Week 9: Cardiac III Flashcards
What is Heart failure
- occurs when the heart cannot pump enough blood fasst enough to meet the metabolic needs of the body
- no longer use the term “congestive” because all heart failure does not result in clinically apparent volume overload
Fast Facts:
- Leading diagnosis for group over 65
- median survival is 3.2 years for men and 5.4 years for women
- most common cause of death is progressive HF, but sudden death may account for up to 45% of all deaths
- Patients with coexisting IDDM have a significantly higher mortality rate
Preload
- the amount of blood the heart must pump with each beat
- determined by: venous return to heart and strength of muscle fibers
- increasing preload–>increased stroke volume in normal heart
- increasing preload–>impaired heart–>decreased SV. Blood is trapped–>chamber becomes enlarged
afterload
- the pressure that must be overcome for the heart to pump blood into the arterial system
- dependent on the systemic vascular resistance
- with increased afterload the heart muscles must work harder to overcome the constricted vascular bed–>chamber enlargement
- increasing the afterload will eventually decrease the cardiac output
dilated congestive cardiomyopathy
heart muscle disorders in which the ventricles enlarge but are not able to pump enough blood for the body’s needs, resulting in HG (example: CAD, myocarditis, etoh, HIV)
hypertrophic cardiomyopathy
heart disorders in which the walls of the ventricles thicken and become stiff, even though the worklaod of the heart is not increased. Ex: congenital HCM, or acquired
restrictive (infiltrative) cardiomyopathy
heart disorders in which the walls of the ventricles become stiff but not necessarily thickened and resist normal filling with blood between heartbeats. EX: ratiation, amyloidosis
adaptive mechanisms of the heart to increase load
- frank sterlin mechanism
- ventricular hypertrophy : increased mass of contractile elemts cuases increased strength of contraction
- increased sympathetic adrenergic activity: increased HR, increased contractility
- increased activity of R-A-A system
systolic cardiac heart dysfunction (systolic HF)
when the heart muscle doesn’t contract with enough force so there is not enough oxygen rich blood to be pumped throughout the body
diastolic cardiac dysfunction (or diastolic HF)
when the heart contracts normally, but the ventricle doesn’t relax properly so less blood can enter the heart
Stages of HF
AHA: ABCD
- A: risk factors but no symptoms
- B: structural changes but no symptoms
- C: patients with structural change symptoms, but they’re treatable with medication
- D: refractory. Structural changes, symptoms, not responsive to medication
New york heart association: class 1, 2, 3, and 4
- Class 1: no obvious symptoms, no limitations on patient physical activity (35% EF or higher)
- Class 2: some symptoms during or after normal activity, mild physical activity limitations (35 %)
- Class 3: symptoms with mild exerction, moderate to significant physical activity limitations (25%)
- Class 4: Significant symptoms at rest, severe to total physical activity limitations (5%)
Cuases of HF
- CAD
- problems with the heart muscle itself (known as cardiomyopathy, myocarditis, et)
- HTN
- problems with any of the heart valves
- abnormal heart rhythms (also called arrhythmias)
- toxic substances (EtOH, cocain)
- Congenital heart disease
- diabetes
- thyroid problems
- HIV
DIastolic HF
- Diastolic HF is defined as a condition caused by increased resistance to the filling of one or both ventricles, this leads to symptoms of congestion from the inappropriate upward shift of the diastolic pressure-volume relation
- 40% patients
- increasing age
- more common in women
- HTN and cardiac ischemia are most common causes
- alterations involve relaxation and or filing and or distensibility
- arterial HTN associated to LV concentric remodeling is the main determinant of DD but several other cardiac diseases, including myocardial ischemia, and extra-cardiac pathologies also possible
Patient differences with HF
- a hemodynamic disorder but there is poor relationship between measures of cardiac performance and patient symptoms
- for ex: pts with very low EF may be asymptomatic while someone with preserved EF may be severely disabled with symptoms
body compensatory mechanisms of HF
- epi and norepi releases which increases HR and contractility which increases myocardial work load
- decrease in salt and water excretion from kidneys which helps maintain BP by increased BV, this leads to stretching of heart’s chambers which can impair ability to contract
- hypertophy and thickening of heart muscle which initially increases contractility but over time leads to stiff chambers
- HF pts have higher levels of epi, norepi, aldosterone, angiotensin 2, enothelin, inflammatory cytokines, and vasopressin which contributes to heart remodeling, progression of HF, and higher levels are associated wiht increased mortality
neurohormonal with HF
- Stimulated by decreased perfusion leadin gto secretion of hormones
- Epi: increases contractility, increases rate and pressure, vasoconstriction leads to SVR
- Vasopressin: pituitary gland, mild vasoconstriction, renal water retention
renin angiotensin mechanism in HF
- Decreased renal blood flow secondary to low cardiac output triggers renin secretion by thte kidneys
- aldosterone is released–> increased sodium retention and water retention
- preload increases
- worsening failure
ventricular hypertophy
- long term compensatory mechanism
- increases size due to increase in work load ie skeletal muscle
potential reasons
- alternation in ventricular distensibility
- valvular regurgitation
- pericardial restrain
- cardiac rhythm
- conduction abnormalities
- rv function
- also several non-cardiac factors including peripheral vascula fxn, reflex autonomic activity, renal sodium handling, etc
HF risk factors history
- smoking
- etoh use
- SM HTN
- dyslipidemia
- thyroid disorder
- chemo
- radiation
- cardiotoxic drugs
- fam HX of sudden death, CAD, conduction problems, HCM
- HIV status
Cardiovascular medical HX
- Hx heart failure
- angina
- mi
- cabg
- pci
- pacemaker/icd
- embolic events
- arrhythmias
- cva
- pvd
- rheumatic dx
- other valvular hx
- congenital
sign and symptoms of HF
- dyspnea
- pnd
- orthopnea
- cough
- exercise intolerance
- edema
- fatigue
- nausea
- abdominal fullness
- rales (usally starts at bases)
- s3 (position patient left lateral to hear)
- pulmonary edema
- jvd
- tachycardia
- cardiomegaly
- hepatojugular reflex (apply pressure, see distention, let go it stays pretty long)
- peripheral edema
- hepatomegaly
physical exam of HF: signs that suggest HF include
- tachycardia
- third heart sound (listen LL recumbent)
- increased jugular venous pressure
- positive hepatojugular reflux
- bilateral rales (not always present, only in L sided HF)
- peripheral edema not due to venous insufficiency
- laterally displaced apical impulse (from midclavicular (normal) to mid-axillary)
- weight gain
HF diagnosis and assessment
- primarily a clinical dx, but additional infor via other diagnostic can be beneficial
- look at CXR, BNP, EKG
- evaluation depends on if this is first presentation, change in clinical symptoms certainty of dx, etc
what we should know about the individual patient’s HF
- identify the patients with HF
- assess for S/S and risk factors for HF
- Initial workup should have been included work up for reversible causes if appropriate (TSH, HIV)
- echocardiogram to determine systolic and diatstolic LV performance, cardiac output (EF) and pulmonary artery and ventricular filling pressures
Elevated BNP levels have been associated with?
reduced LVEF, LVH, and elevated LV filling pressure, and acute MI
evidence supports getting baseline BNP
