Heart Failure Flashcards
Heart Failure defn • Prevalence: about 2% and increasing! – aging population – ↑ post-MI survivors – uncontrolled hypertension ON THE RISE
Chronic, persistent,progressive
few instances of reverse
complex clinical syndrome caused by abnormal heart function that results in clinical symptoms/signs of reduced cardiac output and/or congestion (at rest or during stress)”
– structural or functional disorder that impairs ventricular filling or ejection of blood (↓cardiac output)
– dyspnea, fatigue and fluid retention
– “Congestive” heart failure (CHF), used to be called this (no longer used)
• A persistent, progressive condition (Chronic HF)
– acute decompensated HF (ADHF) or acute HF:
gradual or rapid change in symptoms in need of urgent therapy
Doesn’t fill properly (systole) or eject properly (diastole)
Heart Failure
5-year survival
read
Poor prognosis: high mortality & morbidity
– overall 5-year survival 50%
– death: pump failure or sudden cardiac death (ventricular)
– poor quality of life
• One of the most common reasons for hospitalization
– average length of stay = 8 days
– 20-30% readmission rate (20% readmit within 30 days)
– HF trials incorporate hospitalizations as endpoint
• Economic burden
– Direct costs: $2.8 billion/year
- childbirth 2. COPD exac 3. heart failure
Risk Factors
- Hypertension
- Atherosclerotic Disease: 70% cases
- Diabetes
- Obesity
- Metabolic Syndrome
- Cardiotoxins (smoking, alcohol, cocaine)
- Physical inactivity
what happens to heart in HF
HF is likely the final common pathway for a variety of cardiac disorders:
Loss of viable myocardial tissue: slowly due to
hypertension or coronary artery disease or ‘fast’ due
to myocardial infarctio
damaged muscle
Insult can be fast due to MI
No longer functions as effective pump
Iatrogenic myocardial damage
caused by other therapies
– radiation
– Drugs:
• Anthracyclines (doxorubicin), trastuzumab
• Negative inotropic drugs: beta blockers (at high initial dose),
calcium channel blockers, antiarrhythmics
• Fluid retention: NSAIDS, COX-2 inhibitors, thiazolidinediones
other causes of HF
- Valvular heart disease
- High output failure
- Atrial fibrillation (other tachyarrhythmias)
- Viral myocarditis
- Familial cardiomyopathy
valvular: Prevent forward fill of blood, Reduce cardiac output (some reversible or irrev)
high output failure: cardiac output normal range, demands of body high (pregnancy)
atrial fibrillation: can exacerbate HF, atria contract too quickly wihtout filling themselves, vent filling compromised (1/3 pt)
viral myocarditis: virus attacks heart, induce change to muscle, lead to chronic HF
familial: genetic alterations in various components of myocardium
Pathophysiology
what is stroke vol affected by (3)
Cardiac Output (CO) = heart rate (HR) x stroke volume (SV, amt of blood ejected during systole)
• HR controlled by ANS:
– If HR too fast not enough time to fill left ventricle, ↓SV
• stroke volume is affected by:
– preload
– afterload
– contractility (inotropy) – intrinsic strength of contraction independent of preload/afterload (inherent strength of muscle, dictacted by movement of Ca2+)
Preload
• amount of blood presented to the heart for pumping at the end of diastole (left ventricular end diastolic volume, LVEDV), just before contraction
• amount of blood influences the initial stretching of cardiac myocytes (sarcomere length)
– linear relationship between sarcomere length and myocardial force (the more crosslinks, the greater the strength)
• normally, increasing preload increases cardiac output dramatically
• other terms: LVED pressure, pulmonary capillary wedge pressure
Preload and Starling’s Law of
the Heart
see diagram slide 9
as preload increases, cardiac output increases
• In a “HF heart”, increasing the preload doesn’t
increase cardiac output, and, in fact, will decrease it by
overwhelming the pumping capacity of the heart
- increasing preload makes CO worse in HF
• Note: an increase in preload is both the cause and
effect of heart failure
Afterload
systemic vascular resistance (SVR), total peripheral
resistance
what happens in pt of HF
• afterload is the resistance against which the heart must work to pump blood (resistance to blood exiting the heart)
– related to arteriolar tone and is reflective of, but not the sole determinant of BP (BP = CO x SVR)
– increasing afterload increases myocardial work
– In a normal heart, increasing afterload doesn’t change CO much, but in the “HF heart”, increased afterload makes the already weakened
heart work harder, and can actually decrease CO
– increase in afterload can cause HF, or occur as a result of HF
Afterload can weaken the heart, can cause HF and exacerbate it
CO = HR x SV
– Since HR is an inefficient way to increase
CO, you are left with altering ____________
which paremeters were altered
• Case #1: patient watched hockey all day, ate 2
large bags of potato chips and drank ~ 8 beer
• Case #2: patient had a stuffed up nose and
took pseudoephedrine for the past 3 days
• Case #3: patient was started on diltiazem for
hypertension 3 days ago
preload,, afterload or contractility
Why is this important?
– Patient seen in the emergency department with extreme shortness of breath and determined to have pulmonary edema:
Case 1: increased preload, (fluid, salt increases return to the heart)
Case 2: increased afterload (vasoconstrictor, fluid overloaded state)
Case 3: reduction in contractility (diltiazem works by relaxing blood vessels in the body and heart and lowers the heart rate, CCB)
Compensatory Mechanisms In HF
Reflective of signs and symptoms pt see
symp NS –> NE increases that causes increase HR and contractility –> vasoconstiction
in HF, increasing HR and vasoconstriction further reduces CO
- body will preserve blood to heart and brain
kidneys interpret not enough bloodflow, renin activated, RAAS –> increase Ang II which further increases vasoconstriction = increase afterload
aldosterone leads to sodium and water retention which increases preload
makes it worse
Ventricular Remodeling
maladaptive change
- activation of neurohormonalcompensatory responses promotes remodeling process.
- AT II, NE, aldosterone, vasopressin, endothelian, inflammatory cytokinesexert direct toxic effects on cardiac cells
- results in changes to the structure (size, shape, composition) and function of ventricle.
- remodeling responsible for progression of HF, mortality
Ventricular Remodeling
normal heart
2 forms of remodelling
hypertrophied heart: thicker muscle, chamber inside is smaller, (diastolic HF)
dilated heart: changed shape, not elliptical, now sphere, larger chamber size but thinner muscle (systolic HF)
Signs and Symptoms of HF
no single sign, smyptom, blood test that points to HF
pt can change over time
categories general CVS resp GI GU MSK/EXT labs diagnostics
Congestion, hypoperfusion
General: rapid weight gain, fatigue, weakness, exercise
intolerance
CVS: tachycardia, ↓ BP, jugular venous distension, hepatojugular reflux (reliable indicator), S3 gallop rhythm
Resp: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, rales/crackles
GI: ascites, hepatomegaly, abdominal pain, nausea, bloating, anorexia, early satiety
GU: Nocturia, increased Scr
MSK/EXT: pitting edema, cool extremities
Labs: BNP > 400pg/ml (NT-proBNP), CBC, lytes, creatinine/BUN, thyroid function
Diagnostics X-ray: cardiomegaly, pleural effusion,
pulmonary edema, fluid in lungs .ECG. Echocardiogram: chamber fxn, structure,valves (prob most useful)
