CV physiology for Sedation Flashcards

1
Q

What are the 2 circulations that the heart is the pump for?

A

 Pulmonary circulation is short- oxygen depleted blood leaves RV, reaches the lung, becomes oxygenated in lung then reaches LA

 Systemic- arterial blood leaves LV, supplies whole body (including heart) and returns to the RA

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2
Q

What does force of contraction increase?

A

Pressure

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3
Q

How is back flow avoided in the heart?

A

Valves- close by pressure created as a result of contraction

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4
Q

What are the 4 valves present in the heart?

A

 Tricuspid- between RA/RV
 Pulmnory- between RV/Pulmonary circulation
 Mitral- between LA/LV
 Aortic- between LV and systemic circulation

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5
Q

What blood vessels supply the myocardium?

A

Left and right coronary arteries and their branches (come from aorta)

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6
Q

How is the heart drained?

A

Via coronary veins into Right atrium

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7
Q

How does the conducting system of the heart cause contraction?

A

Contraction does not happen in all chambers at the same time- atrium contract together first, then there is a delay and ventricles contract
 SA node (natural pacemaker for cardiac rhythm)- electrical stimulation of upper right side (RA) initiates contraction of both atria
 AV node- the signal travels here, there is a delay which gives time for both atria to contract and fill both ventricles
 The electrical signal travels through R+L bundle of HIS to the apex and stimulate contraction of the ventricles via Purkinje fibres

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8
Q

What is the effect of parasympathetic nerve supply to the heart?

A

Actions on SAN, AVN via muscarinic cholinergic receptors
-> Negative chronotropic (HR) and dromotropic effect (conduction speed)

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9
Q

Which neurotransmitter is involved in parasympathetic neurotransmission in the heart?

A

Acetylcholine

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10
Q

What is the effect of sympathetic nerve supply to the heart?

A

Actions on SAN, AVN, myocytes via B1 adrenoreceptors
-> Positive chronotropic and dromotropic effect
-> Positive inotropic effect (force of contraction)
-> relaxation of mycoytes

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11
Q

What are the phases is ventricular systole?

A

First phase involves contraction but no change in volume of ventricle (termed isovolumetric)

Second phase is ejection (pushes blood out of ventricle)

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12
Q

What are the phases of ventricular diastole?

A

 Phase 1- isovolumetric relaxation allows AV valve to open (no change in volume but ventricle relaxes)
 Phase 2- Valve open and blood flows in (passive filling)
 Phase 3- atrial systole causes blood to fill ventricles

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13
Q

What is required for diastole to occur?

A

Requires pressure changes over period of time, variation of volumes, mechanical events (opening and closing of valves), preceded by contraction and before that electrical events

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14
Q

What are the stages of the cardiac cycle? (does not necessarily have a starting point)

A
  1. Atrial systole- both together (triggered by SAN, with delay via AVN to allow ventricle to fill)
  2. Signal from AVN travels to apex of heart to start contraction of the ventricles, however contraction does not change volume of ventricles but only pressure. This forces AV valves to close and avoid reflux of blood (isovolumetric ventricular contraction)
  3. Continuation of ventricular contraction- allows opening of pulmonary/aortic valves and causes ejection
  4. Relaxation of ventricles without any change in volume allows reduced pressure (systemic blood returns to RA and pulmonary blood to LA)
  5. Difference in pressure between A and V allows AV valves to open and start filling ventricles (starts again)
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15
Q

What are the different points on an ECG?

A

P wave before atrial systole (atrial depolarisation)

QRS complex- before ventricular systole (ventricular depolarisation)

T wave- ventricular repolarisation

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16
Q

When is coronary blood flow the greatest?

A

During ventricular diastole (as CA are compressed during systole)

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17
Q

What factors cause a decrease of coronary blood flow?

A

Increased heart rate

Low aortic diastolic BP
-> less force to sustain coronary blood flow

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18
Q

How is Blood pressure calculated?

A

BP= CO x TPR

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19
Q

How is cardiac output measured?

A

Stroke volume (volume of blood ejected from ventricle on every beat) x Heart rate

20
Q

Which factors can affect SV?

A

End Diastolic volume- how much blood fills ventricles

Preload- which depends on venous return and HR

Ventricular contractility

Afterload- related to TPR

21
Q

What is venous return?

A

Blood returning to RA

22
Q

What are push and pull forces in venous return ?

A

Push- systole and muscle pumping (limb muscles/valves)

Pull- thoracic pump (neg intrathoratic pressure)- links to respiratory system (pos pressure causes reduced venous return)

23
Q

What is preload?

A

Stretching of cardiac muscle- tension in heart wall due to filling
-> determined by End diastolic volume

24
Q

What is starling’s law?

A

Starlings law- more blood (EDV) = greater stroke volume -> due to length and tension relationship (overlap of actin/myosin filaments)

25
Q

What occurs as a result of increased and reduced contractility in the heart?

A

If contractility and force increased- the end diastolic volume will increase with same SV (more efficient pumping blood)

If contractility is reduced (HF)- heart becomes less efficient

26
Q

What is after load?

A

Force that heart must develop to pump blood (eject) against the arterial BP and peripheral resistance

27
Q

What are the results of increased after load seen in hypertension?

A

Increased cardiac ‘work-load’
-> Can affect coronary blood flow

28
Q

How does blood pressure vary in different BV?

A

Decreases as it passes from arteries-> arterioles-> capillaries-> venules-> veins

29
Q

What are they typical blood pressure values for different parts of CVS?

A

Pulmonary circulation:
Heart to lungs- 25/12mmHg
Lungs to heart- 0-4mmHg

Systemic circualtion:
Arteries- 120/80mmHg
Veins- 0-5mmHg

30
Q

How is arterial BP measured?

A

done on brachial artery with sphygmomanometer

31
Q

How does a sphygmomanometer function?

A
  1. Cuff pressure exceeds arterial pressure- no sound as arterial flow is occluded
  2. When arterial pressure exceeds cuff pressure- blood flows intermittently (turbulent)
  3. Sound becomes louder but is still intermittent
  4. Lasting muffed and continuous sound when cuff reaches diastolic blood pressure level
  5. No sound- as cuff does not have pressure to obstruct bloodflow or generate turbulence
32
Q

Which vessels can be used to measure pulse?

A

External carotid artery
Facial artery
Superficial temporal artery
Radial artery
Internal Jugular

-> depends on accessibility

33
Q

How is flow calculated? (Poiseuille’s Law)

A

Delta P x Pi x (radius)4

 Divided by            

8 x Viscosity x length

34
Q

What is delta P?

A

change in pressure between each side of vessel

35
Q

How is radius related to flow?

A

Diameter of blood vessel (increasing diameter, increases flow)

36
Q

What factors can affect arteriolar radius?

A

Local- O2, CO2, pH, temp, vasoactive agents

Sympathetic nerves (A/B receptors)

Hormones- Adrenaline, ADH, Angiotensin II

37
Q

What is TPR?

A

The combined resistance of all the systemic blood vessels (provided when blood flows through all organs)

-> reducing diameter, increases resistance

38
Q

What are the effects of vasodilation in some organs on TPR?

A

Vasodilation within organs reduces TPR in some organs
-> However, compensatory vasoconstriction can occur in other organs causing TPR and therefore BP to remain the same

39
Q

What are the effects of changing posture on BV?

A

When standing there is an additional hydrostatic pressure (depending on height) of around 80mmhg- as veins are more compliant than arteries the hydrostatic pressure is converted which causes veins distend causing venous pooling and reduced venous return

-> Tilting table- changes venous return

40
Q

What is hypovolaemia and its effects?

A

Reduced intravascular volume

-> SV, CO, MABP are reduced so there is a compensatory increase in HR and TPR by vasoconstriction (may not return it to normal)

41
Q

What are the venous cannulation sites?

A
  • Cubital fossa- cephalic vein, median cephalic vein, median basilic and basilic vein (AND brachial artery)
  • Dorsum of hand- basilic vein, cephalic vein, dorsal venous network
42
Q

What are the ADV of using dorsum of hand?

A

-Easy access
-no nearby arteries
-no nearby nerves
-no joints

43
Q

What are the DIS of using dorsum of hand?

A

-small veins
-susceptible to cold/anxiety
-mobile veins
-more painful

44
Q

What are the ADV of using the cubital fossa?

A

-big vein
-well tethered to connective tissue (less mobile)
-less painful
-less venoconstriction

45
Q

What are the DIS of using the cubital fossa?

A

-access
-potential nerve damage
-potential intra arterial injection
-joint immobilisation