Determinants and Cardiac basics Flashcards
Determinants of Cardiac Output
Heart and Stroke Volume
What is SV?
SV is the amount of blood ejected by the ventricle with each contraction.
Preload is the
precontractile fiber length of myocardial fiber augmented
Preload can be augmented by
End diastolic volume
Venous return is directly proportional to
EDV
Some factors that affect venous return
Factors that affect venous return include blood volume, venous tone, intrathoracic pressure, pulmonary vascular resistance, and right heart function
What is afterload?
Afterload, the force against heart contraction,
What are the 3 determinants of afterload?
Ventricular wall stress
Systemic vascular resistance
Blood viscosity.
Afterload and SV relationship is
Inversely proportional; As afterload increases, SV decreases.
Contractility is the
intrinsic ability of the myocardial fiber to contract.
What is the main role of Intracellular calcium
main mechanism which influences the binding strength of actin and myosin filaments that determine the force of myocardial contraction
Cardiac output (CO) is the
amount of blood delivered to the tissue in 1 min.
Starling’s law
The stronger the stretch, the greater output
Normal CO
5-6L/min
What is CI ?
CO/BSA
Normal CI
2.5 to 3.5⋅L⋅min−1⋅m−2
CO formula is
HR x SV
What is the primary determinant of HR?
the rate of phase 4 depolarization of the SA node of pacemaker cells
Rate of discharge of SA node is a determinant of HR and determined by
humoral and neural (Epi, NE) mechanisms
In children how is the CO determinants different?
the myocardium is less contractile and less compliant; therefore HR is critically important for maintenance of CO
How does significant tachycardia affect CO?
significant tachycardia can negatively affect CO because increased HR (> 170 beats/min) disproportionately decreases diastolic ventricular filling time relative to decreases in systole, which then contributes to a lower CO.
Heart rhythm also is an important determinant of cardiac output because the atrial contraction inherent in sinus rhythm contributes of _______CO in normal hearts and up to in the case of reduced ventricular compliance or delayed relaxation.
20% to 25%; 40% to 50%
What is a normal SV?
70-80ml per contraction
What are determinants of SV?
Preload, afterload and contractility. and SOMETIMES 4th wall motion abnormalities
What is the formula of SV?
EDV - ESV
What are the determinants of EDV?
Preload
What are the determinants of ESV?
Afterload and contractility
3 determinants of Preload
Venous return
Ventricular filling time
Intrathoracic pressure
3 determinants of Afterload?
SVR
Wall tension
Blood viscosity
2 determinants of contractility
Sympathetic nervous system
Catecholamines drugs.
Preload is directly proportional to
end-diastolic myocardial fiber length
Normal EDV
120 ml
If no obstruction or loss of volume in circulating pathways is present, venous return should equal
CO
Venous return is regulated by according to the formula
peripheral venous pressure (Pv), right atrial pressure (Pra), and venous resistance (Rv)
Formula venous return VR =
(Pv − Pra)/Rv
Useful estimate of contractility is
ejection fraction.
What exerts the most important influence on contractility?
The adrenergic nervous system
Provide 95% of resistance to ejection.
Systemic vascular resistance (SVR) accounts for approximately
What is the formula of SVR
80 x (MAP - RAP ) / CO)
What is afterload defined by?
Afterload, as defined by ventricular wall stress, is represented by LaPlace’s law:
Afterload represented by what law?
La Place’s Law
Laplace law and variable
T = P r / 2h
where T is tension in the LV wall
P is pressure
r is ventricular radius, and h is wall thickness.
From LaPlace’s law, it is apparent that 3 are primary determinants of afterload.
ventricular volume
LV wall thickness, and
systolic intraventricular pressure
A failing ventricle effect on afterload and CO.
dilate and significantly increase afterload, which significantly reduces CO.
Important goal in managing congestive heart failure
Reducing afterload
A change in contractility is considered to be a change in the
contractile force of the heart in the presence of unchanged diastolic dimensions and pressure
The sympathetic division of the autonomic nervous system increases the HR via stimulation of
Beta-1 adrenergic receptors,
Parasympathetic division of the autonomic nervous system decreases the HR by stimulating
muscarinic M2 cholinergic receptor
Stroke volume and afterload have an _________
relationship
inversely proportional
What happens to SV and CO when the ventricular
wall tension increases,
Decreased SV and CO.
Which has the most profound effect on myocardial contractility ? and Why?
The sympathetic nervous system as the sympathetic adrenergic fibers release norepinephrine, which stimulates the myocardial beta-1 adrenergic receptors to enhance contractility and CO
Inotropism or contractility is affected by the
of SV and CO
rate of myofibril shortening as well as by the rate of calcium release from the smooth sarcoplasmic
reticulum.
Faster rates of myofibril shortening and
calcium release into the intracellular space contribute
to an
increased strength of contractility and augmentation
The various degrees of wall motion abnormalities range from 3 different types
toand finally to akinesis, which refers to
the absence of contractility.
hypokinesis, dyskinesis, akinesis
Refers to the diminished force of contractility,
Hypokinesis
A paradoxical and asynchronous pattern of contraction,
Dyskinesis,
How does wall motion abnormalities affect LV?
Affect the ability of the left ventricle to adequately fill with the blood volume delivered by the atria, subsequently reducing its SV capacity and CO potential
Myocardial contraction occurs as a result of crossbridge
formation between
two contractile proteins, actin (thin
filaments) and myosin (thick filaments
The intracellular release of calcium from the sarcoplasmic reticulum facilitates the conformational change in what? and what does it allow?
two regulatory proteins (troponin and tropomyosin) to allow the cross-bridge formation between actin and myosin
Explain the process of calcium release?
-Initial calcium release from the sarcoplasmic reticulum is triggered by the electrical depolarization of dihydropyridine, voltage-gated calcium channels.
-As the intracellular calcium concentration increases, it triggers an even greater release of calcium from the sarcoplasmic reticulum via ryanodine, nonvoltagegated
calcium channels
What determine the strength as well as rate of the contraction?
overall calcium concentration
rate of release from the sarcoplasmic reticulum
Calcium regulation and Sympathetic nervous system stimulation (via norepinephrine) activates
beta-1 adrenergic receptors, leading to an increase in the intracellular calcium concentration and strength of contraction.
In contrast to SNS, calcium regulation of parasympathetic nervous system
stimulation (via acetylcholine) activates M2 cholinergic receptors, which enhance the Ca2+- ATPase activity to pump calcium back into the sarcoplasmic reticulum, thus effectively lowering the intracellular calcium
concentration and decreasing the strength and rate of the myocardial contraction.
The cardiac cycle can be divided into alternating periods of
myocardial contraction, or systole
myocardial relaxation, or diastole.
Ventricular SYSTOLIC function is best understood by 2 parameters
CO and EF
Diastolic function of the ventricle is best understood by
ventricular isovolumetric relaxation time
ventricular capacitance during filling
Ventricular pressure–volume diagrams:2 main point of interests are
EDV and ESV
What does EDV really indicates?
diastolic function, ability of the ventricular myocardium to relax to fill with blood;
What does EDV really indicates?
end-systolic volume (ESV), reflects systolic function, including the ability of the ventricular myocardium to contract to eject a fraction of the end diastolic ventricular volume.
Generally, as both the right and left ventricle
depolarize in synchronous fashion, the pulmonary and
systemic COs generated are
usually equal.
The normal range for the left ventricular EF is usually .
59%-75%
The overall net effect of systolic failure translates into a
down and right shift of the pressure–volume loop (negative inotropy)
What happens to the EDV and ESV as the systolic function of the ventricle is failing,
there is an increase in EDV and ESV because
EF (the ability of the ventricle to eject a fraction of the EDV) is significantly reduced.
Systolic augmentation (positive inotropy) shifts the pressure volume loop
up and left.
The ventricular capacitance can be estimated via
transesophageal echocardiography
The assess ventricular capacitance you look at those 2 parameters?
ventricular isovolumetric relaxation time and the flow velocity across the mitral valve during diastole (ventricular filling).
A stiff and less compliant ventricle is indication by 2 things
Prolonged isovolumetric relaxation times and high flow velocities across the mitral valve
As the diastolic function of the ventricle is failing, the EDV of the ventricle decreases and the less-compliant ventricle becomes
unable to accommodate the blood volume delivered by the atrial depolarization.
In contrast, a compliant ventricle is
able to accommodate a larger EDV and augments SV and CO, thus shifting the loop up and left.
Are responsible for the delivery of oxygenated blood to the myocardium.
right and left coronary arteries
What does the RCA supplies?
right atrium, the right ventricle, and the inferior portion of the left ventricle, SA and AV nodes.
What does left coronary artery (LCA) includes the
left atrium, the interventricular septum, and the anterolateral walls of the left ventricle.
Circumflex artery, which supplies the
Lateral wall of the left ventricle,
Left anterior descending artery (LAD), which supplies the
Anterior wall of the left ventricle
Interventricular septum
To supply the myocardium with oxygen, the blood flows from the _______ to the _______and then returns to the _______via the _______
Epicardial vessels to the endocardial vessels, and then returns to the right atrium via the coronary sinus.
The coronary perfusion pressure (CPP) is dependent on the
difference between the aortic diastolic pressure (ADP) and the left ventricular end-diastolic pressure (LVEDP),
CPP formula
CPP = ADP − LVEDP.
What is the LVEDP?
The LVEDP is an approximation of the resistance to coronary blood flow during diastole
CPP is directly proportional to____, but inversely proportional to ______and ______
ADP; LVEDP as well as heart rate (HR).
CPP increases with:
(1) increases in ADP; (2) decreases in LVEDP; and (3) decreases in HR as the diastolic time
CPP decreases with:
1) decreases in ADP; (2) increases in LVEDP; and
(3) increases in HR.
Myocardial oxygen consumption at rest is between
7 and 10 mL/100 g tissue/min;
CPP ranging from
50 to 120 mm Hg, produces coronary blood flows of 60-80 mL/100 g tissue/min
Myocardial oxygen consumption increase with
exercise
In contrast to other organ beds, myocardial arterial oxygen extraction is quite high, about
70%-80%, compared to about 25% for the rest of the body.
This system has minimal effects on the tone of the coronary vasculature.
The parasympathetic nervous system
The 4 important factors affecting myocardial oxygen
supply are as follows: CHAC
(1) HR (in particular, diastolic time);
(2) CPP (as determined by ADP as well as by LVEDP)
(3) arterial oxygen content (including both oxygen tension as well as hemoglobin concentration); and
(4) coronary vessel diameter.
The rate of oxygen supply to the myocardium increases
with
ncreases in the diastolic time, increases in CPP, increases in oxygen and hemoglobin concentration, and coronary vasodilation
Myocardial oxygen demand is affected by the following
important factors:
(1) HR;
(2) ventricular wall tension (as determined by preload, afterload, and wall thickness); and
(3) myocardial contractility
The rate of myocardial oxygen consumption (Mv . O2)
increases with
increases in HR, increases in wall tension, and
increases in contractility
