tamponade, constriction, CHG Flashcards
tamponade vs. constriction: duration, symptoms, BP, HR, pulsus paradoxus, JVP, Y descent, Kussmaul’s sign, impairment of filling, equalization of diastolic pressures, heart size, echo
duration: tamponade is acute; constriction subacute/chronic
symptoms: t- dyspnea and cough; c- edema, ascites
BP: t- low; c- low to normal
HR: incr. in both
pulsus paradoxus: present in t; abscent in c
JVP raised in both
Y descent: t- attenuated; c- accentuated
Kussmauls: t- abscent; c- often present
impairment of filling: t-pan-diastolic; c- second 2/3
equalization of diastolic pressures in both
heart size: markedly increased; c- mildly increased
echo: t: echo-free space and collapse; c: thickened pericardium with early diastolic septal bounce
What is the definition of CHF?
clinical syndrome in which CV function derangement limits patient activities because the CV system can’t meet metabolic needs, or can only do so at elevated filling pressures
usually causes fatigue and/or dyspnea
systemic abnormalities with CHF
systemic disease with abnormalities in vascular reactivity, structural and functional abnormalities of skeletal muscle, venous congestion, and high circulating levels of neurohumoral mediators
acute CHF: clinical presentation
abrupt onset dyspnea, orthopnea, pallor, fatigue, and diaphoresis
often tachycardia or tachyarrhythmias
BP may be high or low
may have a giant v wave of tricuspid regurg from RV enlargement
pleural effusion is common
S3 and S4 often heard
cool and clammy skin
Symptoms of chronic CHF
lethargy, easy fatigue, exertional dyspnea, and peripheral edema
breathing in the supine position is often labored- paroxysmal nocturnal dyspnea
signs of chronic CHF
may appear ill with wasted muscle mass
often tachycardic if not medicated
often have cool skin
JVP raised if right heart failure is present
often have an S3 gallop with a displaced apex
edema in dependent areas if right heart failure is bad.
What is the best way to quantitate severity of CHF?
oxygen consumption (V02 max) basically, as you start to execrise, the rate of O2 consumption and the rate of CO2 production rises in tandem. at some point, however, the rate of oxygen consumption cannot rise further (the blood isn't getting there fast enough, the tissues can't extract it, whatever), and this is the VO2 max. It is about 30 mg/kg/min in normal people and lower in more severe CHF
high output failure
cases like myxedema and AV fistula that impose an abnormally high level of demand on the heart. clinical syndrome develops but there isn’t actually a problem with the heart per se
systolic vs diastolic failure
systolic failure: CHF with low LVEF
diastolic failure: stiff LV (usually) from LVH but normal LVEF
what are the factors that influence progression of CHF?
usually myocardial injury, degeneration, or stresses on the myocardium. these stresses cause:
1. incr. starling forces
2. hypertrophy
3. incr. sympathetic input
4. activation of renin-angiotensin-aldosterone system to retain Na and water and to vasoconstrict
These are maladaptive in the long term:
1. starling causes greater wall stress and more oxygen demand on heart
2. hypertrophy causes lowered myocardial capillary density and causes stiffness such that greater diastolic pressures are needed for filling
3. SNS: may aggravate the underlying problem. High plasma norepinephrine levels are strong prognostic indicators. Also, this causes down reg of beta receptors on the heart and uncouples receptor from its message.
4. salt, water retention, vasoconstriction = burden on the heart (preload and afterload). Also, vasoconstriction may be inappropriate- skeletal muscle arterioles may not dilate appropriately in response to metabolic need. Cuases skeletal muscle atrophy and incr. local vasoconstriction.
Angiotensin is directly toxic to the myocardium
edema conprresses vessels and limits dilation
Why can’t pts with heart failure exercise well?
- Heightened pulm venous pressures raise pulm vascular resistance during exercise
- abnormalities of diastolic properties of the left ventricle
- Intense and inappropriate vasoconstriction- little access to increased cardiac output if skeletal muscles are all vasoconstricted. Thus, ACE-Is help
complications and treatments for CHF
ACE-Is to increase flow to skeletal muscle
implantable cardioverter-defibrillators to reduce risk of sudden cardiovascular death through VFib unless QRS is very wide (>0.16 s)
LBBB is common. dyssynchrony hampers ventricular emptying- try cardiac resynchronization therapy
Treatment for “diastolic” heart failure
we know very little
normalize bp and try to maintain them in sinus rhythm
ACE-I and BBs (no evidence, just theory)
diuretics help symptomatically
treatment of asymptomatic LV systolic dysfunction (reduced LVEF tx and LVH tx)
reduced LVEF but no symptoms: about 10%/yr progress to CHF
warrant treatment to forestall symptomatic CHF and mortality
ACE-I reduced combined endpoint of CV death and progression to symptomatic CHF
LVH patients with good LVEF: reverse LVH progression with ARBs (then CCBs, ACE-I, diuretics, BBs)
tx for asymptomatic post-MI pts with reduced LVEF
ACE-I, esp. when given soon after acute MI, delays death and onset of symptomatic CHF
mortality and recurrent MIs reduced with BBs (even in pts w/o reduced LVEF)
