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CVS > Lecture 20 > Flashcards

Lecture 20 Flashcards

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
Q

What is cardiac arrest?

A

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
Q

What is the most common form of cardiac arrest?

A

Ventricular fibrillation (caused by MI/electrolyte imbalance/arrhythmias)

27
Q

How do you treat cardiac arrest?

A

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
Q

What is distributive shock?

A

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
Q

What is toxic shock?

A

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
Q

Symptoms/signs of septic shock:

A

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
Q

What is anaphylactic shock?

A

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
Q

Symptoms of a patient with anaphylactic shock:

A

-difficulty breathing
-collapsed
-rapid HR
-red, warm extremities
Acutely life threatening

33
Q

What is given to a patient in anaphylactic shock?

A

Adrenaline (EpiPen) in pharmacological dose (at physiological doses acts on B2 receptors)
-vasoconstriction via alpha1 adrenoceptors in vascular smooth muscle

CVS (16 decks)

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