Cardiomyopathy and HF Flashcards
clinical features of HD syndrome
- dyspnea
- fatigue
- signs of circulatory congestion
- hypoperfusion
systolic HF more common among
middle-aged men (associated with CAD)
diastolic HF usually seen in
elderly women (HTN, obesity and Diabetes after menopause)
most common discharge dx with more dollars and medicare spent on dx and tx than any other disease
Heart failure
principle pathophysiological feature of HF
inability of heart to fill or empty
HF syndrome may result from these 5 things
- impaired contractility
- valve abnormalities
- systemic HTN
- pericardial disease
- pulmonary HTN (cor pulmonale)
what BBB and which type of HF in combination has a high risk for sudden death
LBBB + systolic HF
Hallmark of chronic LV systolic dysfunction
DEC EF
symptomatic patients with normal/near normal LV systolic function (EF > 40%) most likely due to ___ ___
diastolic dysfunction
DHF prevalence for these ages:
<45
50-70
>70
<45 — <15%
50-70 — 35%
>70 —- > 50%
in diastolic dysfunction, hypertrophied LV is prone to ischemia; therefore maintenance of a ___ (low/high) MAP and ___ (low/high) normal HR is crucial.
high MAP
slow normal HR
DHF: factors that predispose to poor LV distensibility
- myocardial edema
- fibrosis
- hypertrophy
- aging
- pressure overload
most common causes of DHF:
- ischemic HD
- long-standing HTN
- progressive Ao stenosis
DHF more common in which sex
women > men
characteristic heart sound or gallop rhythm present in SHF and DHF
SHF – 3rd heart sound
DHF – 4th heart sound
most common cause of left side HF
Right side HF
most prominent signs in right HF
peripheral edema
congestive hepatomegaly
this type of output failure have may normal CI at rest but inadequate for stress
low-output failure
type of output failure from INC hemodynamic burden
high-output failure
most common causes of low-output failure
CAD cardiomyopathy HTN valvular dis pericardial dis
most common causes of high-output failure
anemia pregnancy a-v fistulas severe hyperthyroidism beriberi Paget's
HF: adaptive mechanisms to maintain CO
- INC SV (frank starling)
- SNS activation
- alt INOTROPY, HR, afterload
- humorally mediated response
key change in progression of HF
remodeling
according frank starling, SV is directly related to
LVEDP
HF compensatory mechanisms: how does SNS activation affect CO
(RAAS) inc venous tone - shift blood from peripheral to central = VR enhanced = CO maintained via frank starling
what activates RAAS (kidney related)
DEC in renal blood flow
what does RAAS activation do in renal tubuls
reabsorption of Na and H2O
inc blood volume = inc CO by FS relationship
good for short-term but contributes to deterioration long term
HF: in SNS activation what is happening to beta-adrenergic receptors and CAT. Ultimately this causes ____.
- down-regulation of beta-adrenergic receptors
- inc CATS (urine and plasma)
- high NE levels (directly cardiotoxic)
- leads to remodeling
- what Beta-Blockers aim at reducing
Systolic HF + LOW CO = SV is ___
any INC in CO depends on what?
SV is fixed
INC HR
(SHF + low EF) tachycardia is expected finding
goal of HR in DHF
prevent tachycardia (inadequate filling time)
humorally mediated response: generalized vasoconstriction initiated by 5 things:
- SNS activity and RAAS
- PSNS withdrawal
- High vasopressin levels
- endothelial dysfunction
- inflammatory mechanisms
function of BNP production in HF
promotes BP
protects form effects of volume/pressure overload
physiologic effects of BNP in HF:
(VANDI) vasodilation anti-inflammatory natriuresis diuresis inhibitinon of RAAS and SNS
both ANP and BNP inhibit what
(even thou blunted over time)
can give exogenous in acute HF
hypertrophy
fibrosis
remodeling
most common cause of myocardial remodeling
ischemic injury
1st line tx in HF
ACE inh aldosterone inh (promote reverse-remodeling)
earliest subjective finding of HF
dyspnea
-starts with exertion
why orthopnea in HF
inability of failing LF to handle increased VR when supine
Hallmark Sx of LOW cardiac reserve and CO
fatigue and weakness at rest
or with minimal exertion
“classic” findings of LV failure
tachypnea
moist rales
- mild HF - bases
- pulm edema - diffuse
what is S3 sound known as and what causes (physiological)
- ventricular gallop
- blood entering and distending a noncompliant LV
sign of severe chronic HF
-due to high metabolic rate, anorexia, nausea, dec intestinal absorption, dec splanchnic venous congestion, HIGH CYTOKINES (interferon and interleukins)
cardiac cachexia
BPN levels and indications
can be affected by gender, adv age, renal, obesity, PE, dysrhythmia
<100 negative
100-500 probable HF
> 500 consistent with HF
2 drug classes favorable influence on long term outcomes
ACE inh
Beta Blockers
benefits of ACE inh
promote vasodilation
reduce water and sodium reabsorption
supports potassium conservation
dec ventricular remodeling (potentiates reversal)
side effects of ACE inh
BP, syncope, renal dysfx, HYPERkalemia,
non productive cough, angioedema
similar but NOT superior to ACE inh
given ONLY to those who cant tolerate ACE inh
benefit to those with returning angiotensis increase
ARBs
aldosterone does what
also potassium levels
sodium and H2O retention
hypokalemia
remodeling
monitor what levels with aldosterone antagonist (which are incorpoprated as 1st line therapy in all HF)
renal fx
potassium
excessive doses of diuretics may lead to 3 things
hypovolemia
prerenal azotemia (high cr, bun, waste)
undesirable LOW CO w/ worst clinical outcomes
digoxin improves survival (t/f)
F
this is uncertain
