CHF Part 2 Flashcards
Major Common Signs and Symptoms for CHF (10)
Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Ankle Edema Pulmonary Edema Fatigue Exercise Intolerance Cachexia Tachycardia Elevated venous pressure Positive Hepato-jugular reflex Pulmonary rales Tachypnea S3 Hepatomegaly Ascites Pleural Effusion
Minor Common Signs and Symptoms for CHF (10)
Weight Loss Cough Nocturia Palpitations Peripheral edema Depression Mitral Regurgitation Cardiomegaly Splenomegaly Hypotension Pulsus alterans Extrasystoles (PVCs, PACs) Atrial fibrillation
New York Heart Association 4 Functional Classes
Class 1Symptoms of HF only at activity levels that would limit nml individuals
Class 2 Symptoms of HF with ordinary exertion
Class 3Symptoms of HF with less than ordinary exertion
Class 4 Symptoms of HF at rest
ACC/AHA 4 Stages of Development of HF
Stage A High risk of HF, without structural heart disease or symptoms
Stage B Heart Disease with asymptomatic left ventricular dysfunction
Stage C Prior or current symptoms of HF
Stage D Refractory end stage HF
Kerley B Lines (3)
When fluid leaks into the peripheral interlobular septa it is seen as Kerley B or septal lines.
Kerley-B lines are seen as peripheral short 1-2 cm horizontal lines near the costophrenic angles.
These lines run perpendicular to the pleura.
Creatine Kinase
peaks 4-8 hours post infarction and declines after 2-3 days. Peak is usually after 24 hours
CK isoenzymes
MM (skeletal and cardiac), BB (brain and kidney) and MB (cardiac and skeletal (1-3%), small amounts in small intestine, tongue, diaphragm, uterus and prostate)
A ratio of 2.5 or greater of MB is usually indicative of an MI (CK-MB index)
Inaccurate in the setting of skeletal breakdown and large CK release or in chronic skeletal injury resulting in release of MB or when the CK is in the nml range and the MB in elevated ? Microinfarctions.
Troponins
Three types that regulate calcium-mediated contractile process of striated muscles
Troponin C which binds calcium
Troponin I which binds to actin and inhibits actin-myosin interactions
Troponin T binds to tropomyosin thereby attaching the troponin complex to the thin filament.
Released when a myocyte is damaged after about 3 hours and persist for 7 to 10 days (Trop I) and can last upwards of 10-14 days. (Trop T)
B type Natretic Peptide
released from the ventricle
< 100 pg/dL is nml (accuracy of 81.2%)
>400 pg/dL has a high predictive value for CHF
Elevated levels does not rule out other causes in addition to CHF of dyspnea
Maybe chronically elevated, need to compare to previous
Can be elevated due to cor pulmonale which does not necessarily indicate HF
Levels are lower in obese pts and elevated in renal failure pts and in sepsis
Lipid Panel
Total Cholesterol, HDL, LDL, Triglycerides
EKG Findings in CHF (5)
Evidence of ischemia LVH Heart block Tachycardias A fib with RVR
Echocardiography Findings in Heart Failure (8)
Size and Shape of the ventricle
LV ejection Fraction
Regional wall motion, synchronicity of ventricular contraction (Hypokinesis, akinesis)
LV remodeling (concentric versus eccentric)
LV or RV hypertrophy (DDx-HTN, COPD, Valve disease)
Morphology ad severity of valve lesions
Mitral inflow and aortic outflow properties, RV pressure gradient
Output state
Systolic Dysfunction–Echocardiography Findings in Heart Failure (6)
Reduced LVEF ( < 45%) Enlarged LV Thin LV wall Eccentric LV remodeling Mild or moderate mitral regurgitation Pulmonary hypertension Reduced mitral filling Signs of increased filling pressure
Diastolic Dysfunction–Echocardiography Findings in Heart Failure (8)
Normal LVEF ( >45%) Normal LV size Thick LV wall, dilated atria Concentric LV remodeling No or minimal mitral regurgitation Pulmonary Hypertension Abnormal mitral filling pattern Signs of increased filling pressure
4 Medications in Heart Failure
Remove extra fluid
Diuretics
Loop
Potassium sparing
Work Directly on calcium movements in and out of the SR
Digitalis
Calcium channel blockers
Decrease Cardiac Work Ace Inhibitors (decrease afterload) Decreases mortality from 39 to 30% in pts with LV dysfunction
Increase contractility
Beta agonist have a inotropic strength
Inotropic Support– Medications in HF (7)
Isoprosterenol Norepinephrine Dopamine Dobutamine Phosphodiesterase inhibitors Amrinone Milrnone
Who gets Hospitalized for Acute HF? (10)
Hypotension, AKI, altered MS Dyspnea at rest Dangerous Arrhythmia ACS Worsened Pulmonary or Systemic Congestion, wt gain ≥ 5 Kg Electrolyte disturbances Presence of pneumonia, PE, DKA, TIA/CVA ICD firings Previously undiagnosed HF with signs and symptoms of systemic or pulmonary congestion
Goals of Treatment are for Hospitalized Pts with Acute HF (8)
Improve Symptoms Optimize Volume Status Identify Etiology Identify Precipitating Factors Optimize Chronic Oral Therapy Minimize Side Effects Identify pts whom may benefit from revascularization Educate pts Initiate a disease management program
4 Hemodynamic monitoring– Acute HF Treatment
Vitals
Possible Swan, Arterial lines, Central lines
Echo
EKG
Systolic and Diastolic Dysfunction– Acute HF Treatment (10)
ABCs IV access Upright position Oxygen Diuresis Lasix Vasodilator Therapy Nitroglycerin Morphine Monitor UOP ”MONA” (Morphine, oxygen, Nitro, ASA)
Oxygen– Acute HF Treatment
Only give when needed
Noninvasive positive pressure ventilation (NPPV), may prevent pt from being intubated, but do not withhold mechanical ventilation if needed or if the pt fails NPPV (continues to have or has worsening respiratory distress or failure)
Diuretics– Acute HF Treatment (6)
ONE OF MAINSTAY
Pts are usually volume overloaded and this extra volume needs to be removed.
Used in most situations,
Pt is hypotensive and LVOT obstruction should be diuresed with caution because they are preload dependent.
Loop diureticsFurosemide, Bumetaninde, Torsemide
By decreasing the circulating volume it will decrease ventricular pressures promoting forward flow
Monitor UOP, BP, and Renal Function
ACE- I and ARBs– Acute HF Treatment (3)
Used for pts with systolic dysfunction, mainstay for chronic failure
Continue therapy if pt has no contraindications (hypotension, AKI, Hyperkalemia)
Should be started once pt is stable rather than early in an unstable pt
Nitrates– Acute HF Treatment (3)
Nitroglycerin- Venodilator and reduces LV filling pressure, lowers systemic vascular resistance and increases CO and SV
Nitroprusside- Venous and arterial vasodilator. Used when afterload needs to be reduced dramatically (hypertensive emergency, acute aortic regurg, acute mitral regurg, acute ventricular septal rupture).
Nesiritide- recombinant human BNP causes arterial and venous vasodilation MAY increase mortality!! Not frequently used
In addition to Diuretics– Acute HF Treatment (7)
Sodium and fluid restriction < 2 gm of sodium/day Fluid restrictions of < 2 L/day A Reminder that the fluid overload can cause hyponatremia Increase the diuretic dose Add a Thiazide diuretic Start a Loop diuretic gtt
Inotropic Agents– Acute HF Treatment (8)
used in pts with severe systolic dysfunction
2009 ACC/AHA guidelines suggest starting in pts with hypoperfusion (low output syndrome), LV Dilation, reduced LVEF and elevated PAOP.
May cause ischemia in High output states by increasing HR and myocardial O2 consumption
Dobutamine
Works on Beta 1 adrenergic and less on beta 2 or alpha 1
Increases SV and CO with some decrease in SVR
Milrinone
Phosphodiesterase inhibitor that inhibits the degredation of cAMP, Causing more intracellular calcium and stronger contractions
Decreases SVR (peripheral phosphodiesterase inhibition)
