Cardiac Function Flashcards
Required for the Ca2+ release from the SR that leads to Contraction
Influx of Ca2+
In the heart, what is required for contraction?
-Distinguishing feature between cardiac and skeletal muscle
Extracellular calcium
The mechanism by which an AP initiates Ca2+ release in cardiac muscle is called
Calcium-Induced Calcium Release (CICR)
In a cardiac myocyte, increased intracellular Ca2+ is sensed by the Ca2+-sensitive
Ryanodine Receptors (RYR)
Does NOT have CICR
Skeletal muscle
SR calcium release in skeletal muscle is independent of
Ca2+
In cardiac muscle, relaxation requires removal of Ca2+ from the cytoplasm. This occurs via
SERCA (back to SR) and NCX (out of cell)
Returns Ca2+ to the Sarcoplasmic Reticulum (SR)
SERCA
Calcium is removed from the cardiac cell via
NCX
The intrinsic ability of myocardial cells to develop force at a given muscle length
Contractility (inotropy)
Most mechanisms that affect inotropy affect how
Ca2+ is handled by the cell
What are the three measures of ventricular function?
Stroke volume, Ejection fraction, and Cardiac Output
The volume of blood ejected per contraction
-difference between EDV and ESV
Stroke Volume (SV = EDV - ESV)
A way to look at the efficiency of ventricular contraction
Ejection fraction
Determines the percent EDV ejected with each beat
Ejection Fraction
The total volume of blood ejected by the heart in one minute
Cardiac Output (CO)
How do we calculate Cardiac Output (CO)?
CO = SV x HR
The biggest contributor to increased CO during exercise is
Increased HR
In order for CO to increase, we also need some increase in
SV
An increase in HR alone can cause CO to
Fall
Which three factors influence stroke volume?
Preload, afterload, inotropy
A cardiac myocyte can generate more force when it is
Stretched
This stretch-induce inotropy is related to
Ca2+
Increases TN-C Ca2+ affinity and stretch-activated Ca2+ channels
Stretch
Stretch activated Ca2+ channels increase Ca2+ release from the
Sarcoplasmic Reticulum (SR)
Increasing volume increases the
Maximal pressure
Increasing the ventricular volume regulates the
Contractile force
Does not change when preload is decreased
ESPVR
The Frank-Starling law of the heart is that the SV is determined by the
LVEDV
Increasing the PRELOAD (EDV) increases the
Force of contraction
Increasing the force of contraction increases the
Stroke Volume (and thus CO)
Increases as cardiac filling increases
SV
Altering the preload DOES NOT affect the
ESPVR
Increased venous return raises
EDV
HR and atrial contraction are two factors which regulate the
Ventricular Preload
Ventricular filling varies with
HR
Atrial contraction is only an important component of ventricular filling when
HR is high or we have decreased ventricular compliance
In the normal heart, PRELOAD correlates with
End-Diastolic Pressure (EDP)
Affects the relationship between EDP and EDV
Compliance of the heart
How easily the heart expands when it is filled with a volume of blood
Compliance
The slope of the volume vs pressure plot is the
Compliance
Ventricular compliance can be altered by
Disease
Reflects stiffness of the ventricle
End-Diastolic Pressure-Volume Relationship (EDPVR)
An increased EDPVR shows a
Stiff ventricle
A stiff ventricle is harder to
Fill
With a stiff ventricle, we have a higher pressure for any given
Volume
With a stiff ventricle, we have a lower volume for any given
Pressure
Under conditions of decreased compliance, the left ventricle does not
Relax
When we have a stiff ventricle, we will have an increase in LVEDP, this leads to an increase in
Pulmonary capillary pressure
Heart failure with preserved ejection fraction
“Diastolic” Heart Failure
We can see concentric hypertrophy with
Hypertension and valvular disease
Amyloidosis, glycogen storage diseases, hemochromatosis, and mutations in sarcoma result proteins can all result in
Restrictive cardiomyopathy
Blood pressure in the thoracic vena cava near the right atrium
Central Venous Pressure (CVP)
A major determinant of filling of the right ventricle
CVP
CVP determines the
Preload
The load against which the heart must contract to eject blood
Afterload
A larger afterload causes
Decreased SV
Makes the ventricle work harder to eject blood
Increased afterload
Increasing the afterload DOES NOT affect the
ESPVR
Decreases velocity and extent of fiber shortening
Increased afterload
We can see chronic elevations in afterload with
Hypertension and aortic stenosis
What are three examples of afterload reducing agents?
ACE inhibitors, Hydralazine, Sympathomimetics
Determined by cellular mechanisms that affect the intrinsic contractility
Inotropy (contractility)
Will INCREASE stroke volume independent of changes in preload or afterload
Increased inotropy
Inotropy alters the slope of the
ESPVR
Increases the intrinsic contractility
Inotropy
The maximal pressure generated for any specific volume
Intrinsic contractility
Inotropy causes the slope of the ESPVR to
Increase
Sympathetic nervous system inner action of the heart influences
Inotropy
Inotropy is also influenced by increased circulating
Catecholamines
What is the effect on inotropy of sympathetic nervous system stimulation?
Increases inotropy
Heart failure with reduced ejection fraction
Systolic Heart failure
Activation of muscarinic ACh receptors decreases
cAMP
What are three examples of positive inotropic agents for the heart?
Beta-agonists, phosphodiesterase-3 inhibitors, Digoxin
