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Causes of Congestive Heart Failure

Contents
  1. Congestive Heart Failure: Introduction
  2. List of Causes
  3. Drugs/substances (15 causes)
  4. Drug interaction (221 causes)
  5. Hidden causes
  6. Risk factors
  7. Excerpts from book chapters
  8. Complication causes
  9. Causes of symptoms
  10. News
  11. Related cause information

List of causes of Congestive Heart Failure

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Congestive Heart Failure) that could possibly cause Congestive Heart Failure includes:

More causes: see full list of causes for Congestive heart failure

Congestive Heart Failure Causes: Book Excerpts

Congestive Heart Failure as a complication of other conditions:

Other conditions that might have Congestive Heart Failure as a complication may, potentially, be an underlying cause of Congestive Heart Failure. Our database lists the following as having Congestive Heart Failure as a complication of that condition:

Congestive Heart Failure as a symptom:

Conditions listing Congestive Heart Failure as a symptom may also be potential underlying causes of Congestive Heart Failure. Our database lists the following as having Congestive Heart Failure as a symptom of that condition:

Medications or substances causing Congestive Heart Failure:

The following drugs, medications, substances or toxins are some of the possible causes of Congestive Heart Failure as a symptom. This list is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

See full list of 15 medications causing Congestive Heart Failure


Drug interactions causing Congestive Heart Failure:

When combined, certain drugs, medications, substances or toxins may react causing Congestive Heart Failure as a symptom.

The list below is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

  • Advil (Ibuprofen) and Bumex (Bumetanide) interaction
  • Advil (Ibuprofen) and Diachlor (Chlorothiazide) interaction
  • Advil (Ibuprofen) and Diuril (Chlorothiazide) interaction
  • Advil (Ibuprofen) and Diucardin (Hydroflumethiazide) interaction
  • Advil (Ibuprofen) and Saluron (Hydroflumethiazide) interaction
  • more interactions...»

See full list of 221 drug interactions causing Congestive Heart Failure

Medical news summaries relating to Congestive Heart Failure:

The following medical news items are relevant to causes of Congestive Heart Failure:

Related information on causes of Congestive Heart Failure:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Congestive Heart Failure may be found in:

Causes of Congestive Heart Failure: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Congestive Heart Failure.

Cardiomegaly: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Congestive heart failure
  • Ischemic heart disease
  • Hypertension (with left ventricular hypertrophy)
  • Valvular disease (primarily MR, AS, AR)
  • Hypertrophic cardiomyopathy
  • Congenital heart disorders (e.g., ASD, VSD, PDA, coarctation of the aorta, Ebstein's anomaly, tetralogy of Fallot)
  • Idiopathic cardiomyopathy
  • Alcoholic cardiomyopathy
    • Lung disease (leading to right-sided enlargement)
      –Pulmonary embolus
      –COPD
      –Cor pulmonale
      –Primary pulmonary hypertension
    • Subacute bacterial endocarditis
    • Myocarditis
    • Renal failure (risk of pericardial effusion)
    • Anemia
    • Scleroderma
    • Systemic lupus erythematosus
    • Sickle cell disease
    • Marfan's syndrome
    • Pregnancy
    • Drugs (numerous drugs are cardiotoxic)
    • Postradiation
    • Normal, “athletic” heart
    • Mediastinal mass
    • Kyphoscoliosis
    • Rheumatoid arthritis
    • Less common etiologies include infiltrative diseases (e.g., amyloidosis, hemochromatosis, atrial myxoma, endocardial fibroelastosis, Fabry's disease, Hurler's syndrome, Pompe's disease), epicardial fat pad, carcinoid, acromegaly, hyper- or hypoparathyroidism, and severe cases of hypocalcemia, hypomagnesemia, and/or hypophosphatemia

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Paroxysmal Nocturnal Dyspnea: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • CHF is the most common cause
    –Etiologies include uncontrolled HTN, pulmonary embolus, endocarditis, hyperthyroidism, pericardial disease, endocardial disease (e.g., valvular stenosis, insufficiency, rupture, endocarditis), and myocardial disease (e.g., MI, ischemia, arrhythmias)
  • Mitral stenosis
    –Almost always secondary to rheumatic heart disease (after 15–40 years)
    –Advanced cases result in pulmonary hypertension and right heart failure
    –Dyspnea is the most significant symptom
    –Classic triad: Diastolic rumble, opening snap, and loud first heart sound
  • Aortic regurgitation
    –Most commonly due to rheumatic fever
  • Cardiomyopathies
    –Abnormal myocardium, resulting in impaired cardiac output and CHF
  • Aortic stenosis
    –Due to senile valve degeneration, rheumatic disease, or congenital
    –Associated with angina, syncope, and CHF
  • Congenital heart disease
    –May see failure to thrive, progressive CHF symptoms, cyanosis, and/or murmur
    • “Cardiac asthma”
      –Bronchospasm secondary to pulmonary congestion and interstitial edema that compresses small airways
      –Standing decreases lung congestion
    • Anxiety
    • Severe COPD and emphysema
    • Asthma
    • Obstructive sleep apnea
    • Obesity/hypoventilation
    • Tropical pulmonary eosinophilia (filariasis)

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Heart Failure: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Increased afterload

  • Most common in the neonate due to left-sided obstructive lesions, which present acutely
  • Aortic coarctation is most common
    –Increased pulse/BP in right arm
    –Decreased pulse/BP in lower extremities
  • Critical aortic stenosis
    –Poor pulses, loud murmur
    • Hypoplastic left heart syndrome, aortic arch interruption

    Left-to-right shunt lesions
  • Normal cardiac muscle funtion but overcirculation of lungs due to a congenital connection between the right and left side of the heart and low PVR
    • Usually presents at 1–2 months of age
      –PVR drops and systemic resistance becomes higher than PV
      –Blood shunts from left to right (systemic circulation to pulmonary circulation)
      –Pulmonary overcirculation and poor systemic output (poor peripheral perfusion, low urine output)
  • Ventricular septal defect (most common)
  • Atrioventricular septal defect (AV canal, endocardial cushion defect), associated with Down syndrome
  • Patent ductus arteriosus
    • Atrial septal defect (usually asymptomatic)

    Intrinsic myocardial disease
  • More common cause of heart failure in older children and adolescents
    • Myocarditis
      –Acute inflammation and dysfunction of cardiac muscle, usually postviral
      –1/3 remain stable, 1/3 return to normal cardiac function, and 1/3 deteriorate
    • Cardiomyopathy
      –Dilated most common, but also hypertrophic and restrictive
      –Multiple genetic and metabolic causes, often positive family history, some represent old, “burned-out” myocarditis
  • Myocardial infarction (rare)
    –Kawasaki disease
    –Congenital coronary abnormalities (anomalous left coronary artery)

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Paroxysmal nocturnal dyspnea: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Left-sided heart failure

Dyspnea — on exertion, during sleep, and eventually even at rest — is an early sign of left-sided heart failure. This sign is characteristically accompanied by Cheyne-
Stokes respirations, diaphoresis, weakness, wheezing, and a persistent, nonproductive cough or a cough that produces clear or blood-tinged sputum. As the patient’s condition worsens, he develops tachycardia, tachypnea, alternating pulse (commonly initiated by a premature beat), a ventricular gallop, crackles, and peripheral edema.

With advanced left-sided heart failure, the patient may also exhibit severe orthopnea, cyanosis, clubbing, hemoptysis, and cardiac arrhythmias as well as signs and symptoms of shock, such as hypotension, a weak pulse, and cold, clammy skin.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulse pressure, narrowed: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Cardiac tamponade

With cardiac tamponade, a life-threatening disorder, pulse pressure narrows by 10 to 20 mm Hg. Paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds are classic. The patient may be anxious, restless, and cyanotic, with clammy skin and chest pain. He may exhibit dyspnea, tachypnea, a decreased LOC, and a weak, rapid pulse. A pericardial friction rub and hepatomegaly may also occur.

Heart failure

Narrowed pulse pressure occurs relatively late and may accompany tachypnea, palpitations, dependent edema, steady weight gain despite nausea and anorexia, chest tightness, slowed mental response, hypotension, diaphoresis, pallor, and oliguria. Assessment reveals a ventricular gallop, inspiratory crackles and, possibly, a tender, palpable liver. Later, dullness develops over the lung bases, and hemoptysis, cyanosis, marked hepatomegaly, and marked pitting edema may occur.

Shock

With anaphylactic shock, narrowed pulse pressure occurs late, preceded by a rapid, weak pulse that soon becomes uniformly absent. Within seconds or minutes after exposure to an allergen, the patient experiences hypotension, anxiety, restlessness, and feelings of doom, along with intense itching, a pounding headache and, possibly, urticaria. Other findings include dyspnea, stridor, and hoarseness; chest or throat tightness; skin flushing; nausea, abdominal cramps, and urinary incontinence; and seizures.

With cardiogenic shock, narrowed pulse pressure occurs relatively late. Typically, peripheral pulses are absent and central pulses are weak. A drop in systolic pressure to 30 mm Hg below baseline, or a sustained reading below 80 mm Hg not attributable to medication, produces poor tissue perfusion. Poor perfusion produces tachycardia; tachypnea; cold, pale, clammy skin; cyanosis; oliguria; restlessness; confusion; and obtundation.

With hypovolemic shock, narrowed pulse pressure occurs as a late sign. All peripheral pulses become first weak and then uniformly absent. Deepening shock leads to hypotension, urine output of less than 25 ml/hour, confusion, a decreased LOC and, possibly, hypothermia.

With septic shock, narrowed pulse pressure is a relatively late sign. All peripheral pulses become first weak and then uniformly absent. As shock progresses, the patient exhibits oliguria, thirst, anxiety, restlessness, confusion, and hypotension. Extremities become cool and cyanotic; the skin becomes cold and clammy. In time, he develops severe hypotension, persistent oliguria or anuria, respiratory failure, and coma.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Paroxysmal nocturnal dyspnea: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Left-sided heart failure

Dyspnea—on exertion, during sleep, and eventually even at rest—is an early sign of left-sided heart failure. This sign is characteristically accompanied by Cheyne-Stokes respirations, diaphoresis, weakness, wheezing, and a persistent, nonproductive cough or a cough that produces clear or blood-tinged sputum. As the patient’s condition worsens, he develops tachycardia, tachypnea, alternating pulse (commonly initiated by a premature beat), a ventricular gallop, crackles, and peripheral edema.

With advanced left-sided heart failure, the patient may also exhibit severe orthopnea, cyanosis, clubbing, hemoptysis, and cardiac arrhythmias as well as signs and symptoms of shock, such as hypotension, weak pulse, and cold, clammy skin.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Pulse pressure, narrowed: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Aortic stenosis

Narrowed pulse pressure occurs late in significant stenosis. This disorder also produces an atrial or ventricular gallop; chest pain; a harsh, systolic ejection murmur; angina; dyspnea; paroxysmal nocturnal dyspnea; and syncope. Crackles, palpitations, fatigue, and diminished carotid pulses may also occur.

Cardiac tamponade

With this life-threatening disorder, pulse pressure narrows by 10 to 20 mm Hg. Paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds are classic. The patient may be anxious, restless, and cyanotic, with clammy skin and chest pain. He may exhibit dyspnea, tachypnea, decreased LOC, and a weak, rapid pulse. Pericardial friction rub and hepatomegaly may also occur.

Heart failure

Narrowed pulse pressure occurs relatively late and may accompany tachypnea, palpitations, dependent edema, steady weight gain despite nausea and anorexia, chest tightness, slowed mental response, hypotension, diaphoresis, pallor, and oliguria. Assessment reveals a ventricular gallop, inspiratory crackles and, possibly, a tender, palpable liver. Later, dullness develops over the lung bases, and hemoptysis, cyanosis, marked hepatomegaly, and marked pitting edema may occur.

Shock

With anaphylactic shock, narrowed pulse pressure occurs late, preceded by a rapid, weak pulse that soon becomes uniformly absent. Within seconds or minutes after exposure to an allergen, the patient experiences hypotension, anxiety, restlessness, and feelings of doom, along with intense itching, a pounding headache and, possibly, urticaria. Other findings include dyspnea, stridor, and hoarseness; chest or throat tightness; skin flushing; nausea, abdominal cramps, and urinary incontinence; and seizures.

With cardiogenic shock, narrowed pulse pressure occurs relatively late. Typically, peripheral pulses are absent and central pulses are weak. A drop in systolic pressure to 30 mm Hg belowbaseline, or a sustained reading below 80 mm Hg not attributable to medication, produces poor tissue perfusion. Poor perfusion produces tachycardia; tachypnea; cold, pale, clammy skin; cyanosis; oliguria; restlessness; confusion; and obtundation.

With hypovolemic shock, narrowed pulse pressure occurs as a late sign. All peripheral pulses become first weak and then uniformly absent. Deepening shock leads to hypotension, urine output of less than 25 ml/hour, confusion, decreased LOC and, possibly, hypothermia.

With septic shock, narrowed pulse pressure is a relatively late sign. All peripheral pulses become first weak and then uniformly absent. As shock progresses, the patient exhibits oliguria, thirst, anxiety, restlessness, confusion, and hypotension. Extremities become cool and cyanotic; the skin becomes cold and clammy. In time, he develops severe hypotension, persistent oliguria or anuria, respiratory failure, and coma.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Cardiomegaly/Congestive Heart Failure: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Congestive heart failure

❑ Hypertensive left ventricular hypertrophy

❑ Anterior myocardial ischemia

❑ Athlete’s heart

❑ Mitral regurgitation

❑ Aortic stenosis

❑ High output

❑ Hypertrophic obstructive cardiomyopathy

❑ Pulmonary hypertension

❑ Cor pulmonale

❑ Dilated cardiomyopathy

❑ Endocarditis

❑ Pericardial effusion

❑ Left ventricular aneurysm

❑ Mitral stenosis

❑ Amyloidosis

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Heart failure: Causes
(Handbook of Diseases)

Heart failure may result from a primary abnormality of the heart muscle (such as an infarction), inadequate myocardial perfusion due to coronary artery disease, or cardiomyopathy. Other causes include:

❑ mechanical disturbances in ventricular filling during diastole when there’s too little blood for the ventricle to pump, as in mitral stenosis secondary to rheumatic heart disease or constrictive pericarditis and atrial fibrillation

❑ systolic hemodynamic disturbances such as excessive cardiac workload due to volume overloading or pressure overload that limit the heart’s pumping ability.

These disturbances can result from mitral or aortic insufficiency, which causes volume overloading, and aortic stenosis or systemic hypertension, which results in increased resistance to ventricular emptying.

Reduced cardiac output triggers three compensatory mechanisms: ventricular dilation, hypertrophy, and increased sympathetic activity. These mechanisms improve cardiac output at the expense of increased ventricular work.

Cardiac dilation

In cardiac dilation, an increase in end-diastolic ventricular volume (preload) causes increased stroke work and stroke volume during contraction, stretching cardiac muscle fibers beyond optimum limits and producing pulmonary congestion and pulmonary hypertension, which lead in turn to right-sided heart failure.

Ventricular hypertrophy

In ventricular hypertrophy, an increase in muscle mass or the diameter of the left ventricle allows the heart to pump against increased resistance (impedance) to the outflow of blood.

An increase in ventricular diastolic pressure necessary to fill the enlarged ventricle may compromise diastolic coronary blood flow, limiting the oxygen supply to the ventricle and causing ischemia and impaired myocardial contractility.

Increased sympathetic activity

As a response to decreased cardiac output and blood pressure, increased sympathetic activity occurs by enhancing peripheral vascular resistance, contractility, heart rate, and venous return.

Signs of increased sympathetic activity, such as cool extremities and clamminess, may indicate impending heart failure. Increased sympathetic activity also restricts blood flow to the kidneys, which respond by reducing the glomerular filtration rate and increasing tubular reabsorption of sodium and water, in turn expanding the circulating blood volume. This renal mechanism, if unchecked, can aggravate congestion and produce overt edema.

Chronic heart failure may worsen as a result of respiratory tract infections, pulmonary embolism, stress, increased sodium or water intake, and failure to comply with the prescribed treatment regimen.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Pulse pressure, narrowed: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Aortic stenosis

Narrowed pulse pressure occurs late in significant stenosis. Aortic stenosis also produces an atrial or ventricular gallop; chest pain; a harsh, systolic ejection murmur; angina; dyspnea; paroxysmal nocturnal dyspnea; and syncope. Crackles, palpitations, fatigue, and diminished carotid pulses may also occur.

Cardiac tamponade

With cardiac tamponade, a life-threatening disorder, pulse pressure narrows by 10 to 20 mm Hg. Paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds are classic. The patient may be anxious, restless, and cyanotic, with clammy skin and chest pain. He may exhibit dyspnea, tachypnea, decreased LOC, and a weak, rapid pulse. Pericardial friction rub and hepatomegaly may also occur.

Heart failure

Narrowed pulse pressure occurs relatively late in heart failure and may accompany tachypnea, palpitations, dependent edema, steady weight gain despite nausea and anorexia, chest tightness, slowed mental response, hypotension, diaphoresis, pallor, and oliguria. Assessment reveals a ventricular gallop, inspiratory crackles and, possibly, a tender, palpable liver. Later, dullness develops over the lung bases, and hemoptysis, cyanosis, marked hepatomegaly, and marked pitting edema may occur.

Shock

With anaphylactic shock, narrowed pulse pressure occurs late, preceded by a rapid, weak pulse that soon becomes uniformly absent. Within seconds or minutes after exposure to an allergen, the patient experiences hypotension, anxiety, restlessness, and feelings of doom, along with intense itching, a pounding headache and, possibly, urticaria. Other findings include dyspnea, stridor, and hoarseness; chest or throat tightness; skin flushing; nausea, abdominal cramps, and urinary incontinence; and seizures.

With cardiogenic shock, narrowed pulse pressure occurs relatively late. Typically, peripheral pulses are absent and central pulses are weak. A drop in systolic pressure to 30 mm Hg belowbaseline, or a sustained reading below 80 mm Hg not attributable to medication, produces poor tissue perfusion. Poor perfusion produces tachycardia, tachypnea, cyanosis, oliguria, restlessness, confusion, obtundation, and cold, pale, clammy skin.

With hypovolemic shock, narrowed pulse pressure occurs as a late sign. All peripheral pulses become first weak and then uniformly absent. Deepening shock leads to hypotension, urine output of less than 25 ml/hour, confusion, decreased LOC and, possibly, hypothermia.

With septic shock, narrowed pulse pressure is a relatively late sign. All peripheral pulses become first weak and then uniformly absent. As shock progresses, the patient exhibits oliguria, thirst, anxiety, restlessness, confusion, and hypotension. Extremities become cool and cyanotic; the skin becomes cold and clammy. In time, he develops severe hypotension, persistent oliguria or anuria, respiratory failure, and coma.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Paroxysmal nocturnal dyspnea: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Left-sided heart failure.Dyspnea—on exertion, during sleep, and eventually even at rest—is an early sign of left-sided heart failure. This sign is characteristically accompanied by Cheyne-Stokes respirations, diaphoresis, weakness, wheezing, and a persistent, nonproductive cough or a cough that produces clear or blood-tinged sputum. As the patient's condition worsens, he develops tachycardia, tachypnea, alternating pulse (commonly initiated by a premature beat), a ventricular gallop, crackles, and peripheral edema.

With advanced left-sided heart failure, the patient may also exhibit severe orthopnea, cyanosis, clubbing, hemoptysis, and cardiac arrhythmias as well as signs and symptoms of shock, such as hypotension, a weak pulse, and cold, clammy skin.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulse pressure, narrowed: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Cardiac tamponade.In cardiac tamponade, a life-threatening disorder, pulse pressure narrows by 10 to 20 mm Hg. Paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds are classic. The patient may be anxious, restless, and cyanotic, with clammy skin and chest pain. He may exhibit dyspnea, tachypnea, decreased LOC, and a weak, rapid pulse. A pericardial friction rub and hepatomegaly may also occur.

Heart failure.Narrowed pulse pressure occurs relatively late with heart failure and may accompany tachypnea, palpitations, dependent edema, steady weight gain despite nausea and anorexia, chest tightness, slowed mental response, hypotension, diaphoresis, pallor, and oliguria. Assessment reveals a ventricular gallop, inspiratory crackles and, possibly, a tender, palpable liver. Later, dullness develops over the lung bases, and hemoptysis, cyanosis, marked hepatomegaly, and marked pitting edema may occur.

Shock.With anaphylactic shock, narrowed pulse pressure occurs late, preceded by a rapid, weak pulse that soon becomes uniformly absent. Within seconds or minutes after exposure to an allergen, the patient experiences hypotension, anxiety, restlessness, and feelings of doom, along with intense itching, a pounding headache and, possibly, urticaria. Other findings include dyspnea, stridor, and hoarseness; chest or throat tightness; skin flushing; nausea, abdominal cramps, and urinary incontinence; and seizures.

With cardiogenic shock, narrowed pulse pressure occurs relatively late. Typically, peripheral pulses are absent and central pulses are weak. A drop in systolic pressure to 30 mm Hg below baseline, or a sustained reading below 80 mm Hg not attributable to medication, produces poor tissue perfusion. Poor perfusion produces tachycardia; tachypnea; cold, pale, clammy skin; cyanosis; oliguria; restlessness; confusion; and obtundation.

With hypovolemic shock, narrowed pulse pressure occurs as a late sign. All peripheral pulses become first weak and then uniformly absent. Deepening shock leads to hypotension, urine output of less than 25 ml/hour, confusion, decreased LOC and, possibly, hypothermia.

With septic shock, narrowed pulse pressure is a relatively late sign. All peripheral pulses become first weak and then uniformly absent. As shock progresses, the patient exhibits oliguria, thirst, anxiety, restlessness, confusion, and hypotension. Extremities become cool and cyanotic; the skin becomes cold and clammy. In time, he develops severe hypotension, persistent oliguria or anuria, respiratory failure, and coma.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Congestive Heart Failure: Congestive Heart Failure - pathophysiology
(The 5-Minute Pediatric Consult)

  • Basic mechanisms:
    • Diminished ejection from the systemic ventricle
      • Cardiomyopathy
      • Pressure load (hypertension, pulmonary hypertension, outflow obstruction coarctation)
    • Normal to increased ejection with diminished systemic output:
      • Severe atrioventricular (AV) valve or semilunar valve regurgitation
      • Left-to-right shunt (atrial septal defect [ASD], ventricular septal defect [VSD], patent ductus arteriosus [PDA])
      • Arteriovenous malformation (AVM)
    • High cardiac output CHF:
      • Anemia and other noncardiovascular causes
  • Neurohormonal activation:
    • CHF leads to activation of the renin–angiotensin–aldosterone system.
      • Vasoconstriction, intended to raise BP, leads to increased oxygen consumption and workload on the heart.
      • Angiotensin II receptors are involved in cardiac myocyte apoptosis pathway.
      • Fluid retention, intended to raise preload and improve cardiac contractility by Frank-Starling mechanism, is ineffective at restoring normal blood flow.
      • Aldosterone activates fibroblasts, causing collagen deposition, which can lead to worsening diastolic function.
    • Sympathetic nervous system activation
  • Right vs. left heart failure:
    • Left ventricles are sensitive to acute volume loads and ischemia.
    • Right ventricles are compliant, but sensitive to pressure loads.

Congestive Heart Failure - etiology

  • Classification:
    • Structural heart disease vs. myocardial disease
    • Acquired vs. congenital:
      • Acquired: Myocarditis, Kawasaki disease, rheumatic heart disease, polyarteritis nodosa, other transient conditions
      • Congenital: Heart defects, cardiomyopathy, inborn errors of metabolism
    • In utero (hydrops):
      • Arrhythmias: Supraventricular tachycardia (SVT), ventricular tachycardia (VT), complete heart block (CHB)
      • Volume overload: AV valve regurgitation, AVM
      • Primary myocardial disease: DCM, HCM, myocarditis
      • Anemia: Rh isoimmune disease, thalassemia, twin–twin transfusion
      • Premature closure of the ductus arteriosus or foramen ovale
    • In neonates:
      • Myocardial dysfunction: Asphyxia, sepsis, myocarditis, hypoglycemia, acidosis, DCM, HCM, ischemia (anomalous left coronary artery from the pulmonary artery), metabolic defects (carnitine deficiency, other inborn errors of metabolism)
      • Outflow obstruction: Aortic stenosis, coarctation of the aorta
      • Volume overload: Large ASD, large VSD, moderate to large PDA, truncus arteriosus, aortopulmonary window, total anomalous pulmonary venous return, AVM
      • Arrhythmias: SVT, VT, or CHB
      • Left heart inflow obstruction: Mitral stenosis, cor triatriatum, pulmonary venous obstruction
    • In infants:
      • Myocardial dysfunction: DCM, HCM, restrictive cardiomyopathy, metabolic disease, mitochondrial disease, glycogen storage disease, myocarditis, Kawasaki disease, anomalous left coronary artery from the pulmonary artery
      • Outflow obstruction: Right or left heart
      • Volume overload: ASD, VSD, PDA, common AV canal defect, partial anomalous pulmonary venous return
      • Secondary causes: Renal disease, hypertension, hypothyroidism, sepsis
      • Arrhythmias: SVT, VT, or CHB
      • Pericardial effusion owing to systemic lupus erythematosus (SLE), juvenile rheumatoid arthritis (JRA), other inflammatory diseases, postpericardiotomy syndrome
    • In childhood and adolescence:
      • Unrepaired congenital heart disease (CHD) with volume and/or pressure overload
      • Repaired CHD with a residual defect that results in volume and/or pressure overload
      • Acquired heart disease: Pericarditis, myocarditis, endocarditis, rheumatic fever
      • Cor pulmonale: Pulmonary hypertension, Eisenmenger syndrome, pulmonary disease
      • Cardiomyopathy: Primary or secondary (anthracyclines, sickle cell anemia, etc.)

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008


 » Next page: Risk Factors for Congestive Heart Failure

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