Congestive Heart Failure Flashcards
CHF
Clinical Syndrome in which an abnormality of cardiac structure or function is responsible for the inability of the heart to eject or fill with blood at a rate sufficient to meet the demands of the metabolizing tissues.
“pump failure”
preload and HF
systolic failure
= (EDV)
The more heart fibers are stretched the more difficult it is for them to contract increasing work/pressures and causing hypertrophy (Starling law)
afterload and HF
Resistance against heart contraction/ejection of blood
heart rate and HF
too slow = decreased CO
too fast = not enough time to fill (low CO due to very low SV)
components of diastolic dysfunction?
- impaired relaxation
- impaired compliance (stiff ventricle): due to hypertrophy and HTN
high output failure?
normal heart function, but due to increased metabolic demands, or increased peripheral blood flow from decreased PVR
- Metabolic disorders: thyrotoxicosis
- excessive bloodflow: anemia, AV fistula, BeriBeri
pathophys of heart failure?
heart damage/ventricular overload/ decreased ventricular contraction –> tachycardia, ventricular dilation, myocardial hypertrophy –> decreased CO –> decreased renal perfusion –> increased sodium retention –> increased pressure –> increased ADH –> increased water reabsorption –> fluid overload/edema –> heart damage
what do chatecholamines do in HF?
increased NE and epi seen in CHF –> this is why Beta blockers have shown to be helpful
systolic vs. diastolic HF?
systolic HF: results from inadequate CO (SVxHR) or EF (SV/EDV)
- Dilated CM = decreased contractility
- valvular insufficiency = increased preload
- severe acute HTN, valvular stenosis –> increased after-load
- arrhtymias = change in HR
diastolic HF: results from inability of ventricles to relax and fill normally w/ blood during diastole
- chronic HTN
- HOCM
- RCM
- ischemic fibrosis
- pericardial disease
forward vs. backward HF?
**forward failure - decrease in perfusion of the organs/tissues downstream of heart
= left HF results in no perfusion (hypotension, weakness, exercise intolerance, end organ damage: cardiac ischemia, renal failure, bowel ischemia, shock liver)
- *backward failure = backing up of blood into the organs upstream, increasing hydrostatic pressure –> leads to congestion and edema
- LH backward failure = pulmonary edema
- RH backward failure = peripheral edema
left sideHF?
caused by: CAD/MI, aortic/mitral valve problems, HTN, CMs
forward failure = problems in systemic circulation
backward failure = congestion of lungs
sx: paroxysmal nocturnal dyspnea, elevated pulmonary capillary wedge pressure, pulmonary congestion (cough, crackles, wheezes, blood-tinged sputum, tachypnea), resltessness, orthopnea, tachycardia, exertional dyspnea, fatigue, cyanosis
right sided HF?
caused by: pulmonary diseases/cor pulmonale, tricuspid/pulmonary valves, pulmonary HTN, pulmonary emboli
- results in congestion in systemic circulation (upstream)
sx: fatigue, increased peripheral resitsnance, ascites, enlarged liver/spleen, may be secondary to chronic pulmonary problems, distended JVP, anorexia/GI distress, weight gain, dependent edema - can result in end organ damage: congestive hepatopathy/nutmeg liver, splenomegaly with hypersplenism, intestinal congestion/GI sx
- can affect lungs as well as 20% of blood is received from bronchial artery off of the aorta
acute vs. chronic HF?
acute:
- due to sudden event: MI, chorda tendinae rupture, large PE
- usually forward failure
- flash pulmonary edema (frothy sputum)
chronic: progressess slowly, usually results in backward failure (congestion)
causes of dilated cardiomyopathy?
- CAD or MI: Due to death or functional ischemic dysfunction of myocardial tissue due to complete or partial blockage of coronary arteries
- results in an “ischemic cardiomyopathy” - HTN: causes increased workload –> LVH –> diastolic dysfunction –> ventricular dilation –> systolic dysfunction
- Valvular Heart Disease:
aortic regurg –> increased preload/EDV –> increased workload –> LVH –> left ventricular dilation –> systolic dysfunction - Infective myocarditis:
- a main cause of DCM
- usually viral, cardiac sx preceded by URI 2 weeks earlier
- suspect when see young people with DCM
- will have viral synd. that goes away then developes SOB
(older people with DCM, think ischemic HD) - non-infective myocarditis
- alcoholic cardiomyopathy
non-infective myocarditis
results in DCM
1. Toxic MC: Chemotherapy Doxorubicin (Adriamycin) Heavy metals (copper, iron, lead) Lithium – used for bipolar disorders Malaria drugs Radiation causing inflammation and fibrosis
- AI/CTD associated MC
Giant Cell Myocarditis
Polyomyocyties/DM
SLE/RA
how does cocaine affect myocardium?
May cause vasospasm leading to MI
May cause arrhythmia
May cause drug-induced myocarditis/cardiomyopathy due to released catecholamines
alcoholic CM?
- type of DCM
- occurs in prolonged chronic alcohol use (10+ years)
- alcohol directly affects myocardium
CAD/MI?
cause DCM
- CAD or MI: Due to death or functional ischemic dysfunction of myocardial tissue due to complete or partial blockage of coronary arteries
- results in an “ischemic cardiomyopathy”
HTN?
cause DCM
2. HTN: causes increased workload –> LVH –> diastolic dysfunction –> ventricular dilation –> systolic dysfunction
aortic regurg?
DCM
3. Valvular Heart Disease:
aortic regurg –> increased preload/EDV –> increased workload –> LVH –> left ventricular dilation –> systolic dysfunction
infective myocarditis?
DCM
4. Infective myocarditis:
- a main cause of DCM
- usually viral, cardiac sx preceded by URI 2 weeks earlier
- suspect when see young people with DCM
- will have viral synd. that goes away then developes SOB
(older people with DCM, think ischemic HD)
peripartum CM
- type of DCM
- occurs b/w last month of pregnancy and first 5 mos after delivery
- likely due to immune-mediated process
- over 1/2 improve within 6 mos.
Takotsubo CM
type of DCM
“stress CM” or “broken heart snd”
- triggered by acute medical illness or intense emotional/physical stress
mechanism: stress –> catecholamine xs (NE ) –> coronary aa. vasospasm –> microvascular dysf or dynamic left ventricular outflow tract obstruction which contribute to apical balooning
sx are similar to acute MI: CP, SOB, syncope
HOCM
- genetic hypertrophic CM
- group of disorders causing myocardial hypertrophy unrelated to any pressure or volume load
- due to diff. gene mutations: myosin heavy chains, proteins regulating Ca2+ handling
- most autosomal dominant
- inter-ventricular septum often disproportionally enlarged
- sub-aortic stenosis often present
- mostly causes diastolic, not systolic dysfunction
- ex. athletes dropping dead during a game
- patients don’t die from the hypertrophy but from the arry.
clinical sx of HOCM?
- affects younger people
sx: SOB, c/p, syncope after exercise, arrhythmias (a fib, v arr, sudden death)
systolic murmur along left sternal border that increases with valsalva maneuver and decreases with squatting
- valsalva decreases volume inside of heart, if have lots of hypertrophy, then the lumen is small and blood volume thats decreased makes murmur louder
NOTE: when have aortic stenosis the murmur is louder if there is more blood in it (squatting)
valsalva maneuver?
The Valsalva maneuver or Valsalva manoeuvre is performed by moderately forceful attempted exhalation against a closed airway –> reduces venous return –> CO remains low
non-genetic Hypertrophic CM?
hypertensive cardiomyopathy: similar to HOCM except for a more generalized thickening with no disproportional involvemnt of septum
- aortic stenosis related hypertrophy
sx:
- related to diastolic dysfunction, SOB, edema
- related to obstruction: syncope (decrease in CO ), c/p (decreased flow to cardiac aa.)
restrictive CM
- impaired filling causing predominantly diastolic dysfunction
- genetic forms are uncommon, most forms are secondary conditions:
ex. amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disease, metabolic disorders, radiation, scleroderma. Loffler’s endocarditis, endomyocardial fibrosis
pulmonary HTN
- normal pulmonary circulation is 20/10
- pulmonary HTN is precursor to RHF
- cor pulmonale = primary pulmonary HTN
pulmonary arterial HTN?
idiopathic/familal portal HTN drugs/toxins mediated HIV infection CTD left to right shunt
pulmonary HTN due to left heart disease?
valvular heart disease
LVH/LAH disease
cor pulmonale
pulmonary disease –> pulmonary HTN –> increased RV afterload –> RV hypertrophy –> RV failure
ex. COPD, sleep disorders, ILD, alveolar hypoventilation disorders
idiopathic pulmonary HTN?
- uncommon, females>males
age 30-50 onset - 12-20% is autosomal dominant genetic disorder
- mean survival of 2-3 years
Left to right shunt?
ASD, VSD, PDA, AVSD
- results in left high pressure being transmitted to right high pressure
- Esenmenger syndrome: results when the flow reverses due to severe HTN in lungs
what weight loss pill is associated w/ pulmonary HTN?
fenfluramine weight loss pill –> secondarily causes right sided valvular heart disease
- also cocaine and amphetamines
pulmonary embolism
originates from lower extremities –> causes pulmonary HTN and right sided HF
thyrotoxicosis
causes increase in HR and increase in SV due to thyroid storm which overwhelms the heart –> high output failure
anemia
causes high output heart failure b/c tissues aren’t being well perfused so heart works harder
AV fistula
causes high output HF b/c it decreases the peripheral resistance and causes more blood to stay in periphery, so decreased SV means that heart has to increase HR to compensate
Beriberi
a cluster of symptoms caused primarily by a nutritional deficit in vitamin B1 (thiamine).
wet beriberi causes peripheral tissues to become edematous –> decreased total SV –> results in heart having to work harder –> HOHF
** New YOrk Health ASsosocation (NYHA) Functional Class. of CHF ***
Class I: Symptoms with more than ordinary activity (extreme exercise)
Class II: Symptoms with ordinary activity (walking upstairs)
Class III: Symptoms with minimal activity
Class IIIa: No dyspnea at rest (can’t click remote control)
Class IIIb: Recent dyspnea at rest (fluctuates)
Class IV: Symptoms at rest
Stages of HF ACC/AHA guidelines
Stage A: At high Risk for Heart Failure, but without structural heart disease
Stage B: Structural Heart Disease, but without symptoms or signs of heart failure
Stage C: Structural Heart Disease, with prior or current symptoms of heart failure
Stage D: Refractory Heart Failure Requiring specialized intervention
physical findings of CHF
VS: BP may be low in advanced CHF, tachycardia, tachynpea and hypoxia
Neck: see JVD, hepato-jugular reflux, thyroid enlargment
Lungs: crackles/rales bilaterally, usually bi-basilar (the higher you hear them the worse the CHF)
- decreased breath sounds at bases
- dullness to percussion
- tactile fremitus (decreased in b/l pleural effusion= space surrounding lungs, increased in alveolar interstitial edema)
heart changes in CHF?
PMI displaced if LV is enlarged
parasternal heave if RV is enlarged
arr. is common
S1 may be diminshed if LV fn is poor
P2 accentuated?
pulmonary HTN
S3
present with low EF - due noncompliant ventricle
S4
present with diastolic dysfunction due to floppy atria
which test is better for ascites?
shifting dullness:
tympanic on top, dull on bottom, this should shift because water shifts
CHF EKG findings?
LVH, RVH, biventricular Hypertrophy, atrial fibrillation, PVC’s
cor pulmonale: see RV strain and RVH (upslope of PR), see RAD
look at slides
BNP?
hormone produced by heart cells in ventricles
used as a marker for HF, but not specific. only can prove that there is prob. not HF if its low
High false positive rates: Increased in other conditions Old age Renal failure Cor pulmonale Pulmonary hypertension Pulmonary embolism
Kerley B lines
often seen on CXR in CHF
Diuretics?
Loop diuretics
Help with “congestion” part of CHF
Improvement of symptoms, but not mortality (live better, but not longer)
May worsen renal function and cause electrolytes abnormalities
ACEIs?
Decrease after-load –> increase ventricular function
Improves symptoms and mortality.
which groups improve mortality?
ACEIs, beta blockers, ARBs, aldo antagonists
nitrates + hydralazine improve mortality in AA’s
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
beta 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?
Upregulate beta receptors improving inotropic and chronotropic responsiveness of the myocardium and improvement in contractile function.
Reduce the level of vasoconstrictors causing decreased after-load.
Have a beneficial effect on LV remodeling causing improvement in LV geometry 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
aldo 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 (decreases afterload)
