Lecture 20 Flashcards

(33 cards)

1
Q

What is mean arteriole BP equal to? (Equation)

A

CO x TPR (to increase BP, you increase CO/increase TPR-constrict arterioles)
Cardiovascular system can choose to constrict arterioles to maintain arteriole blood pressure in order to perfuse vital organs e.g. brain secure supply
(CO= SV x HR)

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2
Q

How would you calculate mean arteriole blood pressure?

A

(Diastole lasts 2/3 of time, systole lasts 1/3 of the time)

Mean ABP: diastolic pressure + 1/3 pulse pressure

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3
Q

What is the pulse pressure?

A

The difference between the diastolic and systolic pressure

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4
Q

What is haemodynamic shock?

A

Blood pressure drops so that there is inadequate blood flow through the body (acute condition)
-due to catastrophic fall in arterial BP so vital organs are not being perfused

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5
Q

How can you get a drop in the mean arterial pressure?

A

Cardiac output falls

TPR falls

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6
Q

Why would you get a fall in CO?

A

Mechanical: heart can’t fill properly
Heart not pumping properly
Loss of blood volume

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7
Q

Why would you get afl in peripheral resistance?

A

Excessive vasodilation: more blood vessels open in peripheries, not enough blood to fill all of the vessels

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8
Q

What are the 3 types of shock due to fall in CO?

A

Cardiogenic shock: pump failure, ventricle can’t empty properly
Mechanical shock: obstructive, ventricle can’t fill properly
Hypovolaemic shock: reduced blood volume leads to poor venous return to heart= drop in cardiac output

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9
Q

What are some causes of cardiogenic shock (pump failure)?

A
  • following an MI (damage to LV)
  • serious arrhythmias (third degree heart block)
  • tachycardia/ventricular fibrillation (not enough time for ventricles to fill in diastole so CO decreases)
  • worsening of heart failure
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10
Q

What happens to CVP (central venous pressure) in cardiogenic shock?

A

Can be normal/raised
Heart fills but fails to pump effectively
-end systolic volume and pressure will be high

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11
Q

Give some examples of tissues which may be poorly perfused in cardiogenic shock:

A

Coronary arteries: exacerbates problem

Kidneys: reduced urine production (oliguria)

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12
Q

What is cardiac tamponade?

A

Blood/fluid build up in pericardial space
Restricts filling of the heart, limiting EDV (nothing wrong with contraction)
-high central venous pressure (jugular veins bulge)
-low arteriole BP
(Affects both sides of heart)

Here SV is reduced and therefore CO is reduced

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13
Q

Is there continued electrical activity in cardiac tamponade?

A

Yes, heart still attempts to beat

-HR may increase to increase arteriole BP

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14
Q

What other than cardiac tamponade can cause mechanical shock?

A
Massive pulmonary embolism 
-Occludes large branch of pulmonary artery 
-increase in pulmonary artery pressure 
-right ventricle can’t empty
-CVP high 
-reduce return of blood to left side of heart
-limiting filling of left heart 
-left atrial pressure is low 
-arteriole BP is low 
= SHOCK
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15
Q

What other symptoms do people with pulmonary embolism causing mechanical shock get?

A
  • Chest pain

- dyspnoea

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16
Q

How does a pulmonary embolism reach the lungs?

A

Due to DVT

  • part of thrombus breaks off and travels in venous system to right side of heart
  • pumped out through pulmonary arteries to lungs
  • effect will depend on size of embolus
17
Q

What is the most common cause of hypovolaemic shock?

A

Haemorrhage- reduced blood volume
>20% of blood loss shows some signs of shock
30-40%= substantial decrease in mean aBP and shock response

18
Q

What is the severity of shock related to in hypovolaemic shock?

A

Amount and speed of blood loss

19
Q

What is the body’s response to hypovolaemic shock?

A

Venous pressure drops and therefore so does the SV due to Starling’s Law.
-causes a drop in arteriole pressure
-this is detected by baroreceptors
Response
- increase HR and contractility via sympathetic nervous system steepening Starling’s curve
-peripheral vasoconstriction to maintain arteriole BP
-venoconstriction

20
Q

What pressure changes does hypovolaemic shock cause?

A

Reverse of a small net movement of fluid out of the capillaries (Normal)

  • reduced blood volume/constriction of arterioles before capillaries= reduced hydrostatic pressure
  • causing net movement into capillaries (reabsorption rather than filtration) to increase volume
21
Q

Symptoms/signs of hypovolaemic shock:

A
  • tachycardia
  • weak pulse
  • pale skin (peripheral vasoconstriction)
  • cold/clammy extremities
  • low CVP
22
Q

What else (other than haemorrhage) can cause hypovolaemic shock?

A
  • severe burns

- severe diarrhoea and vomiting

23
Q

What are the dangers of hypovolaemic shock? (If not treated by fluids)

A

Danger of decompensation-when compensation fails (compensation works up until a certain time)

  • tissue damage due to hypoxia (peripheral tissues not being perfused)
  • release of chemical mediators: vasodilators
  • TPR falls
  • BP falls and vital organs stop being perfused
  • multi system failure= death
24
Q

What are the body’s long term adjustments to hypovolaemia?

A

-RAAS activation to promote salt and water retention via kidneys
-ADH released
Work over a longer time (3 days)

25
What is cardiac arrest?
Unresponsivness associated with lack of pulse -heart has stopped/ceased to pump effectively Asystole (loss of electrical and mechanical activity) PEA (pulseless electrical activity) Ventricular fibrillation often following an MI
26
What is the most common form of cardiac arrest?
Ventricular fibrillation (caused by MI/electrolyte imbalance/arrhythmias)
27
How do you treat cardiac arrest?
Basic life support (chest compressions/external ventilation) until you get advanced life support Advanced life support -defibrillation (deliver and electrical current to heart depolarising all cells at once, putting them into refractory period, causing coordinated electrical activity to restart) -adrenaline given enhancing myocardial function, and increases TPR (acting on alpha 1 adrenoreceptors causing constriction)
28
What is distributive shock?
Low resistance shock/normovolaemic shock No change in volume of blood, but profound peripheral vasodilation, reducing TPR, reducing peripheral BP -due to toxic/septic shock -due to anaphylactic shock
29
What is toxic shock?
Sepsis: can lead to septic shock (serious life threatening response to infection) Endotoxins released from bacteria or cytokines/chemokines as an inflammatory repsonse -profound inflammatory response -profound vasodilation -fall in arterial BP -impaired perfusion of vital organs -capillaries also become leaky: reducing blood volume -increased coagulation and localised hypo-perfusion in extremities often
30
Symptoms/signs of septic shock:
Decreased arterial pressure - detected by baroreceptors= increased sympathetic output - vasoconstrictor effect overridden by mediators of vasodilation - HR and SV increased Patient has - tachycardia - warm red extremities initially, later stages vasoconstriction due to localised hypo-perfusion
31
What is anaphylactic shock?
Severe allergic reaction Due to release of histamine from mast cells -powerful vasodilator effect= fall in TPR, causing drop in mAP -increased sympathetic response, increased CO to maintain mAP but this can’t overcome vasodilation -impaired perfusion of vital organs Mediators also cause bronchoconstriction/ laryngeal oedema = difficulty breathing
32
Symptoms of a patient with anaphylactic shock:
-difficulty breathing -collapsed -rapid HR -red, warm extremities Acutely life threatening
33
What is given to a patient in anaphylactic shock?
Adrenaline (EpiPen) in pharmacological dose (at physiological doses acts on B2 receptors) -vasoconstriction via alpha1 adrenoceptors in vascular smooth muscle