As already mentioned, hemodynamics are the forces which circulate blood through the body.

Specifically, hemodynamics is a term used to describe the intravascular pressure and flow that occurs during a cardiac cycle. It is important to remember that the vascular system is a closed circuit. Pressure and flow variations in the venous compartment will necessarily affect the arterial compartment and vice versa.

Therefore, hemodynamic measurement is not simply a number value in relation to a norm. Rather, hemodynamics are the beat to beat variations of pressure and flow that occur within and between the arterial and venous compartments. The decision to treat a hemodynamic value in one compartment depends on the status of the other compartments and should always be undertaken with careful consideration of the potential unintended effects of the proposed treatment.

• Cardiac output (CO) is the main focus of many hemodynamic studies. CO is defined as the amount of blood pumped into the aorta each minute. CO is stroke volume (SV) multiplied by the heart rate (HR); CO = (SVXHR) is the amount of blood pumped per minute. On average, a healthy resting adult heart will eject about 5 liters of blood from the left ventricle, through the aortic semilnar valve and into the aorta every minute. On average a healthy adult has a blood volume of about 5 liters, therefore the healthy heart recirculates the entire blood volume every minute.
  
  
• Venous return (VR) on average, must equal CO. The body can compensate for temporary minor decreases in VR due to blood loss, dehydration, diuresis etc., by increasing sympathetic activity. Increased sympathetic response causes peripheral vasoconstriction driving blood to the core and it increases heart rate which together are intended to increase CO. However, because the circulatory system is a closed system, continuing decreased VR will diminish CO. If the imbalance is not corrected the sympathetic neurohormones: norepinephrine (NE); angiotensin II (AII) and endothelin will continue to provoke a response while CO is reduced.
  
  
• Inotropy or contractility is a measure of the amplitude of myocardial contractions. The strength of contraction is determined by the amount of ATP available to drive reactions and the amount of Ca++ available for binding of myosin to actin. During systole, cardiomyocytes contract because their sarcomeres shorten as a result of Ca++, actin, myosin interactions. The presence of Ca++ allows the myosin heads to bind to actin. ATP causes myosin head flexion which moves of actin filaments toward the M-line. During diastole, passive filling of the heart stretches the cardiomyocytes, resetting the cardiomyocyte for another contraction.
  
  As a cardiomyocyte is stretched by preload pressure, the sarcomeres within the myofibrils are also stretched. According to the sliding filament theory, a major determinant of inotropy is the distance that myosin can travel along the actin fiber. Increasing sarcomere length, produces increased tension within the muscle fiber, a little like a rubber band (see Starling effect). It is also believed that stretching the cardiomyocyte increases external Ca++ flow into the cell and Ca++ release stored in the sacroplasmic reticulum close to the sarcomeres, both of which would tend to increase Ca++ availablity for myosin/actin binding.
  Inotropy is affected by venous return, exercise, stress and positive chronotropic agents: including adrenergic agonists, atropine, dopamine, epinephrine, isoproterenol and by negative chronotropes including: beta blockers, acetylcholine, digoxin and calcium channel blockers.

• Vasoactivity is the ability of blood vessels to increase or decrease their internal diameter. Relaxation of vascular smooth muscle can increase flow and lower systemic blood pressure by increasing vessel caliber, decreasing resistance to flow and increasing compliance. Conversely, contraction of vascular smooth muscle reduces vessel caliber, increases resistance to blood flow, decreases compliance, resulting in an reduced blood flow and increased systemic blood pressure.
  Poiseuille's Law states that "that the volume of a homogeneous fluid passing per unit time through a capillary tube is directly proportional to the pressure difference between its ends and to the fourth power of its internal radius, and inversely proportional to its length and to the viscosity of the fluid. Therefore, vessel radius is one of the most important factors determining blood flow. If the radius of a vessel doubles, blood flow could increase 16 fold. If the radius is reduced by half there could be a 16 fold reduction in flow.
  
  
• Chronotropy is the timing, and frequency (rate) of cardiac contractions. Change in the heart rate is regulated by a dynamic balance of sympathetic (epinephrine and norepinephrine) and parasympathetic (vagal acetylcholine) influences on the pacemaker and conduction cells of the heart.
  
  Heart rate is a major determinant of cardiac output. Under stress or when cardiac output fails to meet metabolic requirements the autonomic system compensates by supressing vagal activity and releasing the catecholamine norepinephrine to elevate heart rate by lowering the action potential threshold of the pacemaker cells in the sinoatrial and atrioventricular nodes. Conduction velocity is also enhanced.

The entire blood volume of a healthy resting adult is circulated in one minute.

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