Your SlideShare is downloading. ×
Cardiac output
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Cardiac output

8,118

Published on

2 Comments
6 Likes
Statistics
Notes
No Downloads
Views
Total Views
8,118
On Slideshare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
366
Comments
2
Likes
6
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 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 end diastolic volume …EDV) 
    • This value is related to right atrial pressure.
    •  
    • The most important determining factor for preload is venous return .
  • 4. Cardiac Vocabulary
    • Afterload :  Afterload is the tension (or the arterial pressure ) 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
    • Cardiac Output is 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 :
    • An increase in parasympathetic activity via M 2 cholinergic receptors in the heart will decrease the heart rate.
    • An increase in sympathetic activity via B 1 and B 2 adrenergic receptors throughout the heart will increase the 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. 
  • 9. Preload
  • 10. afterload
  • 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.  
  • 19. How (TPR)Total Peripheral Resistance effects CO
  • 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
  • 24. Cardiac Neurotransmitters & Receptors
  • 25. Chemical Regulation of the Heart
    • The hormones epinephrine and thyroxine (T 4 ) increase heart rate
    • 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)
  • 30. Coronary Artery Bypass Surgery
  • 31. Heart Auscultation Normal Heart Beat Mid Systolic Click Diastolic Murmur Aortic Stenosis

×