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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
Classification of heart failure is based on the ejection fraction of the __
left ventricle
26
What are the three classifications and LVEF levels of heart failure?
HFrEF: /=50%
27
What is cardiomyopathy?
An acquired or inherited disease of the myocardium associated with mechanical or electrical disfunction, leading to an enlarged/rigid heart muscle
28
In hypertrophic cardiomyopathy, ventricles become __
larger and thicker
29
In dilated cardiomyopathy, ventricles become __
weaker and larger
30
In restrictive cardiomyopathy, ventricles __
stiffen, but do not thicken
31
In left ventricular non-compaction, the LV becomes __
thick/spongy
32
In arrythmogenic right ventricular dysplasia __ leads to arrhythmias
fibrous tissue
33
What are examples of Primary non-ischemic cardiomyopathies?
Genetic: HCM Congenital heart defect Ion channel disorders ARVC/D LVNC Acquired: Peripartum Takotsubo Inflammatory (myocarditis) Arrhythmias Mixed: DCM Restrictive
34
What are ischemic cardiomyopathy examples?
CAD ACS
35
What are examples of secondary non-ischemic cardiomyopathies?
Infiltrative Neuro-muscular Obesity Hypertension Toxicity Auto-immune Anemia Endocrine Electrolyte imbalance Chronic lung disease Cardiac tumor Inflammatory CKD Pericardial disease VHD
36
What are the most common etiologies of HFrEF?
CAD/ACS Hypertension
37
What is the most common etiology if HFpEF?
Hypertension
38
What is involved in the pathophysiology of HFrEF?
SNS: neurohormonal activation Frank-Starling mechanism RAAS: neurohormonal activation Ventricular hypertrophy and remodeling
39
Compensatory mechanisms in heart failure are initiated by __
acute reductions in blood pressure or reduced renal perfusion (due to low CO)
40
What is the purpose of the compensatory mechanisms in heart failure?
To provide short-term support to maintain circulatory homeostasis
41
Long activation of heart failure compensatory mechanisms results in __
functional, structural, biochemical, and molecular changes in the heart Further stress results in deterioration of ventricular function
42
What neurohormones are involved in the SNS activation leading to heart failure? What effects to they precipitate?
NE: tachycardia, vasoconstriction, contractility AVP: vasoconstriction, water retention Renin: vasoconstriction, water retention
43
What is the result of SNS activation leading to heart failure?
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
44
What are the results of cardiomyocyte contraction in heart failure?
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
45
Which neurohormones are involved in the RAAS activation that leads to heart failure? What are their effects?
Angiotensin II: Na and water retention, stimulates aldosterone release Aldosterone: Sodium and water retention, cardiac fibrosis
46
What is the Kallikrein-kinin system?
Cross talks with RAAS to cause vasodilation Bradykinin increases release of other vasodilatory molecules
47
What are the types of natriuretic peptides?
Atrial NP: high affinity, short half-life Brain or B-type: lower affinity but longer half-life N-terminal: biologically inactive, longest half-life
48
What is the purpose of natriuretic peptides in response to volume overload?
To promote natriuresis/diuresis and inhibit RAAS and SNS
49
Chronic activation of hemodynamic and neurohormonal compensatory responses leads to __ (ventricular remodeling).
Eccentric hypertrophy Change in ventricle composition Oxidative stress and inflammatory cytokines Altered myocardial contraction Alterations in geometry
50
What is the benefit of increased preload volume (Frank-Sterling) response?
Increased stroke volume (CO)
51
What is the harm done by increased preload volume (Frank-Sterling) response?
Pulmonary and systemic congestion (edema) Myocardial O2 demand
52
What is the benefit of vasoconstriction (RAAS) response?
Increased SVR to increase BP Shunts blood to vital organs (CO)
53
What is the harm of vasoconstriction (RAAS) response?
Myocardial O2 demand increases Decrease stroke volume (activates compensatory mechanism)
54
What is the benefit of tachycardia/increased contractility (SNS) response?
Increased HR (CO)
55
What is the harm with tachycardia/increased contractility (SNS) response?
Myocardial O2 demand increases Decrease diastole time (less volume) Increase risk of arrhythmias Increase myocardial cell death Decrease beta1 receptor regulation
56
What is the benefit of ventricular remodeling (hypertrophy) response?
Increase CO Decrease myocardial wall stress Decrease myocardial OR demand
57
What is the harm with ventricular remodeling (hypertrophy) response?
Diastolic/systolic dysfunction Increase myocardial cell ischemia/death Increase fibrosis and arrhythmias
58
What is included in the pathophysiology of HFpEF?
Systemic Inflammation: aging, DM, obesity Pressure Overload: hypertension Hormonal Activation: SNS, RAAS, NP Endothelial Dysfunction: Microvasculature Concentric Hypertrophy: remodeling
59
What is the most common protein that attributes to amyloidosis?
transthyretin
60
What is the most common genetic cardiac disease that commonly causes HFpEF?
hypertrophy cardiomyopathy
61
What are key findings in hypertrophic cardiomyopathy?
Myosin protein defects Mutant sarcomere genes trigger myocardial changes Leads to hypertrophy and fibrosis
62
What is included in a differential diagnosis of heart failure?
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
What is the acronym for symptoms of heart failure?
FAILURE
64
What are symptoms of heart failure?
Fatigue Abdominal pain, appetite loss, anorexia Impaired memory (confusion) Lower ability to exercise/do daily activities Urination at night Respiration issues Edema
65
What is the acronym for signs of heart failure?
HEART CMP
66
What are signs of heart failure?
Hepatomegaly, hepatojugular reflux Edema Ascites Regurgitation, S3 gallop Tachypnea, tachycardia Cool extremities, cardiomegaly, cachexia Mental status changes Pulmonary rates, pleural effusion, positive JVD
67
How is NYHA Class I defined? Limitation of Physical Activity: Clinical Assessment:
Limitation of Physical Activity: None Clinical Assessment: ordinary physical activity does not cause undue fatigue, dyspnea, palpitations, or angina
68
How is NYHA Class II defined? Limitation of Physical Activity: Clinical Assessment:
Limitation of Physical Activity: Mild Clinical Assessment: Comfortable at rest, ordinary physical activity may cause symptoms
69
How is NYHA Class III defined? Limitation of Physical Activity: Clinical Assessment:
Limitation of Physical Activity: Moderate Clinical Assessment: Comfortable at rest, less than ordinary physical activity leads to symptoms
70
How is NYHA Class IV defined? Limitation of Physical Activity: Clinical Assessment:
Limitation of Physical Activity: Severe Clinical Assessment: Symptoms present at rest and worsened with any activity
71
What is stage A of heart failure?
At risk No objective evidence of CVD and no symptoms or limitations in ordinary physical activity
72
What is stage B of heart failure?
Pre-HF No symptoms/signs of HF, but objective evidence of CVD
73
What is stage C of heart failure?
Symptomatic HF Structural heart disease with current or previous signs/symptoms of HF
74
What is stage D of heart failure?
Advanced HF Marked HF symptoms interfering with daily life and with recurrent hospitalizations
75
Who is considered at risk for heart failure?
Hypertension CVD DM Obesity Hereditary cardiomyopathies Exposure to cardiotoxins
76
What is evidence of CVD?
Structural heart disease increased filling pressures Risk factors AND elevated BNP or persistent elevated cardiac troponin levels
77
What are lab markers in heart failure?
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
What are non-invasive diagnostic tools used for heart failure?
ECG Chest x-ray Echo CMR
79
What is an ECG useful for in diagnosing HF?
Left ventricular hypertrophy Q waves/ST-T wave changes Atrial fibrilation
80
What is a chest X-ray useful for in diagnosing HF?
Cardiomegaly Pulmonary venous congestion Pleural effusion
81
What in an echo is useful for diagnosing HF?
LV size, ejection fraction Valve function Wall motion abnormalities Pericardial effusion
82
What in a CMR is useful for diagnosing HF?
LV mass Volume status Anatomical/functional abnormalities Identify cause of HF
83
What are invasive diagnostic tools for HF?
Pulmonary artery catheter Right heart catheterization Left heart catheterization Left ventriculography
84
What in a pulmonary artery catheter is useful in diagnosing heart failure?
Bedside hemodynamic monitoring Swan Gan: catheter Evaluate response to IV vasopressors, diuretics, intropes
85
What in a right heart catheterization is useful in diagnosing HF?
Hemodynamic monitoring in cath lab Assess oxygen saturations Evaluate response to medications
86
What in a right heart catheterization is useful in diagnosing HF?
Rule out ischemic heart disease Reverse LV dysfunction due to ACS Assess LV/valve function
87
What in a left ventriculography is useful for diagnosing HF?
Uncommon, useful if ECHO images are suboptimal Assess LV size, function, valve function
88
What is acute decompensated heart failure?
Acute worsening of chronic HF requiring medical intervention
89
What is the underlying problem in ADHF?
Low cardiac output Volume overload
89
What are the signs/symptoms of ADHF?
Same as chronic HF bus exacerbated
90
What causes ADHF?
Dietary indiscretion Medications GDMT nonadherence Non cardiac illness (infection, AKI)
91
What are specific cardiac causes of ADHF?
MI Arrhythmias Hypertensive crisis Myocarditis Acute valvular insufficiency
92
What is considered Subset I in ADHF?
Warm and dry PCWP <18 CI 2.2 or greater
93
What is considered Subset II in ADHF?
Warm and wet PCWP 18 or greater CI 2.2 or greater
94
What is considered Subset III in ADHF?
Cold and dry PCWP <18 CI <2.2
95
What is considered Subset IV in ADHF?
Cold and wet PCWP 18 or greater CI <2.2
96
How do you control subset I ADHF?
Optimize chronic oral medications
97
What is considered Subset II in ADHF?
IV loop diuretic +/- IV vasodilator PAC to guide management
98
What is considered Subset III in ADHF?
Assess volume status/SBP IV fluids, IV inotrope, IV vasodilator
99
What is considered Subset IV in ADHF?
Assess PAC/SBP IV diuretic, IV inotrope, IV vasopressor, vasodilator
100
What are the three ways drugs exacerbate HF?
Negative inotrope Cardiotoxic Na/H2O retention
101
What drugs are negative inotropes that exacerbate HF?
Antiarrhythmias Beta blockers Non-DHP CCBs Itraconazole TCAs Ketamine Propofol
102
What drugs are cardiotoxic and exacerbate HF?
Anthracyclines Alkylating agents Carbamazepine Ethanol Amphetamines
103
What drugs cause Na/H2O retention and exacerbate HF?
NSAIDs Glucocorticoids Angrogens/estrogens Thiazolidinediones IV: Flagyl, Zosyn, Unasyn OTC: omeprazole alendronate, Mirilax
104
What are goals of HF treamtent?
Prevent development of HF Improve quality of life Relive/reduce symptoms Prevent hospitalizations Slow progression of disease Prolong survival
105
What are quality markers in HF?
30 day mortality 90 day mortality Excess days in acute care (>30 days)
106
What are nonpharm options for HF treatment?
Education Screening Restriction Exercise
107
What is included in education of HF?
Patient education to facilitate HF self-care Self-monitoring for signs of worsening HF Patient education to adhere to therapies
108
What is included in "Screening" nonpharm HF treatment?
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
What is included in the "restriction" part of nonpharm for HF treatment?
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
What is included in the "exercise" portion of nonpharm HF treatment?
Maintain physical activity as tolerated Exercise training
111
What are risk scores used to predict development of HF?
Framingham HF risk score Health ABC HF score
112
What is the primary focus for treating Stage A HF?
Primary prevention
113
What is the primary focus for treating Stage B HF?
Preventing syndrome of clinical HF Patients still asymptomatic Recommendations from Stage A still apply
114
What is the primary focus for treating Stage C HF?
ARNI/ACE/ARB Beta Blocker Diuretic
115
What is the role of diuretics in HF?
Decrease preload Stimulates neurohormonal release No clear benefit on morbidity or mortality
116
What diuretic should be used in HF?
loop diuretics preferred
117
What is the goal for using loop diuretics in HF?
eliminate clinical evidence of fluid retention using the lowest dose of diuretics possible to maintain euvolemia (dry weight)
118
NYHA Class I/II should have PRN or SCHEDULED loop diuretic dosing
PRN for rapid weight gain
119
NYHA Class III/IV should have PRN or SCHEDULED loop diuretic dosing
Scheduled
120
In ADHF what initial loop diuretic dose should be started?
Double the home dose If not on a diuretic, start with 40-80mg IV furosemide or equivalent
121
What is the urine output goal for loop diuretics in ADHF?
500mL in first 2 hours 2-3L in 24 hours
122
If urine output goal at 2 hours is not met, what should be done with the diuretic?
Double the IV diuretic dose
123
What labs should be monitored with loop diuretics?
K, Mg, Na, Urine Na, Cl, Ca CO2 BUN/Cr ratio, SCr uric acid
124
What should be monitred when a patient is taking a loop diuretic for HF?
Daily weights Urine output
125

IPCS 4 (5 decks)

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