Blood Pressure Cardiac Out Put

      • 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.


        • 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.


      • 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.

Cardiac Output, Heart Rate, Stroke Volume and Blood Pressure
A tutorial looking at heart rate, stroke volume, cardiac output and blood pressure.
Cardiac OutPut, Systolic & Diastolic blood pressure (PART 1
Expert Student Nurse Mentor Mike Linares reveals how to fully understand all the components of systole & diastolic blood pressure.
Blood Pressure and Cardiac Output
Real World: Heart Rate and Blood Pressure
Learn about the physiological effects reduced gravity environments have on the human body. Use multiplication to calculate cardiac output and find out what effect space travel has on sensory-motor skills, stroke volume and heart rates of the astronauts.
Cardiac Cycle – Systole & Diastole
Thanks to McGraw Hill you can watch this video of the cardiac cycle!
High Blood Pressure
Transcript: High blood pressure, or hypertension,
is a common condition in which the force of blood on the walls of your arteries is often too high.
Arteries are the blood vessels that carry blood away from your heart to supply your tissues with oxygen and nutrients.
Peripheral Resistance and Blood Flow
This is an answer to a question that was asked when I did my Anatomy & Physiology Academy on how exactly resistance works when it comes to blood flow. In this video, I explain peripheral resistance in a bit more detail and how there are different factors that are involved in increasing or decreasing Peripheral Reistance