Blood Pressure Cardiac Out Put

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      • Ventricular Action Potential Versus Mechanical Events
        • The QRS complex represent ventricular cell phase 1 depolarizations.(MCQ)
        • The T wave records of all ventricular cell phase 3 repolarizations. MCQ)
        • The T wave begins midway through the ejection phase and continues until the onset of the isovolumetric relaxation phase. (MCQ)
      • Myocardial Cell Structure
        • Cardiac muscle cells
          • contain numerous myofibrils
          • chains of sarcomeres, the fundamental contractile unit.
          • Myocytes are coupled to one another by intercalated disks.
          • cardiac myocytes that comprise the ventricles and atria contract almost in unison, MCQ)
        • Cell-to-cell conduction occurs through gap junctions (MCQ)
        • Low resistance pathways that are a part of the intercalated discs (MCQ)
          • allow for rapid electrical spread of action potentials to cells.
        • Cardiac muscle differs from skeletal muscle in the following ways:
          • Cardiac muscle contains only one or two centrally located nuclei, in contrast to the several nuclei in skeletal muscle.
          • Gap junctions are found only in cardiac muscle. (MCQ)
          • Compared to skeletal muscle, cardiac muscle contains fewer but larger T-tubules, particularly in the atria. (MCQ)
      • Similar Cardiac Output: Right and Left Heart
        • The stroke volume (SV) of the two ventricles must, at steady state, be identical.
        • The rate (HR) of the two ventricles must be identical.
        • output (HR × SV) of the two ventricles must also be identical.
        • Cardiac output is equivalent to the venous return
          • Cardiac output increases during exercise because of the fall in skeletal muscle resis- tance and increased venous return.
      • Excitation-Contraction Coupling
        • This coupling links the electrical activities of the myocyte to the force- generating actin-myosin reaction.
        • Ca2+ enters the myocyte mainly during phase 2 of an action potential via voltage-activated channels. (MCQ)
        • This Ca2+ entry triggers the release of Ca2+ from intracellular (MCQ)sarcoplasmic reticulum (SR) stores, increasing intracellular Ca2+ levels.
        • Ca2+ binds to troponin C, moving tropomyosin away and allowing actin and myosin binding.
        • Actin and myosin bind, the thick and thin filaments slide past one another, and the myocardial cell contracts.
        • The strength of contraction correlates with the amount of SR Ca2+ release. (MCQ)
        • Ca2+ removal by an active Ca2+-ATPase pump is required for relaxation. (MCQ)
      • End-diastolic Blood Pressure Changes with Change in Cardiac Output
        • with an increase in sympathetic activity, the rate and the myocardial contractility (ie, stroke volume) will increase.
        • The result will be decreased ventricular end-diastolic pressure, because these induced cardiac changes are accompanied by a concurrent increase in arteriolar resistance (ie, vasoconstriction). (MCQ)
        • With the increase in cardiac output during exercise, ventricular end-diastolic pressure will not decrease, as a result of reduction in peripheral resistance from dilation in the skeletal muscle beds. (MCQ)
      • Starling’s Law
        • The relation between fiber length and strength of contraction is known as Starling’s law of the heart.

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        • An increase in myocardial fiber length, as occurs with an increased ventricu- lar filling during diastole (ie, preload), produces a more forceful ventricular contraction because more overlap between thick and thin filaments is exposed for cross-bridge formation. (MCQ)
        • Hence, a decreased heart rate, with longer filling time, will result in an increase in stroke volume.
        • Starling’s law is active only to the point at which a maximal systolic pressure is reached at the optimal preload.
        • If diastolic pressure increases beyond the optimal preload, no further in- creases in developed pressure will occur. Thus, the normal heart operates on the ascending portion of the Frank-Starling curve.

Pressure-Volume Loop of the Left Ventricle

The external work of the heart can be approximated as the product of pressure (P) times stroke volume (SV), which is the pressure-volume loop of the heart.

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      • Pressure-volume loop
        • Isovolumetric contraction
          • Occur From points 1 to 2.
          • Point 1
            • is diastole with the ventricular muscle relaxed
            • filled with blood to about 145 mL (end-diastolic volume). (MCQ)
            • Upon excitation, the ventricle contracts but no blood is ejected be- cause all of the valves are closed.
        • Ventricular ejection
          • represented by movement from points 2 to 3.
          • At point 2
            • aortic valve opens and blood is ejected into the aorta.
            • The volume ejected per beat is the stroke volume
            • Graphically depicted by the width of the pressure-volume loop
          • Point 3
            • is the end-systolic volume. (MCQ)
        • Isovolumetric relaxation
          • represented by movement from points 3 to 4
          • At point 3, as the ventricle relaxes, the aortic valve closes.
          • Ventricular volume is constant because all valves are closed.
        • Ventricular filling
          • represented by movement from points 4 back to 1.
          • After left ventricular pressure decreases below left atrial pressure, the mitral valve (AV) opens and filling begins.
          • Ventricular volume increases to about 140 mL (end-diastolic volume), of which only 10–20% results from atrial contraction. (MCQ)
      • Cardiac Work
        • Cardiac work is the amount of work done by the heart on each beat.
        • cardiac work is much greater for the left heart because of the greater afterload, or increase in arterial pressure.
          • Afterload on the left ventricle is equivalent to aortic pressure.
          • Afterload on the right ventricle is equivalent to pulmonary artery pressure.
        • Cardiac work is primarily a function of arterial systolic pressure and stroke volume.
        • Systolic pressure is a function of stroke volume(MCQ)
        • As stroke volume increases, systolic pressure increases.
        • increased afterload results in a decrease in stroke volume.
        • Heart rate is an indicator of stroke volume
          • as heart rate increases, stroke volume usually decreases, due to decreased filling time. (MCQ)
      • Venous Return and Central Venous Pressure
        • The venous return (ie, vascular function) relationship defines the changes in central venous pressure evoked by changes in cardiac output.
        • As cardiac output increases, blood is removed from the central veins at a greater rate, and central venous pressure declines.
        • Central venous pressure is the response, and cardiac output is the stimulus.


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