CHF ppt- Pales Flashcards
syndrome vs 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 defn
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
Systolic components of heart function/ dysfunction
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 ( CO = SV x HR)
Too fast — not enough time to fill ( CO = SV x HR)
diastolic components of heart function/ dysfunction
Impaired relaxation –functional problem
Ischemia
Impaired compliance (“stiff” ventricle) –anatomical problem related to interstitial fibrosis
Hypertrophy
Hypertension
High output failure
Normal heart function with
increased metabolic demand
Increased peripheral blood flow from decreased PVR
systolic vs diastolic 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.
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 failure is decrease in perfusion of the organs/tissues down-stream from the heart
Backward 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
Forward 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 Failure
End result of left and right failure
Acute heart faillure
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
Heart Failure vs. Cardiomyopathy
Heart failure is a syndrome
Cardiomyopathy is a large group of heterogeneous disorders of myocardial function in the absence of abnormal loading conditions such as with hypertension, CAD or valvular disease.
Left Heart Failure.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 (Old term, still widely used)
Infectious Myocarditis
One of the main causes of dilated cardiomyopathy and left heart systolic failure in young patients.
Multiple etiological agents
- Viral
- Bacterial
- Fungal
- Helminthic
Febrile illness or URI frequently precedes cardiac symptoms by few weeks
Symptoms can present acutely (fulminant) or gradually
Non-infective Myocarditis
Toxic Myocarditis
- Chemotherapy
- Doxorubicin (Adriamycin)
- Heavy metals (copper, iron, lead)
- Lithium
- Malaria drugs
- Radiation causing inflammation and fibrosis
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
No preexisting cardiac disease
More than ½ of patients improve within 6 months
Takotsubo Cardiomyopathy
A.K.A. Stress cardiomyopathy
A.K.A. Apical Ballooning Syndrome
A.K.A. Broken Heart Syndrome
stress- neurogenic –> myocardial stunning, heart failure, angina, coronary spasm, arrhythmias, stress cardiomyopathy
80% are women
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 CardiomyopathyGenetic (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
May cause diastolic or systolic dysfunction
Valsalva maneuver
decreases pre-load
with aortic stenosis the murmur decreases
with HOCM it increases
HOCM. Clinical manifestations
Affects younger people
Symptoms/signs SOB Chest Pain Syncope (often after exercise) Arrhythmias Atrial Fibrillation Ventricular arrhythmias Sudden death Systolic murmur along the left sternal border increases with Valsalva maneuver/upright position decreases with squatting
Restrictive Cardiomyopathy
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 Hypertension
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
Idiopathic Pulmonary Hypertension(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
(congenital) Pulmonary Hypertension.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
Drugs-associated Pulmonary HTN
Fenfluramine (weight loss pill) Direct effect on pulmonary vasculature Secondary effect via right sided valvular heart disease Amphetamines Cocaine
Cor Pulmonale
most common cause of pulmonary HTN
pulmonary disease–> pulmonary HTN–> increased RV afterload–> RV Hypertrophy–> RV failure
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)
Left-sided failure symptoms
paroxysmal nocturnal dyspnea
elevated pulmonary capillary wedge pressure
pulmonary congestion (cough, crackles, wheezes, blood-tinged sputum, tachypnea, restlessness, confusion, orthopnea, tachycardia, exertional dyspnea, fatigue, cyanosis)
symptoms of right-sided failure
fatigue increased 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 dependent edema
backward failure from left heart failure CHF symtoms
Pulmonary edema SOB, cough (frosty) PND Orthopnea Pleural effusions
Right heart failure
symptoms
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
Forward failure
symptoms
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 (NYHA)Functional Classification
Class I: Symptoms with more than ordinary activity
Class II: Symptoms with ordinary activity
Class III: Symptoms with minimal activity
- Class IIIa: No dyspnea at rest
- Class IIIb: Recent dyspnea at rest
Class IV: Symptoms at rest
Stages of heart failure
Stage A- at risk 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
CHF. Physical findings.
VS:
BP may be low in advanced CHF
Tachycardia is often present
Tachypnea and hypoxia in severe cases
Jugular Vein Distention
Hepato-jugular (Abdominal-jugular) reflux
Thyroid enlargement in toxic goiter may be present
Lungs
Crackles/rales.
- Usually bilateral
- Bi-basilar
- The higher you can hear them, the worse CHF is
Sometimes decrease breath sounds on bases
Dullness on percussion
Tactile Fremitus
- Decreased in case of bilateral pleural effusion
- Increased in case of alveolar/interstitial edema
Heart
PMI is displaced if LV is enlarged
Parasternal lift (heave) if RV is enlarged
Arrhythmia is common
CHF. Physical findings.Heart Auscultation
S1 may 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
S4 is 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 diagnostic testsBNP
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 drawbacks
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
Shown benefit in CHF clinics
Echocardiogram
Ultrasound examination of the heart
Looks at: Size of the heart chambers Thickness of the walls Contractility Ejection fraction Wall motion abnormality Septal defects Valvular structures and their integrity Intracardiac structures (clots, tumors) Diastolic dysfunction Pulmonary pressures
CHF treatment: diuretics
Loop diuretics
Help with “congestion” part of CHF
Improvement of symptoms, but not mortality
May worsen renal function and cause electrolytes abnormalities
CHF treatment: ACE inhibitors
Decrease after-load –> increase ventricular function
Improves symptoms and mortality.
CHF treatment: ARBs
Decrease after-load
Improve symptoms and mortality
CHF treatment: digoxin
The oldest drug used for CHF Increases contractility Improves symptoms, decrease hospitalizations No effect on mortality May cause arrhythmia Narrow therapeutic index
CHF treatment: 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 beta blockers work in heart failure?
Upregulate beta receptors improving inotropic and chronotropic responsiveness of the myocardium improvement in contractile function.
Reduce the level of vasoconstrictors after-load.
Have a beneficial effect on LV remodeling 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
CHF treatment: 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 after-load
All mortality improvements are for CHF patients with
decreased systolic function/ejection fracture.
