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
digoxin caution in
elderly
impaired renal
dig toxicity Sx:
tx:
Sx: anorexia, nausea, blurred vision and dysrhythmias
Tx: reverse HYPOkalemia, antidigoxin antibodies, TPM (pacer)
vasodilators' action on: LV ejection: venous capacitance ventricular filling pressures SV
DEC resistance to LV ejection
INC venous capacitance
DEC ventricular filling presures
INC SV
benefit of statins in HF
anti-inflammatory and lipid lowering
DEC morbidity and mortality in SH
BEST treatment for DHF
prevention
- most tx is empirical/experimental
- no drug selectively diastolic fx
what caution to use with diuretics in DHF
want to relieve pulm congestion w/o significantly reducing preload (bc u want to optimize ventricular filling)
what physiologically causes cough in ACE inh (NH 202)
breakdown of bradykinin
-this does not occur in ARBs
CRT (cardiac reshynch therapy): where are leads introduced?
ventricular leads introduced via coronary sinus into epicardial coronary vein
-advanced to LATERAL WALL of LV
CRT (cardiac resynch therapy) recommended for:
NYHA Class III or IV
EF < 35%
QRS > 120 - 150 ms
caveat to CRT to keep in mind
therapy fails to improve 2/3 of patients that receive therapy!
ICD indication in HF from CAD
EF < 35%
EF < 40% w/ EP study demonstrating inducable ventricular dysrhythmias
ICD indications in all other causes of HF (excluding CAD)
after first episode of syncope or aborted ventricular tachycardia/v-fib
major differences btw 1st and 2nd generation LVADs
2nd Gen (NONpulsatile)
quieter
smaller
less thromboebolic risks
LVAD: percutaneous lead purpose and anesthetic implications.
“drive line”
exists right side of abdomen
connects pump to external console and power
– where exits skin (RUQ) site most likely to be infected
– do not let prep w/ iodine/providone (plastic breakdown) – drape out of field instead
most common LVAD in US
HeartMate II (2nd gen continuous flow)
LVAD: General anesthetic implications
periop anticoagulation mngmt cardiac rhythm devices antibiotic prophylaxis connection to power source AVOIDANCE of chest compression (dislodges cannula) USE BIPOLAR catery instead of MONO (or direct current away) NIBP - no pulse Pulse ox - no pulse USE cerebral oximeter may need US for a-line placement
percutaneous VAD designed for cardiac support up to how many days to bridging to CABG/stenting or stabilization
14
2 types of PVAD
Impalla
Tandemheart
absolute CI to impella (PVAD)
prosthetic valve
severe aortic stenosis
aortic regurge
peripheral vascular disease
complications of impella (PVAD) due to centrifugal force
hemolysis
thrombocytopenia (ie tearing of RBC’s)
complications of TandemHeart (PVAD)
paradoxical emboli
right - left shunt (seen in hypoxemia)
coronary sinus/RA injury
** cannula dislodgement and MV entrapment is the worse complication**
Preop mngmt of these in HF: diuretics: ACEinh: ARBs: digoxin:
- diuretics: may D/C day of surgery
- ACEinh: continue only if treating HTN (not remodeling)
- ARBs: D/C day BEFORE surgery
- digoxin: CONTINUE until day of sugery
described as the most important risk factor for perioperative morbidity and mortality
HF
how can PPV and PEEP be benefitial intraop in HF
decrease pulm congestion
improve arterial oxygenation
cardiomyopathy groups: (primary or secondary)
- confined to heart muscle
- genetic, acquired, or mixed
primary
cardiomyopathy groups: (primary or secondary)
-pathophysiological involvement of heart that is involved in multiorgan disorder
secondary
cardiomyopathy pathological cause: intrinsic or extrinsic
- DEC contractility of heart muscle that cannot be attributed to specif outside source
intrinsic
cardiomyopathy pathological cause: intrinsic or extrinsic
-directly attributed to disease process or toxin that adversely damages cardiac muscle (ischemia, chronic inflammation, congenital HD, metabolic, toxins
extrinsic
4 major forms of cardiomyopathy
1 dilated
2 hypertrophic
3 secondary restrictive
4 arrhythmogenic RV
cardiomyopathy groups: genetic list
*hypertrophic (most common genetic 1/500 incidence)
*arrhythmogenic RV
LV noncompaction
glycogen storage dis
conduction dis (Lenegre’s)
Ion channel issues (brugada, QT)
cardiomyopathy groups: mixed list
dilated cardiomyopathy*
primary restrictive nonhypertrophic
cardiomyopathy groups: acquired list*
- myocarditis (viral, bacterial, rickettsial, fungal, parasitic (chagas’s)
- stress cardiomyopathy
- peripartum cardmpthy
cardiomyopathy groups: infiltrative
amyloidosis*
gaucher’s dis
hunter’s syn
cardiomyopathy groups: storage
hemochromatosis *
glycogen storage dis
niemann-pick dis
cardiomyopathy groups: toxic*
- drugs (cocaine, alcohol
- chemo (doxorubicin, daunorubicin, cyclophospohamide)
- heavy metals (lead, murcury)
- radiation therapy
cardiomyopathy groups: inflammatory
sarcoidosis*
cardiomyopathy groups: endomyocardial
hypereosinophilic (loffler’s syn)
endomyocaridal fibrosis
cardiomyopathy groups: endocrine
DM
hyperthyroidism or hypo
pheo
acromegaly
cardiomyopathy groups: neuromuscular
Duchenne-Becker dystrophy
neurofibromatosis
tuberous sclerosis
cardiomyopathy groups: autoimmune
lupus RA scleroderma dermatomyositis polyarteritis nodosa
most common genetic CV disease
characterized by LVH with no disease (ie HTN, aortic stenosis)
Hypertophic CM
in hypertophic CM, what structures are commonly form hypertrohpy
septum
anterolateral free wall
Hypertophic CM: LVOT is bound anteiorly by ___ and posteriorly by ____ leaflet of MV
IV septum (anterior) anterior leaflet of MV (posterior)
Hypertophic CM: systolic contractiono of hypertophied septum accelerates blood flow thru LVOT creating ___ effect on anteior leaflet of MV (pulls it into LVOT!) –> accentuation LVOT obstruction –> Significant MR
Venturi effect
hypertrophic CM: LV relies on LA for volume and contraction around __ % of total volume. Keep in NSR
75
events that INC outflow obstruction:
Inc HR, Dec BP and volume
- increased contractility
- decresased preload (hypovelemia, vasodilators, tachy, PPV)
- decreased afterload (hypotension, vasodilators)
events that DEC outflow obstruction
- DEC contractility (volatiles, CCB, BB)
- INC preload (hypervolemia, brady)
- INC afterload (HTN, a-adrenergic stimulation)
hypertrophic CM: physical exam findings (not symptoms)
double apical pulse
gallop rhythm
murmur and thrill
hypertrophic CM: risk of sudden death more likely in this age group
10 - 30 yo
hypertrophic CM: ECG
LVH
high QRS voltage
ST/T changes
Qs resembling MI
hypertrophic CM: echo findings
EF > 80% and LVOT obstruction
hypertrophic CM: cardiac cath findings
pressure gradients
decrease in LV cavity
hypertrophic CM: definitive dx
endomyocardial biopsy
DNA analysis
hypertrophic CM: treatment main goal is to minimize LVOT obstruction.. what about goal for diastolic filling?
prolong diastole with:
BB
CCB - improve v-filling
hypertrophic CM: these hemodynamics will worse LVOT
SNS
hypovolemia
vasodilation
Per NH, this cardiomyopathy is the most common cause of sudden death in peds and young adult population
hypertrophic CM
NH: HCM anesthetic considerations regarding: preload: HR: afterload: depth of anesthesia: myocardial depression
- ensure adequate preload (NH says increase)
- HR: AVOID tachycardia
- afterload: increase
- ensure adequate depth of anesthesia (dont want SNS response!)
- myocardial depression IS desirable
NH: how does increasing contractility worsen HCM?
BASICALLY - GREATER LVOT OBSTRUCTION
- exacerbates the outflow obsruction by increasing septal wall contraction and decreasing CO.
- increased BF velocity causes greater degree of systolic anterior motion of MV’s anterior leaflet, causing more obstruction
HCM: which NMB to avoid
pancuronium (tachycardia)
those that release histamine
HCM: contraindicated vasoactives
dopamine
dobutamine
ephedrine
HCM: why avoid vasodilators
can inc LVOT obstruction (by decreasing afterload)
most common form of CM
3rd most common cause of HF
most common indication for transplant
most common in adult, men (esp. black)
dilated CM
in HCM: PCWP goal
maintain 19-25
bc of DEC diastolic compliance, PCWP DOES NOT equal LVEDV
DCM: medication treatment
diuretics
ACEIs
digoxin
anticoags
RCM: causes
genetic (familial CM)
infiltrative (SARCOIDOSIS)
storage dis ( HEMOCHROMATOSIS)
endomyocardial dysfunction (FIBROSIS)
RCM: genetic explanation
INC sensitivity of troponin and tropomysin complex though to be involved
RCM: rarest prevalence in ___
children
A RVDCM: S and Sx manifest in adolescence
tachy ventricular dysrhythmiaa T-wave inversion (V1-3) BBB hypokinetic RV DEC RV ejection JVD syncope peripheral edema
A RVDCM: common dysrhythmia
PVC all way to AFIB
very sensitive to CATs - potentiates lethal rhythms
A RVDCM: which antiarhythmic best
amio
Cor pulmonale: causes
COPD - MOST COMMON
restrictive lung ds
respiratory insuff of central origin (OHS - obesity hypoventilation syn)
Cor Pulmonale: epidemiology
> 50 yo
men 5x > women
Cor Pulmonale: main characteristic
PulmHTN
Cor Pulmonale: 3 signs of severe PHTN
accentuation of pulm component of S2
diastolic murmur dt incompetent pulm valve
systolic murmur dt TR
Cor Pulmonale: ECG signs
peaked P waves (lead I, II, III, avF)
RAD, RBBB
normal EKG does not exclude PHTN
Cor Pulmonale: med tx
diuretics
digitalis
pulm vasodilators (sildenafil - viagra)
Cor Pulmonale: DEC SVR in patients w/ FIXED PHTN can cause
SEVERE hypotension!
