Cardiac Muscle Dysfunction: Heart Failure Part 2 Flashcards
causes of right HF
increased pulmonary resistance
increased afterload - pulmonary HTN or valve stenosis
low preload or poor pump
causes of left HF
impaired contractility
increased afterload
loss of myocardial tissue
low preload
symptoms of right HF
venous congestion weight gain peipheral edema hepatomegaly jugular venous distension
symptoms L HF
dyspnea orthopnea -need 3 pillows to breathe at night paroxysmal nocturnal dyspnea S3 heart sound excessive weight gain (> 2 lbs/day) decreased exercise tolerance
left-sided HF and dyspnea
- what do you hear during auscultation
- pulmonary edema
crackles (rales)
pulmonary edema
-when pulmonary venous pressure > 20 mmHg, fluid into lungs (increased hydrostatic pressure)
-decreased pulmonary compliance = increased work of breathing
neurohormonal compensatory mechanisms
-decreased CO –>
sympathetic stimulation -increase HR -increase contractility -vasoconstriction stimulate ADH increase vascular volume renin-angiotensin -vasoconstriction -increase BP INCREASING PRESSURE AND VOLUME DO NOT HELP SOMEONE WHO WITH HF
compensatory mechanisms
- purpose
- magnitude eventually leads to…
purpose of compensatory adaptations in HF is to maintain a CO and arterial pressure that adequately perfuses the brain and heart
magnitude of the compensatory adaptations eventually leads to maladaptive processes which lead to a decompensated state or end-stage HF
compensatory mechanisms
-what are they
increase in MAP moderate fluid retention increase in LVEDP decreased stroke volume (decreased ejection fraction) decreased contractility
compensated vs. decompensated HF
compensated
-symptoms are stable and many overt features of fluid retention and pulmonary edema are absent
decompensated
-refers to a deterioration, which may present either as an acute episode of pulmonary edema or as lethargy and malaise, a reduction in exercise tolerance, and increasing breathlessness on exertion
diagnostic marker of HF
B-type natriuretic peptide (BNP)
BNP
- what is it
- purpose
- BNF _____ is diagnostic for HF
what
-endogenous neurohormones that maintain normal fluid status and promote normal cardiac function
-secreted by left ventricle in response to volume expansion and pressure overload - “myocardial stretch”
purpose
-counter-regulation of renin-angiotensin-aldosterone system (RAAS)
-encourages vasodilation, diuresis while inhibiting the RAAS
BNP > 100 pg/ml is diagnostic for CHF
New York Heart Association function classification of HF
class I
-no limitation of physical activity
class II
-slight limitation of activity - OK at rest
-dyspnea and fatigue with “ordinary” physical activity
class III - OK at rest
-symptoms of HF with less than “ordinary” activity
class IV
-symptoms present at rest
control of HF strategies
- preload
- contractility
- afterload
preload - control salt and water retention
-low-sodium diet, diuretics
improve contractility
-B-blockers, inotropic meds, pacemaker or decrease workload
afterload
-reduce peripheral resistance
-lower BP
medications that decrease cardiac workload
- HF triple drug cocktail
- -purpose of each
ACE inhibitors -decrease afterolad diuretics -decrease volume beta-blockers -limit sympathetic stimulation to heart, hold heart rate down
agents that increase cardiac muscle contraction
digitalis (glycosides) - fallen out of favor
- inhibit Na/K pump, increase intracellular Ca++
- increases CO
- signs of digitalis toxicity (N/V, headache, confusion, arrhythmias, sinus bradycardia)
other treatments for HF
ventricular assist
heart transplant
if fluid is pooled in the legs, what is the kidney thinking?
not as much volume in the body (not as much going through the kidney)
- stimulate ADH
- increase renin-angiotension (maybe)
relationship between exercise capacity and measures of HF
most clinical measures of cardiac function correlate poorly with the clinical severity of HF
measurement of exercise capacity in HF
- measurements include…
- peak VO2 threshold for heart transplant candidates
- what tests predicts VO2
- what test is prognostic? How?
measurements include
-peak oxygen uptake
-anaerobic threshold
peak VO2 < 14 ml/kg/min threshold for heart transplant candidates
6 minutes walk predicts VO2
6 min walk is prognostic
-40% who walked <300 m died or were admitted for mechanical support within 6 months
acute cardiac responses to exercise in patients with HF
progressive decrease in CO, SV, and HRR capacity
exercise tolerance limited by reduced CO during exercise
acute circulatory responses to exercise in patients with HF
muscle blood flow is reduced during an acute bout of exercise in patients with HF
- not entirely due to a reduction in CO or local vascular impairment
- change in the distribution of blood flow during exercise
acute skeletal muscle metabolic responses to exercise in patients with HF
higher lactate levels at submaximal workloads
slower on- and off- kinetics with exercise (O2 consumption increases and decreases at a slower rate)
10-year exercise training in chronic HR
- who
- what did they do
- what was measured
- conclusion
123 patients
trained group: supervised exercise training at 60% VO2peak, x2/week, x10 years
nontrained group: “did not exercise formally”
changes in peak VO2
conclusion
-moderate supervised ET performed twice weekly for 10 years maintains functional capacity of more than 60% of maximum VO2
-NT patients, peak VO2 decreased progressively
aerobic interval training versus moderate continuous training
- training types
- results
training
-continuous: 70% peak HR, x3/wk, x12 weeks
-interval: 95% peak HR, x3/wk, x12 weeks
results
-VO2 peak increased: 46% IT, 16% C
-decreased LVEDV and LVESV (IT only): 18% and 25%
-LV EF increased: 35% (IT only)
-BNP (B-type natriuretic peptide) decreased: 40%
