Cardiac Output PowerPoint

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Cardiac OutputWhen the heart contracts

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Cardiac VocabularyContractility:  Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length.

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Cardiac VocabularyPreload:  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.

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Cardiac VocabularyAfterload:  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.

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Cardiac OutputCardiac 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

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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 M2 cholinergic receptors in the heart will decrease the heart rate. An increase in sympathetic activity via B1 and B2 adrenergic receptors throughout the heart will increase the heart rate.

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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. 

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Preload

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afterload

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Cardiac VolumesSV = 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

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Cardiac ReserveCardiac 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)

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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.)

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Frank – Starling PrincipleThe 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).

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How (TPR)Total Peripheral Resistance effects CO

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Regulation of Heart Rate: Autonomic Nervous SystemSympathetic 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

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Bainbridge ReflexBainbridge (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

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Cardiac Neurotransmitters & Receptors

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Chemical Regulation of the HeartThe hormones epinephrine and thyroxine (T4) 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

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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

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Last Updated: 8th March 2018

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