Heart Failure_PATHO Flashcards
Heart Failure
Definition
Change in heart structure results in dysfunction
Not able to pump
Decreased CO
Unable to meet metabolic demands of body, results in systemic symptoms (including pulmonary)
Clinical Syndrome
Chronic and progressive
Heart Failure
Incidence
increase with age
50% die in 5 years
Fomulae
Cardiac output
CO = HR x Stroke volume
4-8L/minute
HR (60-100bpm)
- SNS: beta 1 stimuli NE results in increased heart beat, contraction, conduction
- PNS: acetylcholine stimuli, decrease heart rate, beat, contraction
Stroke volume (70mL/beat)
- preload (blood return to heart, stretch at diastole)
- afterload (pressure pump against, PVR)
- contractility (myocardium force of contraction, Frank starling law)
Beta 1 receptors and HF
Heart and Kidney Compensation
HF: Decrease CO
- anaerobic metabolism = decrease pH = activation medulla = SNS activation
- decrease in BP = activation baroreceptors = SNS activation = NE release = beta 1 receptor activation
beta 1 receptors on heart and kidney
MOA
G protein activation
cAMP signal
Open calcium channels
influx calcium
depolarization
Heart:
increase contractility (phase II fast AP)
increase conduction and heart rate (phase 0 and 4 slow AP)
- increase CO
Kidney
increase renin release (RAAS)
angiotensin II: vasoconstriction, SNS stimuli, remodelling, aldosterone release
aldoesterone: Na/water reabsorption, higher baroreceptor setpoint, NE increased, heart remodelling
- increase preload (venous return)
- increase CO
Stroke Volume and HF
Contractility compensation
HF decrease CO
Decrease blood pressure
trigger activation baroreceptors (medulla)
activation SNS and release NE
activation beta 1 receptors
phase II fast AP
influx calcium
depoloarization and contraction of myocardium
increase force of contraction
Increase vasoconstriction alpha 1 (veins) and arteries; and angiotensin II vasoconstriction (veins) and arteries
- increase preload
- increase stretch, increase force of contraction (normal heart, Frank-starling Law)
Preload
Definition and factors that increase/decrease
Preload
- amount of cardiac stretch at the end of diastole
- venous return to the heart
- blood remaining in ventricles/atrium after contraction
Factors that increase preload
- blood products
- volume expanders
- ADH, aldosterone (absorption water, sodium)
- valvular regurgitation
* increase volume
Factors that decrease preload
- hemorrhages
- vasodilators (CCB), diuretics
*loss of volume
Afterload
Definition factors that increase / decrease
Afterload
- pressure heart has to pump against to eject blood
Factors that increase
- HTN
- stenosis
- vasoconstrictors (ex. dopamine)
Factors that decrease
- hypotension
- vasodilators
- ACE, ARB, nitrates
Frank Starling Curve
Heart Failure vs. Normal
Frank Starling Curve
- Y axis: CO or stroke volume
- X axis: Left ventricular end diastolic volume (preload, stretch)
Normal physiology
- increase stretch (preload), increase contractility, increase cardiac output (stroke volume)
- shift LEFT
Heart failure
- change in structure and function of heart (myocytes)
- increase stretch (preload), no increase/decrease contracitlity, no change/decrease in cardiac output (stroke volume)
- SHIFT RIGHT
Pathogenesis of Heart Failure
Systems involved
- Heart and vasculature
- injury, inflammation
- remodelling
- change in structure and function
- decrease CO - Compensation: SNS, RAAS, ADH
- CO = HR x SV
- SNS: increase HR, conduction; increase contractility (SV)
- RAAS: vasoconstriction (angiotensin II, SNS activation; increase preload/venous return), fluid volume retention (aldosterone release; increase preload)
- ADH: fluid volume retention (preload; SV) - Decompensation: SNS, RAAS, ADH
- SNS: increased workload of heart = ischemia = inflammation = remodelling = damage = decrease CO
- RAAS: vascular / heart remodelling (angiotensin II, aldosterone), increase afterload from vasoconstriction increases workload of heart ischemia, inflammation, remodelling (decrease CO), FVO, edema, back up blood pulmonary and systemic venous system
Natriuretic Peptides
Physiological Antagonists
HF = decrease CO
= increase end diastolic volume (preload)
= atrial and ventricle stretch
release natriuretic peptides
ANP = atrial natriuretic peptide
BNP = bone natriuretic peptide (ventricles)
- excretion salt and water from distal tubules
- vasodilation
*BNP diagnostic for HF
*prognostic for HF
- use to determine therapeutic working
>30% increase from baseline BAD sign
Cycle of HF
- ischemia, injury, remodelling, dysfunction
- decrease CO
- Activation neuro-humoral system (baroreceptors carotid and aortic bodies, activation SNS)
- Activaiton SNS, ADH and RAAS
- Retention fluid, vasoconstriction, vascular and cardiac remodelling, increase SNS activity = self perpetuation
- INcrease cardiac demand, ischemia, necrosis, dysfunction
*self perpetuating
chronic
progressive
PHarmacological treamtnets for HF
- Block SNS
- beta blockers - Block ADH effects
- diuretics - Block RAAS effects
- ACEi
- ARB
- MRA
- CCB?
HF ejection fraction
Definitions
HFpEF
heart failure preserved ejection fraction
>/= 50%
HFrEF
heart failure reduced ejection fraction
< 40%
HFmEF
heart failure mid-range ejection fraction
heart failure recovered ejeciton fraction
between 41-49%
Refers to blood ejected from ventricle in 1 minute?
Normal ejection fraction is >/= 50%
Risk Factors
HF
- age >40 years
- gender (male > female; exception post-menopause)
- HTN (hyptertension)
- DM (hyperglycemia)
- Smoking, alcohol, chemotherapy, radiation therapy (toxins)
- obesity (dyslipidemia), elevated BMI, sedentary lifestyle
- genetics (L hypertrophic cardiomyopathy, L dilated cardiomyopathy, arrhythmogenic R V cardiomyopathy)
- acquired (myocarditis, takotsuba, toxins)
- Valvular (stenosis, regurgitation)
2/3 of HF are due to…
- ischemic (CAD, MI)
- HTN
- Rheumatic fever (GAS) - valve
- COPD
Other causes of HF
Genetic
- cariomyopathy (hypertrophy, dilation LV; arrhythmogenic RV fattyscelerotic deposits)
Acquired
- myocarditis
- toxins
- takotsubo (broken heart syndrome)
Symptoms of HF
Heart failure
- inability of the heart to pump
- decreased cardiac output and perfusion to the body…
Dyspnea
Fatigue
confusion
Orthopnea (difficulty breathing lying down)
paroxysmal dyspnea (wake up first 2 hours at night)
tachycardia and palpitations
nocturnal diuresis
coughing and wheezing (pulmonary congestion, edema)
Nausea, decreased appetite (blood congestion into venous system, liver, spleen, GI)
Physical Exam findings
HF
Extra heart sounds
- S4 - diastolic HF (blood striking the non compliant ventricle)
- S3 - systolic HF (mitral valve regurgitation)
- regurgitations
Cardiomegaly
- shift in LV apex
JVP increased
HJ reflex
- increase venous distention
- hepatomegally
Hypotension
tachycardia
SpO2 low
pale, cold extremities
Rales, crackles, wheezing
peripheral edema and weight gain
Left sided HF vs. Right sided HF
Left sided HF
- Left side of heart (ventricles)
1. systolic HF (reduced CO)
2. diastolic HF (loss of compliance, reduced perfusion)
- blood backs up into pulmonary circulation
Clinical signs and symptoms:
Dyspnea, fatigue, confusion
orthopnea, paroxismal nocturnal dyspnea, crackles/rales, cough
exercise fatigue
Right sided HF
- inability to pump blood into the pulmonary circulation
- blood backs up into the venous circulation (liver, spleen, GI)
Clinical signs and symptoms:
elevated JVP, HJ reflex
anorexia, nausea
hepatomegaly, splenomegaly
peripheral edema
ascites
- can be caused by L sided HF
NYHA Classification of HF
Class I - asymptomatic
Class II - mild, symptomatic with activity
Class II - moderate, symptomatic with normal ADL
Class IV - bed rest, symptomatic at rest
*Subjective rating
Patient report
determine if stable or getting worse
AHA Classification HF
Stage A
Asymptomatic
no structure
just risk factors for HF
Stage B
Asymptomatic
structure changes present
LVEF reduced, LVH present
Stage C
Symptomatic
structural changes present
exercise intolerance
Stage D
Symptmatic
end stage
symptoms at rest
*transplant, LV assist device, end of life care
Work up for HF
- past medical history
- Risk factor assessment
- DM, HTN, obesity, inactivity, alcohol, smoking, toxins, radiation, chemo, genetics, vavular, MI, age, gender, etc. - presenting illness
- clinical signs and symptoms
- L sided HF: dyspnea, exercise tolerance decreased, fatigue, confusion, tachycardia, orthopnea, paroxysmal nocturnal dyspnea
- R sided HF: anorexia, nausea, hepatomegaly, splenomegaly, edema, ascites - Physical findings
- Vital signs: hypotension, tachycardia, SpO2 reduced, pale periphery, cold
- PVS: edema, weight gain, increased JVP, HJ reflex present
- ABDO: hepatomegaly or splenomegaly, ascites
- RESP; crackles lungs
- CARDIO: displaced apex, S3 or S4 - Diagnostics or laboratory values
Blood work
- CBC and diff (anemia, infectious causes)
- electrolytes (Na, K, Ca, Mg, P)
- FPG and A1C
- lipid profile
- TSH (hypo increased DBP? hyper increased SBP?)
- Cr and BUN
- LFTs (AST, ALT)
- BNP (dx. HF)
- Diagnostic BNP
BNP > 400pg/mL (likely)
BNP < 100pg/mL (unlikely)
out of hospital
BNP > 50pg/mL
N-pro-BNP > 125pg/mL
- proceed with imaging below:
- Imaging
ECG
1. rate
2. rhythm
3. ischemia or infarct
4. hypertrophy
Echocardiogram
1. wall motion
2. hypertrophy / diameter
3. valvular regurgitation / stenosis
4. ejection fractions
Chest X ray
1. cardiac sillouette (hypertrophy)
2. pulmonary edema (vascular redistribution (upper), kerly B lines (lower))
3. pleural effusions
Cardiac perfusion studies
1. Stress echocardiogram
2. vasodilator echocardiogram (nuclear perfusion studies)
3. angiogram
4. CT / MRI (better imaging of heart - genetic, acquired causes)
SV =
SV
1. preload = EDV + venous return
2. afterload = PVR + aortic pressure
3. contractility = SNS, EDV, oxygen supply to heart
HR
CNS
SNS
baroreceptors
atrial receptors
hormones (NE, cortisol, thyroid)
Hypertensive hypertrophic cardiomyopathy
Triggers
- Angiotensin II
- catecholamines
- ischemia, inflammation (TNF alpha)
- aldosterone
Pathological remodelling
1. dilation
2. hypertrophy
3. increased ECM, fibrosis
4. thickening
Cycle HF with HFrEF
Mi –> reduced contractility
- decreased ejection fraction
increased LVEDV
increased preload
decreased contraction - decreased ejection and cardiac output
increase SNS, increase RAAS
increase afterload
hypertension
HFrEF vs. HFpEF
HFpEF
- female
- normal EF >. 50%
- no cardiomegaly
- no dilation
*hypertrophy
*decreased chamber size
- S4
HFrEF
- male
- reduced EF < 40%
- cardiomegaly
- dilation
- normal to increase hypertrophy
- increased chamber size
- S3
Etiology
HFpEF
- chronic activation SNS and RAAS
- diastolic dysfunction
- remodelling: thickening, hypertrophy, decreased compliance
Right Ventricular HF
Causes
- Pulmonary pressure
- ARDs (acute respiratory disease)
- COPD
- pulmonic valvular stenosis
-left sided heart failure (increased EDP; blood left in ventricles after pumps)
Pathophysiology
Right ventricular HF
increased pulmonary pressure (HTN)
increased workload of R ventricle
increased oxygen demand
unable to contract and pump
increase RVEDV and Pressure
back up blood into systemic cirucaltin
- increase RVEDP (RVEDV)
- increase RV preload
- increase back up of blood
High output heart failure
Trigger:
Increase in tissue hypoxia / oxygen demand
Causes:
Sepsis
Hyperthyroidism
Anemia
BeriBeri (thyamine deficiency)
Result:
Turns on SNS and catecholamine release
increase HR, conduction, contractility and CO increases
HFrEF
gender
LVEF
LVchamber size
LV hypertrophy?
Chest radiograph
Gallop?
Male
Decreased EF
<40%
LV dilation
cardiomegaly
pulmonary congestion X ray
S3
HFpEF
gender
LVEF
LV chamber size
LV hypertrophy?
chest radiograph
Gallop?
female
normal EF
>50%
Decreased chamber size - thickening
no cardiomegaly
pulmonary congestion on X ray
S4
Treatment HFrEF
Acute myocardial ischemia
MONA - decrease workload of heart
- morphine
- oxygen
- nitroglycerine
- ASA
Inotropic medications - contractility
- dopamine
- dobutamine
Diuretics - decrease afterload and preload
ACEi/ARB/MRA - decrease afterload
LVAD
- left ventricular assist device
first line diuretic for HF
loop diuretic
furuosemide
works with low GFR
profound diuresis
Why use spironolactone/triamtereine in HF?
potassium sparing diuretics
MRA
mineralcorticoid receptor antagonist (aldosterone antagonist)
prevention digoxin toxicity with hypokalemia
prevention cardiac remodeling, SNS activation, baroreceptor dysfunction
First line BP drug for HF
ARNI
angiotensin receptor neprolysin inhibitor
sacubitril/valsartan
- increase natriuretic peptides (vasodilation, diuresis, natriuresis)
- supression RAAS
(blockage aldosterone)
What is quadruple therapy in HF
- ARNI
angiotensin receptor/neprolysin inhibitor
- sacubitril/valsartan - beta blocker
Ex. propranolol - MRA
Mineralcorticoid receptor antagonist
Ex.spironolactone
- SGLT2 inhibitor
- sodium glucose co-transporter inhibitor
- Ex. CanaGLIFLOZIN
