tamponade, constriction, CHG Flashcards Preview

Misc Heart > tamponade, constriction, CHG > Flashcards

Flashcards in tamponade, constriction, CHG Deck (22):

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?

1. Heightened pulm venous pressures raise pulm vascular resistance during exercise
2. abnormalities of diastolic properties of the left ventricle
3. 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)


treatment of acute decompensated systolic CHF

if there are signs of gross fluid excess, give diuretic and/or nitrates. consider priming with a thiazide before giving the loop. mechanical ventilatory support may be needed
if extreme dyspnea and HTN, reduce BP with IV vasodilating drugs (labetolol). If also tachycardic, give IV BB.
hypotensive w/o fluid excess: give bolus of IV fluid
pulm congestion and hypotension: treat cause, then do the best you can. Pheylephrine is a vasoconstrictor but will weaken cardiac output. Diuretics will worsen hypotension.


Advantages and disadvantages of dobutamine and milrinone

positively inotropic
both have peripheral vasodilating properties
dobutamine may invite tachyarrhythmias
dopamine may be used but casues more tachyarrhythmias than dobutamine
digoxin: weak and slow to act. positive inotrope.


Treatment of chronic systolic HF

lifestyle: 2-3000 mg of salt/day, exercise presecribed in a graded fashion
improve mortality with ACE-Is, ARBs, BBs, and hydralzine/nitrates (esp. in African Americans). If advanced, give aldo antagonists
diuretics and digoxin help symptoms but not mortality
you have to choose how to spend your bp carefully, since many of these drugs lower bp


devices in severe heart failure

mechanical ventricular assist devices, esp. as a bridge to transplantation in about 50% of pts
risks include expense, inconvenience, infection, and thrombotic risks
cardiac transplant
giving pacemaker to synchronize the ventricles
defibrillator if pt has very low LVEF, often with cardiac resynchronization


CHF with preserved LVEF treatment

pts decompensate in settings of rapid HR, vol excess, and HTN. tolerate A fib poorly
this should all be explainable by the fact that most of these pts have very stiff LV- rapid HR = less time for ventricular filling, A fib means suddenly the atrium doesn't generate enough pressure to force fluid into the ventricle- can cause flash plumonary edema
diuresing is important to keep lungs clear but must be done carefully, since the patients do need enough volume to get fluid into the stiff ventricle
control HTN
consider ARBs and potentially aldo blockers


causes of high output CHF

thyrotoxicosis, larve AV fistulae, intra-cardiac shunts


hypertrophic obstructive cardiomyopathy

w/o obstruction, this is a stiff LV with a high risk of lethal ventricular arrhythmias
with dynamic outflow obstruction, you can't give positive inotropes, vasodilators, or diuretics. positive inotropes lessen systolic LV diameter, and vasodilators decrease preload.
tx: BB and CCB to keep pre-load relatively high. IV phenylephrine is a vasoconstrictor that may be used in the acute setting.
prophylactic insertion of ICD in high risk pts