Class 24: Heart Failure Flashcards
describe the differences in pressure in the pulmonary arteries, left ventricle, systemic bp, and CVP (around the right atrium)
what does this mean
- pulmonary & CVP = very low
- LV and systemic = higher
= does not take much increase in pressure to cause edema in the pulmonary artery & CVP
what is SBP and DBP
- systolic blood pressure
- diastolic blood pressure
what is pulse pressure
systolic pressure - diastolic
what is MAP
- average blood pressure in arteries during one cardiac cycle
what is the formula for MAP
SBP +DBP + DBP /3
what is CVP
- central venous pressure = pressure around R atrium
what is CVP reflected by
- JVP
what is LVEDV/P
- left ventricle end diastolic volume or pressure from the volume
= preload
what is SVR
-systemic vascular resistance = afterload
what is PVR
- pulmonary vascular resistance
what is SV
- stroke volume
- vol of blood pumped out per contraction
what is EF
- ejection fraction
- what percent of blood in the ventricle is pumped with contraction
- tells us how good the heart is pumping
how is EF determined
SV / EDV
%
what is CO
how much blood pumped per minute
what is CI
- cardiac index
- CO adjusted for body size
- relates the estimation of CO related to someones size
what does the heart need to be effecient
- volume & pressure
- mechanical structures
- electrical conduction
- fuel (O2 and nutrients)
where does fluid in the RV get backed into
- body & JV
where does fluid in the LV get backed into
- lungs = pulmonary edema
what is normal EF? what is significantly low?
- normal = 50-60
- low = less than 30%
what are important mechanical structures of the heart
- heart muscle
- valves
what dont you want to occur in heart muscle
- hypertrophy
- dilation
what dont you want to occur with the heart valves
- no regurgitation (leaky = blackflow)
- no stenosis
what is aortic stenosis
- aortic valve gets smaller = hard to get blood through = increased afterload
what is the formula for CO
= HR x SV
what is the formula for BP
= CO x SVR
= HR x SV x SVR
how does theSNS & kidneys compensate for low bp, CO, and perfusion
- increased HR
- increased contracility
- fill up more = increased preload (thru RAAS)
- carry more stuff: increased Hgb, RR, O2
what occurs if compensation becomes chronic (aka during HF)? what does this lead to?
- remodelling
- changes in shape of heart = further HF & decompensation
what results from the heart pumping faster
- increased workload
= exhaust - consider reserve
what is cardiac reserve
- range between normal pumping & maximum pumping for exertion, SNS, etc.
describe cardiac reserve in an athlete
- high cardiac reserve
describe cardiac reserve in a HF pt
- EF < 30% = low cardiac reserve
- can’t ask too much extra of the heart
what remodelling occurs with the heart squeezing harder
- increased workload = hypertrophy = thickening
what remodelling occurs from the heart filling up more
= stretch = dilation = bigger & thinner
how does the RAAS respond to the low bp
- triggers vasoconstriction & keep more fluid
= increased afterload
what remodeling of the heart occurs after “carrying more stuff”? what does this lead to?
= polycythemia = increased viscosity & risk of clots
what causes dilation of the heart
- chronically increased volume, preload, pressure, and stretch
what changes occur in the myocytes with dilation
- elongation
- think of it like worn out yoga pants that wont snap back
what causes hypertrophy of the heart
- from the ventricle constantly pushing against high afterload
- think of how muscles get from working out = stiff & inflexible
what is cor pulmonale
- abnormal enlargment of the RS of the heart
what causes cor pulmonale
- r/t to hypertrophy
- result of disease of the lungs or pulmonary blood vessels
what is the difference between hypertrophy and hyperplasia
- hypertrophy = increased size
- hyperplasia = increased number
how do the myocytes become less effective (decompensate) in dilation and hypertrophy?
- less stretch when filling
- less contraction in systole
- increased O2 use
recap the process of cardiac compensation if prolonged
cardiac compensation –> prolonged –> cardiac remodeling & decompensation –> HF
define cardiac dilation: describe the cells, walls, cavity
- long cells, baggy walls
- decreased starling response
- large heart size with slightly thicker walls
define hypertrophy: describe the cells, walls, and cavity
- thick cells
- thick walls
- smaller cavity
what is cardiomegaly
- big heart
what is cardiomyopathy
- disease of all heart muscle
- global
= weak heart
how does HF affect CO
- decreases CO
what causes acute HF
- immediate loss or decrease in CO
how can an MI cause acute HF
= stunned heart & loss of tissue
= decreased contractility
how can arrhythmias cause acute HF
- can cause decreased CO
ex. brady, tachy, vfib
how can HTN crisis cause acute HF
- massive increase in bp = increase in afterload heart cannot pump against
how can a PE cause acute HF
= decreased return to LV
what is the function of papillary muscles in the heart
- papillary muscle supports heart valves
- prevents them from opening against resistance & preventing back flow
how can rupture of the papillary muscle cause acute HF
= immediate backflow = decreased forward flow = decreased CO
what is myocarditis
- global inflammation of the heart
how can myocarditis cause acute HF
- inflamed heart = decreased function & contraction = decreased CO
how can chemotherapy cause acute HF
- will destroy heart tissue along w cancer tissue = decreased function
how can pregnancy cause acute HF
- often towards end of pregnancy
= increased strain, demand, etc. & heart cannot cope w it - also get electrolyte imbalances
what is the purpose of the thyroid gland
- “engine of metabolism”
- secretes thyroid hormone which regulates metabolism
what is thyrotoxicosis
- hyperthyroidism
= overactivity of the thyroid gland
how can thyrotoxicosis cause acute HF
- too much thyroid hormone = high metabolism = energy & O2 consuming = increased demand of heart
what is chronic HF
- slow development
how can chronic hypertension cause chronic HF
- heart has to work against constant increased afterload
how can DM cause chronic HF
= increased BP, atherosclerosis
= changes in microvasculature of heat = stiff muscle
what is the number one cause of chronic CF
- ischemic heart disease
how can pulmonary diseases cause chronic CF
- make heart work harder
how can valve disease lead to chronic HF
- chronic regurgitation
- aortic stenosis
what is endocarditis
- infection on the valves
how can endocarditis lead to chronic HF
= valve does not close properly due to vegetation
how can chronic anemia lead to chronic CF
- anemia = poor O2 capacity
= have to increase workload of heart to move blood around - also heart is also suffering from low O2 due to anemia
what can cause cardiomyopathy
- ischemia
- ETOH (alcohol) = toxin to heart
- viral infection –> can permanently injure
- chemo
- idiopathic
what are 3 descriptors from cardiomyopathy
- dilated
- hypertrophic
- restrictive
what are 4 different ways to look at HF
- acute v chronic
- reduced EF v preserved EF
- systolic v diastolic
- RS v LS
what is meant by chronic HF being progressve
- always worsening
- we can slow down but cannot stop
what occurs in the heart with systolic dysfunction
- heart fails to generate enough force to pump blood
= decreased contractility & SV
= back up of fluid
what occurs in the heart w diastolic dysfunction
- reduced ability of ventricles to fill
= increased end diastolic pressure = congestion
what can cause diastolic dysfunction
- failure of myocardium to relax
- increased stiffness of ventricle
do systolic & diastolic dysfunction occur separately?
- often occur together
- a heart that does not fill cannot pump adeqaute blood
- heart does not pump properly becomes overfilled
what is the formula for EF
SV / EDV (preload of LV)
how is EF measured?
use:
- echo
- mri
- angiogram
- muga
- mibi
what does 60% EF mean
- normal
what does 40-59% EF mean
- mild dysfunction
what does 20-39% EF mean
- moderate dysfunction
what does <20% EF mean
- severe dysfunction
how is systolic dysfunction in LS HF assessed
- using EF
is diastolic or systolic dysfunction associated w HF with reduced EF? what is the EF ?
- systolic dysfunction
- < 50%
describe HFrEF
- inability to move blood forward effectively
- unable to overcome SVR (LV) or PVR (RV)
what might cause HRrEF
- loss of muscle cells
- decrease in contractility
- structural changes
- high afterload
what does HFeEF eventually lead to
- not meeting needs of tissue
= decreased CO
does diastolic or systolic dysfunction occur with HFpEF
- diastolic
what is the EF in HFpEF
- symptoms w >50%
describe what occurs during HFpEF
- stiff ventricle = diminished relaxation in early diastole & diminished compliance (stretch) in late diastole
- shifts pressure-volume curve
explain how HFpEF causes decreased CO
- EF is still normal
- but, it is of a smaller volume
ex. 50% of 100 mL = 50 mL –> not bad
ex. 50% of 50 mL = 25 mL forward = bad
what occurs in people w HFpEf during high demand
- when get extra demands, heart cannot stretch to accommodate = tip into HF quickly, get fluid back up etc.
= activity intolerance
what is biventricular HF
- when both sides of the heart are affected
- typically one sided HF leads to the other
what can cause RS HF
- LV failure
- loss of muscle mass
- cor pulmonale
- congenital defects
how can LV failure cause RS HF
- LSHF = pulmonary edema = increased afterload on RV
what can cause loss of muscle mass leading to RSHF
- right ventricular or inferior MI
describe how cor pulmonale can cause RSHF
- impaired ventilation = pulmonary vasoconstriction = increased afterload –> failure
= RSHF secondary to pulmonary disease
what congenital defects can lead to RSHF
- pulmonary obstructions or shunts increase the workload on the RV –> fail
how does RSHF effect CO? what does this lead to?
- RV ventricle weakens and cannot empty = decreased CO
= SNS stim to increase HR, vasoconstriction, etc. = increased workload
how does RSHF effect the kidneys? what does this lead to?
- kidney misinterprets low CO as low volume = triggers RAAS & aldo secretion
= keep H2O = increased workload
how does RSHF effect the JVP and the brain
- fluid backs up:
= increased JVP = distension
= cerebral edema
how does RSHF effect the body system
- get back up of blood into the systemic circulation
where do we see edema in RSHF
- legs
- liver
- brain
- pulmonary edema
- periphery
- abdomen
- organs congested
- JV distension
what are symptoms of RSHF
congest BODY:
- edema (abdominal distension, pedal)
- weight gain
- fatigue
- decreased appetite
- catabolize muscle mass = tiny in frame, hands, etc.
how come decreased appetite is associated with RSHF
- get distended/edematous bowel
= bowel does not digest = no appetite
what type of spacing is fluid in the abdomen (ascites)
- 3rd spacing = difficult to remove
what can cause LVHF
- volume overload
- pressure overload
- loss of muscle mass
- loss of contractility
- restricted filling
what is the most common problem with LSHF
pulmonary edema
how does LSHF effect CO? what does this lead to?
= decreased CO, BP, perfusion
= SNS stimulation = increased hr, contractility, vasoconstriction = more work
how does LSHF affect the kidneys
- kidneys misinterpret decreased CO as low volume = triggers RAAS & aldo secretion = overloads heart
how does LSHF effect the lungs
- get backup of blood into pulmonary vein = get increased pressure in pulmonary capillaries = pulmonary congestion/edema
how does LSHF affect the RV
- increased P in lungs = increased afterload for RV
what effect does pulmonary edema have
- decreased O2 sats
- increased WOB/SOB
- increased RR
- decreased A/E
- fine crackles
- cyanosis
- dry cough (to try and get rid of fluid) that progresses to pink frothy sputum
- orthopnea
- paroxysmal nocturnal dyspnea
- possible angina
- accessory muscle use
how does edema cause pulmonary manifestations
- get high hydrostatic pressure = pushes fluid out
- fluid in alveoli = decreased gas exchange = hypoxia
what causes orthopnea
- when lay down the fluid spread out to effect whole lung instead of just base
what are the symptoms of LSHF
- pulmonary manifestations
- flutter in chest
- angina if also IHD
- nocturia
- fatigue/activity intolerance
- confusion
- pale, cold, sweaty, cyanotic skin
- 3rd heat sound
why is nocturia associated with LSHF
- renal perfusion is reduced especially during the day = decrease in urine produced
- when person is recumbent, renal perfusion improves = urine production
why does confusion occur with LSHF
- reduced perfusion into cerebrum
why do we get pale, cold, sweaty, cyanotic skin with LSHF
- get compensatory vasoconstriction to get more blood flow to important organs = cold
- sweating bc body heat cannot be dissipated thru constricted vascular beds
- mild cyanosis from hypoxia
why do we get a 3rd heart soud with LSHF
- common with fluid overload
what causes paroxysmal nocturnal dyspnea
- when lay down = increased venous return = after few hours = SOB
- sitting up = decreased SOB = recover quick
what are symptoms of HF (R and L) on the nervous system
- difficulty concentrating
- confusion
- dizziness
- pre-syncope, syncope
- lightheaded
- fatigue
what are symptoms of HF (R and L) on CVS
- drop in bp
- orthostatic hypotension
- faint pulse
- increased HR
- palpitations
- lifts, heaves, thrills
- arrhythmia - flutter in chest
- angina (due to decreased O2 sat &
- complicated if anemia or polycythemia
- activity intolerance
what are symptoms of HF (R and L) psychosocially
- anxiety
- depression
- feeling of profound sadness
what are symptoms of HF (R and L) on resp. system
- dyspnea/SOB
- increased RR
- decreased O2 sats
- crackles
- cyanosis
- PND
- orthopnea
- pulmonary edema
- pleural effusion
- cough (dry –> pink, frothy)
what changes in ABGs are seen w HF
- decreased PaO2
- slight increase in PaCO2
what changes in fluid retention are seen w HF (R and L)
- fluid retention due to RAAS, increased Na, decreased albu,in
- increased weight
- increased JVP
- edema
- nocturia
what GI symptoms are seen w HF (R and L)
- ascites
- nausea
- anorexia
- GI bloating
what changes in the kidney do we see w HF
- renal insufficiency / injury due to low CO
how come a thrombus may form during HF
- weak contractions and low EF = blood stasis = form thrombus
- thrombus can become an emboli
where does an emboli in the RV go? LV?
- RV = lungs
- LV = brain
how do we prevent thrombus formation in HF patients
- many pts with EF < 25% on anticoagulants
what is HF functional classification
- similar to angina classes but sees how much activity can be done without SOB, fatigue, or palpitations
what are the HF stages
- 4 stages –> A to D
- one way
what is stage A of HF
- high risk
- no structura changes
- no symptoms
what is stage B of HF
- structural changes
- no symptoms
what is stage C of Hf
- structural changes
- past or present symptoms
what is stage D of HF
- structural changes
- refractory symptoms
- specialized interventions
how do the stages & classes of HF line up
- stage A + B correlate with class 1 = asymptomatic
- stage C = class 2 & 3 where there are symptoms with moderate or minimal exertion
- stage D = class 4 where symptoms at rest
what does increased Na possibly indicate?
- increased Na = increased water retention
- RAAS? diet?
what do we want to look for when considering diagnostics for HF
- look for anything reversible
- IHD? stressor (ex. uncontrolled HTN)? fluid?
why should we just K+ levels
- could be altered by drugs –> ACE-I, ARB, BB, diuretics
- arrhythmia concern
why should we assess BUN/Cr
- tells us about renal function r/t meds, perfusion
what should we assess Mg
- arrythmias
why should we assess Hgb/Hct
- anemia? = decreased O2 carrying capacity
- polycythemia = increased viscosity = increased overload
why shoudl we asses WBC levels
- infection?
ex. myocarditis? endocarditis?
why should we assess myoglobin, CK-MB, troponin?
- indicate an MI
why should we assess thyroid
- to rule out thyrotoxicosis
why should we asses LFTs
- liver function test
- see if congested, how it is functioning
why should we assess BNP
- B-type natriuretic peptide
- biomarker for HF
- released from ventricle with chronic HF stress
- released by stretched vent
- causes diuresis
what is the acronym for MI treatment? what does it stand for>
Morphine
Oxygen
Nitroglycerin
Aspirin
what is the acronym for HF treatment
A prils
B ols
C pines
D iuretics
what does A stand for for HF treatment
- ACE Inhibitors = prils
- aldo
- ARBs (sartans)
- decrease vol
what does B stand for, for HF treatment
Beta blockers "ols" Brady = decreased HR Blood pressure = decreased Bronchi constriction (B2)
what does C mean for HF treatment
Calcium Channel Blockers (pines)
- decrease hardness
what does D mean for HF treatment
diuretics
- lasix/furosemide K+ wasting
- thiazide
- spironolactone = K+ sparing
what do we first want to give as treatment for HF
- ACE inhibitor & BB
what should we give if they are intolerant to ACEI or BB
- ARB (angiotensin receptor blockers)
what are devices used to treat HF
- ICD
- CRT
- VAD
- transplant
what is an ICD? what do we use it for?
- implanted cardioverter defibrillator
- for pts with EF < 30%
what is a CRT? what do we use it for?
- cardiac resynchronization therapy
- for low EF and wide QRS
what is a VAD
- ventricular assist device
what interventions should be used for all patients experiencing symptoms of Hf
- education
- reduce risk factors
- lifestyle modifiation
- salt & fluid control
- diuretic therapy
what should we do if after the pt has been on ACEI and BB, but symptoms are not improving?
- add ARB, digoxin, or nitrates
what are 6 classes of drugs used for HF
- diuretics
- RAASi
- BB
- ivabradine
- inotropic agents
- vasodilators
what are different types of RAASi
- ACE-I
- ARB
- ARNI
- aldosterone antagonists (MRA)
- direct renin inhibitors
what is the first line for volume overload
- diuretics
what do diuretics do
- reduce afterload, edema, and cardiac dilation
what is a caution w diuretics
- not to overeduce CO & BP
what is the goal of using diuretics for HF
- symptoms reduction
what are 3 types of diuretics? do they save or get rid of K
- furosemide = reduced K
- hydrochlorothiazide = reduce K
- spironolactone = K sparing
what should you not give spironolactone with
- ACE-I or ARN
what is the suffix for ACE-I
____pril
what is the first line for HF
- ACE-I &BB
what is the MOA of ACE-I
- prevents conversion of angiotensin 1 to angio 2
how do ACE-I affect Kinins? what does this cause?
- causes increased kinin = causes inflammation
= reduced remodelling but also chronic cough
what do ACE-Is do
- decrease aldo
- & atrial & venous dilation
what are the S/E of ACE-I
- hypotension
- hyperkalemia
- cough
- angioedema
- renal impairment (check BUN/Cr)
how should we start a dose of ACE-I
- start low & titrate up
what are examples of ACE-I
- captopril
- enalopril
- ramipril
- lisinoril
what is the suffix for ARBs
___sartan
describe the use of ARBs
- very similar to ACE-I
- no increased kinin = less reduced remodelling
- used if intolerant of ACE-I
what is ARNI
angiotensin receptor neprilysin inhiibitor
describe use of ARNI
- new, very effective drug
- can replace ACE-I and ARB
- for class 2-4 HF
what does ARNI do
- increases natriuretic peptides (ANP, BNP)
- decreases RAAS
what is a type of ARNI
sacubitril/valsartan (enestro)
what does MRA stand for
mineralcorticoid receptor antagonist
what is MRA often added to
- add to ACE-I or ARB for residual aldo
what does MRA do
- reduces symptoms
- prolongs life
- blocks receptors (not production)
what are side effects of MRAs
- risk of harmful effects on heart
- increased K
- renal impairment risk
what are two types of MRAs
- spironolactone
- eplerenone
what is a side effect w spironolactone
- painful breast development in men
what are direct renins use for
- HTN, no HF
- seems ideal but not proven in trials
what is an example of direct renin inhibitors
- aliskiren
what do BB block
- decreases SNS, decreased arrythmia
what kind of dose should we start w for BB? why?
- low
- watch for bradycardia
describe the use/action of BB
- originally thought as harmful due to decreased contractility
- beneficial with slow congtrol
- slows progression
- increases HF
- prolongs life
what is the suffic for BB
_____olol
what is Ivabradine
- new drug
- for stable, symptomatic HF with low EF, NSR
what might ivabradine replace
- BB if contraindicated
what does ivabradine do
- slows HR in nodal cells
what are 3 types of inotropic agents
- digitalis (digoxin)
- dopamine
- milrinone
why isnt digoxin used too often?
- high toxicity, narrow therapeutic range
what do inotropic agents do
change the force of heart’s contractions
what does dopamine do
- sympathomimetic =increased SNS
what does milrinone do?
- IV & short term use
- for severe HF
what are 2 types of vasodilators
- nitroglycerine
- isosorbide with hydralizine
what does nitro do
- potent vasodilator
- reduced preload
what are 2 concerns w nitroglycerin
- decreased bp
- tachycardia
what does isosorbide with hydralizine do
- reduced afterload & improve renal function
what is the goal of HF management for stage 1
- delay/prevent onset of stage B
how do we delay onset of stage B
- ACE-I or ARB for HTN. DM, and atherosclerosis
- reduce smoking & alcohol use
- exercise
what is the goal of management for someone in stage B of HF
- prevent S&S
- prevent injury
- slow progression/remodelling
how will we prevent S&S, injury, and remodelling in stage B
- add BB to ACE-I or ARB
what type of structural changes are seen in stage B of HF
- LV hypertrophy/fibrosis
- LV dilation
- hypocontractility
- valvular heart disease
- previous MI
what type of symptoms are seen in stage C of Hf
- dyspnea
- fatigue
- edema
- increased JVP
what is the goal of treatment for stage C of HF
- relieve congestive symptoms
- improve functional capacity & QOL
- slow remodelling
- prolong life
what meds might be given for stage C of HF
- diuretic
- ACE-I or ARB
- BB
what do you want to avoid in stage C of HF?
- nsaids
- CCB
- most antiarrhythmics
what do you want to avoid nsaids in stage C of HF
- promote Na retention
- increases toxicity of diuretics/ACE-I
what do you want to avoid CCB during stage C
- bc they suppress contractility
what is the goal of management for stage D of Hf
- symptoms management
what is done for stage D of HF
- monitor weight
- maximize medical therapy
- periodic IV meds
- prn diuretics
what might BB and ACE-I cause during stage D of HF
- bradycardia
- hypotension
- renal failure
what is initiated during stage D of HF
- end of life palliative care
what can acute care of HF include
- bedrest
- O2
- cardiac monitoring
- angina? nitro or morphine
- IV diuretic
- anticoagulants to avoid clots
