CHF Part 2

Question 1

Major Common Signs and Symptoms for CHF (10)

Answer 1

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

Question 2

Minor Common Signs and Symptoms for CHF (10)

Answer 2

Weight Loss
Cough
Nocturia
Palpitations
Peripheral edema
Depression
Mitral Regurgitation
Cardiomegaly
Splenomegaly
Hypotension
Pulsus alterans
Extrasystoles (PVCs, PACs)
Atrial fibrillation

Question 3

New York Heart Association 4 Functional Classes

Answer 3

Class 1Symptoms of HF only at activity levels that would limit nml individuals
Class 2 Symptoms of HF with ordinary exertion
Class 3Symptoms of HF with less than ordinary exertion
Class 4 Symptoms of HF at rest

Question 4

ACC/AHA 4 Stages of Development of HF

Answer 4

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

Question 5

Kerley B Lines (3)

Answer 5

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.

Question 6

Creatine Kinase

Answer 6

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.

Question 7

Troponins

Answer 7

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)

Question 8

B type Natretic Peptide

Answer 8

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

Question 9

EKG Findings in CHF (5)

Answer 9

Evidence of ischemia
LVH
Heart block
Tachycardias
A fib with RVR

Question 10

Echocardiography Findings in Heart Failure (8)

Answer 10

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

Question 11

Systolic Dysfunction–Echocardiography Findings in Heart Failure (6)

Answer 11

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

Question 12

Diastolic Dysfunction–Echocardiography Findings in Heart Failure (8)

Answer 12

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

Question 13

4 Medications in Heart Failure

Answer 13

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

Question 14

Inotropic Support– Medications in HF (7)

Answer 14

Isoprosterenol
Norepinephrine
Dopamine
Dobutamine
Phosphodiesterase inhibitors	
Amrinone
Milrnone

Question 15

Who gets Hospitalized for Acute HF? (10)

Answer 15

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

Question 16

Goals of Treatment are for Hospitalized Pts with Acute HF (8)

Answer 16

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

Question 17

4 Hemodynamic monitoring– Acute HF Treatment

Answer 17

Vitals
Possible Swan, Arterial lines, Central lines
Echo
EKG

Question 18

Systolic and Diastolic Dysfunction– Acute HF Treatment (10)

Answer 18

ABCs
IV access
Upright position
Oxygen
Diuresis
Lasix
Vasodilator Therapy
Nitroglycerin
Morphine
Monitor UOP
”MONA” (Morphine, oxygen, Nitro, ASA)

Question 19

Oxygen– Acute HF Treatment

Answer 19

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)

Question 20

Diuretics– Acute HF Treatment (6)

Answer 20

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 diureticsFurosemide, Bumetaninde, Torsemide
By decreasing the circulating volume it will decrease ventricular pressures promoting forward flow
Monitor UOP, BP, and Renal Function

Question 21

ACE- I and ARBs– Acute HF Treatment (3)

Answer 21

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

Question 22

Nitrates– Acute HF Treatment (3)

Answer 22

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

Question 23

In addition to Diuretics– Acute HF Treatment (7)

Answer 23

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

Question 24

Inotropic Agents– Acute HF Treatment (8)

Answer 24

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)

Question 25

Beta Blockers– Acute HF Treatment (3)

Answer 25

Reduces mortality in long-term management
May continue in acute phase if pt is stable, if unstable either decrease or discontinue the medication
If not on them chronically, hold in the early stage and continue when stable

Question 26

Morphine Sulfate– Acute HF Treatment (3)

Answer 26

Decreases anxiety and work of breathing
Diminish sympathetic outflow and leads to arteriolar and venous dilatation
BE CAREFUL because it effects the respiratory center of the brain and can cause apnea requiring intubation

Question 27

Mechanical Cardiac Assistance– Acute HF Treatment

Answer 27

Pts with cardiogenic pulmonary edema, in cardiogenic shock, Cardiac Index < 2 L/min per m2 SBP < 90 and PAOP > 18
Balloon pump
Ventricular assist device (VAD)

**Control Arrhythmias

Question 28

Ultrafiltration and Vasopressin receptor antagonists– acute HF treatment

Answer 28

Ultrafiltration
Dialysis to remove fluid

Vasopressin receptor antagonists
The “vaptans”
Think anti-antidiuretic hormone (to make you pee)
New form of therapy

Question 29

After Discharge from the Hospital: (3)

Answer 29

Addressed exacerbating factors
Achieve near optimal volume status and pharmacologic therapy
Will need follow up

Question 30

Goals of Chronic HF Treatment (3)

Answer 30

improve symptoms
slow or reverse the deterioration
reduce mortality in addition to treating underlying systemic effects of HF

Question 31

3 Medications used to systolic Dysfunction– Chronic HF Treatment

Answer 31

Loop Diuretics (NYHA III-IV) to first control volume and prevent volume overload resulting in pulmonary and peripheral edema

ACEI/ARBs (NYHA I-IV)
ACEI improve mortality in all severities of myocardial disease
Should be started in symptomatic or asymptomatic pts
ARBS slightly less effective than ACEI

Beta Blockers (NYHA I-IV)
Improve overall and event-free survival in pts with NYHA Class II and III and probably in IV, this improvement is additive to that of the ACEI
Usually Carvedilol or metoprolol succinate ER

Question 32

Nitrates and Aldosterone Antagonist– Chronic HF Treatment

Answer 32

Hydralazine and Nitrates (isosorbide dinitrate/mononitrate) (NYHA Class III-IV based off A-HEFT study) despite the previous therapy
Some data suggests it has better efficacy in blacks rather than whites

Aldosterone Antagonist 
Spironolactone for NYHA class III-IV based off RALES study
Eplerenone for NYHA class II based on EMPHASIS-HF study

Question 33

ARB and Digoxin for Chronic HF Treatment

Answer 33

ARB in addition to ACE
CHARM study used candesartan

Digoxin for NYHA class III-IV
Given to pts with HF to control symptoms (fatigue, dyspnea, exercise intolerance) and afib

Question 34

Statins and CCB for Chronic HF Treatment

Answer 34

Fish Oil may reduce mortality

Statins
Prevent CAD
May prove beneficial

Calcium Channel Blockers
May have no OR even worsen mortality

Question 35

Exercise and Refractory Treatment for Chronic HF

Answer 35

Exercise
To improve Functional Class
Hypoperfusion and reduction of physical activity cause skeletal muscle dysfunction and intolerance to exercise
Serial Assessments
Refractory Treatment
Continuous IV inotropic therapy, cardiac resynchronization, hemodialysis, mechanical circulatory support , surgery, or cardiac transplantation

Question 36

Diastolic Dysfunction treatment for Chronic HF

Answer 36

Treat the underlying process
HTN
REMINDER decreased LV volume and therefore must be cautious as not to decrease preload much.
Digoxin is NOT used as contractility is intact

Question 37

Antihypertensive medications for Chronic HF

Answer 37

Regression of LVH
ARBs 13%
Calcium Channel Blockers 11 %
ACEI 10%
Diuretics 8%
Beta Blockers 6%

Control Afib as pt is dependent of preload and if pt has decreased forward flow from the atria then decreased volume will enter the ventricle, in addition tachycardia shortens diastole
Need to convert to sinus and/or rate control
Amiodarone, CCB, Beta-blockers

Question 38

Beta Blockers and Anti- ischemia therapy for Chronic HF

Answer 38

Anti-ischemia therapy
BB, CCB, Nitrates, PCI, CABG

Beta Blockers
Reduce myocardial oxygen demand
Lower Blood pressure
Cause regression of LVH

Question 39

CCB and ACE/ARB for Chronic HF

Answer 39

Calcium Channel Blockers
Has lusitropic effect
Slows HR
Reduction in or prevention of ischemic episodes

ACEI/ARB
No clear evidence that it improves mortality/morbidity, however, used in treatment underlying Diastolic Dysfunction (i.e. HTN, CAD and DM)

Question 40

Statins and Aldosterone Antagonists for Chronic HF

Answer 40

Aldosterone Antagonists
Aldosterone contributes to hypertrophy

Statins
Recommended in CAD independent of diastolic dysfunction, however may benefit

Question 41

Prognosis of HF (2)

Answer 41

Diastolic Dysfunction is slightly better prognosis than Systolic Dysfunction
Approx 87 vs 156 per 1000

Question 42

Prevention of HF (2)

Answer 42

Early detection and removal of reversible predisposing conditions (cannot reverse age, race and gender )
Prevention is aimed to Class A and B HF