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Cardiac Output
When the heart contracts
Cardiac Vocabulary
• Contractility: Contractility is the intrinsic
ability of cardiac muscle to develop force
for a given muscle length.
Cardiac Vocabulary
• Preload: Preload is the muscle length prior to
contractility, and it is dependent of ventricular
filling (or enddiastolicvolume…EDV)
• This value is related to right atrial pressure.
• The most important determining factor for
preload
is venousreturn.
Cardiac Vocabulary
• Afterload: Afterload is the tension (or the
arterialpressure) against which the ventricle must
contract.
• If arterial pressure increases, afterload also
increases.
• Afterload for the left ventricle is determined by
aortic pressure
• Afterload for the right ventricle is determined by
pulmonary artery pressure.
Cardiac Output
CardiacOutputis the volume of blood pumped
each minute, and is expressed by the following
equation:
• CO = SV x HR
• Where:
• CO is cardiac output expressed in L/min
(normal ~5 L/min)
• SV is stroke volume per beat
• HR is the number of beats per minute
Heart Rate (HR)
Heart rate is directly proportional to cardiac output
• Adult HR is normally 80-100 beats per minute (bpm.)
• Heart rate is modified by autonomic, immune, and local
factors. For example:
7. An increase in parasympathetic activity via M2 cholinergic
receptors in the heart will decreasethe heart rate.
9. An increase in sympathetic activity via B1 and B2 adrenergic
receptors throughout the heart will increasethe heart rate.
Stroke Volume (SV)
SV = EDV - ESV
• Is determined by three factors: preload, afterload, and
contractility.
• Preload gives the volume of blood that the ventricle has
available to pump
• Contractility is the force that the muscle can create at the
given length
• Afterload is the arterial pressure against which the muscle
will contract.
• These factors establish the volume of blood pumped with
each heart beat.
Preload
afterload
Cardiac Volumes
• SV = end diastolic volume (EDV) - end
systolic volume (ESV)
• EDV = amount of blood collected in a
ventricle during diastole
• ESV = amount of blood remaining in a
ventricle after contraction
Cardiac Reserve
• Cardiac reserve is the difference between
resting and maximal CO
• Cardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat)
• CO = 5250 ml/min (5.25 L/min)
Frank – Starling Principle
• This principle illustrates the relationship between
cardiac output and left ventricular end diastolic
volume (or the relationship between stroke volume
and right atrial pressure.)
Frank – Starling Principle
• The Frank Starling principle is based on the length-tension
relationship within the ventricle.
• If ventricular end diastolic volume (preload) is increased,
it follows that the ventricular fiber length is also
increased, resulting in an increased ‘tension’ of the muscle.
• Cardiac output is directly related to venous return, the
most important determining factor is preload.
• The contraction and therefore stroke volume in response
to changes in venous return is called the Frank-Starling
mechanism (or Starling's Law of the heart).
How (TPR)Total Peripheral
Resistance effects CO
Regulation of Heart Rate: Autonomic
Nervous System
• Sympathetic nervous system (SNS) stimulation is
activated by stress, anxiety, excitement, or
exercise
• Parasympathetic nervous system (PNS) stimulation
is mediated by acetylcholine and opposes the SNS
slowing heart rate
• Baroreceptors
a. carotid sinus reflex - maintains BP in brain
• b. Bainbridge reflex – maintains BP in heart
• c. Aortic sinus reflex – maintains BP in aorta
Bainbridge Reflex
• Bainbridge (atrial) reflex – a sympathetic
reflex initiated by increased blood in the
atria
• Causes stimulation of the SA node
• Stimulates baroreceptors in the atria,
causing increased SNS stimulation
Cardiac
Neurotransmitters
& Receptors
Chemical Regulation
of the Heart
• The hormones epinephrine
increase heart rate
and thyroxine (T4)
• Hormonal Regulation of Blood Pressure
1. Renin
2. ADH
3. Aldosterone
• Intra- & extracellular ion concentrations must be
maintained for normal heart function
Homeostatic Imbalances
• Hypocalcemia – reduced ionic calcium depresses the
heart
• Hypercalcemia – dramatically increases heart
irritability and leads to spastic contractions
• Hypernatremia – blocks heart contraction by
inhibiting ionic calcium transport
• Hyperkalemia – leads to heart block and cardiac
arrest
Congestive Heart Failure (CHF)
caused by:
• Coronary atherosclerosis
• Increased blood pressure in aorta
• Successive myocardial infarcts
• Dilated cardiomyopathy (DCM)
Coronary
Artery
Bypass
Surgery
Heart Auscultation
Aortic
Stenosis
Diastolic
Murmur
Mid Systolic
Click
Normal
Heart
Beat

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edit co.pptx

  • 1. Cardiac Output When the heart contracts
  • 2. Cardiac Vocabulary • Contractility: Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length.
  • 3. Cardiac Vocabulary • Preload: Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or enddiastolicvolume…EDV) • This value is related to right atrial pressure. • The most important determining factor for preload is venousreturn.
  • 4. Cardiac Vocabulary • Afterload: Afterload is the tension (or the arterialpressure) against which the ventricle must contract. • If arterial pressure increases, afterload also increases. • Afterload for the left ventricle is determined by aortic pressure • Afterload for the right ventricle is determined by pulmonary artery pressure.
  • 5. Cardiac Output CardiacOutputis the volume of blood pumped each minute, and is expressed by the following equation: • CO = SV x HR • Where: • CO is cardiac output expressed in L/min (normal ~5 L/min) • SV is stroke volume per beat • HR is the number of beats per minute
  • 6.
  • 7. Heart Rate (HR) Heart rate is directly proportional to cardiac output • Adult HR is normally 80-100 beats per minute (bpm.) • Heart rate is modified by autonomic, immune, and local factors. For example: 7. An increase in parasympathetic activity via M2 cholinergic receptors in the heart will decreasethe heart rate. 9. An increase in sympathetic activity via B1 and B2 adrenergic receptors throughout the heart will increasethe heart rate.
  • 8. Stroke Volume (SV) SV = EDV - ESV • Is determined by three factors: preload, afterload, and contractility. • Preload gives the volume of blood that the ventricle has available to pump • Contractility is the force that the muscle can create at the given length • Afterload is the arterial pressure against which the muscle will contract. • These factors establish the volume of blood pumped with each heart beat.
  • 11. Cardiac Volumes • SV = end diastolic volume (EDV) - end systolic volume (ESV) • EDV = amount of blood collected in a ventricle during diastole • ESV = amount of blood remaining in a ventricle after contraction
  • 12.
  • 13. Cardiac Reserve • Cardiac reserve is the difference between resting and maximal CO • Cardiac Output: Example CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) • CO = 5250 ml/min (5.25 L/min)
  • 14. Frank – Starling Principle • This principle illustrates the relationship between cardiac output and left ventricular end diastolic volume (or the relationship between stroke volume and right atrial pressure.)
  • 15.
  • 16. Frank – Starling Principle • The Frank Starling principle is based on the length-tension relationship within the ventricle. • If ventricular end diastolic volume (preload) is increased, it follows that the ventricular fiber length is also increased, resulting in an increased ‘tension’ of the muscle. • Cardiac output is directly related to venous return, the most important determining factor is preload. • The contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism (or Starling's Law of the heart).
  • 17.
  • 18.
  • 20.
  • 21. Regulation of Heart Rate: Autonomic Nervous System • Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise • Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS slowing heart rate • Baroreceptors a. carotid sinus reflex - maintains BP in brain • b. Bainbridge reflex – maintains BP in heart • c. Aortic sinus reflex – maintains BP in aorta
  • 22.
  • 23. Bainbridge Reflex • Bainbridge (atrial) reflex – a sympathetic reflex initiated by increased blood in the atria • Causes stimulation of the SA node • Stimulates baroreceptors in the atria, causing increased SNS stimulation
  • 25. Chemical Regulation of the Heart • The hormones epinephrine increase heart rate and thyroxine (T4) • Hormonal Regulation of Blood Pressure 1. Renin 2. ADH 3. Aldosterone • Intra- & extracellular ion concentrations must be maintained for normal heart function
  • 26. Homeostatic Imbalances • Hypocalcemia – reduced ionic calcium depresses the heart • Hypercalcemia – dramatically increases heart irritability and leads to spastic contractions • Hypernatremia – blocks heart contraction by inhibiting ionic calcium transport • Hyperkalemia – leads to heart block and cardiac arrest
  • 27.
  • 28.
  • 29. Congestive Heart Failure (CHF) caused by: • Coronary atherosclerosis • Increased blood pressure in aorta • Successive myocardial infarcts • Dilated cardiomyopathy (DCM)