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Advanced Patho Exam 3 > Exam 3: HF > Flashcards

Exam 3: HF Flashcards

1
Q

the definition of heart failure

A

a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricles to fill with or eject blood

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2
Q

what symptoms do patients with HF experience? (3) and why?

A
  • sob
  • fluid retention
  • fatigue

because of the changes in ejecting and filling

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3
Q

what are the associations with HF (3)

A
  • reduced exercise tolerance
  • high incidence of ventricular arrhythmias
  • shortened life expectancy
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4
Q

how does body try to compensate with HF

A

 Body tries to compensate by releasing neurohormonal mechanisms (SNS and RAAS) to increase CO (SV x HR)
* Over time the heart loses the ability to compensate

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5
Q

what are structural change that result from HF due to?

A

due to ventricular remodeling
**ventricular remodeling process can take years to occur

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6
Q

clinical characteristics of HF “DROPSY”

A

o Have to have symptoms for it to be HF, otherwise it is Left ventricular dysfunction “a structural problem”
o No cure, managed by therapeutic lifestyle changes and meds
o Progressive disorder-
 Clinical syndrome characterized by specific symptoms;
* Dyspnea and fatigue
* Edema and rales
 Disease progression can be silent
* This is why an echo is done yearly!

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7
Q

define cardiac output

A

 The volume of blood flowing through either the systemic or the pulmonary circuit and is expressed in liters per minute. Cardiac output is calculated by;
* HR x SV = CO

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8
Q

what is the normal cardiac output at rest

A

5 L/min

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9
Q

what is cardiac output

A

the blood pumped each minute

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10
Q

what are four factors that affect cardiac output directly?

A

-preload
-afterload
-myocardial contractility
-heart rate

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11
Q

define ejection fraction

A

 EF is the % of blood ejected by the ventricle or stroke volume relative to the end diastolic volume
* Ventricles don’t eject all of the blood they contain with each heartbeat, the amount ejected is the EF
* Calculated by; dividing SV by EDV
o EF = SV / EDV  EF = (EDV – ESV) / EDV
o Stroke volume= (EDV – ESV)

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12
Q

what is index of contractility and indicator of ventricular function

A
  • Indicates how well the left (or right) ventricle is contracting
  • Healthy heart pumps 2/3 of its end diastolic volume
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13
Q

what does it mean normal EF 55%

A

means 55% of the total blood in the left ventricle is pumped out with each heartbeat

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14
Q

why does HF with reduced EF occur

A

it happens when the muscle of the LV is not pumping as well as normal
o (EF < 40% – inability of the heart to generate an adequate cardiac output to perfuse to vital tissues)

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15
Q

define Left Ventricular End Diastolic Volume (LVEDV)

A

 The volume of the blood in the heart at the end of diastole is directly related to the force of contraction during the next systole
 Stretches the cardiac muscle fibers and in turn develops tension, or force, for contraction
 Increases with decreased contractility or when there is an excess of plasma volume (IV fluid administration, renal failure, mitral valvular disease)
* Increases can actually improve cardiac output up to a certain point, but as preload continues to rise, it causes a stretching of the myocardium that can eventually lead to dysfunction and decrease contractility
 As stated in the Frank-Starling law, the volume of blood in the heart at the end of diastole (the length of its muscle fibers) is directly related to the force (strength) of contraction during the next systole. The greater the stretch from preload blood volume, the stronger the contraction

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16
Q

define Left Ventricular End Diastolic Pressure (LVEDP)

A

 The pressure in the left ventricle just before systole
 This pressure reflects the compliance of the left ventricle, its ability to receive blood from the left atrium during diastole

  • Also known as preload
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17
Q

An increase in left ventricular end-diastolic volume (preload) result in an increase in ____

A

force of contraction

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18
Q

When the left ventricular compliance decreases, the LVEDP _____

A

rises

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19
Q

what are two examples of when left ventricular compliance decreases?

A
  • MI
  • left ventricular failure
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20
Q

in the person with normal mitral valve and normal lung function, LVEDP is also reflected by the pressure in what? (4)

A

-by the pressure in the pulmonary capillary
-left arterial pressure or pulmonary capillary wedge pressure
- and the pressure in the pulmonary artery at the end of diastole

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21
Q

what is the treatment goals in HF

A
  • maintain end diastolic volume/pressure that will maintain or increase CO
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22
Q

what must happen before blood can be pumped out during systole?

A

pressure in the left ventricle must exceed aortic pressure before blood can be pumped out during systole

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23
Q

define Left Ventricular End SYSTOLIC Volume (LVESV)

A

 Minimum volume of cardiac cycle
 The volume of blood in the ventricle at the end of contraction (systole) and at the beginning of filling (diastole)
* the amount of blood that remains in the heart after it contracts
* Example- heart is filled with 100ml, only 60ml is ejected (EF), the remaining is 40ml, this is end-systolic volume.

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24
Q

factors that affect end systolic volume

A

afterload and contractility of the heart

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25
Q

what is stroke volume

A

 The difference between the end-diastolic volume and end-systolic volume

  • The volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction
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26
Q

define Left Ventricular End SYSTOLIC Pressure (LVESP)

A

 Pressure in the ventricle at the end of contraction
 Volume is low but pressure is high
* “At this point in the cardiac cycle, muscles are in their maximally activated state, (think the heart is much stiffer). Blood was just ejected out, there is low volume, and the heart is contracted, or stiff, from just forcing everything out of this chamber. So, we have a low volume, high pressure situation”

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27
Q

define compliance

A

 The ability of a hallow organ or vessel to distend and increase volume with increasing Transmural pressure or the tendency of a hollow organ to resist recoil towards its original dimensions on application of an elastance
 A term used in describing diastolic properties “stiffness” of the ventricles
 Reach the maximal stiffness at the end of systole, becomes less stiff during relaxation (minimal stiffness at end diastole)
 Compliance is greatest at low volume and smallest at high volumes

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28
Q

define preload

A

 Pressure that is generated related to the end of diastole volume
 An increase in left ventricular end-diastolic volume (preload) result in an increase in force of contraction
* The greater the stretch, the greater the contraction
 Preload represents the volume work of the heart and is largely determined by venous blood return
* Degree of stretch of cardiomyocytes at the end of ventricular filling- not measurable this is why we use EDV

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29
Q

what are the two major factors preload are determined by?

A
  • the amount of venous blood return to the ventricle during diastole
  • the amount of blood left in the ventricle after systole or end-systolic volume
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30
Q

how can HF occur because of an increase in preload

A

it causes decline in stroke volume and also increases EDP

  • Increase EDP causes pressure to increase or “back up: into the pulmonary or systemic venous circulation
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31
Q

define afterload

A

 Resistance to overcome to eject blood from the ventricle (during systole)
* the load the muscle must move during contraction
* “pressure in LV must be greater than systemic pressure for aortic valve to open, pressure in RV must exceed pulmonary pressure to open the pulmonary valve”

  • Afterload, also known as the systemic vascular resistance (SVR), is the amount of resistance the heart must overcome to open the aortic valve and push the blood volume out into the systemic circulation
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32
Q

what is a good index of afterload for the left ventricle?

A

aortic systolic pressure
* Low aortic pressures (decreased afterload) enable the heart to contract more rapidly
* High aortic pressures (increased afterload) slow contraction and cause higher workloads against which the heart must function to eject blood

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33
Q

define contractility

A

 Stroke volume is dependent on the force of contraction, which is a function of myocardial contractility (the degree of myocardial fiber shortening)
 The more forceful the contraction, the more blood ejects!

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34
Q

what are the most important predisposing risk factors for HF? (2)

A
  • ischemic heart disease
  • HTN
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35
Q

list other common risk factors for HF

A

 Age, obesity, diabetes
 Renal failure
 Valvular heart disease
 Cardiomyopathies
 Excessive alcohol use
 Black males & females and at a younger age!

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36
Q

List the most common risk factors for heart failure (HF): life simple 7-same RF as CHD

A

 Smoking, physical activity, weight, diet, glucose, cholesterol, bp

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37
Q

List the most common risk factors for heart failure (HF): Genetic polymorphisms

A

 Kinase growth- regulate cell growth, day to day metabolism
 Phosphatase-energetics- regulate daily cell functioning
 Cellular calcium handling- important for contractility any impairment can result in HF

**can affect myocardial performance

38
Q

patient who are exposed to ____and ____develop HF and why

A

patient who are exposed to chemotherapy and alcohol develop HF because they are myocardial toxic

39
Q

exposure to what parasite can develop HF

A

Exposure to a parasite Trypanosoma cruzi- effects heart muscle (Chagas disease)

40
Q

The most common etiologies for HF (6)

A

o Ischemic Heart Disease:
 CAD, coronary dissection, or embolization
* Try to correct these first because can correct or improve HF
o Hypertension:
 HTN is a huge contributing factor because of pressure overload on the heart
 HFrEF and HFpEF
o Primary Cardiomyopathies
 Genetic – hypertrophic, arrhythmogenic, mitochondria myopathies, ion-channel disorders
 Acquired- peripartum (pregnancy), takotsubo (broken heart syndrome), substance abuse, toxin related, myocarditis (bacterial), chagas, viral
* Viral can occur younger patients 50-60 years of age
* Have had a common cold for more than 3 weeks, the cold virus can attack the heart
o Secondary Cardiomyopathies: amyloidosis, constricted heart, stiffness, scleroderma, lupus
o Valvular Disease: rheumatic heart disease
o Prolonged Arrhythmias

41
Q

Describe basic structural and functional changes (overall and in the myocyte) associated with the process of ventricular remodeling (physiologic and pathophysiologic). Discuss these changes in terms of ejection fraction.

A

o Ventricular remodeling results in disruption of the normal myocardial extracellular structure with resultant dilation of the myocardium and causes progressive myocyte contractile dysfunction over time
o When contractility is decreased, stroke volume falls, and left ventricular end diastolic volume (LVEDV) increases
o This causes dilation of the heart and an increase in preload
 As preload continues to rise it causes stretching of the myocardium that eventually can lead to dysfunction of the sarcomeres and decreased contractility
o The pathologic increase in muscle mass results in an increase in oxygen and energy demand, which relies on ATP production.
 ATP production is dependent on myocytes getting enough fuel, having adequate mitochondrial function, and using an effective creatine kinase system
 When demand for energy is greater than the ability to of these systems to supply the necessary ATP, contractility of the myocardium is compromised.
 An energy starved state develops that further contributes to changes in the myocytes themselves and ventricular remodeling that significantly impairs contractility and therefore ventricular function

42
Q

what is remodeling

A

Myocardium & vasculature‐compensatory response that results in structural and functional changes

43
Q

what is left ventricular remodeling defined as?

A

as a change in LV geometry, mass and volume that occurs over a period of time

44
Q

cellular changes associated with ventricular remodeling (7)

A
  • Myocyte hypertrophy (abnormal myocyte growth)
  • Intrinsic myocyte dysfunction – because of the enlargement, the relationship of the organelles to each other change
  • Alterations in gene expression
  • Cell loss with apoptosis
  • Extracellular matrix (ECM) remodeling
  • Calcium handling changes within the myocytes
  • Mitochondrial dysfunction
45
Q

what are types of ventricular remodeling

A
  • hypertrophied heart ( diastolic HF) HfpEF
  • dilated heart (systolic HF) HFrEF
46
Q

what is hypertrophied heart ( diastolic HF) HfpEF

A

o EF > 50%
* Concentric remodeling (round)
* Results in thickened myocardium, reduction in size of chamber (pathologic)
* Physiological hypertrophy:
o d/t chronic exercise or pregnancy
o Myocyte length increases > myocyte width
o No fibrosis or cardiac dysfunction
o Chamber size is still normal

47
Q

what is dilated heart (systolic HF) HFrEF

A

o EF < 40%
* Eccentric remodeling
* Results in thinned myocardium and results with problems with contractility
* Chamber becomes huge, and wall becomes very thin

48
Q

Compare and contrast necrosis and apoptosis.

A

apoptosis:
- 12-24 hrs
- cells shrink
- caspase enzymes
-energy dependent process under genetic control
- condensation of cytoplasm, detachment of cell from ECM nuclear DNA fragmentation, phagocytosis

necrosis:
- 20-30 minutes
- cells swell
- ischemia, toxins, physical stimuli
- depletion of ATP stores
- rupture of cell membrane, clumping chromatin

49
Q

what is the function of extracellular matrix

A

 provides support for actual structure of the heart and cells, segregates tissue, and has effects on cellular communication

50
Q

Discuss how collagen contributes to extracellular matrix (ECM) remodeling and fibrosis.

A

o Fibroblasts dysfunction results in collagen imbalance
 MMP activity –
* matrix metalloproteinases (MMP) become active and start degrading some of the proteins in the extracellular matrix  change in shape and geometry
o Misalignment contractile protein causing slippage and over stretching
o Excessive fibrosis
o Clinical consequence:
 Fibrosis
 Thickening of ventricular wall ‐seen post infarct
 HTN
 Small changes in volume accompanied by LARGE change in pressure
o Remodeling also results in the deposition of collagen between the myocytes which can disrupt the integrity of the muscle, decrease contractility, and make the ventricle more likely to dilate and fail

51
Q

what is myocardial remodeling and what is it caused by (6)?

A

a process mediated by angiotensin II, aldosterone, catecholamines, adenosine, oxidative stress, and inflammatory cytokines, which cause myocyte hypertrophy, scarring, and loss of contractile function

52
Q

what are mechanical signals

A

 Stretch receptors that are being misinterpreted that influence how the myocardium can contract

53
Q

what are neuro-humoral signals

A

 G Coupled Receptors
 Natriuretic Receptors
 Angiotensin II, aldosterone, catecholamines, cytokines

  • The signals induces a number of changes in the heart can use and vasculature that are designed to maintain cardiovascular homeostasis
54
Q

Describe the clinical events that cause the cascade of the renin-angiotensin system.

A

o Drop in blood pressure & drop in fluid volume (decreased stroke volume, decreased cardiac output)
o Decrease in kidney perfusion. Kidney is hypoperfused so it activates the RAAS system
o Activation of RAAS causes not only increase in preload and afterload, it also causes direct toxicity to the myocardium

55
Q

RAAS – Angiotensin II in HF

A

 Mediates remodeling of the ventricular wall, contributing to sarcomere death, loss of the normal collagen matrix, and interstitial fibrosis.
o This leads to decreased contractility, changes in myocardial compliance and ventricular dilation
 Two types:
* Circulating-
o Increase antidiuretic hormone
o Vasoconstrictor
o Increase Na reabsorption
o Increase aldosterone secretion (increase Na and water retention)
* Tissue-Derived-
o Myocyte hypertrophy
o Fibroblast proliferation
o Myocyte necrosis
o Myocyte apoptosis

56
Q

what are the three components to stroke volume?

A
  • preload
  • afterload
  • contractility
57
Q

what is preload

A

deals with stretch, filling pressures

e.g. patient with stiff ventricles will have higher preload–>edema has to do with preload

58
Q

what is afterload?

A

the pressure the heart has to pump against to open the aortic valve

e.g. HTN contributes to afterload

59
Q

what is contractility?

A

the ability to stretch and contract (pump action)

60
Q

what does a fast HR utilize?

A

it utilizes myocardial o2 consumption
**worse thing in ischemic heart

61
Q

RAAS – Aldosterone in HF

A

 Levels are extremely high in HF patients
 Negative consequences;
* Na/water retention  EDEMA!
–»Ang II stimulation causes release of aldosterone from adrenal glands
* K, Mg loss (important to maintain NSR)
* Reduced baroceptor reflex
–» Will not response appropriately to pressure changes
* Cardiac fibrosis
–» Stiffness and inability to stretch
* Ischemia
* SNS activation

62
Q

Digoxin (3)

A

 Increase CO
 slows heart rate
 improves the pumping ability of your heart

*positive inotrope

63
Q

Diuretic

A

 Ex: Lasix, oretic, thiazides
 remove excess fluid from the body to help you breathe easier

64
Q

ACE Inhibitors (angiotensin converting enzyme

A

 Ex: Lisinopril, captopril
 reduce the amount of heart-damaging hormones your body produces
 open blood vessels and lower blood pressure to lessen the workload of your heart
 They decrease preload and afterload, help relieve congestion/low cardiac output symptoms, and restore cardiac performance
-vasodilate and decrease remodeling

65
Q

ARB (angiotensin receptor blocker)

A

 Ex: losartan
 don’t cause the cough that some people have when taking ACE inhibitors.
 Same as ACE-I^^

-vasodilate and decrease remodeling

66
Q

Beta Blockers

A

 Ex: carvedilol, metoprolol
 lower heart rate and blood pressure
 DECREASE HR and DECREASE REMODELING BY BLOCKING SNS  going to increase cardiac output

67
Q

Aldosterone Antagonists

A

 Ex: spironolactone, eplerenon
 prevent your body from producing hormones that can damage your heart

  • decrease fibrosis, Na retention, remodeling, aldosterone release
68
Q

o Neprulysin inhibitor

A

vasodilates

69
Q

what are other body systems involved in HF

A

-lungs
-kidneys
-spleen

70
Q

what causes dyspnea and orthopnea in HF

A

 Fluid volume overload, heart not pumping adequately, fluid in pulmonary vasculature –> inadequate oxygenation
 Increased pressure = backward to LA and pulmonary vessels = pulmonary edema
 Severe respiratory distress, jugular vein distention, and chest pain are symptoms of heart failure, particularly pulmonary edema.

71
Q

clinical manifestations of HF (5)

A
  • dyspnea and orthopnea
  • fatigue
  • weight gain, peripheral edema, JVD
  • abdominal discomfort
  • bilateral crackles
72
Q

what causes weight gain, peripheral edema, JVD

A

 Congestion in systemic veins related to fluid volume overload, heart not pumping adequately
 Third space, heart not adequately pump–>fluid volume overload

73
Q

right side HF: s/s backward effects (6)

A
  • hepatomegaly
  • ascites
  • splenomegaly
  • anorexia
  • subcutaneous edema
  • JVD
74
Q

left side HF: s/s backward effects (6)

A
  • DOE
  • orthopnea
  • cough
  • paroxysmal notcurnal dyspnea
  • cyanosis
  • basilar crackles
75
Q

Distinguishing characteristics: HFrEF (Systolic HF)

A
  • Caused by underlying disease that causes the death of cardiac muscle cells (myocytes). For example:
    o Cardiomyopathies
    o Reduced blood supply to heart r/t CAD
    o Valve diseases
    o Arrythmias
  • Walls are THINNER (myocardium thinner)
  • Ventricles/Chambers are BIGGER
  • Ejection Fraction DECREASED < 40%
    • Will need positive inotropic drugs (DIG)
  • Increased LVEDV, preload, and afterload
76
Q

Distinguishing characteristics: HFpEF (Diastolic HF)

What are the physiological and pathological d/t

A
  • Heart is not filling with enough blood (d/t stiffness)
  • Physiological hypertrophy d/t:
    o Exercise or Pregnancy
  • Pathological hypertrophy d/t:
    o Chronic HTN
    o Aortic valve stenosis
  • Walls are THICKER (myocardium thicker)
  • Ventricles/Chambers SMALLER (pathologic)
  • Ejection Fraction NORMAL/ “preserved” > 50%
  • Will NOT need positive inotropic drugs
  • Normal LVEDV, increased LVEDP
77
Q

Neurohormones that are BENEFICIAL to HF

A

 Atrial Natriuretic peptide (ANP)
 C-type Natriuretic peptide (CNP)
 B-type Natriuretic peptide (BNP)*

78
Q

what is B-type Natriuretic peptide (BNP)

A
  • Cardiac hormone that is released by ventricle, in response to ventricle wall stretch (the volume)
    o How much BNP is released will depend on the mass of LV and how healthy the patient is.
  • Biomarker for HF- cut off is 100, although now it is 250
    o Levels can also be elevated in pulmonary and renal conditions
    o Levels correlate with volume overload and NYHA classification 4
  • BNP is beneficial but overtime also doesn’t work
  • positive effect on;
    o BNP (Hemodynamics) helps vasodilate veins, arteries, coronary arteries
    o BNP (Neurohormonal) helps to decrease aldosterone, endothelin, norepi
    o BNP (Renal) increases diuresis and natriuresis
    o BNP (Cardiac) lusitropic, antifibrotic, anti-remodeling
     Basically, helps loosen the heart
79
Q

Neurohormones that WORSEN HF: RAAS and Angiotensin II

A
  • Na and H2O retentions result in EDEMA,
  • K and Mg losses will lead to arrhythmias.
  • Aldosterone will also make one lose potassium, and if K drops below 4 then pt will likely vasodilate.
80
Q

Neurohormones that WORSEN HF: SNS and catecholamines

A
  • Catecholamines (epinephrine, norepinephrine)
    o Sympathetic nervous system activation (when map is low) initially compensates for a decrease in cardiac output by increasing HR and peripheral vascular resistance (vasoconstriction- increasing the BP)
     increase HR, increase stroke volume, increase myocardial contractility increase CO
    o However, after a while it will FAIL!
     will start to down-regulate and cause there to be less receptors, so heart won’t respond as it did before
81
Q

Neurohormones that WORSEN HF: Arginine vasopressin in HF

A

 “Also known as antidiuretic hormone (ADH)”
 causes both peripheral vasoconstriction and renal fluid retention
* exacerbate hyponatremia and edema

82
Q

Neurohormones that WORSEN HF: Inflammatory Cytokines in HF

A

 Endothelial hormones-
* vasoconstrictor
* associated with a poor prognosis
 TNF-a
* elevated and contributes to myocardial hypertrophy and remodeling
* down regulates the synthesis of the vasodilator Nitric Oxide (NO)
* induces myocyte apoptosis
* contribute to weight loss and weakness
 IL-6:
* elevated
* contribute to further deleterious immune activation

83
Q

Neurohormones that WORSEN HF: Myocyte calcium transport in HF

A

 Calcium transport into, out of, and within myocytes is critical to normal contractile function.
 Changes in calcium ion channels, intracellular transport mechanisms in the sarcoplasmic reticulum, and calcium cycling have been implicated in decreased myocardial contractility and heart failure

84
Q

what is compensatory goal?

A

increase CO by either increasing HR or increasing SV

85
Q

frank-starling law for preload

A

increase preload causes increase stroke volume, therefore increase cardiac output

86
Q

what is the problem with increase preload?

A
  • Cardiomyocytes contract with more force but need more energy to do that, therefore they need more blood/oxygen. And if there is no additional blood flow coming into the heart muscle cells, they begin to die off
87
Q

what is myocardial hypertrophy?

A

 Heart gains muscle mass to contract harder because it’s stronger
 To try to make up for the decrease in stroke volume or the death of cardiomyocytes, the surviving cardiomyocytes become elongated and they grow. This causes the heart muscle as a whole to get larger and the “bulked up” cardiomyocytes contract harder, eject more blood, and increase cardiac output

88
Q

what is the problem with myocardial hypertrophy

A
  • the more work, the more oxygen and blood supply needed. But with HF that’s not happening, so the overworked cardiomyocytes start to die off.
  • Also, the heart muscle gets bigger, but the chambers get smaller, so there is less blood that can fill in the chambers
89
Q

hemodynamics: in the frank-sterling mechanism for HF

A
  • normally stroke volume increases with end-diastolic pressure (or volume). But in HF patients it increases minimally and insufficiently, because there is not enough forward blood flow.
  • As the heart contracts harder, there is no increase in stroke volume.
  • Poor stroke volume results in pulmonary congestion.
  • People with advanced HF will have a difficult time laying down because they will feel they are drowning due to pulmonary congestion
90
Q

Three factors determine the force of contraction:

A
  • Changes in the stretching of the ventricular myocardium caused by variations in ventricular volume (preload)
  • Alterations in nervous system input to the ventricles
  • Adequacy of myocardial oxygen supply

Advanced Patho Exam 3 (5 decks)

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