Heart Failure Flashcards
What does CHF stand for?
Congestive Heart Failure
What is the significance of ejection fraction in heart failure?
It helps classify heart failure as either systolic or diastolic.
Is a decreased ejection fraction below 40% indicative of systolic or diastolic heart failure?
Systolic. This results in a dilated cardiomyopathy and tends to be accompanied by an S3 heart sound.
What is the primary cause of systolic heart failure?
The most common cause for heart failure with reduced ejection fraction (HFrEF; systolic dysfunction) is myocardial infarction or ischemic disease. The most common form of HFrEF is dilated cardiomyopathy. Less common causes of dilated cardiomyopathy are myocarditis and stress cardiomyopathy.
What stage, in the progression of heart failure is defined as a high risk for heart failure, but without structural heart disease or symptoms of heart failure (patients with risk factors for diabetes or hypertension, patients exposed to cardiotoxic drugs)?
Stage A
What stage is considered with structural heart disease, but without signs or symptoms of heart failure (patients with prior myocardial infarction or valvular heart disease with left ventricular enlargement or low ejection fraction)?
Stage B
What stage is considered structural heart disease with prior or current symptoms of heart failure?
Stage C
What stage is considered structural heart failure symptoms at rest or refractory end-stage heart failure?
Stage D
What are the two most common causes of dilated cardiomyopathy?
- Most common primary: idiopathic
- Most common secondary: coronary artery disease leading to ischemic cardiomyopathy
What type of heart failure is characterized by preserved ejection fraction?
Heart failure with preserved ejection fraction (HFpEF) is when the ejection fraction stays above 50% and this is more common in patients with obesity, hypertension, diabetes, and advanced age. The two major forms are hypertrophic and restrictive cardiomyopathy. This form of heart failure tends to be accompanied by an S4.
What is the main difference between left-sided and right-sided heart failure?
- Left-sided heart failure primarily affects pulmonary circulation, leading to pulmonary edema.
- Right-sided heart failure affects systemic circulation, leading to marked hypotension.
________ (right/left) heart failure will present with pulmonary findings (i.e., dyspnea, orthopnea, paroxysmal nocturnal dyspnea).
Left heart failure
Left-heart problems cause a backup of pressure onto the pulmonary circulation, leading to increased pulmonary capillary hydrostatic pressure, thus, transudation of fluid into the alveolar spaces (pulmonary edema). Sometimes this can also cause pleural effusion, therefore these patients usually benefit from diuresis or fluid restriction. Right sided heart Cath with indicate increase pulmonary capillary wedge pressure for left sided heart failure. Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, jugular venous distension, and peripheral edema often presents together when right and left sided heart failure occurs (CHF).
What subtype of hypertrophy occurs with left sided cardiomyopathy leading to heart failure?
Dilated cardiomyopathy results from a direct insult to cardiomyocytes that impairs their contractile function. There is an increase in left ventricular volume that is initially compensated for by the Frank-Starling mechanism and later by eccentric hypertrophy to maintain cardiac output. However, overwhelming wall stress eventually leads to marked impairment in myocardial contractile function, reduced cardiac output, and symptomatic decompensated heart failure. The elevated left ventricular end-diastolic pressure (LVEDP) is transmitted backward to the pulmonary veins and capillaries, leading to pulmonary edema (evidenced by crackles on lung auscultation). Patients with advanced heart failure also develop elevated right atrial pressure (RAP). RAP is representative of central venous pressure and elevation is indicative of underlying volume overload and possible right-sided heart failure (which most commonly occurs secondary to left-sided heart failure due to backward transmission of elevated pressure overloading the right ventricle). In addition, since the underlying insult in dilated cardiomyopathy often directly affects the right ventricular myocardium, concomitant right ventricular failure is particularly likely in these individuals. Together, the collective manifestation is increased LVEDP and increased RAP.
What type of cells are these?
These macrophages are sometimes called “heart failure cells” because of their association with pulmonary congestion with congestive heart failure. Pulmonary congestion with dilated capillaries and leakage of blood into alveolar spaces leads to an increase in hemosiderin-laden macrophages. The brown granules of hemosiderin from breakdown of RBCs.
Hemosiderin laden macrophages are also seen in diffuse alveolar hemorrhage syndromes such as granulomatosis with polyangiitis, anti-GBM disease, and other systemic vasculitides.
Why do patients with heart failure experience nocturia?
Nocturia can also be a manifestation of volume overload, as lying supine for a prolonged period (eg, sleeping in bed at night) may promote edema fluid mobilization into the vasculature, resulting in solute diuresis.
Fill in the blank: In heart failure, the body compensates through mechanisms such as ______ and ______, which is driven by central venous pressure.
In heart failure, the body compensates through mechanisms such as sympathetic nervous system activation and ** fluid retention (RAAS activation)**, which is driven by central venous pressure.
Why can pulmonary edema have an insidious onset with heart failure?
Patients with slowly progressive decompensation (eg, months in this patient) may have minimal or no pulmonary edema. This is because the pulmonary lymphatics can gradually increase fluid outflow rate up to 10 times from baseline when needed, effectively offloading fluid from the pulmonary venous system to the central venous system.
What is one potential complication of untreated heart failure?
Cardiac arrhythmias.
What is the most common sign of right-sided heart failure?
The most common sign of right-sided heart failure (RHF) is peripheral edema (bilateral lower extremity swelling).
JVD is more evident in right or left heart failure?
Right-sided heart failure.
What is the normal range for JVP?
Less than 3 cm.
What organ is enlarged with right-sided heart failure?
Liver, leading to hepatomegaly, called nutmeg liver.
Fill in the blank: The most common cause of heart failure in the United States is ______.
Coronary artery disease.
What is the most common cause of coronary heart disease?
Atherosclerosis is the most common underlying cause of coronary heart disease (CHD). However, in regards to the most common risk factor that leads to CHD, then hypertension (HTN) is often considered the primary driver, as it accelerates endothelial damage and atherosclerotic plaque formation.
What are risk equivlents for coronary heart disease?
ASCVD, Diabetes, and Chronic kidney Disease.
Between age, alcohol consumption, diabetes mellitus, gender, hypertension, obesity, and smoking, which has the greatest progrostication for developing coronary artery disease?
Diabetes mellitus is the most significant predictor of adverse cardiovascular outcomes for this patient. Patients with diabetes have a significant risk of atherosclerotic vascular disease and future cardiovascular events, with all-cause mortality equal to patients with established coronary heart disease (CHD) and prior myocardial infarction. As a result, diabetes is considered a CHD risk equivalent. Diabetes has even more prognostic significance for women. In addition, other CHD risk factors (eg, hypertension, smoking, obesity) have a synergistic effect with diabetes and greatly increase the risk. Strict glycemic control significantly lowers microvascular complications (eg, retinopathy, nephropathy, neuropathy) but does not consistently reduce macrovascular complications (eg, CHD, stroke). As a result, diabetes mellitus remains the most significant CHD risk factor.
How does hypertension play into the development of coronary heart disease?
Hypertension is a well-established risk factor. Blood pressure should be kept <140/90 mm Hg in diabetics, especially in the context of coronary heart disease as diabetes is the most significant risk factor. Many guidelines even recommend a blood pressure <130/80 mm Hg in diabetics with nephropathy and proteinuria ≥500 mg/day.
How does advanced age and male gender impact development of coronary artery disease?
Advanced age and male gender are associated with a higher risk of CHD.
At what age does family history of a close family member become significant in the evaluation of coronary artery disease?
- 50 in males
- 60 in females
At what age in the female demographic does the risk for deveoping coronary heart disease increase?
Until menopause, women generally have a lower
CHD risk than men of the same age because premenopausal women have lower CHD risk due to estrogen protection. CHD risk in women increases sharply after menopause (~age 55-60). Diabetes and metabolic syndrome have a more profound impact on CHD risk in women than in men.
How does alcohol consumption contribute to the deveopment of coronary artery disease?
Moderate alcohol consumption is associated with a reduced risk of adverse cardiovascular outcomes.
To what degree does obesity play into the development of coronary heart disease?
Obesity is associated with other CHD risk factors (eg, hypertension, dyslipidemia). The Framingham Heart Study also showed that obesity is an independent CHD risk factor but is not as significant as diabetes.
How does smoking cessation improve the prevention of coronary heart disease?
Smoking is an important modifiable CHD risk factor. However, most studies have shown that the most significant increase in CHD risk is in patients smoking ≥1 packs daily. The risk of cardiovascular events declines rapidly after smoking cessation and approaches that of nonsmokers in 2-3 years. This patient would benefit from smoking cessation, but her diabetes carries a higher CHD risk.
What makes the most common form of heart failure insidious and why would this matter in terms of what needs to occur in the workup and management?
Most cases of dilated cardiomyopathy leading to heart failure are idiopathic (or primary), but coronary artery disease (CAD) leading to ischemic cardiomyopathy is the most common secondary etiology. Many patients with ischemic cardiomyopathy do not have typical anginal symptoms and initially present with symptoms of heart failure (eg, dyspnea, volume overload). Therefore, all patients with unexplained new-onset heart failure should be evaluated for CAD with stress testing or coronary angiography. Although acute myocardial infarction causes irreversible myocardial death, patients with chronic myocardial ischemia often have viable myocardial tissue with reversibly depressed contractility. In these patients, coronary revascularization can lead to improvement in symptoms, systolic function, and long-term mortality.
What is one common diagnostic test used to assess heart failure?
Echocardiogram. A transthoracic echocardiogram is used to evaluate systolic ejection fraction, diastolic function, and valves.
A 58-year-old man presents to the emergency department to be evaluated for 1 month of shortness of breath and abdominal distention. Past medical history is significant for hypertension, morbid obesity, and obstructive sleep apnea.
The patient takes losartan for his hypertension but does not always take it consistently, and he does not use his continuous positive airway pressure (CPAP) device. Temperature is 36.7°C (98.1°F), pulse is 90/min, blood pressure is 144/95 mmHg, respiratory rate is 18/min, and SpOz is 97% on room air. On physical examination, the lungs are clear upon auscultation. The abdomen is nontender to palpation. There is a fluid wave and dullness to percussion. There is bilateral lower extremity edema. Serum white blood cell count and creatinine are normal. Paracentesis is performed, which shows a serum-ascites albumin gradient (SAAG) of 1.5. What measure could confirm the cause of this patient’s ascites?
Clinical history, physical examination, and the serum-ascites albumin gradient can be used to identify the underlying cause of ascites. Right-sided heart failure can cause ascites with SAAG ≥1.1. Ascites (excessive or abnormal free fluid in the peritoneal cavity) usually occurs due to intra-abdominal pathologies, but it is also associated with many different systemic disease processes. Clinical history, physical examination, and serum-ascites albumin gradient (SAAG) can help determine the underlying etiology of the ascites. This patient with dyspnea, abdominal distension, and a SAAG ≥1.1 g/dL likely has ascites secondary to right-sided heart failure. Hypertension, morbid obesity, and untreated sleep apnea can lead to pulmonary hypertension, which eventually causes right ventricular failure. Elevated right atrial pressures on echocardiogram indicates pulmonary hypertension. Careful history and physical examination can give clues to the cause of ascites. History should focus on chronicity and progression of the ascites. Slowly progressive ascites usually suggests more chronic etiologies, such as cirrhosis, peritoneal malignancy, nephrotic syndrome, or right-sided heart failure. Acute onset ascites usually suggest more acute etiologies, such as portal vein thrombosis, acute pancreatitis, or acute liver failure. Assessing for symptoms of volume overload (e.g. dyspnea, lower extremity swelling) and abdominal pain is important. It is also important to inquire about coexisting diseases, such as malignancy as well as kidney, liver, or heart disease. On physical examination, patients should be assessed for signs of volume overload. Patients with cirrhosis or nephrotic syndrome will generally have systemic volume overload, whereas patients with ascites from acute pancreatitis or portal vein thrombosis generally do not. Patients with cirrhosis may have stigmata of cirrhosis. Significant abdominal tenderness to palpation may be seen in acute pancreatitis, acute liver failure, and spontaneous bacterial peritonitis.
Which hormone is often elevated in heart failure and can be used as a diagnostic marker?
The hormone B-type Natriuretic Peptide (BNP) (or its precursor, N-terminal pro-BNP (NT-proBNP)) is often elevated in heart failure and is used as a diagnostic marker with a high negative predictive value (NPV). A normal BNP (<100 pg/mL) has a high NPV and strongly rules out heart failure.
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Tends to be falsely low in pregnancy, obesity, flash pulmonary edema, and pericardial constriction. BNP may be falsely high in CKD, sepsis, or pulmonary hypertension.
What lung condition tends to occur in patients with heart failure?
Chronic obstructive pulmonary disease (COPD) is often seen with heart failure patients especially when there is an extensive history of smoking. This may convolute treatment and management of these patients when they present with exertional dyspnea. Findings that would indicate lung involvement, that is not secondary to pulmonary edema in the setting of heart failure (which otherwise would warrant diuresis with furosemide) is a lung examination revealing prolonged expiration, wheezing, or pursed lips. Instead these signs are suggestive of obstructive lung disease. COPD can present similarly to decompensated heart failure with exertional dyspnea and is not classically associated with volume overload. These features should prompt pulmonary function testing to evaluate for COPD. Additionally BNP test or an NT-proBNP test is mainly used to help diagnose or rule out heart failure in a person who is having symptoms.
What are the effects of ANP and BNP?
Lowers aldosterone, induces diuresis, decreases renin, and increase capillary permeability.
What physiological condition, often secondary to the comorbidities associated with heart failure, leads to an “artificial” elevation of BNP?
Brain natriuretic peptide (BNP) levels is sometimes elevated with volume overload and other underlying conditions.
Which medication leads to an elevation of BNP? What serum marker is used instead to assess heart function?
Levels of BNP are unreliable in patients taking an angiotensin receptor-neprilysin inhibitor (ARNI) (eg, sacubitril-valsartan) because neprilysin normally degrades BNP; therefore, ARNI use leads to BNP accumulation regardless of volume status.
N-terminal proBNP, not degraded by neprilysin, is a more accurate marker of volume expansion.
List the MOST sensitive symptom for heart failure.
Dyspnea (shortness of breath) on exertion.
What is the clinical sign MOST specific for heart failure?
S3 gallop
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This will sound like “KEN-tuck-Y” where the extra heart sound is early diastole.
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An S3 is a low-frequency heart sound that may be heard during LV diastolic filling. It commonly indicates ventricular enlargement and heart failure (cardiomyopathy) and is best heard with the bell of the stethoscope.
True or False: Edema is a common sign of congestive heart failure.
True. This is a common finding in the lungs with left-sided heart failure and peripherally with right-sided heart failure.
Fill in the blank: Patients with heart failure often experience ______ at night due to fluid redistribution.
Orthopnea. This is a common finding in left-sided heart failure.
Severe shortness of breath that occurs at night while sleeping is due to right or left sided heart failure?
Paroxysmal nocturnal dyspnea (PND) is a sudden, severe shortness of breath that occurs at night while sleeping, causing the patient to wake up gasping for air. Fluid leaks into the alveoli, impairing gas exchange and causing hypoxemia and dyspnea. It is a hallmark symptom of left-sided heart failure and pulmonary congestion. This occurs hours after falling asleep and improves when the patient sits up.
What lifestyle modifications have been recommended for patients with heart failure, have these been shown to reduce hospital readmissions?
Typically patients are limited to 2 liters per day and significant sodium restriction. These may generally be a good measure. However, intensive dietary sodium (eg, 2 g/day) or fluid restriction in patients with heart failure has not been shown to reduce hospitalizations.
In heart failure, what effect does this have on adrenal hormones?
Increases aldosterone!
What role does aldosterone play in heart failure?
It promotes sodium retention and contributes to fluid overload. Elevated aldosterone will deplete potassium.
What medication class is commonly used as first-line treatment for heart failure?
ACE inhibitors.
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In order to manage symptoms patients are advised to reduce salt intake, are often prescribed loop diuretics such as furosemide, and may be given digoxin if these measures do not help abate symptoms. For guideline directed medical therapy the initial therapy is with an ace inhibitor, ARB, or angiotensin receptor-neprilysin inhibitor. Beta blockers such as carvedilol or Metoprolol can also be added as first line medications.
When is isosorbide dinitrate with hydralazine indicated as a first-line medication for heart failure?
The combination of a long-acting nitrate (eg, isosorbide dinitrate) with hydralazine is effective in controlling symptoms of heart failure in patients who cannot take ACE inhibitors or ARBs.
Aside from the most common first-line medication for heart failure, what are the other first line medications that tend to be coupled?
Generally all angiotensin system inhibitors are the first-line medications, such as, sacubitril-valsartan, however, beta blockers (eg, metoprolol succinate), and a loop diuretics (eg, furosemide) are also prescribed for heart failure (HFrEF).
therefore, an should be added to her medication regimen.
What are the secondary medications given to heart failure patients and when are they given?
The secondary medications include aldosterone antagonists (spironolactone or eplerenone). Hydralazine or nitrates can also be added in addition to aldosterone antagonists. Aldosterone antagonists (eg, spironolactone, eplerenone) are given when patients develop New York Heart Association (NYHA) class Il symptoms, or worse. Subjectively, in the clinically relevant sense, the accompanying symptom for New York Heart Association (NYHA) class Il is slight limitation of physical activity, such as dyspnea with climbing stairs. Objectively, in the clinically relevant sense, this is a recent echocardiogram showing left ventricular ejection fraction (LVEF) of 30%.
What is the role of beta-blockers in heart failure management?
These are first-line medications that decrease heart rate and improve cardiac output. They have been shown to improve mortality.
What heart failure medication selective funny current (If) channel inhibitor is given to patients who either have symptoms despite maximum beta blocker medication, or if beta blockers are contraindicated?
Ivabradine
What is the third line medication for heart failure?
SGL2 inhibitors.
What is the overall benefit of digoxin in heart failure?
Reduces hospitalization, but will not improve mortality.
What are the indications for ICD?
When the ejection fraction is below 30-35% or patients experience dangerous rhythms.
Implantable cardioverter-defibrillator therapy is indicated for patients at high risk for ventricular fibrillation or tachycardia.
When is a Bi-ventricular pacer indicated?
When the ejection fraction is < 35% with a LBBB and QRS greater than 120 milliseconds.
What is the purpose of diuretics in the management of heart failure?
To reduce fluid overload and relieve symptoms of congestion. They can be beneficial in both HFpEF and HFrEF.
What medication is used in both HFrEF and HFpEF?
SGLT-2 inhibitors.
Fill in the blank: The New York Heart Association (NYHA) classification system categorizes heart failure into ______ classes.
four
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I: asymptomatic –> ACEi, ARB, ARNI, Beta-bloacker
II and III: moderate exertion causes symptoms –> Spironolactone, hydralazine, nitrates, SGLT-2, ICD, Biventricular pacer
IV: symptoms at rest —> advanced therapies (inotropes like dobutamine or milrinone, LVAD, transplant)
ICD for heart failure is indicated under what set of conditions?
Primary prevention Indications for implantable cardioverter-defibrillator placement are either a prior myocardial infarction & LVEF ≤30% or the patient is at NYHA class II or III symptoms with LVEF ≤35%. Secondary prevention indications are either prior VF or unstable VT without reversible cause or prior sustained VT with underlying cardiomyopathy.
Biventricular pacer is indicated under what circumstances?
The current guidelines recommend biventricular pacing devices for patients in sinus rhythm who meet all of the following criteria: 1) LV ejection fraction <35%, 2) NYHA class II, Ill, or IV heart failure symptoms (ie, the presence of any symptoms), and, 3) Left bundle branch block with QRS duration >150.
What is an important non-pharmacological treatment for heart failure?
Cardiac rehabilitation
True or False: Heart failure can be completely cured.
False
Which heart failure medications are known to decrease mortality?
ACEi (lisinopril), BBs (metoprolol), MRAs (spironolactone).
Acute worsening of new or underlying heart failure is called … ?
Acute heart failure exacerbation.
What are common risk factors for acute heart failure exacerbation?
Medication noncompliance, Dietary indiscretion, infection, trauma, surgery, ischemia, arrhythmias, and NSAIDs.
Acute decompensated heart failure (ADHF) results from a critical elevation in intracardiac filling pressures that most commonly occurs due to left ventricular (LV) systolic and/or diastolic dysfunction (eg, coronary ischemia, hypertensive cardiomyopathy). Other causes include valvular disease and marked elevations in preload (eg, excessive volume resuscitation) or afterload (eg, severe hypertension).
What are the clinical features of acute heart failure exacerbation?
Dyspnea, peripheral edema, exercise intolerance, weight gain, rales, and elevated jugular venous pressure (JVP).
What is the diagnostic approach for acute heart failure exacerbation?
Clinical diagnosis based on history, physical exam, elevated JVP, and CXR showing pulmonary edema.
What are the primary components of management for acute heart failure exacerbation?
- Respiratory support: Supplemental O₂ with NIPPV/intubation if needed.
- Diuretics: IV furosemide at 2.5x home dose (monitor for renal failure, low BP, and low K+).
- Afterload reduction: Nitrates or hydralazine.
- Inotropes: Dobutamine or milrinone for refractory cases.
Early therapeutic goals include hemodynamic stabilization, improved oxygenation (ie, with supplemental oxygen or positive pressure ventilation), and optimization of volume status. Intravenous diuretics (eg, furosemide) are an important part of initial therapy as they reduce intravascular volume, lower intracardiac filling pressures, and improve pulmonary edema. Beta blockers (eg, metoprolol) are important in the management of chronic heart failure due to LV systolic dysfunction. They are also used in certain patients with tachyarrhythmias or ST-elevation myocardial infarction. However, they are usually contraindicated in ADHF due to the negative inotropy and chronotropy causing a potential worsening of pulmonary edema. The addition of an intravenous vasodilator is recommended in patients with acute decompensated heart failure (ADHF) who have an inadequate response to initial diuretic therapy. Nitroglycerin is most commonly used; as primarily a venous dilator, it leads to a rapid decrease in cardiac preload, resulting in reduced intracardiac filling pressures and improvement in pulmonary edema. Nitroprusside is less commonly used due to the risk of adverse effects (eg, cyanide toxicity and severe hypotension); it decreases intracardiac filling pressures through balanced vasodilation and reductions in both cardiac preload and afterload because intravenous vasodilator therapy often results in rapid improvement of acutely symptomatic pulmonary edema, it is indicated right away (prior to or instead of intravenous diuretics) in patients with “flash” pulmonary edema due to severe hypertension (>180/120 mm Hg) (ie, hypertensive emergency). Milrinone is a selective phosphodiesterase-3 inhibitor that causes positive inotropy as well as reductions in preload and afterload. It can be useful for ADHF due to LV systolic dysfunction; however, it is associated with increased risk of hypotension and atrial or ventricular arrhythmia, and is typically reserved for severe ADHF that is refractory to other management. Intravenous vasodilators (eg, nitroglycerin) reduce intracardiac filling pressures and are recommended in patients with acute decompensated heart failure who have an inadequate response to initial diuretic therapy. In addition, they are indicated as initial therapy (prior to or instead of intravenous diuretics) in patients with “flash” pulmonary edema due to severe hypertension. Transthoracic echocardiogram should be performed in patients with acute decompensated heart failure (ADHF) of uncertain etiology. In this patient it will allow for confirmation of suspected left ventricular dysfunction (ie, hypertensive cardiomyopathy) and provide an assessment for valvular abnormalities (eg, mitral regurgitation) that may contribute to ADHF.
What is the acronym ‘NO LIP’ for the management of acute heart failure exacerbation?
N - Nitrates (afterload reduction).
O - Oxygen (respiratory support including NIPPV, intubation if required).
L - Loop diuretics (IV furosemide at 2x the home dose).
I - Inotropes (e.g., dobutamine, milrinone for refractory cases).
P - Positioning (upright to reduce preload).
What are the two general causes of high output heart failure?
- Elevated cardiac output secondary to increased volume status.
- Elevated cardiac output secondary to decreased peripheral vascular resistance.
What are the etiologies of high output heart failure?
- Severe anemia
- Hyperthyroidism
- Arteriovenous shunting (e.g., PDA, AVF)
- Beriberi
- Sepsis
- Pregnancy
- Erythroblastosis fetalis
What is the most common cause of high output heart failure?
Obesity
What MSK pathology can cause high output heart failure?
Paget’s disease of bone is a musculoskeletal (MSK) pathology that can cause high output heart failure. This condition leads to the formation of structurally weak and highly vascularized bone, resulting in increased blood flow through these AV connections and arteriovenous (AV) shunting. The increased vascular demand places a significant burden on the heart, leading to high output heart failure in severe cases.
What is the pathophysiology in Beriberi and why does this cause high output heart failure?
This overarchingly is due to the profound effects of thiamine (vitamin B1) deficiency, as thiamine deficiency has a significant effect on the energy metabolism, biochemically. Thiamine is a crucial cofactor for several enzymes in carbohydrate metabolism, including, Pyruvate dehydrogenase (converts pyruvate to acetyl-CoA), Alpha-ketoglutarate dehydrogenase (part of the Krebs cycle), and Transketolase (in the pentose phosphate pathway). A lack of thiamine leads to impaired energy production (ATP synthesis), especially in energy-demanding tissues like the myocardium and skeletal muscles. This results in profound myocardial dysfunction and vasodilation due to reduced vascular tone regulation. Then what occurs is significant increase in nitric oxide production and impaired vascular smooth muscle energy metabolism. The vasodilation decreases systemic vascular resistance (SVR), leading to low afterload and a compensatory increase in cardiac output to maintain perfusion. Vasodilation causes pooling of blood in the periphery, which increases venous return and places additional stress on the heart. This increased preload further contributes to volume overload in the heart. Prolonged thiamine deficiency can lead to wet beriberi, characterized by direct myocardial depression (cardiomyopathy), reduced stroke volume due to impaired cardiac energy metabolism, and this combination leads to fluid overload and symptoms of heart failure. Symptoms include fatigue and dyspnea (due to volume overload and reduced cardiac reserve), peripheral edema, orthopnea and paroxysmal nocturnal dyspnea, bounding pulses, warm extremities (due to peripheral vasodilation), and tachycardia. The two types of of Beriberi depend on the system involved. Wet Beriberi has cardiac involvement with symptoms of high output heart failure (dyspnea, edema, tachycardia), while Dry Beriberi has neurological involvement (e.g., peripheral neuropathy, muscle weakness).
What are the clinical features of high output heart failure?
- Heart failure symptoms such as elevated JVP and peripheral and pulmonary edema.
- Hyperdynamic circulation (increased PP, warm extremities, systolic flow murmur).
- Laterally displaced PMI
What would be the effect of the systemic vascular resistance in high output heart failure?
Lowered, especially with AVMs.
What are the ECHO finding associated with high output heart failure?
- Dilated ventricles (LV and RV)
- Dilated inferior vena cava
- Increased cardiac index
What is the management approach for high output heart failure?
Treat the underlying condition and use diuretics as needed to manage volume overload.
What is the general definition of cor pulmonale?
Isolated right heart failure caused by advanced pulmonary hypertension due to a mechanism other than left heart failure.
What are the clinical features of cor pulmonale?
Exertional dyspnea, angina, syncope, JVD, peripheral edema, prominent S2, RV heave, and hepatomegaly.
What are the diagnostic findings in cor pulmonale?
ECG: RBBB, RVH, right axis deviation; TTE: RV dilation and possible tricuspid regurgitation; Confirmed with right heart catheterization.
What is the management approach for cor pulmonale?
Diuretics and treatment of the underlying pulmonary hypertension.
What are the most common precipitating factors for acute heart failure exacerbation?
Ischemia, infection, arrhythmias, medication noncompliance, and excessive salt or fluid intake.
Why is nitrates’ role important in acute heart failure exacerbation?
Nitrates reduce afterload and preload, improving symptoms of pulmonary congestion and dyspnea.
What is the role of inotropes in acute heart failure exacerbation?
Inotropes like dobutamine and milrinone are used in refractory cases to improve cardiac output and perfusion.
What form of heart failure occurs after severe emotional distress (high catecholamines) ?
Takotsubo
This is stress cardiomyopathy and presents with chest pain and symptoms of acute HF. This condition is diagnosed after a full history and physical exam followed by and ECG (which may show changes) and troponins (which may also be elevated). A TTE is used to confirm the diagnosis as it often shows an apical ballooning.
Treatment is supportive, as cardiac function often returns.
What are patients with chronic heart failure (HF) at risk for due to the progressive nature of the disease?
Patients with chronic HF are at risk for frequent hospitalization and hospital readmission due to the progressive nature of the disease, burdensome lifestyle modifications, and complex medication regimens.
What are examples of highly effective strategies associated with reduced hospitalization in heart failure patients?
- In-person patient monitoring (home or clinic setting) and medication management by nurse case managers.
- Multidisciplinary HF clinics featuring team-based care (eg, cardiologist, pharmacist, nurse, social worker).
- Enhanced transitions of care after hospital discharge (eg, directly coordinating care with outpatient teams).
- Early postdischarge follow-up (<1-2 weeks) to assess fluid status and provide education.
- Building of patient skills for self-management with longitudinal, patient-centered approaches (eg, motivational interviewing, personalized HF action plan), including useful skills such as weight monitoring, daily symptom (eg, edema) checks, and dietary education.
What are the features of multidisciplinary HF clinics?
Multidisciplinary HF clinics feature team-based care, including cardiologists, pharmacists, nurses, and social workers.
What is the importance of enhanced transitions of care for HF patients after hospital discharge?
Enhanced transitions of care involve directly coordinating care with outpatient teams to reduce the risk of readmissions.
Why is early postdischarge follow-up important for HF patients?
Early postdischarge follow-up (within 1-2 weeks) assesses fluid status, provides education, and helps prevent readmissions.
How can patient skills for self-management in HF be improved?
Patient skills for self-management can be improved through longitudinal, patient-centered approaches like motivational interviewing, personalized HF action plans, weight monitoring, daily symptom checks, and dietary education.
Why is physician counseling alone insufficient to reduce HF hospitalizations?
Physician counseling must be comprehensive, addressing multiple aspects of HF care (eg, diet, symptoms) rather than focusing on a single component (e.g., dietary sodium restriction).
What is the role of outpatient intravenous diuresis in HF management and is this an effective method for reduction for future hospitalizations?
Outpatient intravenous diuresis may be used for acute decompensated HF but is not effective in preventing HF hospitalizations in most patients.
Why are remote data collection strategies less effective than in-person monitoring in HF management?
Remote data collection (e.g., standing lab orders, remote BP monitoring) provides useful information but is less comprehensive and less effective compared to in-person monitoring and medication adjustment by clinical providers.
What is the educational objective for reducing hospitalization in HF patients?
The risk of hospitalization in chronic HF can be mitigated through multidisciplinary strategies targeting the home environment and health literacy, with in-person monitoring and nurse-led medication management being highly effective.
