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Y1 - CVS > Haemoodynamic Shock > Flashcards

Haemoodynamic Shock Flashcards

1
Q

What are the 2 equations for Mean Arterial BP (MAP)?

A

MAP or maBP = CO x TPR
Can be written as
MAP or maBP = SV x HR x TPR

Or

maBP = diastolic pressure + 1/3 pulse pressure

TPR = Total Peripheral Resistance

CO = Cardiac output

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2
Q

What is the equation for cardiac output (CO)?

A

CO = SV x HR
(L/min) (ml) (per min)

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3
Q

What is the equation for pulse pressure?

A

Systolic pressure - diastolic pressure

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4
Q

What is haemodynamic shock?

A

Acute condition of inadequate blood flow around the body leading poor perfusion of tissues leading to poor oxygen supply to cells and organs

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5
Q

What leads to the inadequate blood flow causing haemodynamic shock?

What 2 factors could be the cause of this?

A

A catastrophic drop in arterial blood pressure

Shock due to fall in:
CO
or
TPR beyond capacity of heart to cope

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6
Q

What causes the fall in TPR that leads to Haemodynamic shock?

A

Excessive vasodilation

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7
Q

What are the 3 possible ways by which cardiac output can fall leading to haemodynamic shock?

What are these 3 types of haemodynamic shock called?

A

Cardiogenic shock = pump failure, ventricle cant empty properly

Mechanical shock = pump is obstructed/cant fill

Hypovolaemic shock = loss of blood volume (poor venous return drop in CO)

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8
Q

What type of failure of the heart to maintain cardiac output occurs in cardiogenic shock, how does this compare to heart failure?

A

Cardiogenic shock is ACUTE failure to maintain cardiac output (pump failure)

Whereas heart failure is chronic failure

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9
Q

What are some potential causes of Cardiogenic shock?

How do they lead to cardiogenic shock?

A

MI (damage to LV):
LV cant pump properly
Arterial BP is greatly reduced
Leads to inadequate perfusion of organs

Serious arrhythmias:
Very profound tachycardia means not enough time to fill in diastole

Very profound Bradycardia lowers BP

Acute worsening of heart failure

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10
Q

How does a very profound tachycardia cause cardiogenic shock?

A

With tachycardia, diastole shortens
Shortens so much heart cant fill with blood properly
Not enough blood pumped out = decreased MAP

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11
Q

Why can central venous pressure be raised in cardiogenic shock?

A

More blood left in heart following systole since heart fails to pump effectively, so its harder for heart to fill
Raised CVP as a result

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12
Q

What is oliguria?

A

Reduced urine production

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13
Q

Why may oliguria present with cardiogenic shock?

A

Kidneys poorly perfumed with blood so reduced urine production

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14
Q

What is the definition of cardiac arrest?

What does this mean?

A

Unresponsiveness associated with lack of pulse

Heart has stopped or has ceased to pump effectively

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15
Q

What are the 3 types of Cardiac arrest?

A

Asystole
Pulseless Electrical Activity (PEA)
Ventricular fibrillation

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16
Q

What is asystole?

A

Loss of electrical and mechanical activity

Its when the heart stops

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17
Q

What is pulseless electrical activity (PEA)?

A

Still electrical activity on ECG by no mechanical function of heart = no pulse

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18
Q

What is ventricular fibrillation?

A

Un-coordinated activity in ventricles so the ventricles dont contract

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19
Q

What usually leads to Ventricular fibrillation?

A

MI
Electrolyte imbalanced
Arrhythmias (long QT and Torsades de Pointes)

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20
Q

What are the 2 types of life support and drug that can be given to help with a cardiac arrest?

A

Basic life support

Advanced life support

Adrenaline

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21
Q

What is basic life support?

When is it given?

A

Chest compressions and external ventilation

Given when no advanced life support is available for a Cardiac Arrest

22
Q

What is done in advanced life support?

How does this work to help with the cardiac arrest?

A

Defibrillation

Gives an electrical current to the heart depolarising all of the cells putting them in the refractory period to allow the heart to restart in a coordinated fashion

23
Q

How is adrenaline useful for a cardiac arrest?

How does it do this?

A

Enhances myocardial function
+
Increases peripheral resistance

Its concentrations are high enough to activate alpha-1 adrenoreceptors of the smooth muscles of veins. This causes vasoconstriction of the peripheral veins increasing peripheral resistnace helping increase/maintain a high Arterial BP

24
Q

What are 2 ways mechanical shock can occur?

A

Cardiac tamponade

Pulmonary embolism

25
Q

What is Cardiac tamponade?

What sides of the heart does it affect?

A

Blood or fluid QUICKLY builds up in the pericardial space RESTRICTING filling of the heart

Both sides of heart affected

26
Q

In Cardiac Tamponade:

How is End Diastolic Volume (EDV) affected?

How is Central Venous pressure affected?

How is mean Arterial Blood pressure affected?

A

EDV reduced/limited

CVP = high (hard for blood to enter heart

maBP = Low (less blood can fill heart and be pumped out into arteries, lower SV)

27
Q

What is an indicator that somebody has a high central venous pressure?

A

Distended neck veins

28
Q

How can a massive Pulmonary Embolism lead to mechanical shock?

How is Central Venous Pressure affected?

How is mean arterial BP affected?

A

Embolus occludes large branch of pulmonary artery
Right ventricle cant empty properly so CVP increases
Less blood flows to left side of heart
So reduced maBP since less blood gets pumped through aorta
Leads

29
Q

What are some signs of a massive pulmonary embolus?

A

Shock
Chest pain
Dyspnoea

30
Q

What usually leads to a pulmonary embolus?

What veins do these normally form from?

A

Deep Vein Thrombosis (DVT)

Thrombus usually breaks off from veins down in the calves

Flows up to the heart through the Inferior Vena Cava into the RHS of the heart and gets pumped through the pulmonary artery

31
Q

What is the most common cause of Hypovolaemic shock?

A

Haemorrhage

32
Q

What percentage of blood loss are you likely to start seeing signs of shock (Hypovolaemic)?

A

More than 20% blood loss

33
Q

When somebody haemorrhages, leading to Hypovolaemic shock, how does CVP, CO and maBP get affected?

A

CVP falls (less blood to fill veins)

CO falls

maBP falls

34
Q

What detects the fall in maBP (fall in Blood pressure/volume)?

Where are these cells located?

A

Baroreceptors

Carotid sinus and aortic arch

35
Q

What is the bodies compensatory response to Hypovolaemic shock once its been detected by baroreceptors?

What branch of the nervous system is activated?
What affect does this have?

A

Increased sympathetic stimulation
Leads to:
-tachycardia
-inotropy (inc strength of contraction)
-peripheral vasoconstriction
-venoconstriction

All of this done to help preserve mean arterial Blood Pressure

36
Q

What is internal transfusion?

Why does this happen in Hypovolaemic shock?

A

The net movement of fluid into the capillaries (normally its out since it returns to venous system via lymphatics via subclavian vein)

Since peripheral resistance increased, theres a lower capillary hydrostatic pressure, so net movement of fluid into capillaries

37
Q

What are the signs a patient is in Hypovolaemic shock?

Why do they get these signs?

A

Tachycardia (sympathetics stimulated)
Weak pulse (less blood volume)
Pale skin (peripheral vasoconstriction)
Cold clammy extremities (adrenaline stimulates sweating from sweat glands)

38
Q

What are some causes of Hypovolaemic shock?

A

Haemorrhaging
Severe burns
Severe diarrhoea
Vomiting and loss of Na+

39
Q

Why can the Hypovolaemic shock response not be maintained forever?

A

Peripheral vasoconstriction impairs tissue perfusion

So theres a danger of decompensation

40
Q

How does prolonged Hypovolaemic shock get decompensated?

A

Due to impaired tissue perfusion of peripheries (hypoxia), damaged tissue release vasodilators
TPR falls
BP falls
Vital organs cant be perfused
Multi system failure

41
Q

What are the long term responses to restore blood volume?

A

Renin-angiotensin-aldosterone system (RAAS)

Anti-diuretic hormone

42
Q

What is distributive shock?

What component of the Cardiac Output equation does it affect?

A

Low resistance shock where blood volume is normal

Where theres Profound peripheral vasodilation leading to massive drop in TPR

43
Q

What are thee 2 types of distributive shock?

A

Toxic/septic shock

Anaphylactic shock

44
Q

What is sepsis?

A

Life threatening organ dysfunction due to a dysregulated host response to infection

45
Q

How can sepsis lead to septic shock?

A

Endotoxins made by circulating bacteria

PROFUND INFLAMMATORY RESPONSE
Leads to drop in TPR
Drop in maBP
Impaired perfusion of vital organs
Leaky capillaries reduce blood vol

Inc coagulation (DIC) and localised hypo-perfusion

46
Q

What are the signs that a patient is in Septic shock?

A

Tachycardia
Warm red extremities at early stages

Later stages - vasoconstriction

47
Q

With septic shock, what is the bodies response?

A

Baroreceptors detect fall in BP
Inc sympathetic stimulation
However, the vasoconstriction affect is overridden by mediators of vasodilation

HR and SV inc

48
Q

How does Anaphylactic shock occur?

What cells are involved?

A

Severe allergic reaction
Mast cells release histamine
Leads to MASSIVE vasodilation
Fall in TPR
Drop in maBP

49
Q

What is the bodies response to anaphylactic shock?

A

Inc sympathetic stimulation
So CO Inc but cant overcome Vasodilation

Leads to impaired perfusion of vitals

50
Q

What are other problems produced by mediators in anaphylactic shock except for vasodilation?

A

Bronchoconstriction
Laryngeal oedema (difficulty breathing)

51
Q

What will a patient present with whose in anaphylactic shock?

A

Difficulty breathing
Collapsed
Rapid heart rate
Red, warm extremities

52
Q

What is given to a patient in anaphylactic shock?
Why is this given?
How does it do this?

A

Adrenaline (via epipen normally)

Leads to vasoconstriction

Is at high enough Conc to bind to alpha 1 adrenoreceptors leading to vasoconstriction helping counteract the vasodilatory affects helping preserve maBP

Y1 - CVS (21 decks)

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