Congestive Geart Failure Flashcards
CHF syndrome not disease
Syndrome is a constellation of signs and symptoms occurring together and characterizing a particular abnormality or condition
The same syndrome may occur with different diseases, which may have distinctly different etiologies and pathogenesis
CHF definition
Clinical Syndrome in which an of is responsible for the of the heart to with blood at a rate sufficient to of the metabolizing tissues.
Pump failure
heart failure epidemiology
Prevalence is 5,000,000 patients
Incidence is 500,000 patients per year
1 million of hospital admissions a year
50,000 death a year
Pathophysiology of systolic heart failure
Myocardial function
How strong the muscle is
Preload (EDV)
The more heart fibers are stretched the more difficult it is for them to contract increasing work/pressures and causing hypertrophy (Starling law)
After-load
Resistance against heart contraction/ejection of blood
Heart rate
Too slow—decreases cardiac output ( decCO = SV x decHR)
Too fast —not enough time to fill ( decCO = decSV x incHR)
pathophysiology of diastolic heart failure
Impaired relaxation –functional problem
Ischemia
Impaired compliance (“stiff” ventricle) –anatomical problem related to interstitial fibrosis
Hypertrophy
Hypertension
pathophysiology of high output failure
Normal heart function with
increased metabolic demand
Increased peripheral blood flow from decreased PVR
pathophysiology of heart failure
steps
heart damage, ventricular overload, decrease vent contraction
tachycardia, ventricular dilation, myocardial hypertrophy
decrease co
decreased renal perfusion
increased na retention
increased osmotic pressure
increased adh
increased water reabsorption
fluid overload edema
heart failure classification
Systolic vs. Diastolic Heart Failure
Low Output vs. High Output Heart Failure
Left vs. Right vs. Biventricular failure
Acute vs. Chronic Heart Failure
Forward vs. Backward Heart Failure
systolic heart failure
Systolic Heart failure results from inadequate cardiac output (C.O.)/Ejection Fracture (E.F.)
C.O. = S.V. x H.R.
S.V. = E.D.V. –E.S.V.
E.F. = S.V./E.D.V.
we measure the ejection fracion to determin 55 is normal
diastolic heart failure
results from inability of the ventricles to relax and fill normally with blood during diastole.
forward vs backward heart failure
Relates to clinical manifestations of the heart failure as a result of pump failure
forward heart failure
is decrease in perfusion of the organs/tissues down-stream from the heart
backward heart failure
is “backing up” of the blood into the organs upstream, increasing hydrostatic pressure, which leads to congestion/edema
left sided heart failure
Left ventricle primarily affected. Caused by conditions primarily affecting left ventricle CAD/MI Aortic/Mitral valves problems HTN Cardiomyopathies
forrward failure symptoms are primarily in systemic circulation (downstream)
Backward failure symptoms/congestion in the lungs (upstream)
right sided heart failure
Right ventricle primarily affected.
Caused by conditions primarily affecting right ventricle
Pulmonary diseases/cor pulmonale
Tricuspid/pulmonary valves
Pulmonary Hypertension
Pulmonary emboli
Backward failure symptoms/congestion in the systemic venous circulation (upstream)
biventricular heart failure
end result of left and right failure
acute heart failure
due to a sudden and severe event
Massive MI
Chorda tendinae rupture
Large PE
Predominantly forward failure
Flash Pulmonary Edema
chronic heart failure
Progresses slowly
Has exacerbation
Predominantly backward failure
Causes of high output heart failure
Metabolic disorders
thyrotoxicosis
excessive blood flow
anemia
av fistula
beriberi
causes of right heart failure
cor pulmonale
pulm art htn
causes of left heart failure
systolic
decreased contractility
dilated cmp
increased preload
valvular insufficiency
increased after load
sever acute htn
valvular stenosis
change in heart rate
arrhythmias
causes of left heart failure
diastolic
chornic htn
hypertrophi cmp
restrictive cmp
ischemic fibrosis
pericardial diseases
restrictive cardiomyopathy causes
infiltrative disorders
storage/metabolic disorders
fibrotic disorders
endomyocardial disorders
hypertrophic cardiomyopathy causes
with obstruction
genetic
hypertensive cardiomyopathy
without obstruction
due to aortic stenosis
dilated cardiomyopathy causes
endstage cardiovascular disease
htn
valvular heart disease
cad/mi
dilated cardiomyopathy causes
systemic disease
sle/ra
scleroderma
polyarteritis nodosa
dermato-myositis
dilated cardiomyopathy causes
toxins-mediated
alcohol
cocaine
radiation
dilated cardiomyopathy causes
other causes
myocarditis
tokosubo cardiomyopathy
perpartum cardiomyopathy
dilated cardiomyopathy
CAD/MI
Due to death or functional ischemic dysfunction of myocardial tissue due to complete or partial blockage of coronary arteries
Degree of dysfunction depends on the percent of myocardium affected
Ischemic cardiomyopathy
Dilated Cardiomyopathy
HTN
HTN
Increase cardiac workload
Left Ventricular Hypertrophy
Diastolic dysfunction
Ventricular Dilatation
Systolic Dysfunction
dialted cardiomyopathy
valvular heart disease
Aortic regurgitation
Increase in EDV/preload
Increase in cardiac workload
Left Ventricular Hypertrophy
Left ventricular dilatation
Systolic dysfunction (very quickly gets to here)
infective myocarditis
One of the main causes of dilated cardiomyopathy
Multiple etiological agents Viral (most common) Bacterial Fungal Helminthic
Febrile illness or URI frequently precedes cardiac symptoms by few weeks
Symptoms can present acutely (fulminant) or gradually
more common in young people
non infective myocarditis
toxic myocarditis
Chemotherapy
Doxorubicin (Adriamycin)
Heavy metals (copper, iron, lead)
Lithium
Malaria drugs
Radiation causing inflammation and fibrosis
non infective myocarditis
Autoimmune/ CTD associated Myocarditis
Giant Cell Myocarditis
PM/DM
SLE/RA
cocaine and myocardium
May cause vasospasm leading to MI
May cause arrhythmia
May cause drug-induced myocarditis/cardiomyopathy due to released catecholamines
alcoholic cardiomyopathy
From prolonged chronic alcohol use (at least 10 years of chronic exposure)
Due to direct toxic effect of alcohol on myocardium
Different from beriberi disease, although thiamine deficiency is frequent in alcoholics
peripartum cardiomyopathy
Between last month of pregnancy and first 5 months after delivery
Likely due to immune-mediated process (from baby antigen)
No preexisting cardiac disease (stay edemic after birth)
More than ½ of patients improve within 6 months
takostubo cardiomyopathy
fun facts
A.K.A. Stress cardiomyopathy
A.K.A. Apical Ballooning Syndrome
A.K.A. Broken Heart Syndrome
Takotsubo” is Japanese name for an octopus trap
takostubo cardiomyopathy
Triggered by an acute medical illness or by intense emotional or physical stress
Postulated mechanisms include catecholamine excess coronary artery spasm microvascular dysfunction OR dynamic mid-cavity or left ventricular outflow tract obstruction which may contribute to apical balooning.
Symptoms are similar to an acute MI
CP, SOB, Syncope
hypertrophic cardiomyopathy
Genetic (hocm)
Group of disorders
Myocardial hypertrophy unrelated to any pressure or volume overload
Due to different genes mutations
Myosin heavy chains
Proteins regulating Calcium handling
Most are autosomal dominant
Inter-ventricular septum often disproportionally involved
Sub-aortic stenosis is often present
Mostly causes diastolic, not a systolic dysfunction (vlave normal but thick septum causes narrowing)
HOCM clinical manifestation
Affects younger people
Symptoms/signs
SOB
Chest Pain
Syncope (often after exercise) (lack of co)
Arrhythmias
Atrial Fibrillation
Ventricular arrhythmias
Sudden death
Systolic murmur along the left sternal border
increases with Valsalva maneuver/upright position
decreases with squatting
valsalva manuever
decreaes venous return to heart
decreases volume of blood in heart
easier to obstruct with less blood in the heart so murmur increases
non genetic cardiomyopathy
Hypertensive cardiomyopathy
Similar to HOCM except for more generalized thickening with no disproportional involvement of the septum
Aortic stenosis-related hypertrophy
happens bc increased workload
non genetic cardiomyopathy
symptoms
Related to diastolic dysfunction
SOB
Edema
Related to Obstruction
Syncope
Chest Pain
Restrictive cardiomyopathy
overview
Characterized by impaired filling causing predominantly diastolic dysfunction
Primary genetic forms are uncommon
Secondary forms are due to other conditions
restrictive cardiomyopathy causes
Infiltrative disease
Amyloidosis
Sarcoidosis
Systemic storage diseases
Hemochromatosis
Glycogen Storage Diseases
Metabolic disorders
Fibrotic
Radiation
Scleroderma
Endomyocardiac
Loffler’s endocarditis
Endomyocardial Fibrosis
pulmonary htn
Pulmonary circulation is a low pressure circulation
20/10 (pulmonary) vs. 120/80 (systemic)
Blood flow is the same as in systemic circulation
Pulmonary vascular resistance is much less than systemic vascular resistance
Pulmonary HTN is increased pressures in the pulmonary circulation
primary pulmonary htn is
idiopathic
secondary pulmonary htn is
other reasons
pulmonary htn means
right side heart
pulmonary arterial htn causes
idiopathic/familial
portal htn
drugs/toxins mediate
left to right shunt
ctd
hiv infection
pulmonary htn causes du to left heart disease
lvh/lah disease
valvular disease
pulmonary htn cor pulmonale causes
copd
sleep disorders
ild
alveolar hypoventilation disorders
pulmonary htn other cause
due to chronic thrombotic/embolic disease
idiopathic pulmonary htn (primary)
Uncommon (2 cases per million)
Females>males
30-50 is predominant age of onset
12-20% is autosomal dominant genetic disorders with incomplete penentrance
Mean survival is 2-3 years from diagnosis
pulmonary htn left to right shunt
Communication between left and right heart
High pressure systemic circulation gets dumped into low pressure pulmonary circulation
Due to various heart defects
Ventricular septal defect
Patent ductus arteriosus
Atrial septal defect
Atrioventricular septal defect
drug associated pulmonary htn
Fenfluramine (weight loss pill)
Direct effect on pulmonary vasculature
Secondary effect via right sided valvular heart disease
Amphetamines
Cocaine
pulmonary htn/right heart failure due to left heart problems
left ventricular failure
increase lv volumes/pressures
increase la volumes/pressure
increase artery pressure
r vent hypertrophy
r vent failure
cor pulmonale
Most common cause of pulmonary HTN
these are backwards:
RV Failure RV Hypertrophy Increase RV after-load Pulmonary Hypertension Pulmonary Disease
pulmonary embolism
Usually originates from lower extremities
May also come from upper extremities, abdominal veins, heart
Results in increase in pulmonary artery pressure therefore increasing after-load for right ventricle
May lead to right ventricular failure
high output failure
Normal heart
Increase metabolic demand doesn’t match with cardiac output
Thyrotoxicosis
Excessive blood flow overwhelms normal abilities of the pump
Anemia
AV fistula
Conditions decreasing peripheral vascular resistance (Beriberi, sepsis etc)
beriberi disease
thiamine deficiency
dry
wet is chf
CHF Clinical manifestation left sided heart failure
parosyxmal nocturnal dyspnea
elevated pulmonary capillary wedge pressure
restlessness
confusion
orthopnea
tachycardia
exertional dyspnea
fatigue
cyanosis
pulmonary congestion cough crackles wheezed bloodtinged sputum tachypnea
chf clinical manifestation right sided heart failure
cor pulmonale
fatigue
inc peripheral venous pressure
ascites
enlarged liver and spleen
may be secondary to chronic pulmonary problems
distended jugular veins
anorexia and complaints of gi distress
weight gain
dependant edema
symptoms of chf
backward failure
Left heart failure Pulmonary edema SOB, cough (frosty) PND Orthopnea Pleural effusions
symptoms of chf
right heart failure
Lower extremity swelling/edema
Anasarca/ascitis/pleural and pericardial effusion
Could affect lungs as well
End organ damage
Congestive hepatopathy/nutmeg liver
Splenomegaly with hypersplenism
Intestinal congestion leading to GI symptoms
symptoms of chf
forward failure
Mostly in left heart failure
Hypotension
Weakness
Exercise intolerance
End organ damage
Cardiac ischemia
Watershed infarcts
Renal failure Bowel ischemia Shock liver
new York heart association functional classification
Class I: Symptoms with more than ordinary activity
Class II: Symptoms with ordinary activity
Class III: Symptoms with minimal activity (brushing teeth)
Class IIIa: No dyspnea at rest
Class IIIb: Recent dyspnea at rest
Class IV: Symptoms at rest
stages of heart failure
stage a
At high Risk for Heart Failure, but without structural heart disease
stages of heart failure
stage b
Structural Heart Disease, but without symptoms or signs of heart failure
stages of heart failure
stage c
Structural Heart Disease, with prior or current symptoms of heart failure
stages of heart failure
stage d
Refractory Heart Failure Requiring specialized intervention
chf physical findings
vs
BP may be low in advanced CHF
Tachycardia is often present
Tachypnea and hypoxia in severe cases
chf physical findings neck
Jugular Vein Distention
Hepato-jugular (Abdominal-jugular) reflux
Thyroid enlargement in toxic goiter may be present
chf physical findings
lungs
Crackles/rales.
Usually bilateral
Bi-basilar
The higher you can hear them, the worse CHF is
Sometimes decrease breath sounds on bases (bc fluid is there)
Dullness on percussion
Tactile Fremitus
Decreased in case of bilateral pleural effusion
Increased in case of alveolar/interstitial edema
chf physical finding
heart palpation
PMI is displaced if LV is enlarged
Parasternal lift (heave) if RV is enlarged
Arrhythmia is common
chf physical findings
heart auscultation
S1may be diminished if LV function is very poor
P2 (Pulmonic component of S2 ) may be accentuated when pulmonary hypertension is present.
An apical third heart sound (S3) with low EF
S4is usually present with diastolic dysfunction
Murmurs may indicate the presence of significant valvular disease as the cause of heart failure or the result of it.
chf physical findings
abdomen
shifting dullness is the good test for ascites
CHF PHYSICAL FINDINGS LE
EDEMA
chf ekg finding
lvh
rvh
biventricular hypertrophy
corpulmonale
afib
ventricular ectopy
v1 up
rvh
post mi
rbbb
ekg cor pulmonale
up in v1
very tall p wave in lead II
ventricular ectopy ekg
triplet pvcs occur in groups of three can get doublets etc
chf diagnostic tests bnp
Brain Natriuretic peptide
Hormone produced by heart cells (ventricles)
Alone with ANP (atrial natriuretic peptide, which is produced by atrial cells) released in response to increased ventricular filling pressures
Both BNP and ANP have diuretic, natriuretic and hypotensive effect (compensatory effect in response to increase in ventricular filling pressures)
BNP is used as a marker of heart failure
bnp
High false positive rates
Increased in other conditions Old age Renal failure Cor pulmonale Pulmonary hypertension Pulmonary embolism
Doesn’t rule out other causes of dyspnea
Chronic elevation in cardiomyopathy doesn’t help with diagnosing exacerbations
very sensitive but not specific
heart failure chest cray
cardiomegaly
fuzzy hilum
basal congestion
pleural effusion
kerley b lines
echocardiogram
main test for chf
mogaskin nucleotides you putin
Ultrasound examination of the heart Looks at Size of the heart chambers Thickness of the walls
Contractility
Ejection fraction
Wall motion abnormality
Septal defects (bubble study)
Valvular structures and their integrity
Intracardiac structures (clots, tumors)
Diastolic dysfunction
Pulmonary pressures
chf meds
ARBs
Digoxin
b -Blockers
Aldosterone antagonists
Nitrates
hydralazine
ARBs
Decrease after-load
Improve symptoms and mortality
Digoxin
The oldest drug used for CHF
Increases contractility
Improves symptoms, decrease hospitalizations
No effect on mortality
May cause arrhythmia
Narrow therapeutic index
heart blocks and vision changes (yellow)
b -Blockers
Used only with low EF
Improves symptoms
Prolongs life
Started only in stable patients
Counter-intuitive treatment
Usually decrease contractility and C.O.
Only 3 beta-blockers have a proven effect on mortality
Metoprolol Succinate
Carvedilol
Bisoprolol
WHY B BLOCKES WORK IN HEART FAILURE
Upregulate beta receptors improving inotropic and chronotropic responsiveness of the myocardium >improvement in contractile function.
Reduce the level of vasoconstrictors> decrease after-load.
Have a beneficial effect on LV remodeling >improvement in LV geometry > increase contractility.
Reduce myocardial consumption of oxygen.
Decrease the frequency of ventricular premature beats and the incidence of sudden cardiac death (SCD), especially after a myocardial infarction
Aldosterone antagonists
Diuretic and a final piece of the renin-angiotensin-aldosterone axis
Decreases mortality in severe heart failure
Nitrates
Decrease preload and somewhat after-load
Improve symptoms of acute CHF
In combination with hydralasine improve mortality in African-Americans
hydralazine
decrease afterload
if you cant tolerate acei bc of renal failure
overview of chf meds
All mortality improvements are for CHF patients with decrease systolic function/ejection fracture
