Cardiovascular Physiology Flashcards
(298 cards)
1
Q
What is shock?
A
An abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation.
Ultimately it leads to cellular failure.
2
Q
How do you calculate the Mean arterial pressure?
A
MAP= Cardiac output (CO) x Systemic vascular resistance (SVR)
3
Q
Define the cardiac output
A
volume of blood pumped by each ventricle of the heart per minute.
4
Q
How do you calculate the cardiac output
A
stroke volume x heart rate
5
Q
Adequate tissue perfusion depends on what?
A
- Adequate blood pressure.
2. Adequate cardiac output.
6
Q
Define stroke volume.
A
The volume of blood ejected by each ventricle per heart beat
7
Q
What types of shock are there?
A
- Cardiogenic
- obstructive
- distributive
- Hypovolemic
8
Q
What happens during hypovolaemic shock?
A
- Blood loss causes decrease in blood volume
- Decrease in venous return
- decreased end diastolic volume
- decreased stroke volume
- decreased cardiac output and decreased blood pressure.
- inadequate tissue perfusion.
9
Q
What happens during cardiogenic shock?
A
Sustained hypotension caused by decreased cardiac contractility.
- decreased cardiac contractility
- decreased stroke volume
- decreased cardiac output and decreased blood pressure
- inadequate tissue perfusion.
10
Q
What happens in obstructive shock?
tension pneumothorax
A
- increased intrathoracic pressure.
- decreased venous return
- decreased end diastolic volume
- decreased stroke volume
- decreased cardiac output and decreased blood pressure.
- inadequate tissue perfusion
11
Q
What happens in neurogenic shock?
A
- loss of sympathetic tone to blood vessels and heart
- Massive venous &arterial vasodilation- effects heart rate
- Decreased Venous Return
Decreased SVR (TPR)
Decreased Heart Rate - Decreased Cardiac Output
Decreased blood pressure - Inadequate Tissue Perfusion
12
Q
What happens during vasoactive shock?
A
- release of vasoactive mediators
- massive venous and arterial vasodilation also increased capillary permeability
- decreased venous return and decreased systemic vascular resistance.
- Decreased Cardiac Output
Decreased blood pressure - Inadequate Tissue Perfusion.
13
Q
How should you treat shock?
A
- ABCDE approach
- high flow oxygen
- volume replacement- except for cardiogenic shock
- call for HELP early
- Inotropes for cardiogenic shock- makes contractility better.
- immediate chest drain for tension pneumothorax (2nd intercostal space)
- Adrenaline for anaphylactic shock
- Vasopressors for septic shock
14
Q
What is the difference between the two main types of hypovolaemic shock?
A
- Non haemorrhagic shock causes ECFV to decrease. Haemorrhagic shock does not
15
Q
When can compensatory mechanisms maintain blood pressure till?
A
When blood volume loss is greater than 30%
16
Q
How many classes of haemorrhagic shock are there?
A
4
17
Q
what are the two types of hypovolaemic shock?
A
- Haemorrhagic shock- haemorrhage from trauma, surgery or GI haemorrhage
- non haemorrhagic shock- vomiting, sweating and diarrhoea
18
Q
What are the characteristics of haemorrhagic shock?
A
- tachycardia- via baroreceptor reflex
- small volume pulse- decreased stroke volume
- cool peripheries - CO decreases and Increase in SVR via baroreceptor reflex
- MAP decrease after >30% of blood loss
19
Q
How can mean arterial pressure be calculated using the diastolic blood pressure?
A
MAP= DBP + 1/3 Pulse pressure
20
Q
What is SVR regulated by?
A
vascular smooth muscles
21
Q
What is the main site of SVR?
A
Arterioles.
22
Q
Contraction of vascular smooth muscles causes what?
A
Vasoconstriction
Increases SVR and MAP
23
Q
What does relaxation of vascular smooth muscle cause?
A
Vasodilation
Decrease SVR and MAP
24
Q
Resistance to blood flow is directly proportionate to what?
A
Blood viscosity and length of blood vessel
25
Resistance to blood flow is indirectly proportionate to what?
Inversely proportional to the radius of blood vessel to the power 4.
26
Write the equation relating to resistance to blood flow.
R ∝ η.L
| r4
27
What is the vasomotor tone.
Describes the smooth muscle being partially contracting at rest.
28
Resistance to blood flow is mainly controlled by what?
Vascular smooth muscles through changes in the diameter of arterioles
29
What type of nerve fibres are vaso smooth muscles supplied by?
ii. What is the neurotransmitter used and what receptor?
Sympathetic.
ii. Noradrenaline and alpha receptor
30
What causes the noradrenaline to be released?
tonic discharge
increased tonic discharge= vasoconstriction
decreased tonic discharge= vasodilation
31
When is there parasympathetic intervention of arterial smooth muscles?
For the penis and clitoris.
32
Where is adrenaline produced from?
The adrenal medulla.
33
What occurs if adrenaline acts on an alpha receptor?
ii. Where would this be found normally?
vasoconstriction.
ii. Skin, gut and kidney arterioles.
34
What occurs if adrenaline acts on a beta 2 receptor?
ii. where would this be found normally?
Vasodilation.
ii. Cardiac and skeletal muscle arterioles.
35
What do each hormones cause:
i. Angiotensin II
ii. Antidiuretic
i. Vasoconstriction
| ii. Vasoconstriction
36
What factors lead to vasodilation and metabolic hyperaemia?
Decreased local PO2
Increased local PCO2
Increased local [H+] (decreased pH)
Increased extra-cellular [K+]
Increased osmolality of ECF
Adenosine release (from ATP)
37
Give examples of Humoral agents which cause vasodilation.
Histamine
Bradykinin
Nitric Oxide (NO) - continuously released
38
Give examples of Humoral agents which cause vasoconstriction.
1. serotonin
2. Thromboxane A2
3. Leukotrienes
4. Endothelin
39
What is a local humoral agent
ii. when are they released?
Local chemicals released in an organ.
ii. Response to Tissue injury or inflammation
40
What is blood pressure?
The hydrostatic pressure exerted by the blood on vessel walls.
41
# Define systemic systolic arterial blood pressure.
ii. What value should it not exceed?
Is the pressure exerted by blood on the walls of the aorta and systemic arteries when the heart contracts.
ii. 140 mm Hg
42
# Define systemic diastolic arterial blood pressure?
ii. What value should it not fall below?
Is the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes
ii. 90 mm Hg
43
What are the values of hypertension?
i. clinically
ii. day time average?
i. 140/90 mm Hg
| ii. 135/85 mm Hg
44
What is the pulse pressure?
ii. What is its average value?
Difference between systolic and diastolic pressure.
ii. 30-50 mm Hg
45
What is laminar flow?
ii. is it audible in a artery through a stethoscope?
Normal blood flow moving in its vessels through layers. with each layer moving smoothly past the adjacent layers with little or no mixing
ii. No- not in a healthy subject anyway
46
How would you be able to hear arterial blood pressure?
If the cuff pressure(external presure) is in between the values of the systolic and diastolic pressures. This makes the blood flow turbulent.
47
Is turbulent blood flow audible in a stethoscope?
yes.
48
What are the 5 korotkoff sounds?
ii when do you hear them?
Sound 1 - Is heard at peak systolic pressure. It is the systolic BP value
Sound 2/3 - Intermittent sounds ,Heard when turbulent spurts of flow exceeds cuff pressure
Sound 4 -Muffling sound
Sound 5 - No sound here but is the diastolic pressure's value. Smooth laminar flow is now occuring
ii. Sound 1,2,3 - Cuff pressure is in between the 120-80 mm Hg
Sound 4 and 5 when cuff pressure is lower than 80 mm Hg
49
what is the role of the Pressure gradient?
ii. How do you calculate?
Gradient between aorta and the right atrium drives the blood around the systemic circulation
ii.MAP- Central venous pressure (CVP)
(RA pressure is close to 0 so main driving force for blood flow is MAP)
50
The systolic period of the cardiac cycle is just as long as the diastolic period true or false?
false- diastolic period is twice as long as the systolic period in the cardiac cycle.
51
Normal systolic pressure is?
<140 mm Hg
52
Normal systolic pressure is?
<90 mm Hg
53
Normal range of mean arterial pressure is?
ii. What happens if it is below 60 mm Hg
70-105 mm Hg
ii. Need to perfuse coronary arteries and kidneys.
54
What is the second equation when calculating the mean arterial pressure?
CO (or SV x HR) x Stroke volume
55
What is the role of the baroreceptor reflex?
Short-term Regulation of Mean arterial Blood Pressure.
| includes prevention of postural changes
56
What are the two types of baroreceptors?
ii. What nerves do they use to send signals to the medulla?
Carotid sinus
Aortic arch
ii. Carotid - IXth Glossopharyngeal nerve
Aortic - Xth vagus nerve
57
Describe what the baroreceptor reflex does to prevent decrease in blood pressure.
e.g. when a person stands up suddenly when lying down for a long time
Gravity effect:
1. Gravity causes venous return to decrease
2. MAP decreases - reduces rate of firing from baroreceptors
Response:
3. Vagal tone decreases/ sympathetic tone increases
4. This leads to Increase in HR and SV (stroke volume)
5. Sympathetic constrictor tone increases- SVR increases
6. Sympathetic constrictor tone to the vein increases the venous return and the stroke volume
Result:
rapid correction of MAP transient fall
HR increases
SV increases
SVR increases
n.b. response and result are opposite if reflex is for blood pressure to high
58
What are the causes of postural (orthostatic) hypotension?
When baroreceptors fail to respond to gravitational shift in blood from horizontal to vertical position.
59
Give examples of risk factors for postural hypotension?
```
Age related
Medications
Certain diseases
Reduced intravascular volume
Prolonged bed rest
```
60
Symptoms for postural hypotension
```
lightheadedness
dizziness
blurred vision
faintness
falls
```
61
Why do baroreceptors only work work on acute related blood pressure issues?
Baroreceptors firing decreases if high blood pressure is sustained
fire again only if an acute change in MAP above the new higher steady state level (they re-set)
Baroreceptors cannot supply information about prevailing steady state blood pressure
Control of MAP in the longer-term is mainly by control of Blood Volume
62
What is stenosis?
narrowing of the vessel lumen
63
Describe the pathophysiology of renal artery stenosis.
Reduced lumen diameter decreases the pressure at the afferent arteriole in the kidney and reduces renal perfusion. This stimulates renin release by the kidney, which increases circulating angiotensin II and aldosterone. These hormones increase blood vlume and causes vasoconstriction and enhances sympathetic activity. This leads to both an increase in systemic vascular resistance and increase cardiac output.
64
Describe how stress causes an increase in hypertension.
Activation of Sympathetic nervous system. Release of noradrenaline from nerves increases cardiac output and systemic vascular resistance. Adrenal medulla secretes more noradrenaline and adrenaline . Circulation of angiotensin II is increased and if prolonged, can lead to cardiac hypertrophy.
65
What is the definition of haemostasis?
arrest of blood loss from a damaged vessel – at the site of injury involves in sequence
66
Describe the process of haemostasis
i Vascular wall damage exposing collagen and tissue factor (TF, thromboplastin)
ii Primary haemostasis
local vasoconstriction
platelet adhesion, activation and aggregation (by fibrinogen)
iii Activation of blood clotting (coagulation) and the formation of a stable clot (by fibrin enmeshing platelets)
67
What does vessel damage expose?
ii. What reacts to this exposure?
Collagen.
This causes platelets to bind and become activated.
68
What does the activation of platelets cause?
1. extend pseudopodia
| 2. synthesise and release thromboxane A2 (TXA2)
69
What does TXA2 bind to?
1. platelet GPCR TXA2 receptors (aka TP receptors) causing mediator release [5-hydroxytryptamine (5-HT – aka serotonin) and adenosine diphosphate (ADP)]
2. vascular smooth muscle cell TXA2 receptors causing vasoconstriction that is augmented by mediator 5-HT binding to smooth muscle GPCR 5-HT receptors
70
What does ADP bind to?
ii. What does this cause?
Purine receptor
ii. Act locally to activate further platelets
Cause increased expression of platelets glycoprotein receptors causing aggregation of platelets into a soft plug
expose acidic phospholipids on the platelet surface that initiate coagulation of blood and solid clot formation
71
What is inactive factor X converted to ?
ii. What activates it?
Active factor Xa
Tenase
72
What is inactive factor II converted to?
ii. What activates it?
thrombin
Prothrombinase
73
What is thrombosis
ii. What are its causes?
Pathological haemostasis - a haemotological plug in the absence of bleeding.
ii. Predisposing factors are Virchow's triad :
Injury to vessel wall
ABNORMAL BLOOD FLOW
Increased coagulability
74
What are the two types of thrombus?
White thrombus (arterial)
Red thrombus (venous)
75
Describe the process of white thrombus.
mainly platelets in a fibrin mesh
forms an embolus if it detaches from its site of origin (e.g. left heart, carotid artery) often lodges in an artery in the brain (stroke), or other organ
primarily treated with antiplatelet drugs
76
Describe the process of red thrombus.
red thrombus: white head, jelly-like red tail, fibrin rich
if detaches forms an embolus that usually lodges in the lung (pulmonary embolism)
primarily treated with anticoagulants.
77
What does Warfarin do to the clotting factors?
Prevents activation of clotting factor II VII, IX and X
78
What are the roles of anticoagulants?
ii. What is a major risk of using them?
deep vein thrombosis (DVT)
prevention of post-operative thrombosis
patients with artificial heart valves
atrial fibrillation- when atria aren't pumping efficiently causing blood to be static and therefore will coagulate.
ii. Cause haemorrhage.
79
What is warfarin structurally related to?
ii. What does it compete for
Structurally related to vitamin K with which it competes for binding to hepatic vitamin K reductase preventing production of the active hydroquinone
80
Describe warfarins characteristics?
is administered orally and is very well absorbed
has a slow onset of action (2-3 days) whilst inactive factors replace active -carboxylated factors that are slowly cleared from the plasma. Heparin may be added for rapid anticoagulant effect
has a long (and variable) half-life (usually about 40 hr)
81
Warfarin has a high therapeutic index true or false?
false - Can be very difficult to strike the balance between anticoagulant effect and haemorrhage.
82
What factors increase the risk of haemorrhage when using warfarin?
liver disease – decreased clotting factors
high metabolic rate – increased clearance of clotting factors
drug interactions
agents that inhibit hepatic metabolism of warfarin by CYP2C9 (consult BNF)
drugs that inhibit platelet function (e.g. aspirin, other NSAIDs)
drugs that inhibit reduction
83
What factors increase the risk of thrombosis and weaken the effect of warfarin?
physiological state – pregnancy (increased clotting factor synthesis) – hypothyroidism (decreased degradation of clotting factors)
vitamin K consumption
drug interactions
agents that increase hepatic metabolism of warfarin (consult BNF)
84
What is the role antithrombin III?
Antithrombin III (AT III) is an important inhibitor of coagulation which neutralises all serine protease factors in the coagulation cascade by binding to their active site in a 1 to 1 ratio
Heparin binds to antithrombin III, increasing its affinity for serine protease clotting factors [particularly Xa and IIa (thrombin)] to greatly increase their rate of inactivation.
85
Give examples of special adaptations of coronary circulation.
High Capillary density
High basal blood flow
High oxygen extraction ( approx 75% compared to 25% whole body average) at rest .
86
What does high oxygen extraction mean?
This means extra O2 (when required) cannot be supplied by increasing O2 extraction
Can only be supplied by increasing coronary blood flow .
87
Describe the effect of intrinsic mechanism on coronary blood flow.
decrease Po2 causes vasodilatation of the coronary arterioles
Metabolic hyperaemia matches flow to demand
Adenosine (from ATP) is a potent vasodilator
88
Describe the effect of extrinsic mechanism on coronary blood flow.
Coronary arterioles supplied by sympathetic vasoconstrictor nerves.
However:
Over-ridden by metabolic hyperaemia as a result of increased heart rate and stroke volume
So sympathetic stimulation of the heart results in coronary vasodilatation despite direct vasoconstrictor effect (functional sympatholysis)
Circulating adrenaline activates beta 2 adrenergic receptors, which cause vasodilatation.
89
when does peak left coronary flow occur?
ii. what does this do?
iii. what vessels are not compressed during this period to allow peak flow to occur?
during diastole.
ii. shortens diastole.
the subendocardial vessels from the left coronary artery are not compressed.
90
How is blood supplied blood?
via internal carotids and vertebral arteries.
91
Grey matter is very sensitive to hypoxia true or false?
true-irreversible cell damage occurs within 3 minutes.
92
Give examples of special adaptations of cerebal circulation?
BASILAR (formed by two vertebral arteries) & CAROTID arteries anastomose to form CIRCLE OF WILLIS
Major cerebral arteries arise from Circle of Willis
Cerebral perfusion should be maintained even if one carotid artery gets obstructed.
AUTOREGULATION of cerebral blood flow guards against changes in cerebral blood flow if mean arterial blood pressure changes within a range (~ 60 - 160mmHg)
Direct sympathetic stimulation has very little effect in overall cerebral blood flow
Participation of the brain in baroreceptor reflexes is negligible, which is just as well!- otherwise constant vasoconstriction would occur.
93
What happens if mean arterial blood pressure in cerebal blood rises?
Resistance vessels automatically constrict to limit blood flow.
94
What happens if mean arterial blood pressure in cerebal blood falls?
Resistance vessels automatically dilate to maintain blood flow.
95
When does autoregulation fail?
If MABP falls below 60 mm Hg (falls)
If MABP rises above 160 mm Hg (rises)
96
What happens if MABP falls below 50 mm Hg?
confusion, fainting, and brain damage if not quickly corrected.
97
What happens if PCO2 increases?
cerebral vasodilatation
98
What happens if PCO2 decreases?
ii. what happens if hyperventilation occured?
cerebal vasoconstriction
ii. constant change in partial pressure = fainting.
99
What is the normal range in intercranial pressure?
8-13 mm Hg
100
How do you calculate Cerebral perfusion pressure?
CPP= Mean arterial pressure- Intercranial pressure.
101
What happens if ICP increases?
Auto regulation of cerebral blood flow fails.
102
What is the blood brain barrier?
Intercellular junctions between cerebal capillaries.
103
What are BBB permeable to?
ii. what are they impermeable to? whats good about this?
oxygen co2
Cerebral capillaries have very tight intercellular junctions- This helps protect brain neurones from fluctuating levels of ions etc in blood.
104
What is the normal range of pulmonary artery BP?
systolic : 20-25 mm Hg
Diastolic : 6-12 mm Hg
105
What are the special adaptations of pulmonary circulation?
pulmonary pressure is lower than systemic pressure
Absorptive forces exceed filtration forces - protects against pulmonary oedema
Hypoxia causes VASOCONSTRICTION of pulmonary arterioles. this is opposite to effect on systemic arterioles. this diverts blood from poorly ventilated parts of lungs.
106
Why is the resting blood flow of skeletal muscle blood flow?
Resting blood flow is low because of sympathetic vasoconstrictor tone.
107
Skeletal muscle blood flow doesn't decrease during exercise true or false?
false.
108
What mechanisms occur to allow for skeletal muscle blood flow to increase during exercise?
During exercise, local Metabolic hyperaemia overcomes sympathetic vasoconstrictor activity
Circulating adrenaline causes vasodilatation (beta 2 adrenergic receptors)
Plus increase cardiac output during exercise, these could increase skeletal muscle blood flow many folds.
109
Describe the role of the skeletal muscle pump.
Large veins in limbs lie between skeletal muscles
Contraction of muscles aids venous return
One-way venous valves allow blood to move forward towards the heart
Skeletal muscle pump reduces the chance for postural hypotension & fainting
110
What are Varicose veins?
Varicose veins are swollen and enlarged veins that usually occur on the legs and feet. They may be blue or dark purple, and are often lumpy, bulging or twisted in appearance.
111
why do Varicose veins usually not lead to reduction of cardiac output.
because of chronic compensatory increase in blood volume
112
What is the expected value of total cholesterol for a person with a previous MI?
3.5-4 mmol.
113
What are capillaries made of?
single layer of endothelial cells.
114
What is the function of capillaries?
Allow rapid exchange of gases,water and solutes with interstitial fluid.
115
What is the role of terminal arterioles?
Regulate regional blood flow to the capillary bed in most tissues.
116
What is the role of Precapillary Sphincters?’
Regulate flow in some tissues such as Mesentry.
117
Blood flow through capillary bed is very slow true or false?
true-allows time for exchange.
118
Explain how each of the following types of molecues move across the capillary wall?
i. Water soluble
ii. lipid soluble
iii. Exchangeable proteins
iv. plasma proteins.
i. pass through pores
ii. Pass through the endothelial cells
iii. Vesicular transport
iv. Cannot travel through wall. (too big)
119
How do fluids travel through capillary wall?
Bulk flow. pressure gradient
120
How do gases and solutes travel through capillary wall?
diffusion concentration gradient.
121
Trans capillary fluid flow is controlled by what?
passively driven by pressure gradients across the capillary wall
122
How does Protein free plasma travel across the capillary wall?
ultra filtration.
123
What factors effect the net filtration pressure?
Forces favouring filtration - fi Forces opposing filtration
A Filtration coefficient (Kf) also affect net fluid filtration
124
What forces support filtration?
PC - capillary hydrostatic pressure
pi i - interstitial fluid osmotic pressure
125
What forces oppose filtration?
pi C capillary osmotic pressure
interstitial fluid hydrostatic pressure
126
How do you calculate NFP?
(PC + pi i) - (pi C + Pi)
127
What is the normal NFP value at the arteriolar end and venular end?
Arteriolar = + 10 mm Hg
Venular = - 8 mm Hg
128
How is excess fluid returned to circulation?
Via the lymphatics system.
129
what is autorhythmicity?
when the heart is capable of beating rhythmically in the absence of external stimuli
130
Where does excitation of the heart normally originate from?
Pacemaker cells- initiate the hear beat
found in the sino-atrial node
131
Where is the sino atrial node found?
Upper right atrium close to SVC enters it.
132
what is sinus rhythm?
when heart rate is controlled by SA node
133
why do cells within the SA node have spontaneous pacemaker potential?
they do not have a stable resting membrane potential so the drift through depolarisation spontaneously
134
what happens when the pacemaker cells take the membrane potential to a threshold?
ii. what does this result in?
an action potential is generated
ii. generation of regular spontaneous APs in the SA nodal cells
135
what factors affect the pacemaker potenial (the slow depolarisation of membrane potential to a threshold)?
1. decrease in K+ efflux
2. Na+ influx ( the funny current)
3. Transient Ca 2+ influx (T type Ca2+ channels)
136
What causes the rising phase of action potential ( i.e threshold has been reached - depolarisation)
ii. what does this cause?
Activation of long lasting L type Ca 2+ channels
ii. Ca 2+ influx
137
What causes the falling phase of action potential (repolarisation) ?
ii. what does this cause
Inactivation of L type Ca 2+ channels
ii. activates K+ channels and therefore causes efflux in K+
138
what is the role of gap junctions?
low resistance protein channels which allow for cell to cell current flow
139
Where is the AV node located?
base of the right atrium just above the junction of atria and ventricles
only point of electrical contact between atria and ventricles
140
What are the two main properties of AV node cells in regards to electrical conduction?
1. small in diameter
| 2. slow conduction velocity
141
discuss the spread of excitation in the heart
1. Atria cell to cell conduction mainly occurs via gap junction
2. from SA node to AV node conduction mainly occurs via gap junctions but there is also some internodal pathways
3. Conduction is delayed in AV node- allows atrial systole to precede ventricular systole
4. Bundle of his and its branches and the network of purkinje fibres allow rapid spread of action potential to the ventricles
5. ventricular cell to cell conduction
142
action potential in contractile cardiac muscle cells (myocytes) is different compared to the action potential in pacemaker cells true or false?
TRUE
143
What is the resting membrane potential on atrial ventricular myocytes?
-90mV (until excited)
144
What causes the rising phase of action potential in myocytes ( depolarisation)
ii. what value doe the membrane potential rise to?
iii. what is this called?
Fast influx of Na+
ii. +20 mV
iii. phase 0
145
what causes phase 1 of the ventricular muscle action potential?
1. closure of Na+ channels
| 2. Transient K+ efflux
146
What causes phase 2 of ventricular muscle action potential ( Plateau phase of action potential)?
Influx of Ca 2+ through L type Ca 2+ channels
147
What cause phase 3 of ventricular muscle action (Falling phase of action potential/repolarisation)?
efflux of K+
caused by activation of K+ channels and inactivation of Ca2+ channels
148
Which nervous system has the main affect on the heart?
autonomic nervous system
149
what is phase 4 of the ventricular muscle action potnential?
membrane rests at resting membrane potential
| -90mV
150
which nerve supplies the parasympathetic innervation to the heart?
vagus nerve
151
under normal conditions what regulates the heart?
vagal tone
152
What is the role of the vagal tone?
slows intrinsic heart rate from ~ 100 bpm to produce a normal resting heart rate ~70 bpm
153
what is the normal resting heart rate?
between 60-100 bpm
154
What is the term to describe a heart rate below 60 Bpm?
Bradycardia
155
what is the term to describe a heart rate above 100 bpm?
tachycardia
156
what exactly does the vagus nerve supply in the heart?
ii. what is the effect of vagal stimulation?
SA node and AV node
ii. slows heart rate and increases AV nodal delay
157
what neurotransmitter is involved in parasympathetic stimulation of the heart?
Acetylcholine
158
What receptors are involved in the parasympathetic stimulation of the heart?
Muscarinic M2 receptors
159
What is the role of atropine
ii. when is it used?
Competitive inhibitor of acetylcholine
ii. extreme bradycardia- speeds up heart
160
what is the effect of vagal(parasympathetic) stimulation on pacemaker potentials?
1. Cell hyperpolarises longer to reach threshold
2. Slope of pacemaker potential decreases
3. Frequency of action potnetials decrease
4. negative chronotopic effect
161
what exactly do the cardiac sympathetic nerves supply?
1. SA node and AV node
AND
2. MYOCARDIUM
162
What is the effect of sympathetic stimulation on the heart?
1. increases heart rate
2. decreases AV nodal delay
3. increases force of contraction
163
which neurotransmitters are involved in the sympathetic stimulation of the heart?
Noradrenaline
164
which receptors are involved in the sympathetic stimulation of the heart?
Beta one adrenoceptors
165
what is the effect of sympathetic stimulation on pace maker cells?
1. Slope of pacemaker potential increases
2. Pacemaker potential reaches threshold quicker
3. frequency of action potential increases
4. Positive chronotropic effect
166
what does the sympathetic system do to the rate of K+ efflux during pacemaker potential?
decreases the rate of K+ efflux
| allowing membrane potential to depolarise and reach threshold faster
167
what does the parasympathetic system do to the rate of K+ efflux during pacemaker potential?
increases the rate of K+ efflux
| causing membrane potential to take more time to depolarise and reach threshold
168
what does the sympathetic system do to the rate of Na+ influx during pacemaker potential?
increases the rate of Na+ influx
| allowing membrane potential to depolarise and reach threshold faster
169
what does the parasympathetic system do to the rate of Na+ influx during pacemaker potential?
decreases rate of Na+ influx
| causing membrane potential to take more time to depolarise and reach threshold
170
decreases rate of Na+ influx
| causing membrane potential to take more time to depolarise and reach threshold
decreases the rate of Ca++ influx
| slowing the impulse down
171
what does the sympathetic system do to the rate of Ca++ influx through voltage gated channels during the rapid depolarisation phase of the action potential of the pacemaker cells?
increases the rate of Ca++ influx
| speeding the impulse up
172
what are the wires that make up Lead I in an ECG?
1. Right arm (RA)
| 2. Left arm (LA)
173
What are the wire that make up Lead II in the ECG?
1. Right arm (RA)
| 2. Left leg (LL)
174
What are the wires which make up Lead III in the ECG?
1. Left arm (LA)
| 2. Left Leg (LL)
175
What does the P wave represent?
Atrial depolarisation
176
What does the QRS wave represent?
ventricular depolarisation ( covers atrial depolarisation at same time)
177
what does the T wave represent?
ventricular repolarisation
178
What does the PR interval represent?
ii. how do you measure it?
AV nodal delay
ii. beginning of P wave to beginning of QRS complex
it is between 0.12-2 seconds
179
What does the ST segment represent?
ventricular systole
180
What does the TP interval represent?
Diastole
181
what type of muscle is the cardiac muscle
striated- caused by regular arrangement of contractile protein
182
What joins to adjacent cardiac myocytes together?
1. Gap junctions- for electrical conduction
2. Desmosomes- found within intercalated discs used for mechanical adhesion (i.e tension developed by one cardiac cell is transmitter to the next)
183
What are myofibrils?
Found within each muscle fibre (cell)
they are the contractile unit of muscle
184
What do myofibrils consist of?
1. Actin (thin filaments)- lighter appearance
| 2. Myosin (thick filaments)- dark appearance
185
What are actin and myosin arranged into?
sarcomeres (functional unit of muscle)
186
How is muscle tension produced?
Sliding of actin filaments on myosin filaments- causes muscle to shorten
187
what is the role of ATP in the contraction cycle?
Allows for contraction and relaxation of muscle
188
What occurs in the contraction cycle?
1. Energised muscle filament myosin with Ca 2+ presence binds to actin filament ( BINDING stage)
2. overlapping of both filaments causes release of energy in the form of ADP and Pi ( Power stroke/BENDING)
3. Available ATP allows the detachment of myosin from actin ( DETACHMENT)
4. Myosin now energised again
189
What happens if no Ca 2+ is available for Binding of Myosin and actin?
Muscle fibres go into resting phase
190
once bending has occured, what happens to the myosin and actin if there is no ATP available?
forms a rigor complex
| which can no longer be used
191
What is the role of Ca2+ in the contraction cycle?
calcium binds to the troponin and moves the troponin-tropomyosin complex out the way thus exposing the cross-bridge binding sites.
myosin cross bridge can now bind to the actin binding sites
192
What does the sarcoplasmic reticulum release?
ii. what is this dependent on?
1. Ca 2+
| ii. presence of extracellular Ca 2+
193
what is needed to switch off the cross bridge formation and cause relaxation?
removal of calcium (either back into SR or out of cell)
194
when the muscle fibre is relaxed why is there no cross-bridge binding?
because the cross bridge binding site on actin is physically covered by the troponin-tropomyosin complex
195
what is the refractory period?
the amount of time it takes for an excitable membrane to be ready for a second stimuli following an exictation
196
what is a tetanic contraction?
continuous contraction
197
What is the role of the refractory period?
Protects the heart by preventing generation of tetanic contractions in the cardiac muscle
198
How do you calculate stroke volume?
End diastolic volume - End systolic volume
199
What is the stroke volume regulated by?
1. intrinsic mechanism= within heart itself (frank-starling mechanism)
2. Extrinsic mechanism = Nervous and hormonal control
200
What does intrinsic control consist of?
Diastolic length/ diastolic stretch of myocardial fibres (cardiac preload)
201
What effects the diastolic length?
End diastolic volume- "volume of blood within each ventricle at the end of diastole"
202
What effects the end diastolic volume?
Venous return
203
What does the frank-Starling mechanism/Starling's law of the heart state?
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)
204
as venous return increases what happens to the stroke volume?
as venous return increases:
1. EDV increases
2. stretch increases
3. stroked volume increases (to a max force)
205
How do you obtain optimal length in cardiac muscle?
Stretching the muscle
206
If Venous return to right atrium increases what happens to EDV of right ventricle?
ii. what will this mean to the stroke volume?
Increases
ii. increases Stroke volume into pulmonary artery
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If venous return to left atrium increases what happens to EDV of left ventricle?
ii. What will this mean to the stroke volume?
increases
ii. increases stroke volume into aorta
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what is the difference between skeletal muscle and cardiac muscle in terms of optimal fibre length?
skeletal muscle: optimal fibre length is resting muscle length
cardiac muscle: optimal length is achieved by stretching the muscle
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What is the afterload?
is the pressure that the heart must work against to eject blood during systole (ventricular contraction)- the extra load is imposed after the heart has contracted
210
If the afterload increases what effect has this got on the SV/EDV?
Heart is unable to eject the full SV so the EDV increases
211
What happens if Afterload continues to increase?
Ventricular hypertrophy will occur to overcome resistance
212
what does a positive inotropic effect mean?
Increases the force of contraction
213
what does a positive chronotropic effect mean?
Increases the heart rate
214
What is the the effect of sympathetic stimulation on ventricular contraction?
1. Shifts frank starling curve left
2. Peak ventricular pressure rises
3. Duration of systole decreases- Rate of pressure change (dP/dt) during systole increases
4. Duration of diastole decreases - rate of ventricular relaxation increases(rate of Ca2+ pumping increases)
5. contractility of heart at a given EDV rises
215
What does heart failure do to frank starling curve?
shift right
216
What effects do adrenaline and noradrenaline have on the heart?
inotropic
chronotropic
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What is the resting cardiac output value of a healthy adult?
5 litres per minute
70 ml (SV) x 70bpm = 4900 ml (CO)
218
when do valves make a sound?
when they are closed
219
What is the cardiac cycle?
all events that occur from the beginning of one heart beat to the beginning of the next one
220
What is the diastole?
Heart ventricles are relaxed and fill with blood
221
what is systole?
Heart ventricles contract and pump blood into the: Aorta and pulmonary artery respectively
222
At a heart rate of 75 beats/min what are the values of:
1. Diastole
2. systole
1. ~ 0.5 sec
| 2. ~0.3 sec
223
What are the 5 main events of the cardiac cycle?
1. Passive filling
2. Atrial contraction
3. Isovolumetric ventricular contraction
4. Ventricular ejection
5. Isovolumetric ventricular relaxation
224
What occurs during passive filling?
1. Pressure in atria and ventricles close to zero
2. AV valves open so venous return flows into the ventricles
3. Aortic pressure ~ 80 mmHg and aortic valve is closed
4. Same occurs in right side of heart but pressure values is much lower
5. Ventricles become ~ 80% full by passive filling
225
What occurs during atrial contraction?
1. P-wave in the ECG signals atrial depolarisation
2. Atria contracts between P wave and QRS
3. Atrial contraction complete the end diastolic volume (~ 130 ml in resting normal adult) - the end diastolic pressure is few
226
What occurs during Isovolumetric ventricular contraction?
1. Ventricular contraction starts after QRS in the ECG
2. Ventricular pressure rises
3. When the ventricular pressure exceeds atrial pressure the AV valves shut (lub sound)
4. No blood can enter or leave the ventricle
5. Tension rises around a closed volume - isovolumetric contraction
6. ventricular pressure rises very steeply
227
What occurs during Ventricular ejection?
1. When ventricular pressure exceeds aorta/pulmonary pressure
2. Aortic and pulmonary valve open ( silent event)
3. Stroke volume is ejected - leaves behind end systolic volume
4. aortic pressure rises
5. Ventricles relax and pressure decreases. Falls below aortic/pulmonary pressure
6. Aortic/pulmonary valves shut (Dub sound)
228
What does the aortic/pulmonary valves closure cause?
valve vibration creates the dicrotic notch in the aortic pressure curve
229
What occurs during isovolumetric relaxation?
1. Closure of aortic valves/pulmonary valves signal start of isovolumetric ventricular relaxation
2. Ventricle is again closed- no blood can leave or enter
3. tension falls around a closed volume- isovolumetric relaxation
4. Ventricular pressure falls below atrial pressure , AV valves open ( silent event)- new cycle starts
230
When are the heart sounds heard?
1. "Lub" sound- caused by closure of mitral and tricuspid valves (S1) SIGNALS START OF SYSTOLE
2. "Dub" sound - caused by closure of aortic and pulmonary valves (S2) SIGNALS START OF DIASTOLE
231
what are the 4 areas that must be auscultated in a cardiac exam?
aortic
pulmonary
tricuspid
mitral
232
why do arterial pressures not fall to zero during diastole?
due to the arterial stretch and recoil
233
When does JVP occur (jugular venous pulse)
Occurs after right atrial pressure waves
234
What do each waves mean on the JVP waveform?
a - atrial contraction
c - bulging of tricuspid valve into atrium during ventricular contraction
v- rise of atrial during atrial filling: release as AV valves
235
What happens if cuff pressure is greater than 120 mmHg and is greater than the blood pressure throughout the cardiac cycle?
No blood flows through he vessels
No sound is heard
236
What is the Mean arterial pressure?
the average arterial blood pressure during a single cardiac cycle, which involves contraction and relaxation of the heart.
237
What is the systemic vascular resistance/total peripheral resistance?
Sum of resistance of all vasculature in the systemic circulation
238
what type of feedback mechanism is the baroreceptor reflex?
negative feedback
239
what happens to the systolic blood pressure when healthy people stand from lying position?
No change
240
what happens to the diastolic blood pressure when healthy people stand from lying position?
slight increase due to the increased SVR (baroreflex)
241
What makes up the total body fluid?
Intracellular fluid (2/3rd)- fluid which bathes the cells
extracellular fluid (1/3rd)
242
How do you calculate Extracellular fluid volume (ECFV)?
Plasma volume + Interstitial fluid volume
243
What are the two main factors which affect extracellular fluid volume?
1. Water excess or deficit
| 2. Na + excess or deficit
244
What are the three main hormones which regular Extracellular fluid volume?
1. RAAS
2. NPs ( natriuretic peptides)
3. ADH ( antidiuretic hormone)
245
What does RAAS consist of?
1. Renin
2. Angiotensin
3. aldosterone
246
What is the function of Renin?
1. Released from kidneys
| 2. Stimulates the formation of angiotensin I from angiotensinogen
247
Where is angiotensinogen produced?
Liver
248
What is the role of ACE enzyme?
Converts Angiotensin I to Angiotensin II
249
Where is ACE enzyme produced?
Pulmonary vascular endothelium
250
What is the role of Angiotensin II?
1. Stimulates release of aldosterone from adrenal cortex
2. Causes systemic vasoconstriction - Increases SVR
3. Stimulates thirst and ADH release i.e contributes to increasing plasma volume brought about by aldosterone
251
What is the role of aldosterone?
Acts on the kidneys to increase sodium and water retention - increases plasma volume
252
What is the rate limiting step for RAAS?
Renin secretion
253
what is Renin usually secreted in response to?
1. hypotension
2. stimulation of renal sympathetic nerves
3. decreased [Na+] in renal tubular fluid
254
What are NPs?
Natriuretic peptides- protein hormones synthesised by heart
255
What are NPs released in response to?
Cardiac distention
or
neurohormonal stimuli
256
What do NPs cause?
1. excretion of salt and water in the kidneys - reducing blood volume and blood pressure
2. Decrease renin release- decrease blood pressure
3. Acts as a vasodilator- decreases SVR and Blood pressure
acts a counter regulatory system for RAAS
257
What are the two main NPs released by the heart?
1. Atrial natriuretic peptide (ANP)
| 2. Brian-type natriuretic peptide (BNP)
258
What is ANP?
28 amino acid peptide
259
Where is ANP stored and synthesised?
atrial myocytes
260
When is ANP released?
In atrial distension (hypervolemic states)
261
What is BNP?
32 amino peptide
262
where is BNP synthesised?
ii. when is it produced?
ventricles and brain
ii. Released from heart under stretching conditions
263
What can BNP used for in terms of diagnosing a disease?
Can be measured in patients with suspected heart failure
264
Where is ADH stored and synthesised?
1. Synthesised- hypothalamus
| 2. stored- posterior pituitary
265
When is ADH released?
1. Increased ECF osmolality (Main)
| 2. decreased ECFV
266
What is plasma (ECFV) osmolality monitored by?
Osmoreceptors- most found in the brain in close proximity to hypothalamus
267
What is the role of ADH?
1.Acts in kidney tubules to increase the reabsorption of water
this increases extracellular and plasma volume- increases cardiac output and Blood pressure
2. Causes vasoconstriction which increases SVR and blood pressure
268
What is the vasomotor tone caused by?
Tonic discharge of sympathetic nerves- causes continuous release of noradrenaline
269
What effect does increasing the sympathetic discharge have on the vasomotor tone?
ii. what does this result in?
Increase vasomotor tone
ii. vasoconstriction
270
What effect does decreasing the sympathetic discharge have on the vasomotor tone?
ii. What does this result in?
Decrease vasomotor tone
ii. vasodilation
271
Where is NO produced?
ii. what process is this catalysed by?
Vascular endothelium from the amino acid L-arginine
ii. Nitric oxide synthase
272
What is the role of NO?
Vasodilator - regulates blood flow.
Only effective for few seconds
273
What stimulates NO fomration?
1. flow dependent NO formation- Stress on vascular endothelium - caused by increased blood flow
2. receptor stimulated NO formation-Chemical stimuli -
274
When is NO released once formed?
adjacent smooth muscle cells
275
What does NO do once when in smooth muscle cells?
Activates the formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation
276
What are the properties of Endothelial produced vasodilators?
1. Anti- thrombotic
2. Anti- Inflammatory
3. Anti - oxidants
277
What are the properties of Endothelial produced Vasoconstrictors?
1. pro thrombotic
2. Pro inflammatory
3. Pro- oxidants
278
What happens to the resistance vessels in organs with a myogenic response if MAP rises?
Automatically constrict
279
What happens to the resistance vessels in organs with a myogenic response if MAP falls?
Automatically dilates
280
What are the main organs involved in Myogenic response?
Brain and Kidneys
281
What are the four main factors which increase venous return?
1. Increased Venomotor tone
2. Increased skeletal muscle pump
3. Increased blood volume
4. Increased respiratory pump
282
The term capacitance vessels describes what?
Veins- contain most volume of blood during rest conditions
283
What effect does an Increased Venomotor tone have?
1. Increases venous return
2. Increases Stroke Volume
3. Increases MAP
284
What effect does an increased vasomotor tone have?
1. Increased Systemic vascular resistance
| 2. Increased MAP
285
What effect does inspiration have on the pressure gradient for venous return?
Increases it due to pressure difference between intrathoracic pressure and intraabdominal pressure.
causes suction effect for blood to enter heart from veins
286
What effect does muscle activity have on venous return?
Increases venous return
287
during exercise what autonomic system dominates?
sympathetic nervous system
288
What effect does noradrenaline have on pacemaker cells?
1. Slope of pacemaker potential increases
2. Pacemaker potential reaches threshold quicker
3. Positive chronotropic effect - frequency of AP increases
289
What are the 6 main chronic CVS responses to exercise?
1. reduction in sympathetic tone and noradrenaline levels
2. increased parasympathetic tone to the heart
3. cardiac remodeling
4. reduction in plasma renin levels
5. improved endothelial function (ie increased vasodilators and decreased vasoconstrictors)
6. reduced arterial stiffening
290
during exercise what happens to the SBP, DBP and pulse pressure?
SBP increases
DBP decreases
pulse pressure increases
291
Which way does exercise shift Frank starling curve?
To the left
292
what does the ALTS classification quantify?
Class of haemorrhagic shock
293
What is the role of fascicles in the heart?
Another word for Bundle e.g. of nerves and fibres
294
What does the bundle of His divide into?
left and right branches
295
what does a 3rd heart sound suggest?
If in a healthy individual then can be early diastolic low frequency sound (related to filling of ventricle)
if not patient is not healthy then potentially heart failure
296
What does a 4th heart sound suggest?
Almost always pathological
refers to later diastolic low frequency sound that is related to active filling of a stiff non compliant ventricle by atrial contraction
297
What effect might increased venous return to the right side of the heart during inspiration have to heart sounds?
May hear three heart sounds. The latter two become further away from each other during inspiration
because increased return prolongs closure of pulmonary valve
298
what endogenous substance acts on M2 muscarinic cholinoreceptors in the heart?
acetylcholine
