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CV Test 2 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

The the heart receives normal venous return but has an unexpected CO, what can be assumed?

A

Something is wrong with the heart itself

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2
Q

What is used to measure venous return?

A

Right atrial pressure

CVP

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3
Q

What is hypereffetive heart?

A

Higher CO than expected

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4
Q

What is hypoeffective heart?

A

Lower CO than expected

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5
Q

How can a heart become hypereffective?

A 
SNS stimulation
-increases contractility 
-increases HR
Healthy hypertrophy 
-conditioning
-healthy resting bradycardia
Decreased after load with stable BP
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6
Q

How can a heart become hypoeffective?

A 
SNS inhibition
PNS stimulation - vagal decreases HR
Dysrhythmia
Valve Dz
Increased afterload 
Myocardial dysfunction
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7
Q

What explains a low CO?

A

Hypoeffective heart

Decreased Venous return

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8
Q

What explains decreased venous return?

A

Decreased blood volume
Obstructive
Distributive

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9
Q

What decreases total blood volume?

A

Hemorrhage, hypovolemia

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10
Q

What are some causes of obstruction to venous return?

A

Gravid uterus
Tumor
Cardiac tamponade

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11
Q

What causes altered distribution of blood volume?

A

ACUTE vasodilation
Sudden increase in venous capacitance
Hypotension

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12
Q

What causes high CO?

A 
Hypereffective heart
Chronic reduction in SVR
-hyperthyroidism > incr metabolism > incr BF > peripheral vasodilation
-certain Vit B deficiencies (Beriberi)
-sepsis
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13
Q

What is the relationship between CO and SVR?

A

Inversely related

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14
Q

What does a sudden drop in SVR do to CO?

A

Decreases CO

-it allows blood to pool, so decreased venous return

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15
Q

What initial effect does increased volume have on a euvolemic patient?

A

Initially it increases venous return and therefore SV

-this does not last long

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16
Q

What happens after the initial increase in SV when volume is given to a euvolemic patient?

A

Venous reservoirs are filled
Autoregulated tissues vasoconstriction to reduce incoming volume
Volume returning to RA trigger reflexes
-increased RBF = increased UOP
-Decrease ADH release
-Bainbridge reflex > increased HR
-low pressure receptors >vasodilation to help reduce BP response to incr volume
Increased capillary pressure exudes fluid into interstitial space

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17
Q

How is CO measured?

A

Healthy: right atrial pressure, CVP
Unhealthy: pulmonary artery catheter, PCWP, thermodilution

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18
Q

When does diastolic step up occur on PA catheter insertion?

A

When catheter enters the pulmonary artery

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19
Q

What is the gold standard for CO reading?

A

PCWP with PA catheter

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20
Q

What preexisting heart condition must be considered before placing a PA catheter? Why?

A

LBBB
Conduction to the left ventricle is blocked, if conduction to the right ventricle is affected by catheter insertion you can cause complete heart block

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21
Q

What West zone should a PA catheter be sitting in? Why?

A

West Zone 3

It has the most blood flow, so it is the most accurate

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22
Q

How can you tell if the PA catheter tip is in Zone 3?

A

The PCWP should be the same or less than the pulmonary artery diastolic pressure

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23
Q

What does a big wave mean on PA catheter reading about CO?

A

Big wave mean it takes longer for the temperature change, which means slower blood flow, which means a low CO

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24
Q

If too much injectate is used for PA catheter thermodilution, how will this affect the result?

A

Too much injectate means it will take longer for the temperature change, which will give a false low CO reading

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25
Q

How will too small a volume of injectate affect the PA catheter reading for thermodilution test?

A

Too small a volume will have a rapid temperature change and give a false high CO result

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26
Q

How can preload be measured in a healthy heart? How is this different from an unhealthy heart?

A

Healthy heart: right atrial pressure, CVP

In an unhealthy heart the venous return may no longer reflect preload, a PCWP would be more appropriate

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27
Q

What does Frank Starling mean SV?

A

That SV is dependent upon preload

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28
Q

What determines preload?

A

Venous return

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29
Q

What can be used to guide fluid administration?

A

CVP

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30
Q

Because a hypoeffective heart can’t keep up with venous return, what is a better measurement of CO?

A

LVEDP
LVEDV
PAC - PCWP

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31
Q

In hypoeffective heart, preload contains the venous return and what?

A

The volume remaining in the LV after systole (ESV) accumulates with each contraction since it is not able to eject a normal EF

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32
Q

What measurements can you get with an arterial/peripheral venous hemodynamic monitor?

A

CO
Preload
Contractility

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33
Q

What measurements can you get with an esophageal Doppler?

A

CO

SV

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34
Q

What is cardiac index? Equation? Normal range?

A

CO adjusted for body size
CI = CO/BSA
Normal range: 2.5-4.2 L/min/m^2
Average CI is 3 L/min/m^2

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35
Q

What is the most common clinical measure or systolic function?

A

Ejection Fraction

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36
Q

List 2 equations for EF

A

((LVEDV-LVESV)) / LVEDV) x 100

(SV/LVEDV) x 100

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37
Q

If systolic function is a measure of ventricular ejection, what is diastolic function a measure of? How is it measured?

A

Ventricular filling

TEE: transmittal flow measures

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38
Q

What besides EF is a measure of the strength of heart?

A

SVO2

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39
Q

What is SVO2

A

The saturation of oxygen in the venous blood

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40
Q

Where is an SVO2 sample obtained?

A

The pulmonary artery

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41
Q

What is SVO2 the best determination of?

A

Adequacy of CO

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42
Q

What influences SVO2?

A

Anemia

Hypoxia

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43
Q

What is cardiac work?

A

How much work is done to move blood out of the heart

Work = force x distance

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44
Q

How is cardiac work calculated?

A

Cardiac work = SV x aortic pressure

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45
Q

How can you visualize cardiac work?

A

The area in the ventricular volume loop

  • bigger area means more work
  • small area means less work
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46
Q

What is one of the strongest predictors for peri operative cardiac complications?

A

Active CHF

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47
Q

What is active CHF?

A

Symptomatic

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48
Q

What is the problem in heart failure

A

Forward pumping

Decreased forward flow

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49
Q

Where does the volume go in HF?

A

It backs up

  • LA
  • Lungs
  • Right heart
  • Periphery
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50
Q

What is acute HF?

A

Decreased forward flow

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51
Q

What are the causes of acute HF?

A

Diminished contractility
Valvular disease
Disease of the muscle
External pressure

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52
Q

What are the symptoms of acute HF?

A 
Hypotension
Cool, mottled skin
Nausea
SOB
Fatigue

Signs of poor perfusion

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53
Q

What causes initial compensation with a sudden event leading to HF?

A

Initial compensation is by SNS stimulation

  • increased contractility (by increased preload)
  • increased HR (reflexes)
  • increased venous return (by decreasing venous capacitance)

Initially venous return stays the same by CO decreases

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54
Q

What happens if decreased CO decreases RBF?

A

Not enough RBF for the kidneys to make urine

The kidneys retain fluid

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55
Q

How does the kidneys retaining fluid volume help?

A

Overtime the fluid increases venous return, which increases CO

When RBF is restored and UOP resumes, this is long term compensation

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56
Q

What determines if someone can maintain long term compensation?

A

If the fluid retained by the kidneys is enough to restore CO enough to restore RBF

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57
Q

HF compensation is determined by the relationship of what 2 things?

A

CO and renal function

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58
Q

What EF is found in patients with compensated HF?

A

30-50%

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59
Q

In order for a compensated HF patient to maintain CO and renal function, what measurement is elevated?

A

Right atrial pressure

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60
Q

Why is compensated HF patient’s RAP higher?

A

Increased venous return

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61
Q

What happens with HF if renal fluid retention can’t restore RBF?

A

Decompensated HF:

  • excessive fluid accumulation
  • pulmonary edema
  • hypoxemia
  • peripheral edema
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62
Q

Decompensated HF is seen typically with what EF?

A

<30%

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63
Q

Does a patient with decompensated HF have elevated RAP?

A

Yes, but CO is still not enough to restore RBF

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64
Q

What happens when Frank Starling mechanism has reached it’s limit?

A

Increasing preload no longer increases SV and decompensated HF ensues

65
Q

How do patients with compensated chronic HF handle normal activity? What about stress or lots of activity?

A 
Normal activity: pretty well
Stress or lots of activity: they become symptomatic because their CO is no longer enough
-hypotension
-fatigue
-cool, mottled skin
-SOB
-Nausea
66
Q

Decompensation under stress is due to what?

A

Decreased cardiac reserve

67
Q

What is cardiac reserve?

A

The ability to increase CO over normal

68
Q

How is cardiac reserve assessed?

A

By activity tolerance

  • Hx
  • Stress test
69
Q

What is another name for ventricular function curves

A

Frank Starling Curves

70
Q

What relationship do ventricular function curves show?

A

Filling pressure to pumping ability

-cardiac performance

71
Q

What is on the horizontal axis of a ventricular function curve?

A

Filling pressure

  • RAP
  • CVP
  • PCWP
  • LVEDP
  • PAD (pulmonary artery diastolic pressure)
72
Q

What is on the vertical axis of a ventricular function curve?

A

Pumping ability

  • CO
  • SV
73
Q

What is ultimate decompensated HF?

A

Cardiogenic shock

74
Q

What volume is preload?

A

LVEDV

75
Q

With poor ejection, what happens to LVEDV?

A

It accumulates with each contraction

76
Q

What is optimal filling pressure?

A

The pressure at which the best preload is created for the best cardiac performance

77
Q

How can you decrease preload?

A

Diuretics

Venodilators

78
Q

What is “unloading the heart”?

A

Decreasing afterload

79
Q

Why is saying “increase contractility” just a clinical statement?

A

Because we can not technically alter contractility, it’s Inotropy we can manipulate

80
Q

How can you increase contractility?

A

Inotropes

Afterload reduction

81
Q

Which does NTG dilate more, veins or arteries?

A

Veins

82
Q

NTG decreases, preload or afterload?

A

Preload

83
Q

Which does Nipride dilate more, veins or arteries?

A

Arteries

84
Q

Nipride decreases, preload or afterload?

A

Afterload

85
Q

Nipride AKA?

A

Sodium Nitroprusside

86
Q

What on the ventricular function curves shows optimum filling pressure?

A

The point on the curve

87
Q

To maintain optimum filling pressure what is manipulated? With?

A

Preload

Volume, diuretics, venodilation

88
Q

What describes contractility on a ventricular function curve?

A

The position of the curve

89
Q

To affect contractility what is manipulated? With?

A

Afterload
Arterial dilation
Inotropes

90
Q

In left-sided HF, where does blood accumulate?

A

Lungs

Progresses to right side, peripherally

91
Q

An MI where will significantly affect LV muscle

A

Anterior wall

92
Q

Where does blood accumulate in right-sided HF?

A

Veins and tissues

-neck vein dissension, hepatomegaly, peripheral edema etc

93
Q

What is right-sided HF as a consequence of lung disease called?

A

Cor pulmonale

94
Q

Can HF occur without poor CO?

A

Yes. High output cardiac failure

95
Q

What is HF without poor CO?

A

High output cardiac failure

  • pumping isn’t the problem
  • heart is overcome with excessive volume and can’t keep up
96
Q

List 2 examples of condition that lead to high output cardiac failure

A

Hyperthyroidism

Beriberi

97
Q

What is usually the cause of increased CO?

A

Chronic decreased SVR

98
Q

When tissues are suffering from poor perfusion and necrosis, this is called?

A

Cardiogenic shock

99
Q

All forms of CHF have what?

A

Fluid retention

100
Q

What is activated when RBF is decreased?

A

Activation of Renin-Angiotensin System and increased Aldosterone secretion

101
Q

What is released by the heart to try and diurese this retained fluid?

A

Atrial Natriuretic Factor

-ANF

102
Q

What does atrial stretch do to increased venous return trigger?

A 
Low pressure receptors (in atrial and pulmonary arteries)
-send impulse to vasomotor center
-to vasodilate 
RA Stretch
-increases RBF, ANF and decreases ADH = increase UOP
RA Stretch
-incr HR via SA node stretch
-incr HR via Bainbridge reflex
103
Q

Why is cardiogenic shock a vicious cycle?

A

Low CO > low coronary perfusion > heart gets weaker > infarct extends > progressive failure > progressive shock

104
Q

What is the presentation of compensated HF?

A

Asymptomatic

  • good perfusion (at rest)
  • filling pressures elevated
  • increased circulating volume
  • decreased cardiac reserve
105
Q

Presentation of decompensated HF?

A 
Pulmonary edema
Dyspnea
Rales
Tachycardia
Peripheral edema
106
Q

What is the number 1 CV risk factor for non cardiac surgery?

A

Active CHF

107
Q

What makes CHF active?

A

Decompensation

108
Q

What is HF? What causes HF?

A

Reduced ability of the heart to pump enough blood to meet body’s need.
Usually caused by decreased contractility resulting from diminished BF of coronaries
-damaged valve
-external pressure
-Vit B deficiency
-primary cardiac muscle disease

109
Q

What 2 main effects occur with acute severe myocardial damage?

A

Reduced CO

Damming of blood in veins

110
Q

What SNS reflexes compensate during acute cardiac failure?

A 
Baroreceptor reflex
Chemoreceptors reflex
CNS ischemic reflex
Reflexes that originate in the damaged heart
-Bainbridge reflex
-
111
Q

What does SNS stimulation do to vascular tone? What does this do?

A 
Increases it (constriction)
Mobilizes venous blood to increase venous return > rise in systemic filling pressure
112
Q

What 2 stages characterize the prolonged semi-chronic state of cardiac failure?

A

Retention of fluid by the kidneys

Varying degrees of recovery of heart itself over weeks to months

113
Q

How does fluid retention by the kidneys increase venous return and therefore CO?

A

Increases blood volume

  • increases the mean systemic filling pressure
  • distends veins which reduces the venous resistance
114
Q

What happens when the heart’s pumping capacity is reduced?

A

CO drops and RBF becomes too low for kidneys to excrete enough salt and water, fluid retention ensues, if retained fluid is not enough to restore RBF to make urine retention continues, volume no longer has a beneficial effect and edema occurs

115
Q

In severe cardiac failure, extreme excess fluid causes:

A

Increased workload on damaged heart
Overstretching heart, further weakening it
Filtration of fluid into lungs > pulmonary edema and hypoxemia
Edema in most parts of the body

116
Q

What happens during the natural reparative process?

A

Collateral blood supply penetrates peripheral portions, can cause muscle to function again
Undamaged portions of muscle hypertrophy to offset damaged parts

117
Q

After partial recovery, what happens to RBF and retention of fluid?

A

Once CO is restored so is RBF and fluid is no longer retained. Except for the fluid already retained continues to maintain a moderate excess of fluid

118
Q

What happens in decompensated HF?

A

Compensation by SNS and fluid retention are unable to restore enough CO to perfuse kidneys, so they continue to retain fluid which continues to increase RAP. Eventually the overstretched and edematous heart function no longer increases by declines

119
Q

Clinically, how can one detect decompensation?

A

Progressing edema, especially pulmonary edema

  • dyspnea
  • Rales
120
Q

Treatment for decompensation

A

Strengthen heart
-cardiotonic drugs
Diuretics
-to increase kidney excretion of salt and water

121
Q

MOA of cardiotonic glycosides like Digitalis

A

Strengthens heart contractions by increasing quantities of Ca+ in muscle fibers

122
Q

What is more common, left or right sided HF?

A

Left

123
Q

What does severe acute cardiac failure do to peripheral capillary pressure?

A

Initially capillary pressure falls (17 to 13mmHg)

-this explains why it almost never causes immediate development of peripheral edema

124
Q

Causes of reduced renal output of urine during cardiac failure?

A

Decreased GFR
Activation of Renin-Angiotenin system and increased reabsorption
Increased Aldosterone secretion
Activation of SNS

125
Q

Why does a decrease in CO decrease glomerular pressure?

A

Reduced arterial pressure

Intense SNS constriction of the afferent arterioles of the kidney

126
Q

Reduced BF to the kidneys causes increase in secretion of what?

A

Renin > increased Angiotensin II > acts on arterioles of the kidney to decrease BF more which reduces peritubular capillary pressure promoting increased reabsorption

127
Q

What 2 mechanism increase aldosterone secretion in chronic HF?

A

Mainly from Angiotensin II, but also from excess K+

128
Q

What effects occur with secretion of Aldosterone in HF?

A

Aldosterone further increases reabsorption of Na from the renal tubules
-which secondarily increases water reabsorption, and ADH secretion is elicited

129
Q

What effect does SNS stimulation play in retention of fluid by the kidneys?

A

Constriction of renal afferent arterioles > decreased GFR
Stimulation of renal tubule reabsorption by activating alpha adrenergic receptors on the tubular epithelial cells
Stimulation of RAAS
Stimulation of ADH release from posterior pituitary

130
Q

What is atrial natriuretic factor? What is it’s effect?

Peptide

A

A hormone released by the atrial walls in response to stretch.
It has a direct effect on the kidneys to increase excretion of water and salt

131
Q

What is cardiac reserve and what is the normal range in health hearts?

A

The maximum % that CO can increase above normal.

300-400%

132
Q

What blood test can provide an estimate of the adequacy of CO?

A

SVO2

133
Q

Norepinephrine enhances contractility primarily via activation of what receptor?

A

Beta 1

134
Q

What depresses myocardial contractility?

A 
Hypoxia
Acidosis
Depletion of catecholamines
Loss of functioning muscle mass
Large doses of most anesthetics and antiarrhythmics
135
Q

How does stenosis of an AV valve reduce SV?

A

By decreasing ventricular preload

136
Q

How does stenosis of an SL valve reduce SV?

A

By increasing ventricular afterload

137
Q

How does valvular regurgitation reduce SV?

A

By allowing back flow

138
Q

When is EF not an accurate measure of ventricular contractibility?

A

Mitral insufficiency

139
Q

How does a health heart respond to increased venous return?

A

Increased SV

140
Q

What could make a heart hypoeffective?

A

Loss of muscle mass
Valve disease
Dysthymia

141
Q

What could make a heart hypereffective?

A

SNS stimulation

Aerobic conditioning

142
Q

How does increased afterload affect the heart?

A

This increases resistance to ejection and can decrease SV. A healthy heart can keep up if it’s not too excessive.

143
Q

How does decreased afterload affect the heart?

A

This decreases resistance to ejection, but vascular tone matters. If afterload is decreased with vasodilation, then venous return is decreased and therefore so is SV

144
Q

How can decreased resistance lead to increased SV?

A

By augmenting the circulating volume, “fill the tank”

145
Q

Other than hypoeffective heart, what are other causes of decreased SV?

A

Decreased venous return: loss of volume, venodilation, obstruction

146
Q

What can you give to decrease preload?

A

Diuretics

Venodilators

147
Q

What if CHF persists with optimal filling pressure?

A

You need to increase contractility

  • inotropes
  • decrease afterload: arterial vasodilators, IABP
148
Q

Causes of systolic HF?

A

CAD
Dilated cardiomyopathy
Chronic pressure overload (aortic stenosis, chronic hypertension)
Chronic volume overload (regurgitative valve, high output heart failure)

149
Q

A patient with LBBB and systolic HF is at high risk for?

A

Sudden death

150
Q

Causes of Diastolic HF?

A

Ischemic heart disease
Long standing systemic hypertension
Progressive aortic stenosis

151
Q

Most common causes of low output heart failure?

A 
CAD
Cardiomyopathy
Hypertension
Valvular disease
Pericardial disease
152
Q

Causes of high output HF?

A 
Anemia
Pregnancy
AV fistula
Severe hyperthyroidism 
Beriberi
Paget’s disease
153
Q

What drugs are used in treatment of systolic HF?

A 
Inhibitors of RAAS
-ACE inhibitors
-ARB
-Aldosterone antagonists
Beta blockers
Statins
Diuretics
Vasodilators
154
Q

How are ACE inhibitors beneficial in HF?

A

Vasodilation
Reduce Na and water retention
Support K+ conservation
Decrease ventricular remodeling and potentially reverse

155
Q

What affect do beta blocks have in HF treatment?

A

Reverse the harmful effects of SNS activation in HF
-with down regulation of B receptors, circulating catecholamines increase
-high plasma levels of NE are directly cardiotoxic and promote myocyte necrosis
Increase the EF
Decrease ventricular remodeling

156
Q

What effect do statins have in HF treatment?

A

Anti inflammatory and decrease lipids

157
Q

What role do diuretics play in HF treatment? Which are recommended?

A 
Relieve circulatory congestion
-pulmonary edema
-peripheral edema
Diuretic induced decreases in ventricular diastolic pressure will decrease diastolic wall stress
Thiazides and Loops
158
Q

What treatment is available for diastolic HF?

A

Low Na diet
Cautious use of diuretics to relieve congestion without excessive decrease in preload
Maintenance of NSR
Correct precipitating factors like ischemia or hypertension

CV Test 2 (3 decks)

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