8 - CARDIAC CYCLE AND OUTPUT Flashcards

1
Q

CARDIAC CYCLE

A
  • Cardiac cycle is one heart beat
  • Systole is contraction. Generally taken to mean ventricular contraction and ejection
  • Diastole is relaxation. Or the rest of the cycle: ventricular relaxation and filling
  • ECG traces the phases by measuring current flow (lecture 3)
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2
Q

CARDIAC CYCLE BASICS

A
  • Atrial contraction
  • isovolumetric contraction
  • ventricular ejection
  • isovolumetric relaxation
  • ventricular filling
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3
Q

CYCLE SUMMARY: TIMINGS

A

• At a heart rate of 75bpm, each whole cardiac cycle lasts 0.8 seconds
• The whole heart is in diastole for 0.4 seconds, atrial systole lasts 0.1 seconds and ventricular systole lasts 0.3 seconds
The heart is physically capable of beating at more than 200bpm, however the volume of blood pumped by the heart starts to decrease above this rate –why?The cardiac cycle at 200bpm would last 0.3 seconds, with the time available for atrial filling, about 0.2 seconds – not enough!

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4
Q

HEART SOUNDS

A

There are 4 heart sounds, but only 2 are loud enough to be heard (auscultation)
First heart sound (LUBB)– turbulence caused by closure of the AV valves (happens when the ventricles contract)
Second heart sound (DUPP) – turbulence caused by semilunar valves closing (when the ventricles stop contracting)
3rd and 4th sounds from ventricular filling and atrial systole. 4th Sound audible when ventricles are stif

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5
Q
  1. Atrial Systole
A

• Atria contract, squeezing blood into the ventricles, through the valves.
• AV valves open. Pulmonic and Aortic closed
• Slight increase in atrial pressures
End Diastolic Volume = ventricular vol + atrial contribution (10% at rest)
EDV= 105ml +25ml = 130ml

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6
Q
  1. Isovolumetric Contraction:
A
  • All valves closed.
  • Beginning of systole- ventricles depolarise.
  • Increase in intraventricular pressure from contraction.
  • Heart shape change but no blood is ejected.
  • Pushes AV valves closed. First sound
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7
Q
  1. Rapid ejection.
A

• AV valves closed , others open.
• When intraventricular P is higher than the aortic and Pulmonary P, the valves open and blood is ejected.
• Atria continue to fill.
- L: LVP exceeds aortic P of 80mm/Hg for SL valves to open and ejection. P increase to 120mm/Hg
- R: RVP exceeds pulmonary P of 20mm/Hg for SL valves to open and ejection. P increases to 25-30mm/Hg
No heart sounds in healthy patient. Ejection sounds indicate a shunt or valve disease.

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8
Q
  1. Reduced ejection.
A
  • Aortic and pulmonary valves stay open and AV valves stay closed. No movement of blood
  • Ventricular repolarisation and muscle relaxation. Ventricular P decreases slightly but blood still leaves the heart (kinetic energy). Atrial P increasing as atria continue to fill
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9
Q
  1. Isovolumetric relaxation.
A

• Valves close ( Heart sound 2). Aortic first, then pulmonic valve.
Ventricle volume remains the same as valves are closed (dicrotic wave). Atrial pressure and volume increase from venous return
End Systolic Volume = volume remaining in the ventricles after ejection
Ie ESV = (EDV)130ml – 70ml = 60ml

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10
Q
  1. Rapid Filling.
A
  • AV valves open. Aortic and pulmonary valves close.
  • Ventricular filling. Relaxation phase still.
  • Amount of filling decreases when HR increases.
  • Atrial P falls
  • Third sound (not usually audible without specialist equipment)
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11
Q
  1. Reduced Filling.
A
  • Difficult to distinguish these phases.
  • When filling is nearly finished , ventricles at full stretch so P rises. P in large vessels drops as blood flows into circulation
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12
Q

CARDIAC OUTPUT

A

To work out a cardiac output you first need to know the Stroke Volume (SV):
SV = End-diastolic vol (EDV) – (ESV) End-systolic vol
EDV: Amount of blood collecting in ventricle (~130ml) Related to filling time and rate of venous return
ESV: amount remaining after contraction (~60ml) Preload, Contractility, Afterload

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13
Q

CALCULATING CARDIAC OUTPUT

A

Cardiac output = stroke volume X Heart rate

CO = (mL/min)
SV = (mL/beat)
HR = (beat/min)
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14
Q

REGULATION OF CARDIAC OUTPUT: HEART RATE

A

Cardiac Output is affected by the control of heart rate
• Neural control: physical or emotional stress
– Sympathetic nervous system stimulates heart rate (SA node). Up to 100-
200%
– Parasympathetic nervous system steadies HR
• Ion levels:
– Calcium: too little: weak. Too much: long contractions
– Potassium: involved in muscle contraction and nerve conduction.
Heart rate increase can increase CO to a point. CO increase not proportional to HR increase.

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15
Q

STARLING’S LAW AND STROKE VOLUME

A

Starlings law: bigger SV ejected if there is a larger degree of filling at the end of diastole.

  • When the rate at which blood flows into the heart from the veins changes, the heart automatically adjusts its output to match the inflow
  • If an increase in end-diastolic volume occurs, the force of ventricular contraction rises, producing an increase in stroke volume and cardiac output
  • Stretching of muscle fibres increases contraction force
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16
Q

REGULATION OF STROKE VOLUME (preload)

A

Preload (how stretchy is the heart at max fill)
The more the heart fills with blood, the more the muscle is stretched
Exercise increases venous return via:
• Rapid breathing forcing reoxygenated blood into heart quicker
• Skeletal muscle pump forcing venous return

17
Q

REGULATION OF STROKE VOLUME (afterload)

A

Afterload (the pressure against which the heart need to pump, to expel blood)

  • The higher the arterial pressure, the lower the stroke volume
  • Arteries are elastic to keep BP stable and absorb volume.
  • If arteries are blocked it increases the amount of force (P) needed to move blood.
18
Q

REGULATION OF STROKE VOLUME (contracticility)

A

Contractility (the ability of the muscle to produce a force)

  • The more forcefully the muscle contracts, the more blood is expelled
    1. Ions like Ca and K affect muscle activity.
    2. Adrenalin and the sympathetic nervous system increase contractility
    3. Increased stretch leads to increased contractility
19
Q

SKELETAL MUSCLE PUMP

A

Lack of muscle in veins limits the force of venous return.
Contraction of skeletal muscle in the tissue surrounding the veins compresses them.
• Compression closes upstream valves and opens downstream valves.
• Compressed veins = increased pressure
• Venous return increases during exercise.
Valves prevent backflow

20
Q

WHAT IS BLOOD PRESSURE?

A

BP is related to Cardiac Output
• Cardiac Output= Heart Rate x Stroke Volume
– HR related to age, exercise, health
– SV related to venous return
Blood Pressure = Cardiac Output. X Total Peripheral Resistance
Blood Pressure describes the pressure of blood on the wall of the Blood Vessels.
It does not describe changes in cardiac pressure during the cardiac cycle

21
Q

PERIPHERAL RESISTANCE

A

Peripheral Resistance (PR) is the degree of friction encountered by blood ie the resistance to flow
What causes friction?
• Constriction or narrowing- initiated by action of the Sympathetic Nervous System or atherosclerosis, or stiffening
• Increased blood volume (increased retention from high NaCl)
• Viscosity (cold, increased red blood cells)
Thus, anything increasing CO or PR, increases BP

22
Q

Pulse pressure (PP)

A
  • massively increases as arteries become less stretchy
    PP = systolic BP – Diastolic BP
    ie = 120-80= 40mm Hg
23
Q

Mean Arterial Pressure (MAP)

A
  • more useful to work out as this is the pressure at which blood is actually delivered to the tissues
    MAP = DP + (PP/3)
24
Q

CONTROL OF BP: CHANGES IN PRESSURE

A
  • Baroreceptors in the Arterial carotids and aortic arch
  • Each receptor is sensitive to a different pressure.
  • Small changes in therefore increase firing frequency
  • A decrease in P is also detected (via decreased frequency)
25
Q

CONTROL OF BP: CHEMORECEPTORS

A
  1. Peripheral chemoreceptors : carotid bodies
  2. Central chemoreceptors: medulla
    - Detect changes in PO2, PCO2, pH
    - Low PO2 is associated with changes in pulmonary pressure, so changes in stretch receptor activity will also respond to low O2 levels.
26
Q

HOW CAN BLOOD PRESSURE BE MODIFIED? - vasoconstriction

A
  • Contraction of smooth muscle in the vessel walls, also precapillary sphincters in arterioles
  • Activation of Sympathetic Nervous activity
  • Causes narrowing of the diameter of the blood vessel
  • Increases the resistance of blood vessels to blood flow
  • Increases Blood Pressure
27
Q

HOW CAN BLOOD PRESSURE BE MODIFIED? - vasodilation

A
  • Relaxation of smooth muscle in the vessel walls, also precapillary sphincters in arterioles
  • Causes widening of the diameter of the blood vessel
  • Caused by withdrawal of sympathetic nerve activity and locally released chemicals e.g. nitrous oxide and lactic acid
  • Decreases the resistance of blood vessels to blood flow
  • Decreases Blood Pressure
28
Q

Why would you need to raise Blood Pressure?

A
  • Counteract the pressure change from getting up too quickly (orthostatic hypotension)
  • Haemorrhage
  • Stress or exercise.
29
Q

How can you decrease Blood Pressure?

A
  • Low salt diet ( regulation of blood volume)
  • Decrease stress and effects of sympathetic nervous system
  • Therapeutically with ACE inhibitors- interacting with the Renin Angiotensin Aldosterone System (RAAS) that regulates blood volume and BV constriction