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Pathophysiology - MD > Week 5 - Cardiac Output > Flashcards

Week 5 - Cardiac Output Flashcards

1
Q

What is the Cardiac Cycle?

A

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

-consists of two periods: diastole (relaxation/filling with blood) + systole (contraction/ejection)

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2
Q

Diastole

(Passive Ventricular Filling)

Cardiac Cycle

A

AV valves are open, blood flows from atria into relaxed ventricles
-accounts for most of ventricular filling
-semilunar valves closed

begins just after ventricular contraction

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3
Q

Diastole

(Active Ventricular Filling)

Cardiac Cycle

A

AV valves open, atria contract + complete ventricular filling
-semilunar valves closed

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4
Q

Systole

(Period of Isovolumic Contraction)

Cardiac Cycle

A

ventricular contraction causes the AV valves to close (beginning of vent. systole)
-semilunar valves remain closed

all 4 valves are closed

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5
Q

Systole

(Period of Ejection)

Cardiac Cycle

A

continued ventricular contraction pushes blood out of the ventricles, causing the semilunar valves to open
-AV valves are closed

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6
Q

Diastole

(Period of Isovolumic Relaxation)

Cardiac Cycle

A

blood flowing back towards the relaxed ventricles causes semilunar valves to close (beginning of vent. diastole)
-AV valves remain closed

all 4 valves are closed

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7
Q

Steps in the Cardiac Cycle

A
  1. Diastole: Passive Ventricular Filling
  2. Diastole: Active Ventricular Filling
  3. Systole: Period of Isovolumetric Contraction
  4. Systole: Period of Ejection
  5. Diastole: Period of Isovolumetric Relaxation
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8
Q

Why is Cardiac Output (C.O.) vital to homeostasis?

A

controls the amount of blood flow to tissues and prevents any undue stress on the heart

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9
Q

Cardiac Output

(C.O)

A

the volume of blood pumped each minute
C.O. = SV x HR
-generally proportional to body surface area
-depends on venous return/rate of flow to tissues
-proportional to energy requirements of the tissues (rate of flow to tissues depends on total peripheral resistance)

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10
Q

Heart Rate

Cardiac Output

A

varied by balance of sympathetic and parasympathetic influence on SA node

-sympathetic: stimulates HR (epinephrine/norepi)
-parasympathetic: inhibits heart by vagus nerve stimulation
-normally 60-100 bpm

directly proportional to C.O.

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11
Q

Filling of the ventricles results in:

Cardiac Output

A

end diastolic volume (EDV) =120-130 mL

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12
Q

Emptying of the ventricles results in:

Cardiac Output

A

stroke volume (SV) output = 70 mL

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13
Q

Remaining blood left over in the ventricles:

Cardiac Output

A

end systolic volume (ESV) = 50-60 mL

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14
Q

Ejection Fraction

(EF)

Cardiac Output

A

fraction / percentage of end-diastolic volume ejected + pumped out by the ventricle
-normal EF = about 55-60%
-less than 55% EF = heart failure
-EF increases during exercise

EF = SV / EDV

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15
Q

At rest, why is C.O. relatively unchanged in a long distance runner?

A

their SV is more effective because the heart muscle is strong + will pump more during systole, effectively decreasing HR

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16
Q

Stroke Volume

(SV)

Cardiac Output

A

the volume of blood pumped out by each ventricle per each contraction
-determined by preload, afterload + contractility
-SV = EDV - ESV

emptying of the ventricles

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17
Q

Cardiac Output is influenced by:

A

intrinsic + extrinsic control
-both factors increase SV by increasing strength of heart contraction

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18
Q

Intrinsic Control

Cardiac Output

A

-heart muscle operates short of optimal sarcomere length
-stretches it by bringing more blood back to the heart, increasing force of contraction (Frank Starling Law)

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19
Q

Extrinsic Control

Cardiac Output

A

Norepinephrine from sympathetic + epinephrine from adernal medulla increase the opening of Ca2+ channels
-more Ca2+ increases the force of contraction

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20
Q

End Diastolic Volume

Regulation of Stroke Volume

A

the amount of blood collected in a ventricle at the end of diastole

EDV = preload

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21
Q

End Systolic Volume

Regulation of Stroke Volume

A

the amount of blood remaining in a ventricle after contraction

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22
Q

Preload

Factors Determining SV

A

volume of blood in ventricles at the end of diastole (EDV)
gives the volume of blood that the ventricle has available to pump

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23
Q

Contractility

Factors Determining SV

A

the force that the muscle can create at the given length
-dependent on stretch and EDV

intrinsic strength of cardiac muscles

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24
Q

Afterload

Factors Determining SV

A

the back pressure exterted by blood in the large arteries leaving the heart
-the arterial pressure against which the muscle will contract
-end systolic wall stress/resistance
-increase in afterload = increased cardiac workload

(resistance left ventricle must overcome to circulate blood)

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25
Q

End Diastolic Volume is Affected by:

Factors Affecting SV

A

venous return or the volume of blood returning to the heart + preload (the amount that ventricles are stretched by the blood = EDV)

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26
Q

End Systolic Volume is Affected by:

Factors Affecting SV

A

-myocardial contractility force due to factors other than EDV
-afterload (back pressure exterted by blood in large arteries leaving the heart)

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27
Q

Increase in Parasympathetic Activity

Autonomic Control of C.O.

A

via M2 cholinergic receptors in the heart will decrease HR
-decrease HR to 20-40 bpm + decrease force of contraction by 20-30%
-releases ACh (increase permeability to K+)
-negative ionotropic effect (hyperpolarization + inhibtion)
-force of contractions reduced = decreased EF

by Vagus nerve stimulation

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28
Q

Increase in Sympathetic Activity

Autonmic Control of C.O.

A

via B1 + B2 adrenergic receptors throughout the heart will increase HR
-increase HR up to 200 bpm + double force of contraction
**-release norepinephrine from sympathetic postganglionic fiber / adrenal medulla **(increase permeability of Ca2+ and Na+)
-ventricles contract more forcefully -> increasing SV + EF, decreasing ESV
-positive ionotropic effect

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29
Q

In what conditions would you see an increase in preload?

A

-hypovolemia
-regurgitation of cardiac valves
-heart failure

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30
Q

In what conditions would you see an increase in afterload?

A

-hypertension
-vasoconstriction

(increase afterload = increase cardiac workload)

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31
Q

Afterload to LV:

A

aortic arterial pressure

afterload LV is greater than afterload RV

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32
Q

Afterload to RV:

A

pulmonary arterial pressure

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33
Q

Factors on C.O.

A

-preload
-afterload
-contractility
-heart rate

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34
Q

How does Preload affect C.O.

A

increased preload = increased C.O.
-more in -> more out

(Frank-Starling Mechanism)

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35
Q

How does Afterload affect C.O.

A

increased afterload = decreased C.O.

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36
Q

How does contractility affect C.O.

A

increased contractility = increased C.O.

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37
Q

How does HR affect C.O.

A

increased HR = increased C.O.
-pumping fast will eventually allow less blood to enter the heart -> decrease C.O.

dual effects; will increase to an extent, then decrease C.O.

38
Q

Cardiac Reserve

A

the difference between resting and maximal C.O.

39
Q

Normal C.O.

Limits of C.O.

A

about 5 L/min

40
Q

Plateau C.O.

Limits of C.O.

A

13 L/min

41
Q

Hypereffective Heart Plateau C.O.

Limits of C.O.

A

20 L/min

42
Q

Hypoeffective Heart Plateau C.O.

Limits of C.O.

A

less than 5 L/min

43
Q

Hypereffective Heart

Limits of C.O.

A

effected by:
-nervous excitation
-cardiac hypertrophy: exercise (marathon runners get 30-40 L/min) + Aortic Valve Stenosis

44
Q

Hypoeffective Heart

Limits of C.O.

A

-valvular disease
-increased output pressure
-congenital heart disease
-myocarditis
-cardiac anoxia
-toxicity

45
Q

Increased Venous Return =

A

increased EDV

(intrinsic control)

46
Q

Frank Starling Law

A

the heart normally pumps out (during systole) the volume of blood returned to it during diastole

-heart muscle is normally (functioning at rest) short of it’s optimal sarcomere length

-increased preload -> increased stretch of muscle -> increased force of contraction -> increased SV

-cardiac muscle fibers contract more forcefully when stretched (preload), thus ejecting more blood (increased SV, decreased ESV)

-SV may increase due to greater contractility (ex. exercise) independent of EDV

only true for a normal, undiseased heart

47
Q

Frank Starling Law: Venous Return (VR)

A

venous return (VR) increases when there is an increase in blood flow through the peripheral organs

-slow heartbeat and exercise increase venous return (VR), increasing SV

-increase VR -> increased EDV
-decreased VR -> decreased EDV
-any decrease in EDV = decrease in SV

-blood loss and extremely rapid heartbeat = decreased SV

peripheral blood flow is a major determinant of C.O.

48
Q

Compensation for Heart Failure

Frank Starling Law

A

sympathetic stimulation: shifts Frank-Starling curve to the left, increasing contractility of the heart (trying to go towards normal heart function)

-compensatory increase in EDV due to increase in blood volume = increase in contraction
-ejects normal SV due to operating at a longer cardiac muscle fiber length

49
Q

Venous Return (VR) + Filling Time Effects on EDV

A

-sympathetic: increased VR = increased EDV
-parasympathetic: decreased VR = decreased EDV
-sympathetic: increased filling time = increased EDV
-parasympathetic: decreased filling time = decreased EDV

EDV directly affects SV

50
Q

Sympathetic + Parasympathetic Effects on Contractility of Muscle Cells

A

-sympathetic: increased contractility = increased ESV
-parasympathetic: decreased contractility = decreased ESV

contractility affects ESV -> affects SV

51
Q

Vasoconstriction (increased cont.) v. Vasodilation (decreased cont.) Effects on Afterload

A

-vasoconstriction (increased contractility/sympathetic): increased afterload = increased ESV
-vasodilation (decreased contractility/parasympathetic): decreased afterload = decreased ESV

afterload effects ESV -> affects SV

52
Q

EDV + ESV Effects on SV

A

-sympathetic: increased EDV = increased SV
-parasympathetic: decreased EDV = decreased SV
-sympathetic: increased ESV = decreased SV
-parasympathetic: decreased ESV = increased SV

53
Q

Increased contractility is due to:

A

-increased sympathetic stimuli
-certain hormones (epi, norepi, thyroxine T4 - positive ionotropic effects)
-Ca2+ and some drugs (elevated by digitalis to interefere w/ Ca2+ removal from sarcoplasm)

54
Q

Decreased contractility is due to:

A

-acidosis
-increased extracellular K+
-calcium channel blockers (beta blockers -olol prevent symp. stimulation - negative chronotropic effect)

55
Q

Peripheral Resistance + C.O.

A

increasing peripheral resistance decreases C.O.
C.O. = arterial pressure / total peripheral resistance

56
Q

Determinants of Venous Return (VR)

A

small increase in RA pressure -> dramatic decrease in VR
(mean systemic pressure)

pressure change is slight

57
Q

VR + C.O.

A

-C.O. increases w/ atrial pressure (normal A. pressure = 10 mmHg)
-venous return decreases w/ atrial pressure
-working C.O. is where venous return curve meets cardiac output curve

58
Q

Compensation for Increased Blood Volume

A
  1. increased C.O. increases capillary pressure, sending more fluid to tissues
  2. vein volume increases
  3. pooling of blood in the liver and spleen
  4. increased peripheral resistance reduces C.O.
59
Q

Effects of Sympathetic Stimulation

A
  1. increases contractility of the heart
  2. decreases volume by contracting the veins
  3. increases filling pressure
  4. increases resistance
60
Q

Disease States Lowering Total Peripheral Resistance

A
  1. Beriberi: insufficient thiamine; tissues starve because they cannot use nutrients
  2. AV fistula: ex. for dialysis
  3. Hyperthyroidism: reduced resistance cause by increased metabolism
  4. Anemia (lack of RBCs): effects viscosity and transport of O2 to the tissues
61
Q

Disease States Lowering Cardiac Output

A
  1. Heart disease, valvular disease, myocarditis, cardiac tamponade, shock
  2. shock = nutrirional deficiency of tissues
  3. decreased venous return by: reduced blood volume, venous dilation (increased circulatory volume), venous obstruction
62
Q

Hormonal Regulation of Blood Pressure

A
  1. renin
  2. ADH
  3. aldosterone

intra + extracellular ion conc. maintained for normal heart function

63
Q

Hypocalcemia

Homeostatic Imbalances

A

reduced ionic calcium depresses the heart

64
Q

Hypercalcemia

Homeostatic Imbalances

A

dramatically increases heart irritability and leads to spastic contractions
-high plasma Ca2+ (ECF)
-positive ionotropic

65
Q

Hypernatremia

Homeostatic Imbalances

A

blocks heart contraction by inhibiting ionic calcium transport
-high plasma Na+ (ECF)
-negative chronotropic

66
Q

Hyperkalemia

Homeostatic Imbalances

A

leads to heart block and cardiac arrest
-high plasma K+ (ECF)
-negative chronotropic
-used in lethal injection

67
Q

Renin

Hormonal Regulation of BP

A

sympathetic stim.. hypotension, decreased sodium delivery -> kidney -> renin -> adrenal glands -> aldosterone -> kidney tubules retain water and increase BP / blood volume, systemic vasoconstriction, cardiac + vascular hypertrophy

68
Q

Angiotensin

Hormonal Regulation of BP

A

angiotensin -> vasoconstrictors -> increased resistance + BP

69
Q

Baroreceptor Reflex

Neural Control

A

stimulated by increase in aterial pressure (stretch)
-regulate the heart when BP increases or decreases
-involved in short term regulation of BP
-effect: negative chronotropic + ionotropic

70
Q

Chemoreceptor Reflex

Neural Control

A

stimulated by decreased O2/pH or increased CO2
-effect: positive chronotropic + ionotropic
-less important in regulating cardiac function

71
Q

Proprioceptor Reflex

Neural Control

A

stimulated by muscle and joint movement
-effect: increase HR during exercise

72
Q

Role of Epinephrine

A

increases HR and contractility
-released from adrenal gland

(sympathetic stimulation)

73
Q

Role of Thyroxin (T4)

A

increases HR
-released from thyroid gland

74
Q

Autoregulation of the Heart

A

SV is autoregulated by ventricular filling (Frank-Starling Law)

75
Q

Preload Increase Effect on EF

A

increased preload = increased EF

preload increase seen in AR, MR + anemia

76
Q

Afterload Increase Effect on EF

A

afterload increase = EF decrease

afterload increase seen in AS

77
Q

Angiographic Assessment

Tests for LV Function

A

determining actual motion of ventricle

78
Q

Echocardiography

Tests for LV Function

A

allows measurement of EF in relation to cardiac filling and visualizing structures that are interfering with C.O. (ex. fluid in pericardial sac)

79
Q

CT Scan

Tests for LV Function

A

excellent visualization of cardiac structures including reproducible measuremenat of wall thickness + ESV + EDV

80
Q

MRI

Tests for LV Function

A

allows visualization even in patients with abnormal anatomy/geometry

81
Q

Heart Failure

A

physiological state in which C.O. is insufficient for body’s needs
-problem with structure or function of heart impairs blood flow / supply
-EF less than 40%

reduction in myocardial efficiency -> produces changes w/in heart

82
Q

Heart Failure Effects on C.O.

A

-reduced contractility (due to overload of ventricle)
-reduced SV (result of failure of diastole, systole, or both)
-reduced spare capacity
-increased HR (stimulated by increased sympathetic activity to maintain C.O.)
-hypertrophy of myocardium (due to terminally differentiated muscle fibers increasing in size in an attempt to improve contractility)
-enlargement of the ventricles (contributing to enlargement + spherical shape of failing heart)

83
Q

Causes of CHF

(Congestive Heart Failure)

A
  1. Coronary Artery Disease (CAD)
  2. heart attack
  3. HTN
  4. Valve disorders
  5. inflammation
  6. kidney disease
  7. abnormal heart rhythms
  8. pulmonary HTN
  9. severe anemia
  10. hyperthyroidism
  11. hypothyroidism
84
Q

Higher than normal EF (greater than 60%)

A

indicates presence of hypertrophic cardiomyopathy

85
Q

Lower than normal EF (less than 55%)

A

heart is weakened (heart failure)

86
Q

Systolic Heart Failure

A

decreased contractility
-enalrged heart fills w/ blood -> ventricles pump less than 50% of the blood
-failure of pump function of the heart
-decreased EF (less than 40-50%) -> inadequate C.O.
-caused by dysfunction of cardiac myocytes
-common mechanism of damage: ischemia -> infarction/scar formation
-EDV + pressure increase
-leads to pulmonary edema (left side of the heart)
-leads to peripheral edema (right side of the heart)

more readily recognized than diastolic HF

87
Q

Diastolic Heart Failure

A

decreased filling of the ventricles
-stiff ventricles fill w/ less blood than normal -> ventricles pump out 60% of blood
-failure of ventricle to relax = stiffer wall
-decreased filling = decreased SV = decreased C.O. (despite normal EF)
-pulmonary edema (LHF)
-peripheral edema (RHF)
-sensitive to increases in HR
-diastolic function worsens with age
-limited exercise tolerance -> elevated pulmonary venous pressure -> increases work of breathing

may be asymptomatic

88
Q

Etiologies of Systolic Heart Failure

A
  1. Coronary Artery Disease (65%)
  2. Idiopathic dilated cardiomyopathy
  3. Alcohol/toxing induced cardiomyopathy
  4. Infectious/inflammatory process
  5. Familial dilated cardiomyopathy
  6. Postpartum cardiomyopathy
  7. Stress induced cardiomyopathy
  8. Endorcine/nutritional causes
  9. Iron overload cardiomyopathy
  10. Tachycardia mediated cardiomyopathy
89
Q

Epidemiology of Diastolic Heart Failure

A

-1/3 pts with CHF have DHF
-prevalence in pts greater than 75 y/old
-mortality = 5-8 % annually
-mortality directly related to absence of CAD

90
Q

Epidemiology of Systolic Heart failure

A

-2/3 pts with CHF have SHF
-mortality rate = 10-15% annually
-mortality rate directly related to presence of CAD

91
Q

Factors that Exacerbate Diastolic HF

A
  1. Uncontrolled HTN
  2. A Fib
  3. noncompliance with medications for HF
  4. myocardial ischemai
  5. anemia
  6. renal insufficiency
  7. NSAID use
  8. deitary indisrection w/ over indulgence of salty foods
92
Q

Diagnosis of Diastolic HF

A

typical signs + symptoms of HF, plus:
-normal LV EF
-no valvular abnormalities on echocardiogram

Pathophysiology - MD (7 decks)

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