Exam 3: HF Flashcards
the definition of heart failure
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
what symptoms do patients with HF experience? (3) and why?
- sob
- fluid retention
- fatigue
because of the changes in ejecting and filling
what are the associations with HF (3)
- reduced exercise tolerance
- high incidence of ventricular arrhythmias
- shortened life expectancy
how does body try to compensate with HF
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
what are structural change that result from HF due to?
due to ventricular remodeling
**ventricular remodeling process can take years to occur
clinical characteristics of HF “DROPSY”
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!
define cardiac output
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
what is the normal cardiac output at rest
5 L/min
what is cardiac output
the blood pumped each minute
what are four factors that affect cardiac output directly?
-preload
-afterload
-myocardial contractility
-heart rate
define ejection fraction
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)
what is index of contractility and indicator of ventricular function
- Indicates how well the left (or right) ventricle is contracting
- Healthy heart pumps 2/3 of its end diastolic volume
what does it mean normal EF 55%
means 55% of the total blood in the left ventricle is pumped out with each heartbeat
why does HF with reduced EF occur
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)
define Left Ventricular End Diastolic Volume (LVEDV)
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
define Left Ventricular End Diastolic Pressure (LVEDP)
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
An increase in left ventricular end-diastolic volume (preload) result in an increase in ____
force of contraction
When the left ventricular compliance decreases, the LVEDP _____
rises
what are two examples of when left ventricular compliance decreases?
- MI
- left ventricular failure
in the person with normal mitral valve and normal lung function, LVEDP is also reflected by the pressure in what? (4)
-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
what is the treatment goals in HF
- maintain end diastolic volume/pressure that will maintain or increase CO
what must happen before blood can be pumped out during systole?
pressure in the left ventricle must exceed aortic pressure before blood can be pumped out during systole
define Left Ventricular End SYSTOLIC Volume (LVESV)
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.
factors that affect end systolic volume
afterload and contractility of the heart
what is stroke volume
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
define Left Ventricular End SYSTOLIC Pressure (LVESP)
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”
define compliance
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
define preload
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
what are the two major factors preload are determined by?
- 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
how can HF occur because of an increase in preload
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
define afterload
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
what is a good index of afterload for the left ventricle?
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
define contractility
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!
what are the most important predisposing risk factors for HF? (2)
- ischemic heart disease
- HTN
list other common risk factors for HF
Age, obesity, diabetes
Renal failure
Valvular heart disease
Cardiomyopathies
Excessive alcohol use
Black males & females and at a younger age!
List the most common risk factors for heart failure (HF): life simple 7-same RF as CHD
Smoking, physical activity, weight, diet, glucose, cholesterol, bp
List the most common risk factors for heart failure (HF): Genetic polymorphisms
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
patient who are exposed to ____and ____develop HF and why
patient who are exposed to chemotherapy and alcohol develop HF because they are myocardial toxic
exposure to what parasite can develop HF
Exposure to a parasite Trypanosoma cruzi- effects heart muscle (Chagas disease)
The most common etiologies for HF (6)
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
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.
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
what is remodeling
Myocardium & vasculature‐compensatory response that results in structural and functional changes
what is left ventricular remodeling defined as?
as a change in LV geometry, mass and volume that occurs over a period of time
cellular changes associated with ventricular remodeling (7)
- 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
what are types of ventricular remodeling
- hypertrophied heart ( diastolic HF) HfpEF
- dilated heart (systolic HF) HFrEF
what is hypertrophied heart ( diastolic HF) HfpEF
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
what is dilated heart (systolic HF) HFrEF
o EF < 40%
* Eccentric remodeling
* Results in thinned myocardium and results with problems with contractility
* Chamber becomes huge, and wall becomes very thin
Compare and contrast necrosis and apoptosis.
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
what is the function of extracellular matrix
provides support for actual structure of the heart and cells, segregates tissue, and has effects on cellular communication
Discuss how collagen contributes to extracellular matrix (ECM) remodeling and fibrosis.
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
what is myocardial remodeling and what is it caused by (6)?
a process mediated by angiotensin II, aldosterone, catecholamines, adenosine, oxidative stress, and inflammatory cytokines, which cause myocyte hypertrophy, scarring, and loss of contractile function
what are mechanical signals
Stretch receptors that are being misinterpreted that influence how the myocardium can contract
what are neuro-humoral signals
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
Describe the clinical events that cause the cascade of the renin-angiotensin system.
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
RAAS – Angiotensin II in HF
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
what are the three components to stroke volume?
- preload
- afterload
- contractility
what is preload
deals with stretch, filling pressures
e.g. patient with stiff ventricles will have higher preload–>edema has to do with preload
what is afterload?
the pressure the heart has to pump against to open the aortic valve
e.g. HTN contributes to afterload
what is contractility?
the ability to stretch and contract (pump action)
what does a fast HR utilize?
it utilizes myocardial o2 consumption
**worse thing in ischemic heart
RAAS – Aldosterone in HF
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
Digoxin (3)
Increase CO
slows heart rate
improves the pumping ability of your heart
*positive inotrope
Diuretic
Ex: Lasix, oretic, thiazides
remove excess fluid from the body to help you breathe easier
ACE Inhibitors (angiotensin converting enzyme
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
ARB (angiotensin receptor blocker)
Ex: losartan
don’t cause the cough that some people have when taking ACE inhibitors.
Same as ACE-I^^
-vasodilate and decrease remodeling
Beta Blockers
Ex: carvedilol, metoprolol
lower heart rate and blood pressure
DECREASE HR and DECREASE REMODELING BY BLOCKING SNS going to increase cardiac output
Aldosterone Antagonists
Ex: spironolactone, eplerenon
prevent your body from producing hormones that can damage your heart
- decrease fibrosis, Na retention, remodeling, aldosterone release
o Neprulysin inhibitor
vasodilates
what are other body systems involved in HF
-lungs
-kidneys
-spleen
what causes dyspnea and orthopnea in HF
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.
clinical manifestations of HF (5)
- dyspnea and orthopnea
- fatigue
- weight gain, peripheral edema, JVD
- abdominal discomfort
- bilateral crackles
what causes weight gain, peripheral edema, JVD
Congestion in systemic veins related to fluid volume overload, heart not pumping adequately
Third space, heart not adequately pump–>fluid volume overload
right side HF: s/s backward effects (6)
- hepatomegaly
- ascites
- splenomegaly
- anorexia
- subcutaneous edema
- JVD
left side HF: s/s backward effects (6)
- DOE
- orthopnea
- cough
- paroxysmal notcurnal dyspnea
- cyanosis
- basilar crackles
Distinguishing characteristics: HFrEF (Systolic HF)
- 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
Distinguishing characteristics: HFpEF (Diastolic HF)
What are the physiological and pathological d/t
- 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
Neurohormones that are BENEFICIAL to HF
Atrial Natriuretic peptide (ANP)
C-type Natriuretic peptide (CNP)
B-type Natriuretic peptide (BNP)*
what is B-type Natriuretic peptide (BNP)
- 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
Neurohormones that WORSEN HF: RAAS and Angiotensin II
- 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.
Neurohormones that WORSEN HF: SNS and catecholamines
- 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
Neurohormones that WORSEN HF: Arginine vasopressin in HF
“Also known as antidiuretic hormone (ADH)”
causes both peripheral vasoconstriction and renal fluid retention
* exacerbate hyponatremia and edema
Neurohormones that WORSEN HF: Inflammatory Cytokines in HF
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
Neurohormones that WORSEN HF: Myocyte calcium transport in HF
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
what is compensatory goal?
increase CO by either increasing HR or increasing SV
frank-starling law for preload
increase preload causes increase stroke volume, therefore increase cardiac output
what is the problem with increase preload?
- 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
what is myocardial hypertrophy?
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
what is the problem with myocardial hypertrophy
- 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
hemodynamics: in the frank-sterling mechanism for HF
- 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
Three factors determine the force of contraction:
- 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
