CHF ppt- Pales Flashcards

1
Q

syndrome vs disease

A

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

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2
Q

CHF defn

A

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

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3
Q

Systolic components of heart function/ dysfunction

A

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)

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4
Q

diastolic components of heart function/ dysfunction

A

Impaired relaxation –functional problem
Ischemia

Impaired compliance (“stiff” ventricle) –anatomical problem related to interstitial fibrosis
Hypertrophy
Hypertension

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5
Q

High output failure

A

Normal heart function with
increased metabolic demand
Increased peripheral blood flow from decreased PVR

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6
Q

systolic vs diastolic heart failure

A

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.

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7
Q

Forward vs. Backward Heart Failure

A

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

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8
Q

Left-sided Heart Failure

A

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)

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9
Q

Right-sided heart failure

A
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)

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10
Q

Biventricular Failure

A

End result of left and right failure

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11
Q

Acute heart faillure

A
due to a sudden and severe event
- Massive MI
- Chorda tendinae rupture
- Large PE
Predominantly forward failure
Flash Pulmonary Edema
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12
Q

chronic heart failure

A

Progresses slowly
Has exacerbation
Predominantly backward failure

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13
Q

Heart Failure vs. Cardiomyopathy

A

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.

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14
Q

Left Heart Failure.CAD/MI

A

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)

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15
Q

Infectious Myocarditis

A

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

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16
Q

Non-infective Myocarditis

A

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
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17
Q

Cocaine and myocardium

A

May cause vasospasm leading to MI
May cause arrhythmia
May cause drug-induced myocarditis/cardiomyopathy due to released catecholamines

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18
Q

Alcoholic Cardiomyopathy

A

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

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19
Q

Peripartum Cardiomyopathy

A

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

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20
Q

Takotsubo Cardiomyopathy

A

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,

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21
Q

Hypertrophic CardiomyopathyGenetic (HOCM)

A

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

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22
Q

Valsalva maneuver

A

decreases pre-load

with aortic stenosis the murmur decreases

with HOCM it increases

23
Q

HOCM. Clinical manifestations

A

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
24
Q

Restrictive Cardiomyopathy

A

Characterized by impaired filling causing predominantly diastolic dysfunction

Primary genetic forms are uncommon

Secondary forms are due to other conditions

25
Q

Restrictive Cardiomyopathy- causes

A

Infiltrative disease

  • Amyloidosis
  • Sarcoidosis

Systemic storage diseases

  • Hemochromatosis
  • Glycogen Storage Diseases

Metabolic disorders
Fibrotic
- Radiation
- Scleroderma

Endomyocardiac

  • Loffler’s endocarditis
  • Endomyocardial Fibrosis
26
Q

Pulmonary Hypertension

A

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

27
Q

Idiopathic Pulmonary Hypertension(Primary)

A

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

28
Q

(congenital) Pulmonary Hypertension.Left to Right Shunt

A

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
29
Q

Drugs-associated Pulmonary HTN

A
Fenfluramine (weight loss pill)
Direct effect on pulmonary vasculature
Secondary effect via right sided valvular heart disease
Amphetamines
Cocaine
30
Q

Cor Pulmonale

A

most common cause of pulmonary HTN

pulmonary disease–> pulmonary HTN–> increased RV afterload–> RV Hypertrophy–> RV failure

31
Q

Pulmonary Embolism

A

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

32
Q

High Output Failure

A

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)
33
Q

Left-sided failure symptoms

A

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)

34
Q

symptoms of right-sided failure

A
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
35
Q

backward failure from left heart failure CHF symtoms

A
Pulmonary edema
SOB, cough (frosty)
PND
Orthopnea
Pleural effusions
36
Q

Right heart failure

symptoms

A

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

37
Q

Forward failure

symptoms

A
Mostly in left heart failure
Hypotension
Weakness
Exercise intolerance
End organ damage
Cardiac ischemia:
- Watershed infarcts
- Renal failure
- Bowel ischemia
- Shock liver
38
Q

New York Heart Association (NYHA)Functional Classification

A

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

39
Q

Stages of heart failure

A

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

40
Q

CHF. Physical findings.

A

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

41
Q

CHF. Physical findings.Heart Auscultation

A

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.

42
Q

CHF diagnostic testsBNP

A

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

43
Q

BNP drawbacks

A
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

44
Q

Echocardiogram

A

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
45
Q

CHF treatment: diuretics

A

Loop diuretics
Help with “congestion” part of CHF
Improvement of symptoms, but not mortality
May worsen renal function and cause electrolytes abnormalities

46
Q

CHF treatment: ACE inhibitors

A

Decrease after-load –> increase ventricular function

Improves symptoms and mortality.

47
Q

CHF treatment: ARBs

A

Decrease after-load

Improve symptoms and mortality

48
Q

CHF treatment: digoxin

A
The oldest drug used for CHF
Increases contractility
Improves symptoms, decrease hospitalizations
No effect on mortality
May cause arrhythmia
Narrow therapeutic index
49
Q

CHF treatment: beta blockers

A
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
50
Q

Why beta blockers work in heart failure?

A

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

51
Q

CHF treatment: aldosterone antagonists

A

Diuretic and a final piece of the renin-angiotensin-aldosterone axis
Decreases mortality in severe heart failure

52
Q

Nitrates

A

Decrease preload and somewhat after-load
Improve symptoms of acute CHF
In combination with hydralasine improve mortality in African-Americans

53
Q

Hydralazine

A

Decrease after-load

54
Q

All mortality improvements are for CHF patients with

A

decreased systolic function/ejection fracture.