The <3 as a Pump Flashcards
The electrical potential
Triggers muscle contraction
When Ca comes in ion potential
Basic unit of muscular system
Myofibril
Mechanism by which the muscle contracts because of the influx of Ca ions
Excitation-Contraction Coupling
Cardiac vs Skeletal Muscle
Cardiac:
Large quantity of Ca ions diffuse into the sarcoplasm
Extra ion concentration affect contraction of muscles
Cardiac events that occur from the beginning of one heartbeat to the beginning of the next
Cardiac cycle
Period of contraction
Systole
Period of relaxation
Diastole
T or F
Flow of blood is dependent on the pressure difference of the valves
True
Blood flows from a lower pressure to higher pressure
T or F
False
Period of Diastesis
Minimim flow of blood from LA to LV
Pressure in ventricle > Pressure in atria
Mitral, tricuspid valve closure (S1, signals the start of systole, first heart sound)
Lub
Contraction
Opposite: Aortic and pulmonic valve closure S2 Dub Relaxation
Augmentation of ventricular pumping effectiveness brought about by atrial contraction
__________?
Atrial Pressure Waves
A wave C wave -systolic event X descent V wave Y descent -opening of the AV valves
Atrial contraction
Bulging of the AV valves into the atria
Filling of the atria
Volume in the ventricles at the end of diastole
110-120 ml
End-Diastolic Volume (EDV)
Volume ejected from the ventricle during systole
70 ml
Stroke volume
S3
Ventricular diastolic gallop
Caused by severe turbulence of blood
Narrowing of aortic valve
Hypertrophy of ventricle
Aortic Stenosis
Leakage of blood
Blood leaks back to the ventricle during diastole
Left ventricle if overwhelmed
Aortic Regurgitation
Rumbling diastolic sound
Calcification of valve
Narrowing of mitral stenosis
Turbulence of blood as blood flows from LA to LV
Mitral Stenosis
CHD
Flow of oxygenated blood from left - sided to right
Left to Right Shunt
Nonoxygenated blood goes to systemic circulation
Continuous murmur
Cyanotic Heart Disease
eg Patent Ductus Arteriosus (PDA)
Alters basic mechanism of cardiac contraction
Calcium
Normal cardiac output
5.2 L/min
These drugs inhibit the cardiac sarcolemmal Na+/K+-ATPase, which leads to an increase in intracellular calcium through the Na+-Ca++-exchanger. Increased intracellular calcium stimulates increased release of calcium by the sarcoplasmic reticulum and thereby makes more calcium available to bind to troponin-C, which increases contractility.
Digitalis compounds have been used for more than two hundred years to treat heart failure.
Ca ion channels open
Ca goes inside
What drugs
Epi, Serotonin?
What causes the plateau phase in contraction
Ca coming in!
Positive Inotropic Effect
Negative Inotropic Effect
Decreased entry of Ca
Entry of K
Amt of calcium bound at these sites depends on
Effect of hormones
Contraction
Sympathomimetic drugs that bind to beta-adrenoceptors located in cardiac nodal tissue, the conducting system, and contracting myocytes. The heart has both beta1 ( β1) and beta2 ( β2) adrenoceptors, although the predominant receptor type in number and function is β1.
These receptors normally bind norepinephrine that is released from sympathetic adrenergic nerves. Additionally, they bind norepinephrine and epinephrine that circulate in the blood.
Beta-agonists
β1 and β2 adrenoceptor activation increases heart rate and contractility, which increases cardiac output. Activation of these receptors also increases conduction velocity within the heart as well as the rate of mechanical relaxation (lusitropy). These drugs are used to treat acute and refractory heart failure, as well as circulatory shock.
Drugs that inhibit the enzyme (cAMP-dependent phosphodiesterase) responsible for breaking down cAMP. This leads to an increase in cAMP. In the heart, this produces positive inotropic and chronotropic responses similar to beta-agonists. These drugs are used to treat acute and refractory heart failure, not chronic heart failure.
Phosphodiesterase inhibitors
These drugs increase the sensitivity of troponin-C for calcium so that more calcium becomes bound to troponin-C, which enhances contractility. At present, these drugs are under clinical investigation for heart failure, and therefore not yet approved.
Calcium sensitizing drugs represent the newest class of cardiostimulatory drugs.
