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OS 205 > The <3 as a Pump > Flashcards

The <3 as a Pump Flashcards

0
Q

The electrical potential

Triggers muscle contraction

A

When Ca comes in ion potential

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1
Q

Basic unit of muscular system

A

Myofibril

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2
Q

Mechanism by which the muscle contracts because of the influx of Ca ions

A

Excitation-Contraction Coupling

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3
Q

Cardiac vs Skeletal Muscle

A

Cardiac:
Large quantity of Ca ions diffuse into the sarcoplasm
Extra ion concentration affect contraction of muscles

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4
Q

Cardiac events that occur from the beginning of one heartbeat to the beginning of the next

A

Cardiac cycle

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5
Q

Period of contraction

A

Systole

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6
Q

Period of relaxation

A

Diastole

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7
Q

T or F

Flow of blood is dependent on the pressure difference of the valves

A

True

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8
Q

Blood flows from a lower pressure to higher pressure

T or F

A

False

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9
Q

Period of Diastesis

A

Minimim flow of blood from LA to LV

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10
Q

Pressure in ventricle > Pressure in atria

A

Mitral, tricuspid valve closure (S1, signals the start of systole, first heart sound)
Lub
Contraction

Opposite:
Aortic and pulmonic valve closure
S2
Dub
Relaxation
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11
Q

Augmentation of ventricular pumping effectiveness brought about by atrial contraction

A

__________?

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12
Q

Atrial Pressure Waves

A wave
C wave -systolic event
X descent
V wave
Y descent -opening of the AV valves
A

Atrial contraction
Bulging of the AV valves into the atria

Filling of the atria

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13
Q

Volume in the ventricles at the end of diastole

110-120 ml

A

End-Diastolic Volume (EDV)

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14
Q

Volume ejected from the ventricle during systole

70 ml

A

Stroke volume

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15
Q

S3

A

Ventricular diastolic gallop

16
Q

Caused by severe turbulence of blood

Narrowing of aortic valve

Hypertrophy of ventricle

A

Aortic Stenosis

17
Q

Leakage of blood

Blood leaks back to the ventricle during diastole

Left ventricle if overwhelmed

A

Aortic Regurgitation

18
Q

Rumbling diastolic sound

Calcification of valve

Narrowing of mitral stenosis

Turbulence of blood as blood flows from LA to LV

A

Mitral Stenosis

19
Q

CHD

Flow of oxygenated blood from left - sided to right

A

Left to Right Shunt

20
Q

Nonoxygenated blood goes to systemic circulation

Continuous murmur

A

Cyanotic Heart Disease

eg Patent Ductus Arteriosus (PDA)

21
Q

Alters basic mechanism of cardiac contraction

A

Calcium

22
Q

Normal cardiac output

A

5.2 L/min

23
Q

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.

A

Digitalis compounds have been used for more than two hundred years to treat heart failure.

24
Q

Ca ion channels open
Ca goes inside

What drugs

A

Epi, Serotonin?

25
Q

What causes the plateau phase in contraction

A

Ca coming in!

Positive Inotropic Effect

26
Q

Negative Inotropic Effect

A

Decreased entry of Ca

Entry of K

27
Q

Amt of calcium bound at these sites depends on

A

Effect of hormones

Contraction

28
Q

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.

A

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.

29
Q

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.

A

Phosphodiesterase inhibitors

30
Q

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.

A

Calcium sensitizing drugs represent the newest class of cardiostimulatory drugs.

OS 205 (18 decks)

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