Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

My Cardiovascular > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do you calculate the Mean arterial pressure?

A

MAP= Cardiac output (CO) x Systemic vascular resistance (SVR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define the cardiac output

A

volume of blood pumped by each ventricle of the heart per minute.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do you calculate the cardiac output

A

stroke volume x heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adequate tissue perfusion depends on what?

A
  1. Adequate blood pressure.

2. Adequate cardiac output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define stroke volume.

A

The volume of blood ejected by each ventricle per heart beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What types of shock are there?

A
  1. Cardiogenic
  2. obstructive
  3. distributive
  4. Hypovolemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens during hypovolaemic shock?

A
  1. Blood loss causes decrease in blood volume
  2. Decrease in venous return
  3. decreased end diastolic volume
  4. decreased stroke volume
  5. decreased cardiac output and decreased blood pressure.
  6. inadequate tissue perfusion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens during cardiogenic shock?

A

Sustained hypotension caused by decreased cardiac contractility.

  1. decreased cardiac contractility
  2. decreased stroke volume
  3. decreased cardiac output and decreased blood pressure
  4. inadequate tissue perfusion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens in obstructive shock?

tension pneumothorax

A
  1. increased intrathoracic pressure.
  2. decreased venous return
  3. decreased end diastolic volume
  4. decreased stroke volume
  5. decreased cardiac output and decreased blood pressure.
  6. inadequate tissue perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens in neurogenic shock?

A
  1. loss of sympathetic tone to blood vessels and heart
  2. Massive venous &arterial vasodilation- effects heart rate
  3. Decreased Venous Return
    Decreased SVR (TPR)
    Decreased Heart Rate
  4. Decreased Cardiac Output
    Decreased blood pressure
  5. Inadequate Tissue Perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens during vasoactive shock?

A
  1. release of vasoactive mediators
  2. massive venous and arterial vasodilation also increased capillary permeability
  3. decreased venous return and decreased systemic vascular resistance.
  4. Decreased Cardiac Output
    Decreased blood pressure
  5. Inadequate Tissue Perfusion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How should you treat shock?

A
  1. ABCDE approach
  2. high flow oxygen
  3. volume replacement- except for cardiogenic shock
  4. call for HELP early
  5. Inotropes for cardiogenic shock- makes contractility better.
  6. immediate chest drain for tension pneumothorax (2nd intercostal space)
  7. Adrenaline for anaphylactic shock
  8. Vasopressors for septic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the difference between the two main types of hypovolaemic shock?

A
  1. Non haemorrhagic shock causes ECFV to decrease. Haemorrhagic shock does not
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When can compensatory mechanisms maintain blood pressure till?

A

When blood volume loss is greater than 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How many classes of haemorrhagic shock are there?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the two types of hypovolaemic shock?

A
  1. Haemorrhagic shock- haemorrhage from trauma, surgery or GI haemorrhage
  2. non haemorrhagic shock- vomiting, sweating and diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the characteristics of haemorrhagic shock?

A
  1. tachycardia- via baroreceptor reflex
  2. small volume pulse- decreased stroke volume
  3. cool peripheries - CO decreases and Increase in SVR via baroreceptor reflex
  4. MAP decrease after >30% of blood loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can mean arterial pressure be calculated using the diastolic blood pressure?

A

MAP= DBP + 1/3 Pulse pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is SVR regulated by?

A

vascular smooth muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the main site of SVR?

A

Arterioles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Contraction of vascular smooth muscles causes what?

A

Vasoconstriction

Increases SVR and MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does relaxation of vascular smooth muscle cause?

A

Vasodilation

Decrease SVR and MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Resistance to blood flow is directly proportionate to what?

A

Blood viscosity and length of blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Resistance to blood flow is indirectly proportionate to what?

A

Inversely proportional to the radius of blood vessel to the power 4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Write the equation relating to resistance to blood flow.

A

R ∝ η.L

r4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the vasomotor tone.

A

Describes the smooth muscle being partially contracting at rest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Resistance to blood flow is mainly controlled by what?

A

Vascular smooth muscles through changes in the diameter of arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What type of nerve fibres are vaso smooth muscles supplied by?

ii. What is the neurotransmitter used and what receptor?

A

Sympathetic.

ii. Noradrenaline and alpha receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What causes the noradrenaline to be released?

A

tonic discharge

increased tonic discharge= vasoconstriction

decreased tonic discharge= vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When is there parasympathetic intervention of arterial smooth muscles?

A

For the penis and clitoris.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Where is adrenaline produced from?

A

The adrenal medulla.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What occurs if adrenaline acts on an alpha receptor?

ii. Where would this be found normally?

A

vasoconstriction.

ii. Skin, gut and kidney arterioles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What occurs if adrenaline acts on a beta 2 receptor?

ii. where would this be found normally?

A

Vasodilation.

ii. Cardiac and skeletal muscle arterioles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What do each hormones cause:

i. Angiotensin II
ii. Antidiuretic

A

i. Vasoconstriction

ii. Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What factors lead to vasodilation and metabolic hyperaemia?

A

Decreased local PO2

Increased local PCO2

Increased local [H+] (decreased pH)

Increased extra-cellular [K+]

Increased osmolality of ECF

Adenosine release (from ATP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Give examples of Humoral agents which cause vasodilation.

A

Histamine

Bradykinin

Nitric Oxide (NO) - continuously released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Give examples of Humoral agents which cause vasoconstriction.

A
  1. serotonin
  2. Thromboxane A2
  3. Leukotrienes
  4. Endothelin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a local humoral agent

ii. when are they released?

A

Local chemicals released in an organ.

ii. Response to Tissue injury or inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is blood pressure?

A

The hydrostatic pressure exerted by the blood on vessel walls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Define systemic systolic arterial blood pressure.

ii. What value should it not exceed?

A

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

ii. 140 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Define systemic diastolic arterial blood pressure?

ii. What value should it not fall below?

A

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

ii. 90 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the values of hypertension?

i. clinically
ii. day time average?

A

i. 140/90 mm Hg

ii. 135/85 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the pulse pressure?

ii. What is its average value?

A

Difference between systolic and diastolic pressure.

ii. 30-50 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is laminar flow?

ii. is it audible in a artery through a stethoscope?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How would you be able to hear arterial blood pressure?

A

If the cuff pressure(external presure) is in between the values of the systolic and diastolic pressures. This makes the blood flow turbulent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Is turbulent blood flow audible in a stethoscope?

A

yes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the 5 korotkoff sounds?

ii when do you hear them?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the role of the Pressure gradient?

ii. How do you calculate?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

The systolic period of the cardiac cycle is just as long as the diastolic period true or false?

A

false- diastolic period is twice as long as the systolic period in the cardiac cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Normal systolic pressure is?

A

<140 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Normal systolic pressure is?

A

<90 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Normal range of mean arterial pressure is?

ii. What happens if it is below 60 mm Hg

A

70-105 mm Hg

ii. Need to perfuse coronary arteries and kidneys.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the second equation when calculating the mean arterial pressure?

A

CO (or SV x HR) x Stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the role of the baroreceptor reflex?

A

Short-term Regulation of Mean arterial Blood Pressure.

includes prevention of postural changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the two types of baroreceptors?

ii. What nerves do they use to send signals to the medulla?

A

Carotid sinus

Aortic arch

ii. Carotid - IXth Glossopharyngeal nerve
Aortic - Xth vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

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

A

Gravity effect:

  1. Gravity causes venous return to decrease
  2. MAP decreases - reduces rate of firing from baroreceptors

Response:

  1. Vagal tone decreases/ sympathetic tone increases
  2. This leads to Increase in HR and SV (stroke volume)
  3. Sympathetic constrictor tone increases- SVR increases
  4. 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the causes of postural (orthostatic) hypotension?

A

When baroreceptors fail to respond to gravitational shift in blood from horizontal to vertical position.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Give examples of risk factors for postural hypotension?

A 
Age related
Medications
Certain diseases
Reduced intravascular volume
Prolonged bed rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Symptoms for postural hypotension

A 
lightheadedness
 dizziness
blurred vision
faintness 
 falls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Why do baroreceptors only work work on acute related blood pressure issues?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is stenosis?

A

narrowing of the vessel lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the pathophysiology of renal artery stenosis.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Describe how stress causes an increase in hypertension.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the definition of haemostasis?

A

arrest of blood loss from a damaged vessel – at the site of injury involves in sequence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe the process of haemostasis

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What does vessel damage expose?

ii. What reacts to this exposure?

A

Collagen.

This causes platelets to bind and become activated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What does the activation of platelets cause?

A
  1. extend pseudopodia

2. synthesise and release thromboxane A2 (TXA2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What does TXA2 bind to?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What does ADP bind to?

ii. What does this cause?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is inactive factor X converted to ?

ii. What activates it?

A

Active factor Xa

Tenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is inactive factor II converted to?

ii. What activates it?

A

thrombin

Prothrombinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is thrombosis

ii. What are its causes?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the two types of thrombus?

A

White thrombus (arterial)

Red thrombus (venous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Describe the process of white thrombus.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Describe the process of red thrombus.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What does Warfarin do to the clotting factors?

A

Prevents activation of clotting factor II VII, IX and X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the roles of anticoagulants?

ii. What is a major risk of using them?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is warfarin structurally related to?

ii. What does it compete for

A

Structurally related to vitamin K with which it competes for binding to hepatic vitamin K reductase preventing production of the active hydroquinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Describe warfarins characteristics?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Warfarin has a high therapeutic index true or false?

A

false - Can be very difficult to strike the balance between anticoagulant effect and haemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What factors increase the risk of haemorrhage when using warfarin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What factors increase the risk of thrombosis and weaken the effect of warfarin?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the role antithrombin III?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Give examples of special adaptations of coronary circulation.

A

High Capillary density

High basal blood flow

High oxygen extraction ( approx 75% compared to 25% whole body average) at rest .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What does high oxygen extraction mean?

A

This means extra O2 (when required) cannot be supplied by increasing O2 extraction

Can only be supplied by increasing coronary blood flow .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Describe the effect of intrinsic mechanism on coronary blood flow.

A

decrease Po2 causes vasodilatation of the coronary arterioles

Metabolic hyperaemia matches flow to demand

Adenosine (from ATP) is a potent vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Describe the effect of extrinsic mechanism on coronary blood flow.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

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?

A

during diastole.

ii. shortens diastole.

the subendocardial vessels from the left coronary artery are not compressed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How is blood supplied blood?

A

via internal carotids and vertebral arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Grey matter is very sensitive to hypoxia true or false?

A

true-irreversible cell damage occurs within 3 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Give examples of special adaptations of cerebal circulation?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What happens if mean arterial blood pressure in cerebal blood rises?

A

Resistance vessels automatically constrict to limit blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What happens if mean arterial blood pressure in cerebal blood falls?

A

Resistance vessels automatically dilate to maintain blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

When does autoregulation fail?

A

If MABP falls below 60 mm Hg (falls)

If MABP rises above 160 mm Hg (rises)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What happens if MABP falls below 50 mm Hg?

A

confusion, fainting, and brain damage if not quickly corrected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What happens if PCO2 increases?

A

cerebral vasodilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What happens if PCO2 decreases?

ii. what happens if hyperventilation occured?

A

cerebal vasoconstriction

ii. constant change in partial pressure = fainting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the normal range in intercranial pressure?

A

8-13 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

How do you calculate Cerebral perfusion pressure?

A

CPP= Mean arterial pressure- Intercranial pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What happens if ICP increases?

A

Auto regulation of cerebral blood flow fails.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the blood brain barrier?

A

Intercellular junctions between cerebal capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are BBB permeable to?

ii. what are they impermeable to? whats good about this?

A

oxygen co2

Cerebral capillaries have very tight intercellular junctions- This helps protect brain neurones from fluctuating levels of ions etc in blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the normal range of pulmonary artery BP?

A

systolic : 20-25 mm Hg

Diastolic : 6-12 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are the special adaptations of pulmonary circulation?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Why is the resting blood flow of skeletal muscle blood flow?

A

Resting blood flow is low because of sympathetic vasoconstrictor tone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Skeletal muscle blood flow doesn’t decrease during exercise true or false?

A

false.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What mechanisms occur to allow for skeletal muscle blood flow to increase during exercise?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Describe the role of the skeletal muscle pump.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are Varicose veins?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

why do Varicose veins usually not lead to reduction of cardiac output.

A

because of chronic compensatory increase in blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the expected value of total cholesterol for a person with a previous MI?

A

3.5-4 mmol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are capillaries made of?

A

single layer of endothelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is the function of capillaries?

A

Allow rapid exchange of gases,water and solutes with interstitial fluid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What is the role of terminal arterioles?

A

Regulate regional blood flow to the capillary bed in most tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is the role of Precapillary Sphincters?’

A

Regulate flow in some tissues such as Mesentry.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Blood flow through capillary bed is very slow true or false?

A

true-allows time for exchange.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

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.

A

i. pass through pores
ii. Pass through the endothelial cells
iii. Vesicular transport
iv. Cannot travel through wall. (too big)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

How do fluids travel through capillary wall?

A

Bulk flow. pressure gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

How do gases and solutes travel through capillary wall?

A

diffusion concentration gradient.

121
Q

Trans capillary fluid flow is controlled by what?

A

passively driven by pressure gradients across the capillary wall

122
Q

How does Protein free plasma travel across the capillary wall?

A

ultra filtration.

123
Q

What factors effect the net filtration pressure?

A

Forces favouring filtration - fi Forces opposing filtration

A Filtration coefficient (Kf) also affect net fluid filtration

124
Q

What forces support filtration?

A

PC - capillary hydrostatic pressure

pi i - interstitial fluid osmotic pressure

125
Q

What forces oppose filtration?

A

pi C capillary osmotic pressure

interstitial fluid hydrostatic pressure

126
Q

How do you calculate NFP?

A

(PC + pi i) - (pi C + Pi)

127
Q

What is the normal NFP value at the arteriolar end and venular end?

A

Arteriolar = + 10 mm Hg

Venular = - 8 mm Hg

128
Q

How is excess fluid returned to circulation?

A

Via the lymphatics system.

129
Q

what is autorhythmicity?

A

when the heart is capable of beating rhythmically in the absence of external stimuli

130
Q

Where does excitation of the heart normally originate from?

A

Pacemaker cells- initiate the hear beat

found in the sino-atrial node

131
Q

Where is the sino atrial node found?

A

Upper right atrium close to SVC enters it.

132
Q

what is sinus rhythm?

A

when heart rate is controlled by SA node

133
Q

why do cells within the SA node have spontaneous pacemaker potential?

A

they do not have a stable resting membrane potential so the drift through depolarisation spontaneously

134
Q

what happens when the pacemaker cells take the membrane potential to a threshold?

ii. what does this result in?

A

an action potential is generated

ii. generation of regular spontaneous APs in the SA nodal cells

135
Q

what factors affect the pacemaker potenial (the slow depolarisation of membrane potential to a threshold)?

A
  1. decrease in K+ efflux
  2. Na+ influx ( the funny current)
  3. Transient Ca 2+ influx (T type Ca2+ channels)
136
Q

What causes the rising phase of action potential ( i.e threshold has been reached - depolarisation)

ii. what does this cause?

A

Activation of long lasting L type Ca 2+ channels

ii. Ca 2+ influx

137
Q

What causes the falling phase of action potential (repolarisation) ?

ii. what does this cause

A

Inactivation of L type Ca 2+ channels

ii. activates K+ channels and therefore causes efflux in K+

138
Q

what is the role of gap junctions?

A

low resistance protein channels which allow for cell to cell current flow

139
Q

Where is the AV node located?

A

base of the right atrium just above the junction of atria and ventricles

only point of electrical contact between atria and ventricles

140
Q

What are the two main properties of AV node cells in regards to electrical conduction?

A
  1. small in diameter

2. slow conduction velocity

141
Q

discuss the spread of excitation in the heart

A
  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
Q

action potential in contractile cardiac muscle cells (myocytes) is different compared to the action potential in pacemaker cells true or false?

143
Q

What is the resting membrane potential on atrial ventricular myocytes?

A

-90mV (until excited)

144
Q

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?

A

Fast influx of Na+

ii. +20 mV
iii. phase 0

145
Q

what causes phase 1 of the ventricular muscle action potential?

A
  1. closure of Na+ channels

2. Transient K+ efflux

146
Q

What causes phase 2 of ventricular muscle action potential ( Plateau phase of action potential)?

A

Influx of Ca 2+ through L type Ca 2+ channels

147
Q

What cause phase 3 of ventricular muscle action (Falling phase of action potential/repolarisation)?

A

efflux of K+

caused by activation of K+ channels and inactivation of Ca2+ channels

148
Q

Which nervous system has the main affect on the heart?

A

autonomic nervous system

149
Q

what is phase 4 of the ventricular muscle action potnential?

A

membrane rests at resting membrane potential

-90mV

150
Q

which nerve supplies the parasympathetic innervation to the heart?

A

vagus nerve

151
Q

under normal conditions what regulates the heart?

A

vagal tone

152
Q

What is the role of the vagal tone?

A

slows intrinsic heart rate from ~ 100 bpm to produce a normal resting heart rate ~70 bpm

153
Q

what is the normal resting heart rate?

A

between 60-100 bpm

154
Q

What is the term to describe a heart rate below 60 Bpm?

A

Bradycardia

155
Q

what is the term to describe a heart rate above 100 bpm?

A

tachycardia

156
Q

what exactly does the vagus nerve supply in the heart?

ii. what is the effect of vagal stimulation?

A

SA node and AV node

ii. slows heart rate and increases AV nodal delay

157
Q

what neurotransmitter is involved in parasympathetic stimulation of the heart?

A

Acetylcholine

158
Q

What receptors are involved in the parasympathetic stimulation of the heart?

A

Muscarinic M2 receptors

159
Q

What is the role of atropine

ii. when is it used?

A

Competitive inhibitor of acetylcholine

ii. extreme bradycardia- speeds up heart

160
Q

what is the effect of vagal(parasympathetic) stimulation on pacemaker potentials?

A
  1. Cell hyperpolarises longer to reach threshold
  2. Slope of pacemaker potential decreases
  3. Frequency of action potnetials decrease
  4. negative chronotopic effect
161
Q

what exactly do the cardiac sympathetic nerves supply?

A
  1. SA node and AV node

AND

  1. MYOCARDIUM
162
Q

What is the effect of sympathetic stimulation on the heart?

A
  1. increases heart rate
  2. decreases AV nodal delay
  3. increases force of contraction
163
Q

which neurotransmitters are involved in the sympathetic stimulation of the heart?

A

Noradrenaline

164
Q

which receptors are involved in the sympathetic stimulation of the heart?

A

Beta one adrenoceptors

165
Q

what is the effect of sympathetic stimulation on pace maker cells?

A
  1. Slope of pacemaker potential increases
  2. Pacemaker potential reaches threshold quicker
  3. frequency of action potential increases
  4. Positive chronotropic effect
166
Q

what does the sympathetic system do to the rate of K+ efflux during pacemaker potential?

A

decreases the rate of K+ efflux

allowing membrane potential to depolarise and reach threshold faster

167
Q

what does the parasympathetic system do to the rate of K+ efflux during pacemaker potential?

A

increases the rate of K+ efflux

causing membrane potential to take more time to depolarise and reach threshold

168
Q

what does the sympathetic system do to the rate of Na+ influx during pacemaker potential?

A

increases the rate of Na+ influx

allowing membrane potential to depolarise and reach threshold faster

169
Q

what does the parasympathetic system do to the rate of Na+ influx during pacemaker potential?

A

decreases rate of Na+ influx

causing membrane potential to take more time to depolarise and reach threshold

170
Q

decreases rate of Na+ influx

causing membrane potential to take more time to depolarise and reach threshold

A

decreases the rate of Ca++ influx

slowing the impulse down

171
Q

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?

A

increases the rate of Ca++ influx

speeding the impulse up

172
Q

what are the wires that make up Lead I in an ECG?

A
  1. Right arm (RA)

2. Left arm (LA)

173
Q

What are the wire that make up Lead II in the ECG?

A
  1. Right arm (RA)

2. Left leg (LL)

174
Q

What are the wires which make up Lead III in the ECG?

A
  1. Left arm (LA)

2. Left Leg (LL)

175
Q

What does the P wave represent?

A

Atrial depolarisation

176
Q

What does the QRS wave represent?

A

ventricular depolarisation ( covers atrial depolarisation at same time)

177
Q

what does the T wave represent?

A

ventricular repolarisation

178
Q

What does the PR interval represent?

ii. how do you measure it?

A

AV nodal delay

ii. beginning of P wave to beginning of QRS complex

it is between 0.12-2 seconds

179
Q

What does the ST segment represent?

A

ventricular systole

180
Q

What does the TP interval represent?

181
Q

what type of muscle is the cardiac muscle

A

striated- caused by regular arrangement of contractile protein

182
Q

What joins to adjacent cardiac myocytes together?

A
  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
Q

What are myofibrils?

A

Found within each muscle fibre (cell)

they are the contractile unit of muscle

184
Q

What do myofibrils consist of?

A
  1. Actin (thin filaments)- lighter appearance

2. Myosin (thick filaments)- dark appearance

185
Q

What are actin and myosin arranged into?

A

sarcomeres (functional unit of muscle)

186
Q

How is muscle tension produced?

A

Sliding of actin filaments on myosin filaments- causes muscle to shorten

187
Q

what is the role of ATP in the contraction cycle?

A

Allows for contraction and relaxation of muscle

188
Q

What occurs in the contraction cycle?

A
  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
Q

What happens if no Ca 2+ is available for Binding of Myosin and actin?

A

Muscle fibres go into resting phase

190
Q

once bending has occured, what happens to the myosin and actin if there is no ATP available?

A

forms a rigor complex

which can no longer be used

191
Q

What is the role of Ca2+ in the contraction cycle?

A

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
Q

What does the sarcoplasmic reticulum release?

ii. what is this dependent on?

A
  1. Ca 2+

ii. presence of extracellular Ca 2+

193
Q

what is needed to switch off the cross bridge formation and cause relaxation?

A

removal of calcium (either back into SR or out of cell)

194
Q

when the muscle fibre is relaxed why is there no cross-bridge binding?

A

because the cross bridge binding site on actin is physically covered by the troponin-tropomyosin complex

195
Q

what is the refractory period?

A

the amount of time it takes for an excitable membrane to be ready for a second stimuli following an exictation

196
Q

what is a tetanic contraction?

A

continuous contraction

197
Q

What is the role of the refractory period?

A

Protects the heart by preventing generation of tetanic contractions in the cardiac muscle

198
Q

How do you calculate stroke volume?

A

End diastolic volume - End systolic volume

199
Q

What is the stroke volume regulated by?

A
  1. intrinsic mechanism= within heart itself (frank-starling mechanism)
  2. Extrinsic mechanism = Nervous and hormonal control
200
Q

What does intrinsic control consist of?

A

Diastolic length/ diastolic stretch of myocardial fibres (cardiac preload)

201
Q

What effects the diastolic length?

A

End diastolic volume- “volume of blood within each ventricle at the end of diastole”

202
Q

What effects the end diastolic volume?

A

Venous return

203
Q

What does the frank-Starling mechanism/Starling’s law of the heart state?

A

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

204
Q

as venous return increases what happens to the stroke volume?

A

as venous return increases:

  1. EDV increases
  2. stretch increases
  3. stroked volume increases (to a max force)
205
Q

How do you obtain optimal length in cardiac muscle?

A

Stretching the muscle

206
Q

If Venous return to right atrium increases what happens to EDV of right ventricle?

ii. what will this mean to the stroke volume?

A

Increases

ii. increases Stroke volume into pulmonary artery

207
Q

If venous return to left atrium increases what happens to EDV of left ventricle?

ii. What will this mean to the stroke volume?

A

increases

ii. increases stroke volume into aorta

208
Q

what is the difference between skeletal muscle and cardiac muscle in terms of optimal fibre length?

A

skeletal muscle: optimal fibre length is resting muscle length
cardiac muscle: optimal length is achieved by stretching the muscle

209
Q

What is the afterload?

A

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
Q

If the afterload increases what effect has this got on the SV/EDV?

A

Heart is unable to eject the full SV so the EDV increases

211
Q

What happens if Afterload continues to increase?

A

Ventricular hypertrophy will occur to overcome resistance

212
Q

what does a positive inotropic effect mean?

A

Increases the force of contraction

213
Q

what does a positive chronotropic effect mean?

A

Increases the heart rate

214
Q

What is the the effect of sympathetic stimulation on ventricular contraction?

A
  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
Q

What does heart failure do to frank starling curve?

A

shift right

216
Q

What effects do adrenaline and noradrenaline have on the heart?

A

inotropic

chronotropic

217
Q

What is the resting cardiac output value of a healthy adult?

A

5 litres per minute

70 ml (SV) x 70bpm = 4900 ml (CO)

218
Q

when do valves make a sound?

A

when they are closed

219
Q

What is the cardiac cycle?

A

all events that occur from the beginning of one heart beat to the beginning of the next one

220
Q

What is the diastole?

A

Heart ventricles are relaxed and fill with blood

221
Q

what is systole?

A

Heart ventricles contract and pump blood into the: Aorta and pulmonary artery respectively

222
Q

At a heart rate of 75 beats/min what are the values of:

  1. Diastole
  2. systole
A
  1. ~ 0.5 sec

2. ~0.3 sec

223
Q

What are the 5 main events of the cardiac cycle?

A
  1. Passive filling
  2. Atrial contraction
  3. Isovolumetric ventricular contraction
  4. Ventricular ejection
  5. Isovolumetric ventricular relaxation
224
Q

What occurs during passive filling?

A
  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
Q

What occurs during atrial contraction?

A
  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
Q

What occurs during Isovolumetric ventricular contraction?

A
  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
Q

What occurs during Ventricular ejection?

A
  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
Q

What does the aortic/pulmonary valves closure cause?

A

valve vibration creates the dicrotic notch in the aortic pressure curve

229
Q

What occurs during isovolumetric relaxation?

A
  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
Q

When are the heart sounds heard?

A
  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
Q

what are the 4 areas that must be auscultated in a cardiac exam?

A

aortic
pulmonary
tricuspid
mitral

232
Q

why do arterial pressures not fall to zero during diastole?

A

due to the arterial stretch and recoil

233
Q

When does JVP occur (jugular venous pulse)

A

Occurs after right atrial pressure waves

234
Q

What do each waves mean on the JVP waveform?

A

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
Q

What happens if cuff pressure is greater than 120 mmHg and is greater than the blood pressure throughout the cardiac cycle?

A

No blood flows through he vessels

No sound is heard

236
Q

What is the Mean arterial pressure?

A

the average arterial blood pressure during a single cardiac cycle, which involves contraction and relaxation of the heart.

237
Q

What is the systemic vascular resistance/total peripheral resistance?

A

Sum of resistance of all vasculature in the systemic circulation

238
Q

what type of feedback mechanism is the baroreceptor reflex?

A

negative feedback

239
Q

what happens to the systolic blood pressure when healthy people stand from lying position?

240
Q

what happens to the diastolic blood pressure when healthy people stand from lying position?

A

slight increase due to the increased SVR (baroreflex)

241
Q

What makes up the total body fluid?

A

Intracellular fluid (2/3rd)- fluid which bathes the cells

extracellular fluid (1/3rd)

242
Q

How do you calculate Extracellular fluid volume (ECFV)?

A

Plasma volume + Interstitial fluid volume

243
Q

What are the two main factors which affect extracellular fluid volume?

A
  1. Water excess or deficit

2. Na + excess or deficit

244
Q

What are the three main hormones which regular Extracellular fluid volume?

A
  1. RAAS
  2. NPs ( natriuretic peptides)
  3. ADH ( antidiuretic hormone)
245
Q

What does RAAS consist of?

A
  1. Renin
  2. Angiotensin
  3. aldosterone
246
Q

What is the function of Renin?

A
  1. Released from kidneys

2. Stimulates the formation of angiotensin I from angiotensinogen

247
Q

Where is angiotensinogen produced?

248
Q

What is the role of ACE enzyme?

A

Converts Angiotensin I to Angiotensin II

249
Q

Where is ACE enzyme produced?

A

Pulmonary vascular endothelium

250
Q

What is the role of Angiotensin II?

A
  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
Q

What is the role of aldosterone?

A

Acts on the kidneys to increase sodium and water retention - increases plasma volume

252
Q

What is the rate limiting step for RAAS?

A

Renin secretion

253
Q

what is Renin usually secreted in response to?

A
  1. hypotension
  2. stimulation of renal sympathetic nerves
  3. decreased [Na+] in renal tubular fluid
254
Q

What are NPs?

A

Natriuretic peptides- protein hormones synthesised by heart

255
Q

What are NPs released in response to?

A

Cardiac distention

or

neurohormonal stimuli

256
Q

What do NPs cause?

A
  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
Q

What are the two main NPs released by the heart?

A
  1. Atrial natriuretic peptide (ANP)

2. Brian-type natriuretic peptide (BNP)

258
Q

What is ANP?

A

28 amino acid peptide

259
Q

Where is ANP stored and synthesised?

A

atrial myocytes

260
Q

When is ANP released?

A

In atrial distension (hypervolemic states)

261
Q

What is BNP?

A

32 amino peptide

262
Q

where is BNP synthesised?

ii. when is it produced?

A

ventricles and brain

ii. Released from heart under stretching conditions

263
Q

What can BNP used for in terms of diagnosing a disease?

A

Can be measured in patients with suspected heart failure

264
Q

Where is ADH stored and synthesised?

A
  1. Synthesised- hypothalamus

2. stored- posterior pituitary

265
Q

When is ADH released?

A
  1. Increased ECF osmolality (Main)

2. decreased ECFV

266
Q

What is plasma (ECFV) osmolality monitored by?

A

Osmoreceptors- most found in the brain in close proximity to hypothalamus

267
Q

What is the role of ADH?

A

1.Acts in kidney tubules to increase the reabsorption of water

this increases extracellular and plasma volume- increases cardiac output and Blood pressure

  1. Causes vasoconstriction which increases SVR and blood pressure
268
Q

What is the vasomotor tone caused by?

A

Tonic discharge of sympathetic nerves- causes continuous release of noradrenaline

269
Q

What effect does increasing the sympathetic discharge have on the vasomotor tone?

ii. what does this result in?

A

Increase vasomotor tone

ii. vasoconstriction

270
Q

What effect does decreasing the sympathetic discharge have on the vasomotor tone?

ii. What does this result in?

A

Decrease vasomotor tone

ii. vasodilation

271
Q

Where is NO produced?

ii. what process is this catalysed by?

A

Vascular endothelium from the amino acid L-arginine

ii. Nitric oxide synthase

272
Q

What is the role of NO?

A

Vasodilator - regulates blood flow.

Only effective for few seconds

273
Q

What stimulates NO fomration?

A
  1. flow dependent NO formation- Stress on vascular endothelium - caused by increased blood flow
  2. receptor stimulated NO formation-Chemical stimuli -
274
Q

When is NO released once formed?

A

adjacent smooth muscle cells

275
Q

What does NO do once when in smooth muscle cells?

A

Activates the formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation

276
Q

What are the properties of Endothelial produced vasodilators?

A
  1. Anti- thrombotic
  2. Anti- Inflammatory
  3. Anti - oxidants
277
Q

What are the properties of Endothelial produced Vasoconstrictors?

A
  1. pro thrombotic
  2. Pro inflammatory
  3. Pro- oxidants
278
Q

What happens to the resistance vessels in organs with a myogenic response if MAP rises?

A

Automatically constrict

279
Q

What happens to the resistance vessels in organs with a myogenic response if MAP falls?

A

Automatically dilates

280
Q

What are the main organs involved in Myogenic response?

A

Brain and Kidneys

281
Q

What are the four main factors which increase venous return?

A
  1. Increased Venomotor tone
  2. Increased skeletal muscle pump
  3. Increased blood volume
  4. Increased respiratory pump
282
Q

The term capacitance vessels describes what?

A

Veins- contain most volume of blood during rest conditions

283
Q

What effect does an Increased Venomotor tone have?

A
  1. Increases venous return
  2. Increases Stroke Volume
  3. Increases MAP
284
Q

What effect does an increased vasomotor tone have?

A
  1. Increased Systemic vascular resistance

2. Increased MAP

285
Q

What effect does inspiration have on the pressure gradient for venous return?

A

Increases it due to pressure difference between intrathoracic pressure and intraabdominal pressure.

causes suction effect for blood to enter heart from veins

286
Q

What effect does muscle activity have on venous return?

A

Increases venous return

287
Q

during exercise what autonomic system dominates?

A

sympathetic nervous system

288
Q

What effect does noradrenaline have on pacemaker cells?

A
  1. Slope of pacemaker potential increases
  2. Pacemaker potential reaches threshold quicker
  3. Positive chronotropic effect - frequency of AP increases
289
Q

What are the 6 main chronic CVS responses to exercise?

A
  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
Q

during exercise what happens to the SBP, DBP and pulse pressure?

A

SBP increases
DBP decreases
pulse pressure increases

291
Q

Which way does exercise shift Frank starling curve?

A

To the left

292
Q

what does the ALTS classification quantify?

A

Class of haemorrhagic shock

293
Q

What is the role of fascicles in the heart?

A

Another word for Bundle e.g. of nerves and fibres

294
Q

What does the bundle of His divide into?

A

left and right branches

295
Q

what does a 3rd heart sound suggest?

A

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
Q

What does a 4th heart sound suggest?

A

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
Q

What effect might increased venous return to the right side of the heart during inspiration have to heart sounds?

A

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
Q

what endogenous substance acts on M2 muscarinic cholinoreceptors in the heart?

A

acetylcholine

My Cardiovascular (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions