Heart Failure Flashcards
Heart failure definition
when the heart can’t meet the body’s O2 demands
- inability to relax enough to receive SV
- inability to deliver SV
LV is the no 1 cause. LV is also the #1 cause of RVHF
Systolic most common in men. Diastolic most common in women
strongest indicator for perioperative cardiac morbidity and mortality
Acute HF
from structural event like MI that causes a valvular dysfunction or a new RWMA
Poorly tolerated bc no time for compensation
manifested by high ventricular filling pressures, low CO, HTN/HypTN
Use diuretics, vasodilators, inotropic drugs, mechanical assist devices
Chronic HF
remodeling of the heart and RAAS activation
BP is maintained and signs of venous congestion are present
LHF
LVED is elevated and leads to pulmonary congestion
S3 gallop hypotension tachycardia cool/pale extremities anorexia/weight loss
RHF
associated with systemic congestion, edema, hepatomegaly
JVD distensible by pressing on the liver - hepatojugular reflex
ascites
weight gain
peripheral edema
High output failure
when the heart can’t keep up with massively increased metabolic demands (anemia, pregnancy, sepsis)
Low output CO
unable to respond to exercise or stress
commonly encountered when trying to come off CPB in pts with severe systolic HF
Starling curve
SV increases as wall tension is increased by contracting muscle
Venous capacitance vessels constrict to increase preload to contribute to this increased wall tension
When contractility becomes impaired then SV is reduced for any given volume put into the ventricle
HF path
initial cause of HF causes an increase in preload to maintain CO but eventually exercise intolerance dvlps
In late stages, CO is sufficient at rest but pt can’t exercise
Neurohormonal reflexes activated to try to maintain CO and SVR
the RAAS system and ADH starts going overtime to increase tone by increasing fluid volume and resting sympathetic vascular tone
Blood is shifted from the peripheral to central circulation and arteriolar constriction redistributes blood from the kidneys, splanchnic circulation, skeletal muscles, skin
The kidneys’ perceive this decrease in BP and pump out more renin, worsening the cycle
As the heart fails in systolic HF you expect a high resting HR to maintain CO
Heart as an endocrine organ
tries to combat cycle
ANP is released in response to increased stretch of the atria.
BNP is released by the ventricles
This causes diuresis, natriuresis, vasodilation, anti-inflammatory effects , inhibition of the RAAS and SNS, inhibits remodeling
body eventually does not respond to this
CVP has to rise to maintain preload and CO and eventually any increase in preload does not result in increased CO and the cycle leads to decompensation and death
DX HF
ECHO
potential cause - such as valve disorders
concurrent pericardial effusions
establish baselines
HF classification
AHA
A - high risk for HF w/o structure disease or symptoms
B- structural disease w/o s/s
C - Structural disease with HF symptoms
D - Refractory HF requiring specialized interventions
HF classification
NYHA
I - no limitation of physical activity; ordinary activity does not cause HF symptoms
II - slight limitations of physical activity; comfortable at rest, but ordinary physical activity results in HF symptoms
III - marked limitations of physical activity; comfortable at rest, but less than ordinary activity causes HF symptoms
IV 0 unable to carry on any physical activity w/o HF symptoms
Managing systolic HF
BB - combat SNS activation
diuretics - relieve circulatory congestion
digoxin
vasodilators - work well in African Americans (hydralazine, NTG)
statins - anti-inflammatory effects
ACEI - RAAS inhibition. beneficial at any stage of HF
aldosterone antagonists
Managing diastolic HF
lifestyle modifications
low dose diuretics
statins
Definitive treatment for HF
transplant
Total artificial heart
implanted in the chest
pulsatile flow
two pumps that simulate ventricles
bridge to treatment or destination
Inotropic support
increases intracellular cAMP but can incrase O2 consumption
Calcium sensitizers
enhance endogenous calcium to incrase contractility
no incrase in O2 consumption or HR
Levosimendan - in Europe currently
Nesiritide
BNP analogue that works at the A and B type receptors
inhibits RAAS
causes vasodilation
promotes diuresis
VAD use
Temporary
bridge to recovery
VAD use
Waiting transplant
bridge therapy
VAD use
Inotropic balloon pump to reversible condition
bridge to decision
VAD use
pats who are not transplant candidates
destination therapy
LVADs
bypass eh LV
RVADs
bypass the RV
VAD pts
typically end stage HF
anticoagulated
- insertion mandates blood products available
- antifibrinolytics administered to decrease blood loss
- Large bore IVs needed
- Art lines mandatory
- PACs should be considered
- Decreases in preload and increases in afterload should be avoided
- Pts have fixed CO and are therefore rate dependent - bradycardia not tolerated
- strict sterile technique
- TEE for placment
- if concurrent repairs, CPB
- NE and Phenyl will increase righ heart afterload from pulmonary vascular constriction - not good
- HTN should be treated to avoid strain on LVAD
VAD
induction
etomidate
NMB
high dose narcotic can be used
VAD considerations
no pulse
- NIBP won’t work
- Pulse ox won’t work
Art lines and oxygenation assessments are needed
- CO2 may be used a s surrogate in short cases
- TEE
Hypotension comes form decreased preload, RV failure, increased afterload - volume is essential. Prevents LV suck down
Afterload increases will also decrease forward flow and should be managed
No chest compressions
PVAD
temporary support devices in cardiogenic shock for up to 14 days (i.e. Impella)
demonstrate better support for end organs than the IABP but not better survival rates
CO 5L/min
contraindicated in prosthetic valves, severe AS/AR, PVD, aneurysms
Complications are stroke, AR, AV injury, tamponade, thrombocytopenia
Tandem Heart
inflow cannula placed in the femoral vein and placed into the RA, then trans-septally into the LA
the outflow catheter is placed in the femoral artery. LA oxygenated blood is drained and ejected retrograde into the abdominal aorta via the outflow cannula
CO is 5L/min
Pt has to have intact RV function
IABP indications
reduces afterload and increase CA perfusion
cardiogenic shock, MI, angina, arrhythmias
What is IABP?
flexible catheter that syncs to ECG and/or art line to allow balloon inflation during diastole
btwn 25-50 mL balloon that is filled with helium or CO2
anticoagulation is needed
Where is IABP placed?
the fem artery is usually accessed and it’s positioned 2 cm distal to the left subclavian artery origin
Timing of IABP
timed with dicrotic notch of the arterial waveform (AV closure) that then seals the descending aorta and forces antegrade flow into the CA.
The balloon is deflated as the R wave occurs on the ECG creating a vacuum effect that reduces afterload and enhances ventricular ejection
*difficult w irregular rhythms
ECMO
temporizing measure to provide perfusion support
cardiogenic shock failure to wean for CPB, resuscitation
Anti coagulation is necessary
Risks bleeding, stroke, infection, hemolysis
veno-venous ECHMO
used for respiratory failure patients
supports the lungs by improving gas exchange
the femoral and internal jugular veins are cannulated
veno-arterial ECMO
bypasses the pulmonary circulation
the carotid artery and jugular vein are cannulated
blood drains into a venous reservoir via centrifugal or roller pumps and circulates 3-6 L/min through an oxygenator. CO2 is removed and O2 is added. Heat exchanger warms blood before returning git
Heart failure anesthesia
All anesthesia types acceptable
Doses are lower
Circulating time is increased from decreased CO
PPV and PEEP can help decrease pulmonary congestion
Fluid use must be judicious
PACs, TEE can be considered
Artline likely
non-invasive CO monitors
Regional is ok as long as anticoag isn’t present
Heart transplant
criteria:
NYHA IV
EF <20%
terminal ESHF
surgical considerations for heart transplant pts
HR dependent
cannot tolerate preload and afterload changes
Induction - etomidate typical with narcotics
RSI with succ
Pts will have prolonged circ times
CPB
glucocorticoids administered
coagulopathies major concern
Bleeding major concern
heart transplant - coming off pump
epicardial pacing
volume status essential when coming off pump as the de-innervated heart is preload dependant
Indirect agents (ephedrine, anticholinergic) ineffective
Pumonary vasodilation may be achieved with NO, prostaglandin, milrinone
Pts with heart transplant
PHTN - so no N2O
Avoid histamine releasing drugs
FFP may be needed to normalize the INR
Do not have vagal nerve innervation, so resting HR of 110 BPM
Preload dependent
no response to indirect drugs
Vasopressin to treat hypotension
have no sympathetic, parasympathetic, veno-sensory innervation to the heart
will have 2 p-waves
have no sympathetic response to DL
Central line insertion is usually in the Left IJ to allow for the RIJ to be available for biopsies
TEE
Inotropic support
