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CR Science 1 > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

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1
Q

Explain the path of blood flow through the heart - the cardiac cycle

A
  • Superior and inferior vena cava
  • Right Atrium
  • Tricuspid Valve
  • Right Ventricle
  • Pulmonary semilunar valve
  • Pulmonary arteries
  • Lungs
  • Pulmonary veins (L+R)
  • Left atrium
  • Bicuspid valve
  • Left ventricle
  • Aortic semilunar valve
  • Aorta
  • Body: arteries -> capillaries -> veins
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2
Q

Electrical conduction pathway of the heart (6)

A
  1. Sinoatrial node
  2. internodal pathways
  3. AV node
  4. AV bundle of His
  5. bundle branches (R+L)
  6. perkinje fibres (R+L)
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3
Q

P-wave

A

atrial depolarisation (atrial repolarisation obscured by QRS complex)

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4
Q

PR interval (PQ)

A

time delay between atrial depolarisation and conduction through AV node for ventricular activation (0.12-0.2s)

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5
Q

QRS complex

A

ventricular depolarisation (0.06-0.1 sec)

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6
Q

ST segment

A

electrical plateau of ventricular activation

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7
Q

T Wave

A

ventricular repolarisation

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8
Q

Normal HR - how to find HR on ECG

A

60-100bpm

- number of QRS complexes in a 6 second strip x 10

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9
Q

Stroke Volume (SV) - definition and normal values, formula

A

amount of blood pumped out of each ventricle during a single beat
○ ~ 70-80ml @ rest
○ EDV - ESV = SV

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10
Q

Heart rate (HR) - definition and normal values, bradycardia, tachycardia

A

number of times the heart beats (per minute)
○ 60-100 bpm
○ Bradycardia = <60 bpm
○ Tachycardia = >100 bpm

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11
Q

Cardiac Output (CO) - definition and formula

A

the amount of blood pumped by each ventricle in 1 minute
○ CO (ml/min) = SV (ml/beat) x HR (beat/min)
The difference between resting and maximal CO is cardiac reserve

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12
Q

End Diastolic volume (EDV) - definition and normal value

A

amount of blood in each ventricle at the end of ventricular diastole (the beginning of ventricular systole)
~ 120ml @ rest

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13
Q

End Systolic Volume (ESV) - definition and normal value

A

amount of blood remaining in each ventricle at the end of ventricular systole (start of ventricular diastole)
○ ~ 50 ml @ rest

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14
Q

Ejection Fraction (EF) - definition and normal value

A

percentage of EDV ejected represented by SV i.e. SV/EDV (x100 to get %)
○ ~ 55-70%
○ Varies with changing demand
○ Represents the efficiency of the heart. A diseased heart will have a reduced EF

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15
Q

Preload - definition, how it affects CO

A

end-diastolic volume/pressure = stretch placed on myocardial fibres just before contraction

○ Greater the end-diastolic volume, the more ventricular muscle fibres are stretched (Frank Starling mechanism)

Affects CO:

  • Preload too low => amount of blood available to pump out is decreased => SV decreased -> CO decreased
  • Preload too high and ventricles stretched out => reduced SV -> reduced CO
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16
Q

Afterload - definition, how it affects CO

A

resistance to ventricular contraction

Affects CO:
- Increased Afterload => increased demands of the heart

17
Q

Blood Pressure (BP) - definition, SBP, DBP definition, normal BP, hypertension, folrmula

A

Pressure the blood exerts against the inner wall of the blood vessels

○ Systolic BP (SBP) - ‘high’ pressure in arterial system
○ Diastolic BP (DBP) - ‘low’ pressure in arterial system
○ Normal arterial BP = 120/80
○ Hypertension = >140/90
○ BP = CO x TPR

18
Q

Pulse pressure

A

Pulse Pressure = SBP - DBP

19
Q

Mean arterial pressure (MAP)

A
  • DBP +1/3 pulse pressure

- Average driving pressure propelling blood from LV to RA

20
Q

What are the (2) determinants of blood flow rate? How do they affect blood flow?

A
  1. Driving pressure - Flow is directly proportional to gradient pressure; blood flow increases when pressure increases and vice versa
  2. Vascular resistance - Flow is inversely proportional to resistance; as resistance increases, blood flow decreases
21
Q

What are the determinants of vascular resistance? How do they affect resistance?

A
  1. Length of blood vessels - longer blood vessel = more resistance
  2. Radius/diameter of the blood vessels (physiological) - smaller radius/diameter = more resistance
  3. viscosity of blood - thicker blood = harder to pump -> increases vascular resistance
22
Q

What causes BP changes (3)?

A

Occur in response to:

  1. baroreceptors and chemoreceptors in the arteries (short term regulation )
  2. renin-angiotensin system (long term regulation)
  3. the kidneys (long term regulation)
23
Q

What are the short term regulators of BP?

define short term and list methods (sensor, control, effectors)

A

short term = regulation of minute to minute changes in arterial pressure due to e.g. postural changes or manoeuvres

methods:

  1. sensors: aortic and carotid baroreceptors via vagus and GP nerves. Sense change -> alert cardiac control centre
  2. control: cardiovascular control centre in the medulla oblongata regulates CV activity through nervous and endocrine systems
    - vasomotor centre = changes arterial diameter of;
    - skeletal muscle arterioles -> vasodilation
    - visceral arterioles -> vasoconstriction
    - cardio-accelerator centre = increased HR and contractility
    - cardio-inhibitor centre = decreased HR and contractility
  3. effectors: sympathetic nerves to heart and blood vessels, vagus nerve, vasomotor nerves
  4. endocrine influence: threat/stress -> sympathetic NS stimulation -> adrenaline & noradrenaline -> increased BP and HR
24
Q

What are the long term regulators of BP?

define long term and list methods

A

Long term = regulating overall arterial bp over time, involving endocrine and renal systems

Controls: (low bp) -> Renin-angiotensin-aldosterone system -> increased total circulating blood volume -> increased BP

25
Q

Controls of CO

A
  • heart rate

- stroke volume

26
Q

How does HR affect CO

A
  • sympathetic activity: increases HR, conduction velocity and ventricular contractility -> increase CO
  • parasympathetic activity: depresses the SA node -> decreases HR and impedes conduction velocity -> decreased CO
  • reflexes: acute changes in BP sensed by stretch receptors in carotid and aortic arch result in an inverse change in HR i.e. increased BP = decrease in HR
27
Q

What determines Stroke Volume?

A
  1. preload 2. afterload 3. contractility

EDV reduced -> SV reduced -> CO reduced

28
Q

How does SV affect CO?

A

increased SV = increased CO

decreased SV = decreased CO

29
Q

How does increased myocardial contractility affect CO? What causes contractility to increase?

A

increased contractility -> increased EF -> increased SV -> increased CO

Increased contractility caused by:

  • circulating adrenaline
  • sympathetic stimulation
30
Q

(3) transport methods of substances into and out of the capillaries

A
  • diffusion
  • transcytosis (transport from one side of a cell to the other within a membrane-bounded carrier)
  • bulk flow (passive movement from high to low pressure)
31
Q

What is filtration? what pressures promote it?

A

Pressure-driven movement of fluid and solutes from blood capillaries

promoted by:

  • blood hydrostatic pressure
  • interstitial fluid osmotic pressure
32
Q

What is reabsorption? what pressures promote it?

A

pressure-driven movement of fluid from interstitial fluid into blood capillaries

promoted by:

  • interstitial fluid hydrostatic pressure
  • blood colloid osmotic pressure
33
Q

What is the net result of capillary exchange?

A

filtration > reabsorption

34
Q

What is net filtration?

A

the balance between the fluid pressure. It determines whether blood volume and interstitial fluid remain steady or change

35
Q

What is oedema? why does it occur?

A

oedema = abnormal increase in interstitial fluid volume

occurs when filtration greatly exceeds reabsorption

excess filtration:

  • increased capillary BP
  • increased permeability of capillaries

inadequate reabsorption:
- decreased concentration of plasma protein

36
Q

When do the AV valves open? phase, cause, function, how

A

In diastole (relaxation)

  • open when ventral pressure is lower than atrial pressure
  • allows blood flow from atria into ventricles
  • occurs when ventricles are relaxed, chordae tendinae are slack and papillary muscles are relaxed
37
Q

When do the AV valves close? phase, cause, function, how

A

in systole (contraction)

  • close when ventricles contract (‘Lub’)
  • prevents backflow of blood into atria
  • ventricles contract, pushing valve cusps closed, chordae tendinae are pulled taught and papillary muscles contract to pull cords and prevent cusps from everting
38
Q

When do the semilunar valves open? phase, cause, function

A

open with ventricular contraction
in systole
allow blood flow into pulmonary trunk and aorta

39
Q

When do the semilunar valves close? phase, cause, function

A

close with ventricular relaxation (‘Dub’)
in diastole
prevents blood from returning to ventricles, blood fills valve cusps, tightly closing the valves

CR Science 1 (3 decks)

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