Heart Failure
Ivabradine
A selective sinus node inhibitor -Used to treat *chronic SYSTOLIC heart failure* -Slows HR without decreasing contractility -Inhibits the *SA node funny current* in phase 4 -Used in patients already on max dose of beta blocker still presenting with high HR -Has limited evidence of decreased mortality and hospitalizations
Metolazone
A thiazide-like diuretic that inhibits Na-Cl reabsorption in the distal tubule -Used to ENHANCE effects of loop diuretics in treatment of *heart failure* -Results in vigorous diuresis -Side effects include additional fluid and potassium loss in conjunction with loop diuretics
S3
Abnormal heart sound associated with HIGH left atrial pressure -Seen in *left heart failure*, *mitral regurgitation*, and *tricuspid regurgitation* -Can be normal in childhood and athletic young adults
S4
Abnormal heart sound associated with STIFF left ventricle -Seen in *diastolic heart failure*, *myocardial ischemia*
Takotsubo
Type of *nonischemic cardiomyopathy* -Occurs after *severe emotional distress* -There is markedly *reduced ejection fraction* -The apex of the heart does not contract, leading to dilation and "ballooning" of the left ventricle -Increases CK, MB, troponin, and ECG changes -Appears on MI like an *anterior MI* but on angiogram there is NO coronary artery disease -Usually recovers in 4-6 weeks -Also called apical ballooning cardiomyopathy -Common in Japan
Dilated cardiomyopathy
Type of SYSTOLIC heart failure *with LV cavity dilation* -Myocytes undergo *eccentric hypertrophy* where myocytes get longer and add in series to result in a NORMAL wall thickness but larger diameter -Hypertrophy occurs in response to *volume overload*
Beta amyloid
Type of amyloid protein that is associated with *Down syndrome* and *Alzheimer's disease* -Appears in the brain as plaques and in cerebral vessels -Can lead to intraparenchymal hemorrhage
AF
Type of amyloid protein that is associated with *familial amyloidosis* -Variant of the *transthyretin hormone* -Transthyretin amyloidosis is a slowly progressive condition -Protein deposits most frequently occur in the peripheral nervous system, resulting in peripheral neuropathy -ANS and CNS can also be affected -Amyloid can also deposit in the heart, kidneys, eyes, and gastrointestinal tract
A Cal
Type of amyloid protein that is associated with *medullary carcinoma of the thyroid* and *pancreatic islet adenoma* -NOT systemically distributed -Is a peptide hormone precursor
AL
Type of amyloid protein that is associated with *multiple myeloma* and *B cell malignant lymphomas* -Protein is composed of *Ig light chains* produced by the neoplastic cells -Protein is deposited in the heart, GI tract, spleen, kidneys, and tongue
AA
Type of amyloid protein that is associated with secondary amyloidosis due to *rheumatoid arthritis* -Progressive accumulation leads to symptoms of *congestive heart failure*
Restrictive heart disease
Type of cardiomyopathy where there are infiltrates in the myocardium -Characterized by *impaired ventricular filling* and *DECREASED LV compliance* -Includes *sarcoidosis* (granulomas) and *amyloidosis* (amyloid deposits) -Classic imaging findings show normal left ventricular function/size and bi-atrial enlargement -Presents with *dyspnea* and *SEVERE diastolic RIGHT heart failure*
Restrictive heart disease
Type of cardiomyopathy where there are infiltrates in the myocardium -Heart cannot relax and fill, leading to *severe diastolic dysfunction* -*Ejection fraction and left ventricular volume is NORMAL* -Restricted filling INCREASES atrial pressure leading to a *dilated right and left atria*
Restrictive heart disease
Type of cardiomyopathy where there are infiltrates in the myocardium -Substances that infiltrate the myocardium can disrupt electrical activity -Rhythms may show *arrhythmias* leading to SUDDEN DEATH or *AV block* -ECG findings may show *low voltage* because myocardium is thickened from infiltrates, NOT hypertrophy
Diastolic
Type of chronic heart failure -Presents with dyspnea, orthopnea, paroxysmal noctural dyspnea, increased JVP, rales, and pitting edema (same as systolic heart failure) -Exact cause is unknown but most cases have *concentric hypertrophy* -Has many associated conditions (age, diabetes, HTN) -There are NO direct therapy for this type of CHRONIC heart failure -Therapies include treating any underlying conditions (HTN, diabetes), monitoring for symptoms, and diuretics
Diastolic
Type of chronic heart failure , causes include: 1. Restrictive cardiomyopathies 2. Hypertrophic cardiomyopathies 3. Myocardial infarction 4. *HTN* 5. Aortic stenosis 6. *Pericardial constriction/tamponade*
Systolic
Type of chronic heart failure characterized by *low flow symptoms* -Presents with dyspnea, orthopnea, paroxysmal noctural dyspnea, increased JVP, rales, and pitting edema (same as diastolic heart failure) -About 50% are idiopathic, non-ischemic -Causes include chemo, HIV, alcoholic, sarcoidosis, tachycardia-mediated, familial, viral, and peri-partum
Biventricular pacemaker
Device enabling ventricles to beat together so that more blood is pumped out of the heart -Used to treat *chronic SYSTOLIC heart failure* -Also called cardiac resynchroniztion therapy
Systolic
Type of chronic heart failure characterized by *low flow symptoms* (cool extremities, cachexia, confusion) and *DECREASED contractility* -Caused by *chronic activation of RAAS and sympathetic beta 1 stimultaion* -Presents with *low stroke volume* that results in *HIGH end diastolic volume/pressure* and and VERY HIGH end systolic volume (blood can't get OUT) -*Ejection fraction is reduced* -There are MANY therapies for CHRONIC heart failure including ACE inhibitors, beta blockers, aldosterone antagonists, defibrillators, and pacemakers
Systolic
Type of chronic heart failure characterized by *low flow symptoms*, common causes include: 1. *Myocardial infarction*: myocytes are replaced by scar tissue resulting in ischemic cardiomyopathy 2. *Mitral/aortic regurgitation* 3. Familial/viral *dilated cardiomyopathies*
Diastolic
Type of chronic heart failure where there is decreased *left ventricular compliance and lusitropy* (blood can't get IN) -Stroke volume and *end diastolic volume DECREASE * -End diastolic pressure INCREASES due to stiff ventricle -*Ejection fraction is NORMAL* -Does NOT has low flow symptoms
High output
Type of heart failure that occurs when the heart is in overdrive -Occurs in cases like *severe anemia, thyroid disease, beriberi* (B1 deficiency), and *postsurgical AV fistulas* -Exact mechanism is unclear but there is *decreased LV filling time*, LOW systemic vascular resistance, and HIGH left atrial pressure -Defining characteristic is *high cardiac output* (only type of heart failure with this hallmark) -Presents with heart failure symptoms despite the absence of the low output (elevated JVP, pulmonary edema, etc)
Chronic
Type of heart failure that presents with clear lungs, NO pitting edema, flat JVP, and a euvolemic appearance -Treatment goal is *reduced mortality/hospitalizations* -Systolic heart failure is treated with ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists, neprilysin inhibitors, and ivabradine -There are no specific therapies for chronic diastolic heart failures
Acute
Type of heart failure that presents with pulmonary edema, pitting edema, increased JVP, and a congested/swollen appearance (*fluid overload*) -Acute exacerbations include *high salt intake*, *poor medication compliance*, *NSAIDs*, infection/trauma/surgery (activates the sympathetic NS), and ischemia (decreased CO) -Treatment goal is *symptom relief* -Treated with *afterload/preload reducers* including loop diuretics, nitroglycerine, and ionotropes (same for systolic AND diastolic heart failure)
Concentric
Type of hypertrophy where there is *pressure overload* causing decreased compliance (STIFF ventricle) -Pressure overload can be caused by HTN, aortic stenosis -Often seen in *diastolic heart failure* -Can also lead to *fibrosis*
Eccentric
Type of hypertrophy where there is *volume overload* causing increased diameter -Often seen in *systolic heart failure* -Can also lead to *fibrosis*
Hydralazine
Vasodilator medication that is used in conjunction with *nitrates* for acute AND chronic heart failure -Nitrates reduce preload and hydralazine reduces afterload -Improves symptoms acutely and reduces mortality chronically -Combination has been largely replaced by ACE inhibitors -Some studies suggest benefit in *black patients*
Afterload reducers
Goal of treatment in heart failure -Medications that do this include: 1. *ACE inhibitors* (Captopril, Lisinopril, Enalapril) 2. *Angiotensin receptor bockers* (Losartan, Valsartan) 3. *Hydalazine* 4. *Nitrates* 5. *Inotropes* (Milrinone)
Preload reducers
Goal of treatment in heart failure -Medications that do this include: 1. Diuretics (don't help with survival) 2. Aldosterone receptor antagonists 3. Nitrates/natriuretic peptides (like Niseritide)
Inotropes
Group of medications that increase contractility -Only used to *systolic heart failure* (diastolic heart failure has normal contractility) -*Activate beta1 pathway* in myocytes -Leads to increased HR and contractility -Can also activate *beta2* pathways in smooth muscle leading to vasodilation and hypotension -Associated with INCREASED mortality -Only given by IV in sick patients under monitored conditions
Low flow symptoms
Group of symptoms of heart failure that occur when the left ventricle is not pumping enough blood forward ("forward failure") -Includes *loss of appetite* (poor gut perfusion), *weight loss* (cachexia), *confusion*, *cool extremities*, and *a narrow pulse pressure* -Seen only with low CO (*SYSTOLIC heart failure*)
CHF
Heart failure associated with myocardial dysfunction that includes signs and symptoms of *volume overload* -Signs of congestion include pulmonary edema, ascites, and peripheral edema, dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Epinephrine
Inotrope used to treat *systolic heart failure* that is highly dose dependent -LOW doses have effects of *beta 1 and beta 2 agonists* leading to increased HR, contractility, and vasodilation -HIGH doses have effects of an *alpha agonist*, leading to vasoconstriction -Given by IV
Dopamine
Inotrope used to treat *systolic heart failure* that is highly dose dependent -LOW doses have effects of a *dopamine agonist*, leading to renal vasodilation -MEDIUM doses have effects of a *beta1 agonist*, leading to increased HR and contractility -HIGH doses have effect of an *alpha agonist*, leading to vasoconstriction -Does NOT cross the blood brain barrier (no CNS effects) -Given by IV
Amyloidosis
Major cause of restrictive heart disease -Amyloid proteins deposit in the cardiomyocytes in a *speckled* pattern -Appears on pathology as a homogenous pink material -Appears with apple green birefringence color when stained with Congo red stain -Can occur in various forms (primary, secondary) -Presents with NORMAL ejection fraction, INCREASED atrial pressure, bi-atrial enlargement, INCREASED wall thickness, and *low voltage of ECG* -Can be caused by *aging*
Sarcoidosis
Major cause of restrictive heart disease -Commonly forms granulomas in the hilar region of the lung -Extra-pulmonary locations of granuloma formation is cardiac tissue
Hypereosinophilic syndrome
Major cause of restrictive heart disease and common cause of death -The acute phase shows *myocarditis* that is often asymptomatic -In the chronic phase, there is *endocardial fibrosis* and myocyte death -Inflammation from the endocardial fibrosis can lead *thrombus* formation and *embolic stroke*
Endocardial fibroelastosis
Major cause of restrictive heart disease in infants -*Endocardial* thickening that occurs in infants -Myocardium is also thickened -There is proliferation of *fibrous collagen* and *elastic fibers* -Differs from restrictive heart disease in that it can have *LOW ejection fraction* and *dilated left ventricle*
Fabry disease
Major cause of restrictive heart disease, lysosomal storage disease -Causes deficiency of *alpha galatosidase A* resulting in accumulation of *ceramide trihexoside*
RAAS
Mechanism to maintain a balance of sodium and water and a healthy blood volume and pressure -Net result is to increase Na/water retention, preload, vascular resistance, and afterlaod -Blocked by *ACE inhibitors* (end in -pril) and *angiotensin receptor blockers* (end in -sartan) -Both classes DECREASE mortality and hospitalizations -Side effects include *hyperkalemia* and *renal failure*
Nitrates
Medication that causes *venous dilation* -Used to treat *heart failure* -Functions to pool more blood in the venous system to take blood away from the left ventricle -Lowers end diastolic volume (preload) and left atrial pressure -There is less pulmonary edema and improved dyspnea -Side effects include *headache* from meningeal vasodilation, *flushing*, and *hypotension*
Bradykinin
Metabolite that causes *dry cough* and *angioemdea* when taking *ACE inhibitors* -ACE inhibitors block its conversion to inactive metabolites, leading to INCREASED levels in the body -Dry coughs occur in ~10% of patients -Angioedema is caused by vasodilatory effects and can be lifethreatening if it affects the larynx
Sacbitril
Neprilysin inhibitor to increase Na/water excretion, cause vasodilation, and reduce sympathetic tone -Used to treat *chronic SYSTOLIC heart failure* -Neprilysin is an enzyme that degrades ANP and BNP -Inhibition leads to INCREASED ANP and BNP
Sodium retention
Response to *low effective circulating volume* (volume effectively perfusing tissue) from heart failure -The sympathetic nervous system, renin-angiotensin-aldosterone system, and ADH stimulate increased Na reabsorption -Leads to water reabsorption that increases total volume in the body -Does NOT correct low effective circulating volume
Systemic vascular resistance
Response to low CO from heart failure -The sympathetic NS and renin-angiotensin-aldosterone system cause vasoconstriction -*Vascular resistance is always high* -This results in a BP that may be high but also can be low -Depends on combined changes in CO and vasoconstriction (*BP=COxTPR*)
Hepatojugular reflux
Sustained, abnormal distention of jugular veins observed with pressure on the abdomen -Normally raises JVP *1-3 cm* -With a failing right ventricle, increase is GREATER
PMI
The point farthest lateral and inferior from the sternum at which the cardiac impulse can be felt -INCREASED in heart failure due to enlarged heart
Nesiritide
A recombinant BNP medications -Causes *vasodilation*, *decreased afterload*, and *increased CO* -Failed to show benefit in clinic trials and is rarely used
ICD
An implantable cardiac defibrillator -Used to treat *chronic SYSTOLIC heart failure* -Improves mortality in appropriate patients -Prevents development of arrhythmias like ventricular tachycardia -Can prevent sudden cardiac death in some patients -Implantation carries risk of bleeding, infection, and innapropriate shocks
Entresto
An oral combination of *sacubitril* (neprilysin inhibitor) and *valsartan* (angiotensin receptor blocker) -Used to treat *chronic SYSTOLIC heart failure* -Side effects include *hypotension, hyperkalemia, and ANGIOEDEMA*, a serious adverse effect -Neprilysin degrades *bradykinin* so increased levels of bradykinin can result in significant vasodilation -CANNOT be given with ACE inhibitors due to similar effects on bradykinin -Decreases mortality and hospitalizations
NSAIDs
Cause of acute exacerbation of heart failure -Medications inhibit COX pathway which DECREASES prostaglandins -Prostaglandins normally help to maintain renal perfusion -Less renal perfusion causes salt/water retention and increase in volume
Dobutamine
Beta1 agonist and weak beta 2 agonist that is an inotrope used to treat *systolic heart failure* -Functions to increase HR and contractility and weakly increase vasodilation -Can cause hypotension -Has similar effects as milrinone -Given by IV
Levosimendan
Calcium sensitizer and INOTROPE that can be administered intravenously (IV) to patients with *acute decompensated congestive heart failure* -Enhances myocardial contractility without increasing oxygen requirements -Causes coronary and systemic vasodilation
Heart failure
Cardiac condition where there is an impaired ability of the heart to pump blood -Diagnosed by typical signs/symptoms (rales, elevated JVP, pitting edema, pulmonary edema) and *elevated BNP* -Heart catheterization is also used for diagnosis to measure left/right ventricular end diastolic pressure
Heart failure
Cardiac condition where there is an impaired ability of the heart to pump blood -Hallmark is *low cardiac output* -Pressure RISE inside of the cardiac chambers that are failing -Histology shows *hemosiderin laden macrophages* -Symptoms include *pulmonary edema*, *pitting edema*, and *INCREASED JVP*
Peri-partum
Cause of *nonischemic cardiomyopathy* -Occurs late in pregnancy or early post-pregnancy -Exact cause is unknown and is likely multifactorial -Women are often advised to avoid future pregnancy
Tachycardia
Cause of *nonischemic cardiomyopathy* -A constant, rapid HR for weeks/months leads to depression of the left systolic function -Reversible with slowing heart rate
Alcohol
Cause of *nonischemic cardiomyopathy* -Chronic consumption can cause cardiomyopathy -Due to toxic metabolites -Can recover with cessation of alcohol
Chemotherapy
Cause of *nonischemic cardiomyopathy* associated with *anthracyclines* (antitumor antibiotic) -Also associated with *doxorubicin* and *daunorubicin*
Familial
Cause of *nonischemic cardiomyopathy* associated with genetic mutations in the *sarcomere proteins*, including the beta myosin heavy chain, alpha myosin heavy chain, or troponin -Many mutations are autosomal dominant -X-linked, autosomal recessive can also occur
Viral
Cause of *nonischemic cardiomyopathy* that is associated with *Coxsackie virus*, *influenza*, and *adenovirus* -Viruses enter the myocyte and cause myocarditis that develops into cardiomyopathy -Myocarditis phase can go undiagnosed -There is no specific therapy
Salt intake
Cause of acute exacerbation of heart failure -Increases plasma osmolarity which increases *ADH* -This increaes free water which leads to normal plasma Na but increased volume -Increased volume can lead to complications of heart failure including pulmonary edema and hospitalization -Eventually, RAAS and ADH are deactivated with increased volume, leading to increased urine output
Loop diuretics
Class of diuretics that inhibit the Na-K-CL pump in the *ascending loop* of Henle -Used to treat *heart failure* -Results in salt and water excretion to releive congestion -IV is better than PO because PO can cause gut swelling -Side effects include *hypokalemia* and *volume depletion* leading to renal failure and hypotension -Includes *furosemide*, bumetanide, torsemide, and ethacrynic acid -All drugs are sulfonamides EXCEPT ethacrynic acid
Beta blockers
Class of medications that block beta1 adrenergic receptors in the heart, used to treat *CHRONIC systolic heart failure* -Not used in ACUTE heart failure because it can worsen CO and symptoms -Specific agents used in CHRONIC heart failure includes *metoprolol*, *carvedilol*, and *bisoprolol* -Decreases mortality and hospitalizations
Rales
Classic lung auscultation finding in *heart failure* -Fluid-filled alveoli pop open with inspiration -Lungs can sometimes be CLEAR in CHF due to increased lymphatic drainage
Elevated JVP
Classic symptom of heart failure caused by back-up of fluid from the right side of the heart -Determined by having patient lay at 30 degree angle and observing the "double bounce" caused by the atrial and ventricular waves of contraction -JVP normally equals *6-8 cm* -JVP is an indicates of *central venous pressure*
Left ventricular dysfuction
Common cause of heart failure -#1 cause is *CAD* -Also can be caused by viruses, alcohol, chronic tachycardia, stress, chemotherapies, and Chagas disease
Pitting edema
Complication of heart failure -Failure of the left ventricle causes backup of blood throughout the heart and venous system (right arial pressure=central venous pressure) -Causes capillary leak of fluid into the interstitium due to *high hydrostatic pressure* -Fluid leaks from the capillaries into tissue, which is pulled to lower extremities via gravity
Pulmonary edema
Complication of heart failure -There is less blood pumped out, leaving to more left behind and a higher pressure in the ventricle -A stiffer ventricle can lead to high pressure -Leads to backup in the pulmonary circulatory system and *increased hydrostatic pressure* in the pulmonary capillaries -When lying *supine*, there is INCREASED venous return to the heart, leading to redistribution of blood volume that transfers fluid from the lower extremities to the lungs (WORSENS pulmonary congestion and breathing) -Shows on CXR with *congestion*, but can be normal due to increased lymphatic drainage
Right heart failure
Complication of restrictive heart disease -Right ventricle is more sensitive to impaired filling -Presents with *elevated JVP*, lower extremity edema, liver congestion, and may lead to *cirrhosis* (*nutmeg liver*) -Can look like liver disease BUT presents with elevated JVP
ANP
Hormone that is released when there is atrial stretch from atrial myocytes -Secretion is increased by volume/pressure overload -Acts as a *vasodilator* and constricts renal efferents and dilates afferents (INCREASES GFR) -Increases *diuresis* -OPPOSITE effect of RAAS system
BNP
Hormone that is released when there is ventriclar stretch from ventricular myocytes -Secretion is increased by volume/pressure overload -Acts as a *vasodilator* and constricts renal efferents and dilates afferents (INCREASES GFR) -Increases *diuresis* -OPPOSITE effect of RAAS system -Can be used to diagnose dyspnea, where HIGH levels indicate heart failure
Left ventricle
Location of heart failure where there is *increased end diastolic pressure in the left ventricle* (systolic pressure may be unchanged) -There is less blood pumped out, leaving to more left behind and a higher pressure in the ventricle -A stiffer ventricle can lead to high pressure -Systolic pressure depends on contractility but can be low -End diastolic volume is always HIGH (hallmark), which causes *high left atrial pressure* and *pulmonary pressure* -Results in *dyspnea* and *pulmonary edema*
Hemochromatosis
Major cause of *dilated cardiomyopathy*, but can rarely cause *restrictive heart disease* -There is *iron excess* in the body -Appears with *golden brown granules* and *blue* color with prussian blue stain
Hypereosinophilic syndrome
Major cause of restrictive heart disease -*Primary* disease is a neoplastic disorder -*Secondary* disease is a reactive process leading to eosinophilic overproduction due to cytokines, occurs in parasitic infection (*Ascars lumbricoides*) or in some tumors/lymphomas -Can be *idiopathic*
Loeffler's syndrome
Major cause of restrictive heart disease -Hypereosinophilic syndrome with a eosinophilic infiltration of organs -Also presents with *eczema* and *lung fibrosis*
Radiation
Major cause of restrictive heart disease -Restrictive cardiomyopathy occurs due to fibrous tissue accumulation leading to *diastolic dysfunction* -Can acutely cause inflammation -Histologically shows *fibroblast recruitment*, *extracellular matrix deposition*, and *collagens and fibronectin* -Pericarditis can occur acutely after therapy -Long term effects include pericardial disease, CAD, valvular disease, and conduction abnormalities
Amyloidosis
Major cause of restrictive heart disease -SYSTEMIC disease is caused by *multiple myeloma* -SENILE cardiac disease is caused by individuals >70 years old -Senile disease has a better prognosis
Digoxin
Only available ORAL inotrope, can be administered acutely OR chronically -Used to treat *systolic heart failure* -INCREASES CO -Improves symptoms and quality of life in heart failure patients -Has NO established mortality benefits
Digoxin
Only available ORAL inotrope, can be administered acutely OR chronically -Used to treat *systolic heart failure* -Showed to have no mortality benefit -Used in *systolic HF* and is not effective for diastolic HR (~50% of cases) -Carries significant risk of side effects -*Inhibits the Na-K ATPase pump* leading to more Na in cells and more Ca in cells -Also *suppresses the AV node conduction* by suppressing parasympathetic tone to the heart (can be used to slow HR in rapid atrial fibrillation)
Milrinone
Phosphodiesterase 3 inhibitor and inotrope used to treat *systolic heart failure* -PD3 breaks down cAMP in myocytes, so this medication *INCREASES cAMP* to increase contraction and vasodilation -Leads to increased contractility, vasodilation, and hypotension -Has similar effects as dobutamine -Given by IV
Heaves
Physical exam finding associated with *ventricular hypertrophy* -Heaves on the right side indicate LEFT ventricular hypertrophy -Heaves on the left side indicate RIGHT ventricular hypertrophy
Kussmaul's sign
Physical exam finding where inspiration causes a RISE in JVP -Classic sign of *restrictive heart disease* -The ventricle cannot accept extra venous return during inspiration -Normally DECREASES during inspiration in healthy patients
Spirolactone
Potassium sparing diuretic that increases Na/water excretion -Used to treat *chronic SYSTOLIC heart failure* -*HYPERkalemia* is a side effect -Has a similar structure to testosterone and blocks its effects, leading to *gynocomasteia* in men -Is a derivative of progesterone so it can activate receptors and cause *amenorrhea* in women -Decreases mortality and hospitalizations
Eplerone
Potassium sparing diuretic that increases Na/water excretion -Used to treat *chronic SYSTOLIC heart failure* -*HYPERkalemia* is a side effect -Is a derivative of progesterone so it can activate receptors and cause *amenorrhea* in women -Does NOT cause gynocomastia unlike spirolactone -Decreases mortality and hospitalizations
Readmission
Recurrence of heart failure after discharge is common -Post discharge followup is very important -There is a high risk of readmission within *30 days* of discharge -Highest risk category occurs among the Medicare population
Left
Side of heart failure where there is *dyspnea on exertion*, *paroxysmal nocturnal dyspnea*, and *orthopnea* (can't breathe lying flat) -Dyspnea results from high pressure in the pulmonary capillaries -When lying *supine*, there is INCREASED venous return to the heart, leading to redistribution of blood volume that transfers fluid from the lower extremities to the lungs (WORSENS pulmonary congestion and breathing) -Patient often has to sleep with multiple pillows in a more upright position
Right
Side of heart failure where there is *increased JVP*, *lower extremity edema*, and *liver congestion* -Most commonly caused by *left heart failure*, but can occur in isolation usually secondary to a lung process such as pulmonary HTN or COPD -Can rarely cause cirrhosis -There is NORMAL left atrial pressure but HIGH pulmonary artery, right ventricular, and right atrial pressure -Often causes *cor pulmonale*
Beta blockers
Specific medications of this class of drugs used to treat heart failure include *Bisoprolol, Carvedilol, Metoprolol succinate, Nebivolol*