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pathophysiology > 2 - cardiac phys HR and contractility > Flashcards

2 - cardiac phys HR and contractility Flashcards

1
Q

diastole

A

cardiac muscle at rest

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2
Q

systole

A

cardiac muscle during contraction

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3
Q

isovolumic ventricular contraction

A

first phase of ventricular contraction when AV valves are pushed closed by pressure within ventricles; semilunar valves remain open

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4
Q

ventricular ejection

A

pressure within ventricles increases forcing semilunar valves open (leaving the heart), allows ejection of blood into the pulmonary or aortic circuit

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5
Q

s1 sound

A

sound due to closure of the AV valves

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6
Q

s2 sound

A

second heart sound due to the closure of the semilunar valves

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7
Q

late diastole

A

both chambers are relaxed and ventricles fill passively

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8
Q

atrial systole

A

atrial contraction forces a small amount of additional blood into the ventricles

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9
Q

isovolumic ventricular relaxation

A

a ventricles relax, pressure in ventricles falls, blood flows back into the cusps of semilunar valves and snaps them closed

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10
Q

Preload

A

myocardial stretch before contraction, preload is a volume = EDV

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11
Q

afterload

A

a pressure, pressure in the aorta or pulmonary artery + EDP

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12
Q

contractility

A

cardiac muscle fibers contract at given fiber length

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13
Q

increase in stretch

A

increase in stretch exposes additional sites for Ca2+ binding and for actin-myosin interaction, increased stretch also effects greater release of Ca2+ from the SR

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14
Q

normal SV number

A

55-100mL

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15
Q

normal ESV number

A

50 mL

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16
Q

normal EDV number

A

120 mL

17
Q

SV =

A

ESV - EDV

18
Q

ESV

A

volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole. ESV is the lowest volume of blood in the ventricle at any point in the cardiac cycle

19
Q

EDV

A

volume of blood in the right and/or left ventricle at end load or filling in (diastole) or the amount of blood in the ventricles just before systole

varies with venous return aided by skeletal muscle and respiratory pump and increases with sympathetic innervation and epinephrine

20
Q

SV

A

volume of blood in millilitres ejected from the each ventricle due to the contraction of the heart muscle

21
Q

Factors affecting EDV (4)

A
  1. skeletal muscle pump - goes against gravity
  2. respiratory pump- helps blood return to the heart - makes pressure gradient less so draws air in and increases the abdominal pressure
  3. sympathetic nervous system innervation of veins - increases sympathetic nerve firing on veins - contracts - goes back to the heart
22
Q

how does diuretic affect blood volume

A

causes blood volume to decrease

23
Q

force of contraction in ventricular myocardium is influenced by

A

contractility and EDV

24
Q

how does SNS increase contractility (NE and EPI)

A

increases the ability of the heart to contract at any EDV
NE is a positive inotropic agent

binds to b1 receptors and activates cAMP - phosphorylating VGCC so calcium entry increases as open time increases

phosphorylating phospholamban reducing inhibiting on Ca-ATPase on SR - increasing stores of Ca in SR which makes a more forceful contraction and removing Ca2+ from the cytosol faster so that Ca and troponin binding time shortens which causes a shorter duration of contraction

25
Q

phospholamban

A

inhibits ca2+ atpase (SERCA - delivers Ca2+ into the ER. Inhibited by PKA to cause an increase in heart rate. Epi is an inhibitor of PKA

26
Q

elevation of cAMP in cardiac myocytes results in

A

PKA activation and phosphorylation of

  1. VGCC that increase Ca2+ induced Ca2+ release from the SR
  2. phospholamban, removes inhibitory effect on SR Ca2+ ATPase (SRCA)
27
Q

verapamil

A

negative ionotropic agent and negative chronotropic agent. inhibits VGCC

28
Q

mirlinone is a phosphodiesterase inhibitor - phosphodiesterase breaks down cAMP

A

makes a more forceful contraction - positive ionotrope- this will increase cAMP which will increase

29
Q

how does afterload affect CO

A

L heart: pulmonary pressure

R heart: aortic pressure

30
Q

Afterload effects on the Frank-Starling Curve

A

Vasoconstriction increases: makes the curve go down, as SV will decrease
relaxes smooth muscle: curve will increase as the SV will also increase but the EDV will decrease

31
Q

signs/symptoms of low cardiac output - heart failure

A

fatigue, weakness
rapid or irregular heart beat ( body is trying to compensate for not enough oxygen getting to the blood)
reduced ability to exercise
difficulty concentrating or decreased alertness
chest pain if your heart failure is caused by a heart attack

32
Q

signs/symptoms of high end diastolic pressure

A

(left ventricle is stiff and impaired relaxation)
shortness of breath (dyspnea) when you exert yourself when you lie down
swelling (edema) in your legs, ankles and feet
persistent cough or wheezing with white or pink blood-tinged phlegm
increased need to urinate at night (antidiuretic - releasing pressure)
swelling of your abdomen (ascites)
very rapid weight gain from fluid retention
sudden, severe shortness of breath and coughing up pink, foamy mucus

33
Q

diuretic effect on the Frank-Starling curve

A

lowers the edv down and to the left - moves pt to a lower cardiac filling pressure along the same ventricular curve- not as much preload to increase SV

34
Q

positive inotropic effect on the frank-starling curve

A

digoxin or dobutamine - straight up - moves patients to a higher ventricular function curve

35
Q

negative inotropic effect on the frank-starling curve

A

straight down

36
Q

vasodilator effect on the frank-starling curve

A

Angiotensin converting enzymes (ACE) inhibitors or nitroprusside - up and left - reduces cardiac filling pressures - decreases afterload, increases sv, decreases edv

37
Q

how does digoxin affect contractility

A

Na/K Atpase provides a conc gradient so that Ca levels can be maintained - maintains a conc gradient - no RMP - narrow TI - more Ca can get pumped into the SR

pathophysiology (11 decks)

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