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Flashcards in Cardio L15 Integrated Responses Deck (32):
1

Central Venous Pressure (CVP):

.1. CVP is the pressure in the great veins at the point they join the heart.
a. SVC joins right atrium
2. CVP is described as the filling pressure of the right ventricle and is a key determinant of preload

2

CVP measurement

Central line into sub-clavian vein with tip near SVC entering the heart.

3

CVP Examination →

patient reclined at 45 degrees. Angle of Louis and he height of the internal jugular vein is filled with blood. RA is 5cm below angle of Louis estimated via JVP distance and the difference.

4

Determinants of central Venous Pressure:

Blood volume
Peripheral venous tone
Gravity
Skeletal muscle pump
Resp pump
Cardiac output

5

Orthostatis: the challenge

1. Gravity increases transmural pressure in lower limb veins →
2. Blood pools in lower limbs
3. Decreased blood volume in central veins ( ~500ml)
4. Decreased CVP/preload
5. Decreased stroke volume/cardiac output
6. Decreased mean arterial pressure
7. Impaired cerebral perfusion and dizziness

6

Orthostatis: The Result

If nothing corrected fainting

7

Orthostatis: The Actual response to avoid this

The Baroreceptor response

8

Orthostatis:The Response explained

1. Fall in BP leads to reduced Baroreceptor firing
→Parasym and sympathetic input altered
2. Degree of venoconstriction
3. R-A-A system activation

9

Aerobic Exercise: the challenge

Increased oxygen demand by skeletal muscle requires increased pulmonary blood flow, increased muscle blood flow and a reasonably stable blood pressure to maintain cerebral and coronary circulations

10

Aerobic Exercise: The Response

1. Increased sympathetic tone and decreased vagal tone produces an increase in heart rate (positive chronotropic effect) and stroke volume (Positive ionotropic effect)
2. The increased cardiac output (5-20 l/min) produces an increase in pulmonary blood flow and the increased stroke volume is partially responsible for an increase in systolic pressure.
3. Increased blood flow to skeletal muscle occurs as the result of active hyperaemia. There may also be effects due to circulating adrenaline acting at beta2 adrenoceptors.
4. The decrease in total peripheral resistance may produce a decrease in diastolic blood pressure.

11

Aerobic Exercise: The response → other systems that have reduced blood flow to compensate.

1. In order to prevent a precipitous fall in blood pressure the sympathetic nervous system produces a “compensatory” vasoconstriction in the splanchnic and renal vascular beds
2. Diverts some blood flow from the gut and kidney to exercising skeletal muscle.

12

Initiating of Responses: in aerobic excercise

1. Central command theory → as the brain sends info to muscle some info goes to medulla to allow it make adjustments
2. Baroreceptor reflex resetting → reset to a higher mean arterial pressure and to achieve increases BP
3. Peripheral reflex hypothesis → metaboloreceptor sin muscles. Detected by sensory nerve fibres and causes adjustments in CNS.

13

Haemorrhage: the challenge

1. Loss of blood volume
2. Decreased blood volume in central veins
3. Decreased CVP/preload
4. Decreased stroke volume/cardiac output
5. Decreased mean arterial pressure

14

Haemorrhage: response

Baroreceptor reflex
Detects low BP
Alters sympathetic tone and decreases parasympathetic tone.

15

Haemorrhage: long term response

Survival of Haemorrhage → need to replace therefore
1. Thirst and increased fluid intake (days)
2. Albumin synthesised by liver hepatocytes (1 week)
3. Erythrocyte production by red bone marrow (several weeks)

16

Shock: Definition



This is an acute failure of the cardiovascular system to perfuse the tissues with enough blood to meet their metabolic requirements.

Potentially Lethal!!

17

Shock: Symptoms and Signs

1. Anxiety, confusion, muscle fatigue and thirst
• Reduced cerebal/skeletal muscle perfusion.

18

Shock: Signs

• Pale/cold skin (vasoconstricted to divert blood away from skin),
• Rapid/weak pulse → positive chronotropic effects of CNS but weak due to low pulse pressure.
• Tachypnoea
• Oliguria
• Eventually Hypotension (Systolic <90 mmHg)
• Cold Shock
• Warm Shock → Sepsis/fever

19

Shock: Classification of shock

1. Hypovolaemic → volume failure
2. Cardiogenic → Pump failure- acutely damaged
3. Obstructive → blockage e.g. PE
4. Distributive (Septic, Neurogenic, Anaphylactic -vasodilation)

20

Hypovolaemic Shock:Definition

Decreased circulating blood volume

21

Hypovolaemic Shock: Example

Haemorrhage
Burns → Loss of SA and volume containment fluid resuss required.
Vomiting, diarrhoea, excessive diuresis (e.g. addisonian crisis),
Intestinal obstruction etc.

22

Hypovolaemic Shock: Key component

Decreased CVP results in decreased cardiac output due to the low Blood volume.

23

Cardiogenic Shock: Definition

A severe reduction in cardiac contractility

24

Cardiogenic Shock: Examples

Infarction
Myocarditis
Arrhythmias
Valve dysfunction

25

Cardiogenic Shock: Factor

Cardiac output is low despite a raised CVP

26

Obstructive Shock:

This is due to a mechanical obstruction to cardiac output such as PE (increased afterload) or impaired cardiac filling such as cardiac tamponade.

27

Distributive Shock: Definition


Results from an increased vascular capacitance above that required accommodating the blood volume.

28

Distributive Shock: Defining factor

This results in a decreased peripheral resistance and a decreased CVP.

29

Distributive Shock: Examples

Allergens (anaphylactic), bacterial toxins (septic), impaired sympathetic function (neurogenic)

30

Septic Shock:Gram negative

Gram negative organisms release endotoxin (a lipopolysaccharide derived from the cell wall) that stimulates a systemic inflammatory response (SIRS)

31

Gram positive

Organisms such as staphylococcus release several exotoxins resulting in the toxic shock syndrome

32

Decompensated Shock: Positive feedback

1. Shock leads to tissue hypoxia
2. Tissue and Organ dysfunction
3. Release of inflammatory mediators

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