1
Q
What are the two circuits of blood flow in body?
A
- Pulmonary circuit and systemic circuit
2
Q
What is the pulmonary circuit?
A
- right ventricle (ejects blood into pulmonary artery)
- goes into lungs (gas exchange), ejects blood into left atrium
3
Q
What is the syswtemic circuit?
A
- Starts with the LEFT VENTRICLE–> aorta—> arterioles–> capillaries–> exchange of nutrients and waste–> back to heart by main veins (vena cavae)
4
Q
First, blood flows through the ____ circuit, then the __ circuit
A
Pulmonary circuit,m systemic circuit
5
Q
In what 3 conditions will you have a fast death?
A
- NO excitation
- NO ventricular contraction
- NO pulse
6
Q
What are desmosomes?
A
Structural component of intercollated disks(the glue)
7
Q
What do gap junctions allow for?
A
- Spread of excitation of heart thus, NO contraction
8
Q
Where is the excitation of the heart initiated?
A
- SA node (sino atrial node)
9
Q
What is the pathway of excitation of heart?
A
- SA node–> internodal pathways–> Bundle of Hiss (in ventricular septum)–> apex–> purkinje fibres –> allows muscle to contract
10
Q
What do the purkinje fibres do ?
A
- transmit electrical impulses to ALL ventricular muscle cells AT SAME TIME so contract at SAME TIME
11
Q
Approx how long does it take for depolarisation/excitation of atria?
A
- approx 0.09 secs for depolarisation
12
Q
Approx how long does it take for dwepolarisation/excitation of ventricles?
A
Approx 0.06 seconds
13
Q
Where is there a significant slowing of rate of conduction?
A
- getting through the AV node (atrioventricular node)
14
Q
Roughly how long does it take to pass through the AV node?
A
- 0.09 secs
15
Q
How come it takes longer to pass through AV node?
A
- Fewer gap junctions between AV node cells (thus slower to pass)
16
Q
Why do we want slow conduction through the AV node?
A
- So ventricles have ENOUGH time to FILL with blood before getting excited (and contracting) (i.e. ventricular filling needs to occur so pulse slows)
17
Q
If an SA node (pacemaker cell) is isolated what happens?
A
- It will generate APs by itself
18
Q
What are the 3 features of ventricular Aps?
A
- Have a plateu
- Much more negative (MDP-maximum diastolic potential -90mV)
- STABLE resting mempot
19
Q
What are the 3 features of SA node APs?
A
- much more positive MDP -65mV
- No stable resting pacemaker potential
- (no plateu)
20
Q
What does aan Ena (nerst) of +70mV
A
If the cell was only permeable to sodium (Na+), it would come to rest at a mempot of +70mV
21
Q
What source of excitation do ventricular muscle cells require?
A
- External source (from K+, Ca2+, Na+)
22
Q
What does TTX inhibit?
A
- Fast Na+ channels
- Selective inhibitor
23
Q
What will TTX do to a ventricular Ap?
A
- NO AP occurs! Heart would stop= death
24
Q
What will TTX do to pacemaker cells?
A
-NOTHING! Fast Na+ channels not involved in pacemaker AP
25
What causes pacemaker cells to have autonomous APs?
- Contain an 'f' (funny) or 'h' (hyperpolarisation current
- Known as pacemaker currnet
SLOW inward flux of Na+ (SLOW Na+ channels)
26
What is special about the slow Na+ channel?
- It is the only voltage dependent channel to be open during hyperpolarisation(negative) (others only during depolarisation)
27
What causes the upstroke in pacemaker AP?
- Ca2+ (L-type)
28
What causes the upstroke in ventricular APs?
- Na+
29
What causes repolarisation in pacemaker cells?
- K+ moving out of cell
30
What is the sympathetic innervation of the heart?
- post ganglionic: entire heart--> release NA (beta cells)
31
What are the arteries supplying the myocardium?
- Coronary arteries
32
Where are the coronary arteries located?
- Behind the aortic valve cusps (first part of aorta)
33
Where do the cardiac veins drain into?
- Coronary sinus (large, single vein) --> empties into right atrium
34
What is the left AV valve also known as?
- Mitral valve
35
What is electrical excitation of the heart coupled with?
- Muscle contraction (Cardiac muscle)
36
What determines the heart rate?
- The discharge rate of SA node(contractions per minute)
37
What does the delay of AP propagation through AV node allow?
- Atrial contraction to finish before ventricles are excited
38
What is the only electrical connection between the atria and ventricles?
- AV node and bundle of Hiss
39
Why does depolarisation in cardiac muscle cells continue for longer than in other cells of body?
- K+ permeability lowers below resting value (K+ channels close that WERE open in resting state)
AND increase in Ca2+ permeability
40
What does membrane depolarisation cause in myocardial cells? (ventricular muscle cells)
- Ca2+ voltage gated channel to OPEN
| - Ca2+ goes into cell
41
What are L-type Ca2+ channels?
- L (long lasting)
- Open slower than Na+ fast channels
- Also known as: DHP (dihydroxypyridine) channels
42
What causes the membrane depolarised at plateu? (ventricular muscle cells)
- Ca2+ ions into cel = K+ ions OUT OF CELL
43
In ventricular muscle cells, how does repolarisation eventualy occur?
- Inactivation of L-type Ca2+ channels
| - Opening of K+ channels (another type) (delayed rectifiers and close once current repolarised to -ve)
44
Are APs of atrial muscle cells similar to ventricular cells?
- SHAPE of APs is similar
| - Plateu duration SHORTER
45
What are the 3 contributors to the pacemaker POTENTIAL?
1. K+ permeability lowers
2. F type channels conduct depolarising Na+ current (only open in negative values)
3. T-type Ca2+ channels (T for transient)
- final depolarising boost to reach threshold (pacemaker)
- channels open BRIEFLY
46
What is another name for F type channel?
- Hyperpolarisation-activated Cyclic Nucleotide-gated channels (HCN)
47
Why do SA node cells initiate APs of the heart rather than AV node cells?
SA node cell threshoold reached more rapidly (determines pace of heart)
48
What is the pathway once threshold is reached for pacemaker cells?
AP occurs--> depolarisation (ca2+ influx via L-type (slow) Ca2+ channels--> Repolarisation (K+ exiting cell)--> PK+ increases --> PNa (f) increases
cycle starts again
49
Why do APs propagate slower along nodal cell membranes?
- Inlfux of L-type (long lasting) Ca2+ channels so slow depolarisation occurs
50
What allows the SA node to have self excitation?
- Pacemaker potential ( and 3 channels)
51
In what circumstances would you need a pacemaker?
- When AV node isn't working properly (reduce AP transmission atria--> ventricles)
52
What is myosin ATP-ase?
- Enzyme (also ATP binding site) that catalyses ATP--> ADP
53
Does contraction always refer to shotening?
- NO! Contraction is activation of force generating sites within muscle fibres (cross bridges form)
54
What does the cytosolic Ca2+ concentration determine?
- Number of troponin sites occupied by Ca2+
| - So number of actin sites for cross bridge binding
55
What is the EDV (End Diastolic Volume)?
- When filling with blood, ventricle is RELAXED
| - the amount of blood in ventricle at this time is EDV
56
What is the ESV (End Systolic Volume) ?
- Amount of blood remaining in ventricle AFTER ejection
57
What is the formula for Stroke Volume?
EDV-ESV
58
What is stroke volume?
- Amount of blood when ventricle is relaxed and filled VS. amount of blood in ventricle after ejection of blood
59
When does early diastole begin?
- When ventricular muscle relaxes and ejection comes to an end
60
How is it good that most ventricular filling is completed during early diastole?
- Makes sure filling happens properly when heart is beating very rapidly
- So TOTAL filling time and duration of diastole reduced
61
Are the stroke volumes (SVs) of the L &RHS of ventricles the same??
YES!!
62
Do the left and right ventricles have different pressures?
- YES! Right ventricular wall MUCH THINNER than left
| - Left ventricular wall at much higher pressure
63
What is the 'lub' sound of the heart?
- Closure of AV valves
64
What is the 'Dub' sound of the heart?
- Onset of diastole (closing of aortic and pulmonary valves)
65
What occurs (generally) in heart murmurs?
- Blood is turbulent instead of laminar (flow)
66
What is stenosis and what main symptom does it produce?
- Abnormally narowed valve
| - High pitched whistling murmur
67
What is 'insufficiency' and what main symptom doesit produce?
- blood flowing backward through damaged, leaky valve
| - Low pitched, gurgling murmur
68
What is a septal defect?
Blood flowing b/w two atria or two ventricels through small hole in septum
69
What is CO (cardiac output) and the formula?
- VOLUME of blood that each ventricle pumps as a function of time (L/min)
- CO= HR * SV
- CO= HR * (EDV-ESV)
70
Is cardiac output the same on both sides of the heart?
-YES! Because under the STEADY STATE, SV and HR are the same
71
What is the effect of stroke volume (SV) and heart rate (HR) with blood loss?
- SV DECREASES
| - HR INCREASES
72
What is the autonomous discharge rate of the SA node?
- 100bpm
| - Occurs without any nervous or hormonal regulation
73
What effect does vagus stimulation have on heart rate?
- REDUCES it
74
What effect does sympathetic stimulation have on pacemaker potential?
- Increases the SLOPE of pacemaker potential
75
How does sympathetic stimulation increase the slope?
- F-type (Na+) channel permeability increases
- Faster depolarisation
- SA node reaches threshold more rapidly --> HR increases
76
How does an increase in parasympathetic current decrease the slope of the pacemaker potential?
- Due to LESS INWARD CURRENT
- threshold reached at slower rate
- So HR decreases
- SA node cell memb. hyperpolarised --> increases perm. to K+ (so potential starts from more negative value)
77
What is a simpler explanation of stoke volume?
- Vol. of blood each ventricle ejects during each contraction
78
With each contraction of heart, do the ventricles empty completely?
- NO!!
79
What would a more forceful contraction of the heart result in?
- Increased SV
| - More emptying of blood
80
What can cause changes in force during ejection of stroke volume? (3 things)
1. EDV changes (preload--> vol. of blood in ventricles just before contraction)
2. Changes in amount of SYMP INPUT TO VENTRICLES
3. Changes in afterload (arterial pressures that ventricles pump against )
81
What is the Frank Starling Mechanism?
- SV increases as EDV increases (given all other factors are in a STEADY STATE--> equal)
82
What is EDV a determinant of?
- How STRETCHED the ventricular sarcomeres are JUST BEFORE contraction.
83
The greater the _____ the greater the stretch and more forceful the contraction
The greater the EDV, the greater the stretch, and the more forceful the contraction
84
Is the normal point for cardiac muscle in resting person at optimal length of contraction?
- NO! It's on the rising phase of curve
85
When do spaces between thick and thin filaments decrease in cardiac muscle?
- When cardiac muscle is stretched towards optimum length (more crossbridging occurs--> twitch)
86
From the Frank Starling mechanism, what does an increase in venous return cause?
- Increase in C.O by increasing E.D.V (End Diastolic Volume) therefore stroke volume
- Left and right cardiac outputs must be same though
87
What will happen if the RHS of heart starts pumping more blood than LHS?
- Increased blood flow (returning to left ventricle) will automatically produce increase in LEFT ventricular output (so blood doesn't acculmulate in pulm, circulation
88
What is ventricular contractility defined as?
- Strength of contraction at any given EDV
89
What does NA act on (which receptors of heart)?
- Beta adrenergic receptors
| - Increases ventricular contractility
90
Does Adrenaline also increase contractility?
- YES!
91
Does the Frank Starling mechanism reflect increased contractility?
- NO! Increased force of contraction + stroke volume from symp. stimulation or Adrenaline are INDEPENDENT of change in EDV --> so frank starling law doesn't apply (Increased SV as EDV increases)
92
How can we quantify contractility?
- Ejection Fraction (EF)
93
What is the ejection fraction equal?
- SV/ EDV
| -
94
what does increased contractility equal?
- Increased ejection fraction
95
What is afterload?
- How hard the heart must work to eject blood
96
What does increased arterial pressure do to SV?
- Increase it **
97
DO the parasympathetic nerves have any significant effect on VENTRICULAR MUSCLE?
- NO!!
98
A man comes into hospital with a pulse rate of 40 pulses/min. The ECG revealed an atrial rate of 90 contractions/min and a blockage of conduction through the AV node. Why was his pulse rate 40 pulses/min?
- Pressure waves down arteries that reflect rate that ventricles are contracting --> Excited by purkinje fibres at lower rate: 40 pulses/min
99
THE SA NODE IS IRREVERSIBLY DAMAGED:
(A) This is not a problem, the autonomic nerves are still stimulating the heart to beat
(B) This person foes not have long to live; without the SA node the heart cannot be excited
(C) The AV node will now initiate the excitation of the heart and the heart rate will be about 50beats/min
(D) The purkinje fibres will now initiate the excitation of the heart, and the heart rate will be about 40beats/min
(C) The AV node will now initiate the excitation of the heart, and the heart rate will be about 50 beats/min
100
What is tachycardia?
- HR>10bpm
101
What is bradycardia?
- HR<60bpm
102
What type of cardiac innervation does a normal sedentary person have?
- Symp and parasymp
103
Why is blood flow out of the heart (left ventricle) intemittent?
- Aortic valve closes after each contraction (BUT blood flow is continuous)
104
When the heart is contracting and emptying, where does 2/3 of the blood go?
- 2/3 of blood goes into stretching walls of arteries (aortic valve open)
105
In systole, where does 1/3 of blood go?
- 1/3 blood goes to arterioles (aortic valve shut)
106
What is the dicrotic notch on the aortic pressure trace due to?
- The closing of the aortic valve
107
What is systolic blood pressure normally (SBP)
120
108
What is disatolic blood pressure normally? (DBP)
80
109
What does pulse pressure equal?
PP= SBP-DBP (40)
110
What does MAP (Mean Arterial Pressure) equal?
- MAP= DBP + 1/3 (PP)
111
What is hypertension?
- Higher than normal blood pressure
| - CONSISTENTLY above approx. 140/90 (140 is systolic and 90 is diastolic)
112
What is hypotension?
- Lower than normal blood pressure
| - CONSISTENTLY below approx. 100/60
113
In the blood pressure (BP) profile (when wearing BP monitor), what is the drop in blood pressure over a period of time associated with?
-SLEEP
114
What do arterioles control?
- Control proportional distribution of blood flow to different organs and tissues of body through changes in DIAMETER (alters resistance to flow)
115
In a relaxed (dilated) arteriole, what is the flow and resistance like?
- Flow INCREASES and resistance DECEREASES
116
In a constricted arteriole, what is the flow and resistance like?
- Flow DECREASES and resistance INCREASES
117
What are the three factors that affect arteriolar radius?
1. Neuronal
2. Hormonal
3. Local
118
What happens in metabolic control (cardiac and skeletal muscle) of arterioles (autoregulation)?
- Dilation of arterioles by H+, Adenosine, incrfeased CO2, decreased O2, K+ acting directly on smooth muscle cells
- Blood flow increased
119
What does the myogenic mechanism allow for?
- Allows for organs to maintain CONSTANT blood flow despite changes in arterial pressure upstream
120
Where in the body is the myogenic mechanism well developed?
- In the brain -cerebral circulation
121
Which two processes control the local needs of specific tissues and organs?
- Metabolic and myogenic control
122
What is the nerve supply to the arterioles?
- Sympathetic (except for genitals)
123
With reflex control of arterioles, what does NA act on and what does this lead to?
- NA (released by sympathetic nerves) acts on arteriolar sm. muscle ALPHA adrenoceptors
- Leads to SMOOTH muscle contraction =CONSTRICTION
124
Is therer always a level of 'resting' sympathetic nerve activity to smooth muscle in arterioles?
- YES!
| - There is so the sm. msucle is aloway PARTIALLY contracted
125
What does increased sympathetic activity to arterioles lead to?
- Constrcition
126
What does decreased sympathetic nerve activity to arterioles lead to?
- Dilation
127
What effect does Adrenaline binding to alpha receptors on smooth muscle have?
- Causes constriction of arterioles (contraction of smooth muscle)
128
What effect does Adrenaline have when it binds to Beta2 Adrenergic receptors on smooth muscle or skeletal muscle?
- Causes relaxation of muscle cells (smooth muscle in arterioles---> Dilation)
129
Which two hormones involved in the renal system constrict arterioles?
- Angiotensin II and Vasopressin (ADH)
130
Which hormone in renal system dilates arterioles?
- ANP (Atrial Naturietic Peptide)
131
What effect does stress have on sympathetic nerve activity?
- Leads to increase in symp. nerve activity
| - Adrenaline secretion increases from adrenal medulla
132
During stress, what happens to arterioles that have little sympathetic innervation and vascular smooth muscle alpha receptors (heart, liver, skeletal msucle) ?
- Arterioles will be dilated
| - Beta2 receptors have a dilating effect so adrenaline will bind and cause dilation
133
During stress, what happens to arterioles with a dense symp. innervation and vascular sm. muscle alpha receptors (gut, kidney)?
- Arterioles will CONSTRICT
| - Alpha receptors have a contracting effect when adrenaline binds
134
What is orthostatic hypotension (also specific BP values)?
- Type of hypotension where person's BP falls suddenly when standing up e.g. Yellow Wiggle
- SYS BP: more than or equal to 20mmHg
- DIA BP: more than or equal to 10mmHg
135
Why is there a sudden drop in MAP with orthostatic hypotension? (In terms of SV EDV CO)
- Venous return DECREASES
- This casues EDV (vol. after filling) to decrease---> leads to SV decreasing ---> leads to CO decreasing
MAP= CO* TPR so big drop
136
What is the total peripheral resistance (TPR) and how is this altered?
- Sum of all vascular resistances of ALL tissues
| - Changed by constricting or dilating blood vessels
137
Would constriction of arterioles increase or decrease the TPR (total peripherals resistance)?
- Constriction would cause INCREASED TPR
138
What causes the MAP to rapidly increase back to normal after someone fainted with orthostatic hypotension?
- Baroreceptor reflex (or Arterial baroreflex) -takes 5-10 seconds
139
What are three ways the MAP can be increased in the body? (sort of three)
1. Increase output of pump (CO) --> increase SV and HR
2. Increase resistance (Increase in TPR)--> changing constriciton/dilation of blood vessels
3. Combination of first two
140
What are two ways in which HR is increased?
1. Reducing parasympathetic activation of SA node
| 2. Increasing sympathetic activation of SA node
141
How can the body increase SV? (which leads to increase in CO and MAP)?
1. INCREASESympathetic activation of VENTRICLES --> increases amount of Ca2+ available for contraction--> more cross bridges--> increase in SV
2. INCREASE sympathetic activation of VEINS
- Increases VENOUS PRESSURE, VENOUS RETURN, EDV + SV
142
How do we increase TRP (and MAP from this)?
- Increase sympathetic activation of arterioles on ALPHA receptors
- this increases arteriolar CONSTRICTION and TPR
143
Which hormones are secreted from adrenal medulla in stress response ans what effect does this have?
- A + NA
- Increase CO (which increases HR and contractility/SV)
- Increases TPR (vasoconstriction)
144
What type of innervation does a normal sedentary person have?
- Sympathetic and Parasympathetic
145
What type of innervation does a receipient of a heart transplant have?
- NO autonomic innervation
146
What type of innervation does a quadriplegic have?
- NO SYMPATHETIC
| - Normal parasympathetic
147
What 4 things is an ECG used to determine?
1. Anatomical orientation of heart
2. Disturbances in cardiac rhythm and conduction
3. Effects of drugs or abnormal contractions of plasm. electrolytes (K+) on heart
4. Location of ischaemic damage to myocardium and the extent
148
When does the P wave occur in a normal ECG and what does it represent?
- EXCITATION of the atria
| - atrial depolarisation
149
When does the QRS complex occur and in which phase?
- Excitation of ventricles
| - Ventricular depolarisation phase
150
When does the T wave occur and in what does it represent?
- Recovery (repolarisation) of ventricles
| - Ventricular repolarisation stage
151
Why is the T wave larger than P wave in aplitude?
- More ventricular muscle cells thus more APs
152
What are the 4 major causes of cardiac arhythmia?
1. Pacemaker goes from SA node--> other pacemaking region (due to damage)
2. Abnormal impulse formation in SA node (Sick sinus syndrome)
3. Blocking or delay of conduction of impulse through heart
4. Ventricular fibrillation (spontaneous generation of abnormal impulses)
153
What are 4 conditions that can block the AV node?
1. Ischaemia (not enough nutrients to heart, blockage of blood supply)
2. Scarr tissue compressing AV-node
3. inflammation of AV node (fever)
4. Extreme stimulation of heart by vagus nerve (very rare)
154
What can ventricular fibrillation be a consequence of ? -
- Myocardial iscahemia and electrocution
155
Does blood pressure increase or decrease with each ventricular systole?
- Increases
| - Left V ejects blood into aorta (p increases)
156
What is microcirculation?
- BLood flow from ARTERIOLE ----> venule
157
What are capillaries the site of?
- Site of exchange of nutrients and waste
158
During exercise, do you get blood flow through the MAJORITY of the capillary bed in SKELETAL MUSCLE (are sphincters open)?
- YES!
| - To increase exchange of nutrients
159
Do multiple RBCs pass adjacently through a capillary?
- NO!!
| - Capillaries are so small that they need to pass through in single file
160
During exercise, do you get blood flow through the majority of the capillary bed in INTESTINES?
NO!!
- Sphincters are closed
(this is what can cause cramps if you've just eaten)
161
Is pressure pulsatile at arterioles?
- NO!
| - Low pressure because thin walled vessels and don't want to rupture
162
What are 4 ways that materials can pass in/out of capillaries?
1. Diffusion (O2, CO2)--> endothelial cells (lipid soluble)
2. Diffuse through pores b/w endothelial cells (for hydrophillic substances e.g. glucose, aas)
3. Bulk flow (H20)
4. Vesicular transport (large molecules--> hormones)
163
What must there be for flow?
-A pressure gradient (delta P)
164
What is the only substance not to be filtered out of the capillary bed?
- Plasma Proteins (too large)
165
What factor drives filtration?
- Hydrostatic pressure (blood pressure in capillaries)
166
What opposes filtration and what is it due to?
- Plasma osmotic (colloidal oncotic) pressure
| - Due to plasma proteins having higher osmotic flow into capillaries (osmotic pressure)
167
What is absorption in capillaries?
- If movement is FROM interstitial fluids ---> Plasma
168
If osmotic pressure is HIGHER than hydrostatic pressure in capillaries, what happens?
- RE-ABSORPTION will occur (movement from interstitial fluid to plasma)
169
What is the role of the lymphatic system in capillary filtration/absorption and which vein does the lymph enter back into?
- Drains solutes that capillaries filter
| - Lymph enters back into subclavian vein and goes back into circulation
170
What is an extracellular odema?
- Failure to maintain correct distribution of body water
| - thus excess acumulation of body fluid
171
What can some causes of odema be?
- Increased hydrostatic pressure (in capillaries) (heart failure)
- Increased osmotic pressure (in capillaries)--> conditions altering plasma protein levels like kidney or liver failure
- Lymphatics with cancerous growth blocking drainage
172
What are the 3 mechanisms that venous return is influenced by? (e.g. in exercise)
1. Pressure gradient
2. Skeletal muscle 'pump'
3. Respiratory 'pump'
BMS2031
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