion and oxygenation
79
Stages in shock
1. Shock 2. Inadequate tissue perfusion 3. Inadequate tissue oxidation 4. Anaerobic metabolism 6. Accumulation of metabolic waste products 7. Cellular failure
80
Hypovolaemic Shock cause by
Loss of blood
81
Steps to hypovolaemic shock
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
Cardiogenic shock is caused by
Decreased cardiac contractility
83
Steps to cardiogenic shock
1. Decreased cardiac contractility 2. Decreased stroke volume 3. Decreased CO and BP 4. Inadequate tissue perfusion
84
Causes of obstructive shock
Tension Pneumothorax
85
Steps to obstructive shock
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
Causes of neurogenic shock
Loss of sympathetic tone to blood vessels and heart
87
Steps to neurogenic shock
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
Causes of vasoactive shock
Release of vasoactive mediators
89
Steps to vasoactive shock
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
Treatment of shock
``` ABCDE High flow oxygen Inatropes of cardio shock Adrenaline in anaphylactic shock Vasopressors in septic shock ```
91
Elevated LDL and decreased HDL are associated with
Cardiovascular disase
92
Lipoproteins
Microscopic spherical particle Hydrophobic core Hydrophilic coat with apoproteins
93
Apoproteins
Recognised by receptors in liver and other tissues allowing lipoproteins to bind to cells
94
4 classes of lipoproteins
HDL LDL VLDL Chylomicrons
95
Examples of HDL
apoA1, apoA2
96
Examples of LDL
apoB-100
97
Examples of VLDL
apoB-100
98
Examples of chylomicrons
apoB-48
99
ApoB containing lipoproteins
Deliver TAG's to muscle for ATP biogenesis and adipocytes for storage
100
Chylomicrons
Formed in intestinal cells Transport dietary triglycerides Exogenous pathway
101
VLDL
Formed in liver cells Transport TAG's Endogenous pathway
102
Life cycle of ApoB
Assembly Intravascular metabolism Receptor mediated clearance
103
Why is LDL bad cholesterol?
Causes atherosclerosis
104
Why is HDL good cholesterol?
Removes excess cholesterol from cells by transporting it in plasma to liver so they can be eliminated
105
Starling forces
favour filtration at arteriolar end, reabsorption at venular end

Phoebe's Cardio (22 decks)

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