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IPCS 4 > Cardio 3 > Flashcards

Cardio 3 Flashcards

1
Q

What is the definition of heart failure?

A

clinical syndrome with symptoms/signs caused by a structural or functional cardiac abnormality AND confirmed by elevated natriuretic peptide levels or evidence of pulmonary or systemic congestion

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2
Q

What is the equation for cardiac output?

A

CO = HR x SV

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3
Q

What is cardiac output?

A

the volume of blood in liters pumped form ventricles per minute

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4
Q

What is the cardiac output goal?

A

maintenance of adequate tissue perfusion

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5
Q

The MAP equation is __
MAP = __ diastole + __ systole

A

MAP = SV x HR x SVR
2/3 diastole
1/3 systole

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6
Q

Heart rate is affected by:

A

Autonomic innervation
Hormone regulation
Fitness level
Age

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7
Q

Stroke volume is affected by:

A

Preload
Afterload
Contractility
Heart size (gender)
Fitness level
Age

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8
Q

Preload:

A

“stretch”
Volume of blood inside ventricles during diastole
Quantify: left ventricle end-diastolic volume (LVEDV or EDV

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9
Q

Afterload:

A

“squeeze”
esistance ventricles must overcome to force blood into systemic circulation
Quantify: systemic vascular resistance (SVR), pulmonary vascular resistance (PVR), end-systolic volume (ESV)

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10
Q

Contractility:

A

“strength”
Contraction of the myocardium through the actin-myosin cross bridge cycle
Quantify: ejection fraction (EF)
EF = (EDV - ESV) / EDV : stroke volume

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11
Q

Preload is affected by:

A

Heart rate
Ventricle compliance
Atrial contraction
Venous/aortic pressure
Total blood volume

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12
Q

Afterload is affected by:

A

Aortic pressure
Systemic vascular resistance
Ventricle wall thickness
Ventricle radius

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13
Q

Contractility is affected by:

A

Sympathetic nervous system
Heart rate
Ca2+
Rhythm

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14
Q

What is an average cardiac output for an adult male?

A

CO = HR x SV
70 bpm x (70ml/1000)
= 4.9 L/min
(4-8 L/min)

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15
Q

LVEDP is a surrogate for __

A

EDV

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16
Q

Decrease in after load or an increase in contractility leads to a HIGHER/LOWER SV

A

Higher SV

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17
Q

Increase in after load or decrease in contractility leads to a HIGHER/LOWER SV

A

Lower SV

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18
Q

CVP is the __ pressure

A

right atrial pressure

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19
Q

LVEDV is the __ pressure

A

Pulmonary-Capillary Wedge pressure

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20
Q

What can impact intracardiac pressures?

A

Heart failure (hypervolemia)
Pulmonary arterial hypertension
Pleural effusion
Cardiac tamponade
Hypovolemia
Shock

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21
Q

HFrEF is due to __ failure

A

systolic (heart contraction)

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22
Q

HFpEF is due to __ fialure

A

diastolic (heart relaxation)

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23
Q

HFrEF is due to:
Loss of __
__ ventricles
__ dysfunction

A

Loss of intrinsic contractility
Overstretched: weak and thin ventricles
Pumping (systolic) dysfunction

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24
Q

HFpEF is due to:
Failure of __
__ ventricles
Reduced __
__ dysfunction

A

Failure of ventricles to relax properly
Thick and stiff ventricles
Reduced ventricle volume in diastole
Filling (diastolic) dysfunction

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25
Q

Classification of heart failure is based on the ejection fraction of the __

A

left ventricle

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26
Q

What are the three classifications and LVEF levels of heart failure?

A

HFrEF: </=40%
HFmrEF: 41-49%
HFpEF: >/=50%

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27
Q

What is cardiomyopathy?

A

An acquired or inherited disease of the myocardium associated with mechanical or electrical disfunction, leading to an enlarged/rigid heart muscle

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28
Q

In hypertrophic cardiomyopathy, ventricles become __

A

larger and thicker

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29
Q

In dilated cardiomyopathy, ventricles become __

A

weaker and larger

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30
Q

In restrictive cardiomyopathy, ventricles __

A

stiffen, but do not thicken

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31
Q

In left ventricular non-compaction, the LV becomes __

A

thick/spongy

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32
Q

In arrythmogenic right ventricular dysplasia __ leads to arrhythmias

A

fibrous tissue

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33
Q

What are examples of Primary non-ischemic cardiomyopathies?

A

Genetic:
HCM
Congenital heart defect
Ion channel disorders
ARVC/D
LVNC
Acquired:
Peripartum
Takotsubo
Inflammatory (myocarditis)
Arrhythmias
Mixed:
DCM
Restrictive

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34
Q

What are ischemic cardiomyopathy examples?

A

CAD
ACS

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35
Q

What are examples of secondary non-ischemic cardiomyopathies?

A

Infiltrative
Neuro-muscular
Obesity
Hypertension
Toxicity
Auto-immune
Anemia
Endocrine
Electrolyte imbalance
Chronic lung disease
Cardiac tumor
Inflammatory
CKD
Pericardial disease
VHD

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36
Q

What are the most common etiologies of HFrEF?

A

CAD/ACS
Hypertension

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37
Q

What is the most common etiology if HFpEF?

A

Hypertension

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38
Q

What is involved in the pathophysiology of HFrEF?

A

SNS: neurohormonal activation
Frank-Starling mechanism
RAAS: neurohormonal activation
Ventricular hypertrophy and remodeling

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39
Q

Compensatory mechanisms in heart failure are initiated by __

A

acute reductions in blood pressure or reduced renal perfusion (due to low CO)

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40
Q

What is the purpose of the compensatory mechanisms in heart failure?

A

To provide short-term support to maintain circulatory homeostasis

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41
Q

Long activation of heart failure compensatory mechanisms results in __

A

functional, structural, biochemical, and molecular changes in the heart
Further stress results in deterioration of ventricular function

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42
Q

What neurohormones are involved in the SNS activation leading to heart failure? What effects to they precipitate?

A

NE: tachycardia, vasoconstriction, contractility
AVP: vasoconstriction, water retention
Renin: vasoconstriction, water retention

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43
Q

What is the result of SNS activation leading to heart failure?

A

Decrease in CO causes unloading of baroreceptors, which decrease parasympathetic tone
Increase in sympathetic tone which releases NE, renin, and AVP
Decrease in Beta1 receptor sensitivity, reduces stimulation over time

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44
Q

What are the results of cardiomyocyte contraction in heart failure?

A

Increase in HR, decrease in diastole time, increase in intracellular Ca2+
Increase in actin-myosin interaction, increase in rate of contraction
Decrease in lusitropy (ability to relax)
Creates greater filament interaction during systole (force), increased wall tension

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45
Q

Which neurohormones are involved in the RAAS activation that leads to heart failure? What are their effects?

A

Angiotensin II: Na and water retention, stimulates aldosterone release
Aldosterone: Sodium and water retention, cardiac fibrosis

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46
Q

What is the Kallikrein-kinin system?

A

Cross talks with RAAS to cause vasodilation
Bradykinin increases release of other vasodilatory molecules

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47
Q

What are the types of natriuretic peptides?

A

Atrial NP: high affinity, short half-life
Brain or B-type: lower affinity but longer half-life
N-terminal: biologically inactive, longest half-life

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48
Q

What is the purpose of natriuretic peptides in response to volume overload?

A

To promote natriuresis/diuresis and inhibit RAAS and SNS

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49
Q

Chronic activation of hemodynamic and neurohormonal compensatory responses leads to __ (ventricular remodeling).

A

Eccentric hypertrophy
Change in ventricle composition
Oxidative stress and inflammatory cytokines
Altered myocardial contraction
Alterations in geometry

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50
Q

What is the benefit of increased preload volume (Frank-Sterling) response?

A

Increased stroke volume (CO)

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51
Q

What is the harm done by increased preload volume (Frank-Sterling) response?

A

Pulmonary and systemic congestion (edema)
Myocardial O2 demand

52
Q

What is the benefit of vasoconstriction (RAAS) response?

A

Increased SVR to increase BP
Shunts blood to vital organs (CO)

53
Q

What is the harm of vasoconstriction (RAAS) response?

A

Myocardial O2 demand increases
Decrease stroke volume (activates compensatory mechanism)

54
Q

What is the benefit of tachycardia/increased contractility (SNS) response?

A

Increased HR (CO)

55
Q

What is the harm with tachycardia/increased contractility (SNS) response?

A

Myocardial O2 demand increases
Decrease diastole time (less volume)
Increase risk of arrhythmias
Increase myocardial cell death
Decrease beta1 receptor regulation

56
Q

What is the benefit of ventricular remodeling (hypertrophy) response?

A

Increase CO
Decrease myocardial wall stress
Decrease myocardial OR demand

57
Q

What is the harm with ventricular remodeling (hypertrophy) response?

A

Diastolic/systolic dysfunction
Increase myocardial cell ischemia/death
Increase fibrosis and arrhythmias

58
Q

What is included in the pathophysiology of HFpEF?

A

Systemic Inflammation: aging, DM, obesity
Pressure Overload: hypertension
Hormonal Activation: SNS, RAAS, NP
Endothelial Dysfunction: Microvasculature
Concentric Hypertrophy: remodeling

59
Q

What is the most common protein that attributes to amyloidosis?

A

transthyretin

60
Q

What is the most common genetic cardiac disease that commonly causes HFpEF?

A

hypertrophy cardiomyopathy

61
Q

What are key findings in hypertrophic cardiomyopathy?

A

Myosin protein defects
Mutant sarcomere genes trigger myocardial changes
Leads to hypertrophy and fibrosis

62
Q

What is included in a differential diagnosis of heart failure?

A

Dyspnea
Chronic lung disease
Pulmonary arterial hypertension
Anemia
Pulmonary embolism
Edema
Venous insufficiency
Nephrotic syndrome
Deep vein thrombosis
Lymphedema
Jugular venous distention
Constrictive pericarditis
Pericardial effusion
Pulmonary embolism
Tension pneumothorax

63
Q

What is the acronym for symptoms of heart failure?

A

FAILURE

64
Q

What are symptoms of heart failure?

A

Fatigue
Abdominal pain, appetite loss, anorexia
Impaired memory (confusion)
Lower ability to exercise/do daily activities
Urination at night
Respiration issues
Edema

65
Q

What is the acronym for signs of heart failure?

A

HEART CMP

66
Q

What are signs of heart failure?

A

Hepatomegaly, hepatojugular reflux
Edema
Ascites
Regurgitation, S3 gallop
Tachypnea, tachycardia

Cool extremities, cardiomegaly, cachexia
Mental status changes
Pulmonary rates, pleural effusion, positive JVD

67
Q

How is NYHA Class I defined?
Limitation of Physical Activity:
Clinical Assessment:

A

Limitation of Physical Activity: None
Clinical Assessment: ordinary physical activity does not cause undue fatigue, dyspnea, palpitations, or angina

68
Q

How is NYHA Class II defined?
Limitation of Physical Activity:
Clinical Assessment:

A

Limitation of Physical Activity: Mild
Clinical Assessment: Comfortable at rest, ordinary physical activity may cause symptoms

69
Q

How is NYHA Class III defined?
Limitation of Physical Activity:
Clinical Assessment:

A

Limitation of Physical Activity: Moderate
Clinical Assessment: Comfortable at rest, less than ordinary physical activity leads to symptoms

70
Q

How is NYHA Class IV defined?
Limitation of Physical Activity:
Clinical Assessment:

A

Limitation of Physical Activity: Severe
Clinical Assessment: Symptoms present at rest and worsened with any activity

71
Q

What is stage A of heart failure?

A

At risk
No objective evidence of CVD and no symptoms or limitations in ordinary physical activity

72
Q

What is stage B of heart failure?

A

Pre-HF
No symptoms/signs of HF, but objective evidence of CVD

73
Q

What is stage C of heart failure?

A

Symptomatic HF
Structural heart disease with current or previous signs/symptoms of HF

74
Q

What is stage D of heart failure?

A

Advanced HF
Marked HF symptoms interfering with daily life and with recurrent hospitalizations

75
Q

Who is considered at risk for heart failure?

A

Hypertension
CVD
DM
Obesity
Hereditary cardiomyopathies
Exposure to cardiotoxins

76
Q

What is evidence of CVD?

A

Structural heart disease
increased filling pressures
Risk factors AND elevated BNP or persistent elevated cardiac troponin levels

77
Q

What are lab markers in heart failure?

A

BNP >100 pg/mL
NT-proBNP >300 pg/mL
CBC: reduced oxygen carrying capacity (anemia)
SCr: elevated due to hyperfusion
Na: low due to volume overload
BUN: elevated due to reduced renal blood flow
LFTs: elevated due to hepatic congestion
Inflammatory markers: Elevated CRP, ESR, and uric acid
Urinalysis: Proteinuria due to HTN or DM

78
Q

What are non-invasive diagnostic tools used for heart failure?

A

ECG
Chest x-ray
Echo
CMR

79
Q

What is an ECG useful for in diagnosing HF?

A

Left ventricular hypertrophy
Q waves/ST-T wave changes
Atrial fibrilation

80
Q

What is a chest X-ray useful for in diagnosing HF?

A

Cardiomegaly
Pulmonary venous congestion
Pleural effusion

81
Q

What in an echo is useful for diagnosing HF?

A

LV size, ejection fraction
Valve function
Wall motion abnormalities
Pericardial effusion

82
Q

What in a CMR is useful for diagnosing HF?

A

LV mass
Volume status
Anatomical/functional abnormalities
Identify cause of HF

83
Q

What are invasive diagnostic tools for HF?

A

Pulmonary artery catheter
Right heart catheterization
Left heart catheterization
Left ventriculography

84
Q

What in a pulmonary artery catheter is useful in diagnosing heart failure?

A

Bedside hemodynamic monitoring
Swan Gan: catheter
Evaluate response to IV vasopressors, diuretics, intropes

85
Q

What in a right heart catheterization is useful in diagnosing HF?

A

Hemodynamic monitoring in cath lab
Assess oxygen saturations
Evaluate response to medications

86
Q

What in a right heart catheterization is useful in diagnosing HF?

A

Rule out ischemic heart disease
Reverse LV dysfunction due to ACS
Assess LV/valve function

87
Q

What in a left ventriculography is useful for diagnosing HF?

A

Uncommon, useful if ECHO images are suboptimal
Assess LV size, function, valve function

88
Q

What is acute decompensated heart failure?

A

Acute worsening of chronic HF requiring medical intervention

89
Q

What is the underlying problem in ADHF?

A

Low cardiac output
Volume overload

89
Q

What are the signs/symptoms of ADHF?

A

Same as chronic HF bus exacerbated

90
Q

What causes ADHF?

A

Dietary indiscretion
Medications
GDMT nonadherence
Non cardiac illness (infection, AKI)

91
Q

What are specific cardiac causes of ADHF?

A

MI
Arrhythmias
Hypertensive crisis
Myocarditis
Acute valvular insufficiency

92
Q

What is considered Subset I in ADHF?

A

Warm and dry
PCWP <18
CI 2.2 or greater

93
Q

What is considered Subset II in ADHF?

A

Warm and wet
PCWP 18 or greater
CI 2.2 or greater

94
Q

What is considered Subset III in ADHF?

A

Cold and dry
PCWP <18
CI <2.2

95
Q

What is considered Subset IV in ADHF?

A

Cold and wet
PCWP 18 or greater
CI <2.2

96
Q

How do you control subset I ADHF?

A

Optimize chronic oral medications

97
Q

What is considered Subset II in ADHF?

A

IV loop diuretic +/- IV vasodilator
PAC to guide management

98
Q

What is considered Subset III in ADHF?

A

Assess volume status/SBP
IV fluids, IV inotrope, IV vasodilator

99
Q

What is considered Subset IV in ADHF?

A

Assess PAC/SBP
IV diuretic, IV inotrope, IV vasopressor, vasodilator

100
Q

What are the three ways drugs exacerbate HF?

A

Negative inotrope
Cardiotoxic
Na/H2O retention

101
Q

What drugs are negative inotropes that exacerbate HF?

A

Antiarrhythmias
Beta blockers
Non-DHP CCBs
Itraconazole
TCAs
Ketamine
Propofol

102
Q

What drugs are cardiotoxic and exacerbate HF?

A

Anthracyclines
Alkylating agents
Carbamazepine
Ethanol
Amphetamines

103
Q

What drugs cause Na/H2O retention and exacerbate HF?

A

NSAIDs
Glucocorticoids
Angrogens/estrogens
Thiazolidinediones
IV: Flagyl, Zosyn, Unasyn
OTC: omeprazole alendronate, Mirilax

104
Q

What are goals of HF treamtent?

A

Prevent development of HF
Improve quality of life
Relive/reduce symptoms
Prevent hospitalizations
Slow progression of disease
Prolong survival

105
Q

What are quality markers in HF?

A

30 day mortality
90 day mortality
Excess days in acute care (>30 days)

106
Q

What are nonpharm options for HF treatment?

A

Education
Screening
Restriction
Exercise

107
Q

What is included in education of HF?

A

Patient education to facilitate HF self-care
Self-monitoring for signs of worsening HF
Patient education to adhere to therapies

108
Q

What is included in “Screening” nonpharm HF treatment?

A

Depression linked to poor self-care, HFH, and mortality
Social isolation associated with higher mortality
Frality associated with increased risk of mortality and self-care

109
Q

What is included in the “restriction” part of nonpharm for HF treatment?

A

1.5-2.3g of sodium restriction
2L fluid restriction
May help with symptomatic congestion but no clinical benefit
Can lead to poor dietary quality

110
Q

What is included in the “exercise” portion of nonpharm HF treatment?

A

Maintain physical activity as tolerated
Exercise training

111
Q

What are risk scores used to predict development of HF?

A

Framingham HF risk score
Health ABC HF score

112
Q

What is the primary focus for treating Stage A HF?

A

Primary prevention

113
Q

What is the primary focus for treating Stage B HF?

A

Preventing syndrome of clinical HF
Patients still asymptomatic
Recommendations from Stage A still apply

114
Q

What is the primary focus for treating Stage C HF?

A

ARNI/ACE/ARB
Beta Blocker
Diuretic

115
Q

What is the role of diuretics in HF?

A

Decrease preload
Stimulates neurohormonal release
No clear benefit on morbidity or mortality

116
Q

What diuretic should be used in HF?

A

loop diuretics preferred

117
Q

What is the goal for using loop diuretics in HF?

A

eliminate clinical evidence of fluid retention using the lowest dose of diuretics possible to maintain euvolemia (dry weight)

118
Q

NYHA Class I/II should have PRN or SCHEDULED loop diuretic dosing

A

PRN for rapid weight gain

119
Q

NYHA Class III/IV should have PRN or SCHEDULED loop diuretic dosing

A

Scheduled

120
Q

In ADHF what initial loop diuretic dose should be started?

A

Double the home dose
If not on a diuretic, start with 40-80mg IV furosemide or equivalent

121
Q

What is the urine output goal for loop diuretics in ADHF?

A

500mL in first 2 hours
2-3L in 24 hours

122
Q

If urine output goal at 2 hours is not met, what should be done with the diuretic?

A

Double the IV diuretic dose

123
Q

What labs should be monitored with loop diuretics?

A

K, Mg, Na, Urine Na, Cl, Ca
CO2
BUN/Cr ratio, SCr
uric acid

124
Q

What should be monitred when a patient is taking a loop diuretic for HF?

A

Daily weights
Urine output

125
Q
A

IPCS 4 (5 decks)

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