Brainscape's Knowledge GenomeTM

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


See full index

CVS > 5 CVS > Flashcards

5 CVS Flashcards

1
Q

How is mean arterial blood pressure defined?

A 
maBP = CO x TPR 
maBP = SV x HR x TPR

or
maBP = diastolic pressure + 1/3 pulse pressure

or
maBP = (SBP + 2 DBP)/3

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

How is haemodynamic shock defined?

A

acute condition of inadequate blood flow throughout the body.
It results from a catastrophic fall in arterial blood pressure.
maBP = CO x TPR, so could result either from a dramatic fall in CO or in TPR

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

Which 3 sources can explain a fall in cardiac output resulting in shock?

A
  1. Mechanical source, ie the pump cannot fill
    = mechanical shock, obstructive
  2. Pump failure
    = cardiogenic shock, originate in the heart itself, the ventricle cannot emoty properly
  3. Loss of blood volume
    = hypovolaemic shock, reduced blood volume leads to poor venous return
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can cause fall in TOR and consequent shock?

A

excessive vasodilation.

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

What is cardiogenic shock?

A

PUMP FAILURE
It is shock in which cardiac output falls dramatically leading to a fall in maBP.
This sort of shock originates in the heart itself, therfore cardiogenic. The ventricle cannot empty properly.
It does fill, doesn’t eject!

It is NOT heart failure! Heart failure is a chronic condition!

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

What is mechanical shock?

A

This is a decrease in cardiac output that leads to fall in maBP because the ventricle can no longer FILL properly. It is an obstructive shock.

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

What is hypovolaemic shock?

A

It is a type of shock in which cardiac output is reduced because of a loss of blood volume. The consequent venous return is poor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Is pump failure defining cardiogenic shock the same as heart failure?

A

No. Heart failure is a chronic condition, and is not immediately life-threatening.
Cardiogenic shock is an acute life-threatening condition in which the heart fails to maintain cardiac output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can the causes of cardiogenic shock be (ie. pump failure, ventricle no longer ejecting sufficiently)

A
  1. Following MI and that has damaged left ventricle.
  2. Serious arrythmias (brady- or tachycardia)
  3. Acute worsening of heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does central venous pressure change with cardiogenic shock?

A

Central venous oressure may be

  • normal
  • raised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do urine levels vary with poor kidney eprfusion?

A

Rediced urine production, ie. oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is cardiac arrest defined?

A

Unresponsiveness associated with lack of pulse.
- heart has stopped or ceased to pump effectively
There are 3 forms of cardiac arrest:
1. asystole (loss of electrical and meachanical activity)
2. pulseless electrical activity
3. ventricular fibrillation - this is the most common form of cardiac arrest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Can you have cardiac arrest and a pulse?

A

No, by definition, cardiac arrest is unresponsiveness associated with lack of pulse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Can you have persistant electrical activity yet be in cardiac arrest?

A

yes! There would be no pulse, but still an electrical activity that can be seen on an ECG. There has been a dissociation between electrical and mecanical activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which is the most common form of cardiac arrest and what does it often follow?

A

Ventricular fibrillation, ie uncoordinated electrical activity is the most common form of cardiac arrest.
It often follows MI, electrolyte imbalance or some arrhythmias (eg. long QT and Torsades de Pointes)

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

What are the 3 steps to cardiac arrest management?

A
  1. basic life support (chest compression and external ventilation)
  2. Advanced life support: defibrilation, electric current delivered to the heart, depolarises all cells and puts them into refractory period. This allow coordinated electrical activity to restart,
  3. Adrenaline: enhances myocardial function and increases perpheral resistance (a1 adrenoceptors on vessels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is mechanical shock?

A

It is a type of shock that induces a fall in cardiac output due to the heart not being able to pump out anymore.
This occurs in cardiac tamponnade, where fluid builds up in pericardial cavity and limits end diastolic volume; or in major pulmonary embolism.
The heart is no longer optimally filling.
- Central vneous pressure high
- arterial pressure is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do the central venous pressure and arterial pressure changes with mecanical shock?

A
  • CVP is high (blood returning to heart but cannot enter

- arterial blood pressure is low, because only little blood is filling heart and being ejected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In which two clinical cases can mecanical shock be seen?

A
  1. Cardiac tamponnade

2. Pulmonary embolism

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

How does a major pulmonary embolism cause shock ,and which sort of shock?

A

Massive pulmonary embolism can cause mecanical shock.
The embolus occludes a alrge pulmonary artery, so rV cannot empty.
Central venous pressur eis high, as blood is not leaving rV.
There is reduced return of blood to the lV seeing as little blood is getting to the lungs. Therefore, lV filling is reduced.
- left atrial pressure is low
- arterial blood pressure is low

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

What is hypovolaemic shock?

A

It is atype of shock reducing CO. It corresponds to a fall in blood volume. It is most commonly due to haemorrhage.
- loss of 20-30% of volume loss will present with some sogns of shock
- 30-40% of volume loss will result in a substantial decrease in maBP and serious shock response.
Severityof shock is related to AMOUNT and SPEED of blood loss

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

Severityof hypovolaemic shock is related to what?

A
  1. Amount of blood loss

2. Speed of blood loss

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

On the starling curve, how is contractility represented?

A

By the cirve of SV/venoupressure.

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

How is hypovolaemic shock detected by the body?

A

Decreased in blood volume is detected by baroreceptors.

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

How does venous pressure change with hypovolaemic shock?

A

Venous pressure falls, consequently SV will also fall, so CO falls too.

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

How does contractility change with hypovolaemic shock response?

A

Contractility increases in response to hypovolaemic shock. This is seen on the Starling curve as a sharper slope.

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

What does one mean by “internal transfusion” when talking about response to hypovolaemic shock?

A

In hypovolaemic shock, there will be vasoconstriction. Normally at capillary level there is small movement of fluid out of the vessel into the interstitium.
But when TPR increases, capillary hydrostatic pressure decreases, and net movement is now into capillaries!

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

A patient in hypovolaemic shock presents with which typical 4 symptoms?

A
  1. Tachycardia
  2. Weak pulse
  3. Pale skin
  4. Cold, clammy extremities (clammy because of sympathetic activation!)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hypovolaemic shock is typically triggered by hemorrhage. But which 2 other causes could trigger this type of shock?

A
  1. Severe burns’2. Severe diarrhoea or vomiting and loss of Na
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which determinant of Blood Pressure is altered in distributive shock?

A

TPR is decreased (massive vasodilation) and so BP decreases too.

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

Profound peripheral vasodilation is susceptible of causing which type of shock?

A

Distributive, or low resistance shock. (vormovolaemic)

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

Which 2 clinical situations are distributive shocks?

A
  1. Septic (toxic) shock

2. Anaphylactic shock

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

Which bodily response causes vasodilation in ,septic shock?

A

Profound inflammatory response (excessive) will cause massive vasodilation in response to bacterial endotoxins. The arterial pressure drops, and perfusion to vital organs is impaired.

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

What happens to capillaries in septic shock that makes the situation worse?

A

The capillaries become mleaky, and so there is not only a big decrease in TPR but there is also loss of volume.

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

How does a patient woth septic shock present?

A
  1. Tachycardia
  2. Warm, red extremities initially, but in later stages of sepsis, there is vasoconstriction and localised hypoperfusion,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which determinant of arterial pressure is affected in anaphylactic shock?

A

TPR decreases massively because of the vasodilator effect of histamine released by mast cells

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

What symptoms does a patient in anaphylactic shock present?

A
  1. Difficulty breathing
  2. Collapsed
  3. Rapid HR (trying to compensate for poor perfusion)
  4. Red, warm extremities
38
Q

What is an epipen and how does it work?

A

An epipen is an injection of adrenaline that will cause vasoconstriction via action on a1-adrenoceptors. It is used in anaphylactic shock to try and counteract the avsodilation mediated by histamine,

39
Q

Which are the 4 types of shock?

A
  1. Mecanical - obstructive
  2. Cardiogenic - pump failure
  3. Hypovolaemic - hemorrhage, burns, or severe diarrhoea or vomiting
  4. Distributive - septic and anaphylactic
40
Q

How is blood pressure regulated short term?

A

Baroreceptor reflex.

  • ajust sympathetic and parasympathetic inputs to the heart to alter cardiac output
  • adjust sympathetic input to peripheral resistance vessels to alter TPR.
41
Q

Where are baroceptors located?

A

Nerve endings in the carotid sinus and the alrtic arch.

They are sensitive to stretch.

42
Q

Where do barorecptors feed back to?

A

Medulla oblongata of the brainstem

43
Q

What are the limitaitons of the baroreceptor reflex?

A

It is efficient in acite changes in BP, but it does not control sustained increases because the threshold for baroreceptor firing resets.
It is the frequency of firing that will be interpreted by the medulla oblongata.

44
Q

What are the medium and long term control mechanisms of blood pressure? (4)

A
  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone ADH
  4. Atrial natriuretic peptide ANP
45
Q

The 4 neurohumoral control mechanisms of blood pressure are directed at controlling the balance of which ion?

A

sodium Na!

46
Q

Where is renin released from?

A

Renin is released from the granular cells of the juxtaglomerular apparatus JGA.

47
Q

Which 3 factors stimulate renin release?

A
  1. Reduced NaCl delivery to the macula densa cells of the distal tubule
  2. Reduced perfusion pressure in the kidney causes the release of renin (detected by baroreceptors in afferent arteriole)
  3. Sympathetic stimulation to JGA increases release of renin
48
Q

Which 3 types of cell make up the juxtaglomerular apparatus that secretes renin?

A
  1. Macula densa cells
  2. Granular cells
  3. Surrounding mesangial cells
49
Q

What is renin’s enzymatic activity?

A

renin activates angiotensinogen into angiotensin I

50
Q

What are the actions of angiotensin II? (3)

A
  1. Vasoconstriction
  2. Stimulates Na reabsorption at midney
  3. Stimulates aldosterone release (from adrenal cortex) => which in turn stimulates Na reabsorption at kidney.
  4. Increases release of noradrenaline by the sympathetic NS
  5. Increases thirst sensation by stimulating ADH release by the hypothalamus.
51
Q

What receptors does angiotensin II bind to?

A

AT1 and AT2

52
Q

Via which receptor ar the majority of angiotensin II’s actions mediated?

A

AT1 receptor, it is a G-protein coupled receptor

53
Q

By which enzyme is angiotensinI converted to angiotensin II?

A

By ACE, angiotensin converting enzyme

54
Q

What are the 4 actions of aldosterone on the kidney?

A
  1. acts on principal cells of collecting ducts
  2. Stimulates Na and therefore water reabsorption
  3. Activates apical Na channel (ENaC) and apical K channel
  4. Increases absolateral Na extrusion via Na/K ATPase
55
Q

What is bradykinin?

A

Bradykinin is a vasodilator which is degraded by ACE.

56
Q

Which action aside from converting AngI into AngIi does ACE exert?

A

It also degrades bradykini, but bradykinin is a vasodilator, so ACE helps AngII with vasoconstriction

57
Q

Captopril is a drug that mimics the brazilian vioers venom, therefore, what does it do?

A

captopril and the venom of the brazilian vioer both block the conversion of AngI into AngII by ACE. Therefore, the vasoconstricting effect of AngII is lost. This drug is consequently an ANTIHYPERTENSIVE ACE inhibitor.

58
Q

On which level of the RAA system do ACE inhibitor act?

A

On ACE, therefore in the conversion of AngI into AngII

59
Q

How does glomerular filtration rate GFR change with sympathetic stimulation?

A

Sympathetic stimulation decreases GFR by arteriole vasoconstriction = conserves volume.

60
Q

What are the actions of antidiuretic hormone ADH.

A

The main role of ADH is the formation of concentrated urine by retaining water to control plasma osmolarity.
It works by increasing water reabsorption in distal nephron AQP2.
It also stimulates Na reabsorption in the thick ascending limb

61
Q

ADH release is stimulated by … (2)

A

Plasma osmolarity or severe hypovolaemia

62
Q

By which cell are atrial natriuretic peptide ANP secreted?

A

ANP is synthesised, stored and secreted by atrial myocytes.

63
Q

What stimulus triggers ANP release?

A

atrial stretch

64
Q

What effect does ANP exert and where?

A

ANP promotes Na excretion and inhibits Na reabsorption by the kidneys.
Causes vasodilation of the afferent arteriole thus increasing GFR.

65
Q

What effect does reduced circulating volume have on ANP release?

A

reduced filling of the heart => less stretch => less ANP release

66
Q

In what does ANP differ in its actions from the other neurhumoral regulators?

A

It causes natiuresis, ie LOSS of sodium. It reacts to high blood pressure, and acts to lower volume.
It is triggered by hypertension.

67
Q

How do prostaglandins influence blood pressure?

A

They act as vasodilators, enhance glomerular filtration and reduce Na reabsorption. Thea re important when AngII is high.

68
Q

How does dopamine influence blood pressure?

A

DA causes vasodilation and increases renal blood flow.

DA reduces NaCl reabsorption.

69
Q

What is hypertension?

A

Hypertension is sustained increase in blood pressure.
>140/90 mmHg in clinic
> 135/85 mmHg at home

70
Q

Ehich are the 3 stages of hypertension?

A

Stage 1 >140/90 in clinic
Stage 2 > 160/100 in clinic
Severe hypertension >180 syst or > 110 dias

71
Q

What causes hypertension?

A

95% of cases don’t know why! This is called essential, or primary hypertension,

72
Q

What is primary or essential hypertension?

A

It is hypertension for which we cannot find and define a particular cause. This is the case for 95% of hypertensive patients.

  • genetic factors
  • environmental factors
73
Q

What is secodnary hypertension?

A 
When the cause of hypertension can be defined, then hypertension is secondary.
Examples
- renovascular disease
- chronic renal disease
- hyperaldosteronism
- Cushing's syndrome
74
Q

What is renovascular disease?

A

Occlusion of the renal artery (eenal artery stenosis) that will cause a fall in perfusion pressure in that kidney.
This will trick the kidney into thinking that BP is low, thus triggering production of renin, and activation of RAAs system.

75
Q

What is renal parenchymal disease?

A

It is a cause of secondary hypertension.
It is due to a loss of vasodilator substances in earlier stages and in later stages there is NA and water retention due to inadequate glomerular filtration.
= volume-dependent hypertension

76
Q

What is Conn’s syndrome?

A

It is an adrenal cause of secondary hypertension. An adenoma is secreting aldosterone causing hypertension and hypokalaemia.

77
Q

What is Cushing’s syndrome?

A

It is an excess secretion of glucocorticoid cortisol.
At high concentrations, cortisol acts on aldosterone receptors causing Na and water retention.
People on steroids (gym or clinical) then they will also get features of Cushing’s.

78
Q

Is there a stronger link between mortality and systolic or diastolic hypertension?

A

diastolic

79
Q

All diseases attributable to hypertension are…

A

vascular!

80
Q

How does hypertension induce heart failure?

A

hypertension induces increased overload. So the heart has to make a bigger effort to punp blood out, this cause left ventricular hypertrophy. This hypertrophy is concentric and even. The heart itself doesn’t get anybogger, only the wall of the LV. So there is narrowing of the ventricular cavity, less filling, and consequent heart failure.

81
Q

Which non-pharmacological approaches are there to treating hypertension?

A
  • exercicse
  • diet
  • reduced Na intake
  • reduced alcohol intake
82
Q

Name 3 pharmacological drug tyoe that target hypertension.

A
  1. ACE inhibitors
  2. Vasodilators
  3. Diuretics
  4. AngII inhibitors
83
Q

Blocking the production or action of AngII is antihypertensive by acting on what?

A

Normally AngII is a powerful vasoconstrictor and has direct action on the kidney and promotes aldosterone release for NaCl retention.
=> if AngII is blocked, then vasodilation, and NaCl excretion

84
Q

Which 2 types of vasodilators could we use to treat hypertension?

A
  1. L-type Ca channel blockers CCBs - they would reduce Ca entry to bascular smooth muscle cells
  2. a1-adrenoceptor blockers could in principle be used too, they would reduce sympathetic tone on the vessels.
    nb. Could cause fainting
85
Q

What is Thiazide and where does it exert its action?

A

Thiazide is a diuretic, it reduces circulating volume.

It acts on NCC, NA-Cl Cotransporter in the apical membrane of kidney tubules.

86
Q

Why are b-blockers not used in hypertension alone?

A

Because blocking b1 receptors in the heart wil lreduce effects of sympathetic output, thus reducing heart rate and contractility.

87
Q

Explain how blood pressure is controlled in the short and longer term.

A
  1. Short term BP control by baroreceptors and beroceptor reflex, via stretch receptros that feedback to medulla oblongata
  2. Longer term BP control by neurohumoral mechanisms such as RAAs, Sympathetic nervous system, ANP atrial natriuretic peptide, ADH.
88
Q

What is the normal range for heart rate?

A

60-100 bpm

89
Q

Waht would happen to the heart rate if you totally de-nervated the heart?

A

The heart rate would increase, as in vivo itnis lowered by parasympathetic tone. Without it, HR is raised to about 100 bpm.

90
Q

What neurotransmitter is released by the sympathetic nervous system acting on the heart and what type of receptor does it act on?

A

Noradrenaline and it acts on b1 adrenoceptors.

91
Q

What is the intracellular signalling mechanism of NA on b1 receptors and what effect does it have on the heart?

A

QIS QIQ SIQ SQS

CVS (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions