Cardiac Flashcards
Numbers to know:
CaO2
DaO2
VO2
CvO2
- CaO2: Arterial oxygen content = 20 mL/O2/dL
- DaO2: Oxygen delivery = 1000 mL/min
- VO2: Oxygen consumption = 250 mL/min
- CvO2: Venous Oxygen content = 15 mL/dL
Ohm’s law
Flow = ∆Pressure
<span><span> Resist</span>ance</span>
Cardiac Output = ∆Pressure (MAP-CVP)
<span><span> Resist</span>ance </span><span>(SVR)</span>
Poiseuille’s law
Q = ˙π * r4(P1 - P2)
8 n l
Flow = (pi) x (radius4) x (P1-P2)
8 x (viscocity) x (length of tube)
Two determinants of Blood Viscocity
- Hematocrit
- Temperature
Cardiac Output
(Formula + Normal Values)
CO = SV x HR
CO = MAP
SVR
(5-6 L/min)
MAP
(Formula + Normal Values)
MAP = (CO x SVR) + CVP
80
MAP = Systolic + 2(Diastolic)
3
(70-105 mmHg)
FICKS PRINCIPAL
Cardiac Output = Total Body Oxygen Consumption
(Pulmonary Arterial O2-Pulmonary Vein O2)
CO = VO2
(Ca02 - Cv02)
VENOUS RETURN
VR = PSF(7)- PRA(0)
RVR(1.4)
VR = MEAN SYSTEMIC FILLING PRESSURE
REYNOLDS #
Renyolds Number = (Density) (Diameter) (Mean velocity)
Viscocity
<2000 = laminar flow
>4000 = turbulent flow
2000-4000 = transitional flow
RESISTANCE/PRESSURE AND FLOW
Q = (PIE)(r to the 4th) / 8Ln ) (P1-P2)
Resistance in Parallel
1/Rtotal = 1/R1 + 1/R2 + …
Capillary Blood Flow
T= Pr
r = radius
Factors that effect Pressures (5)
Aortic Distensibility
Stroke Volume
HR P
eripheral Resistance
Ejection Velocity
Systemic Vascular Resistance
(Formula + Normal Values)
SVR = (MAP - RAP) x 80
CO
SVR = (MAP - CVP) x 80
CO
800-1500 dynes/sec/cm2
Afterload
Tension is proportional to Pressure times radius / wall thickness
Stroke Work
Stroke Work = SV x MAP
Factors that effect inotropy
- HR Sympathetic activation
- Parasympathetic inhibition
- Circulating Catchecholamines
- Afterload
Factors that increase ventricular filling (preload) 5
- Increased atrial contractility
- Increased ventricular compliance
- Increased CVP
- Increased Aortic Pressure - increased after load decreased stroke volume = increased end systolic volume - Secondary increase in preload
- DECREASED Heart Rate
Two things that increase CVP
- Increased thoracic venous volume - total blood volume - Venous return, r/t muscle contraction, respiration and gravity 2. Decreased venous compliance
Stroke volume and increased preload
Increased preload = increased SV r/t increased end diastolic volume
Stroke volume and increased afterload
Increased afterload = Decreased stroke volume r/t increased end systolic volume
Stroke volume and increased isotropy
Increased isotropy = Increased stroke volume r/t decreased end systolic volume
Ejection Fraction
EF = SV / EDV SV = EDV- ESV
Decreased O2 delivery to tissue
Supply / demand mismatch causes: Adenosine Release Increased Co2 - Especially in Brain ATP & ADP Release Histamine Release Increased K+ an Mg++ ions Increased H+ ions, acidosis Ultimately Causing VASODILATION
Cardiac index and Stroke Index
CI = CO / BSA BSA = M2 SI = SV / BSA
02 Delivery
O2 Delivery = CBF x CaO2 CBF = Coronary blood flow (mL / Min) Ca02 = Oxygen concentration of arterial blood (mL 02 / mL Blood)
Cardiac Work
(Formula)
Cardiac Work = SW x HR
- How much work being done for a unit of time
- Cardiac minute work or Ventricular minute work
Cardia Index
(Formula + Normal Values)
CI = CO
BSA
(2.8/4.2 L/min/m2)
Stroke Volume
(Formula + Normal Values)
- Stroke Volume = EDV - SEV
- Stroke Volume = CO x 1000
HR
(50 -110 mL/beat)
Stroke Volume Index
(Formula + Normal Values)
Stroke Volume Index = SV
BSA
(30-65 mL/beat/m2)
Ejection Fraction
(Formula + Normal Values)
Ejection Fraction = EDV -ESV x 100
EDV
Remember SV = EDV - ESV
(60-70%)
Pulse Pressure
(Formula + Normal Values)
SBP - DBP
Stroke Volume Output
Arterial Tree Compliance
(normal = 40 mmHg)
Systemic Vascular Resistance INDEX
(Formula + Normal Values)
SVR = (MAP - RAP) x 80
CI
SVR = (MAP - CVP) x 80
CI
1500-2400 dynes/sec/cm2 / m2
Pulmonary Vascular Resistance
(Formula + Normal Values)
PVR = (MPAP - PAOP) x 80
CO
150-250 dynes/sec/cm2 / m2
Pulmonary Vascular Resistance INDEX
(Formula + Normal Values)
PVR = (MPAP - PAOP) x 80
CI
250-400 dynes/sec/cm2 / m2
Frank Starling Mechanism
INCREASED ventricular volume results in HIGHER cardiac ouput to a point.
(this is based on sarcomere cross bridges)
Contractiliy (inotropy) is and INDEPENDENT variable that is UNRELATED to _______________________________________.
Prelaod and Afterload
Key electrolye in exitation-contraction coupling
Calcium
(think calcum induced calcium-release)
Explain the path of Calcium in myocyte exitation-contraction coupling.
- Depolarization of myocyte membrane opens Voltage gated L-type Ca++ channels
- this is durring PHASE II of the action potential.
-
Calcium Induced Calcium Release
- Influxed Ca activates ryanodine 2 receptor inducing Ca release form the sarcoplasmic retiulum
- Ca++ BINDS to Troponin-C causing CONTRACTION
- Unbinding of Ca++ causes relaxation
- Ca++ returns to SR (MOST) or leaves the myocyte cell (Smaller amount)
- Ca++ enters SR via SERCA2 pump then binds to Calsequestrin (CSQ)
- Ca exits cell via Sodium/Calcium exchanger
Beta 1 stimulation activates adelylate cyclase which then converts ATP to cAMP
cAMP increases production of phosphokinase A.
Explain the three effects of increased Phosphokinase A
Ultimately Phosphokinase A increases intracellular calcium causing
increased contractility in a shorter period of time
_____________________________________________________
- Phosphokinase A Activates MORE L-Type Calcium channels causing MORE calcium to enter the myocyte
- More calcium stimulates the Ryanodine receptor to release MORE calcium
- Stimulation of SERCA2 pump = faster uptake of calcium to sarcoplasmic reticulum
The Law of LaPlace
Used to understand myocardial afterload
Wall Stress = Intraventricular Pressure x Radius
Ventricular Thickness
Coronary Blood Flow Equation
Coronary Blood Flow = Coronary Perfusion Pressure
Coronay Vascual Resistance
(Ohm’s Law)
Coronary Perfusion Pressure
CPP = Aortic DBP - LVEDP
or
CPP = DBP - Pulmonary artery occlusion pressure
Normal Values for Coronary Blood Flow
What is the % of Cardiac Output?
Coronary blood flow = 225-250 mL/min
This is 4-7% of Cardiac Cutput
Coronary vasculature autoregulates between a MAP of ______________________.
Coronary vasculature autoregulates between a MAP of
60-140 mmHg
Myocardial oxygen consumtion rate
8-10 mL/min/100g of tissue
Myocardial Oxygen Extraction Ratio
70%
Coronary Sinus Oxygen Saturation
30%
Explain myocardial supply and demand
Because the myocardiaum has a high extraction ratio of 70% → increasing oxygen extration in times of increased demand is not effective.
In order to adequately profuse the heart coronary blood flow (supply) and CaO2 MUST increase to satify the demand.
Drug therapy for valvular disease
- Digitalis (Digoxin) - Given to increase contractility and slow the ventricular rate in those with a-fib
- Diuretics - May be given for excess intravascular fluid volume, but resultant hypokalemia can place at risk for digitalis toxicity
- Prophylactic Antibiotics - Recommended for the protection against the development of sub-acute bacterial endocarditis
Tests for valvular heart disease? what will they tell us?
-
Doppler Echo -
- valve movement, flow and pressure gradients
-
Cardiac cath
- measure the severity of valvular heart disease
- valve movement, flow and pressure gradients
- ABG→decreased PaO2 and V/Q mismatch
Pathophysiology of mitral stenosis
- Most common in females
- Primary cause = rheumatic fever (slow development over 20-30 years)
-
Valvular manifestations:
- fusion of mitral valve leaflets at the commisures
- calcification of annulus an leaflets
- Senosis with a valve <1 cm2 (normal 4-6cm2) need 25 mmHg to generate adequate cardiac output
- Stenosis over time will lead to
- Left atrial enlargement
- Pulm HTN
- RV enlargement and RF failure
What are some complications associated with Left atrial enlargement?
- Left atrial enlargement - Predisposes to a-fib
- A-fib→stasis and development of thrombi
- Anticoagulants are needed
Severe MS can lead to
CHF
Mitral Stenosis Anesthetic Management GOALS
SLOW, TIGHT, and FULL → prevention and treatment of events that decrease CO or cause pulmonary edema
-
Slow HR 50-60:
- Avoid tachycardia or a-fib with RVR (both decreases CO and cases pulmonary edema d/t increased RA pressure)
-
Tight controll of blood volume:
- Tight fluid administration, give blood or colloids.
-
Full:
- manitain preload→avoid marked increases in blood volume from over-transfusion or head-down positions →still need adequate pressures to overcome the stenosed valve.
- Maintain afterload →Large decreases in SVR will drop preload. More importantly - the compensation for decreased SVR→baroreceptor reflex→increases HR which will generate a LOW CO in this patient! (avoid NTG, and hgh MAC techniques→IAs will drop SVR).
- Manitain full contractility
(also avoid arterial hypoxemia/hypoventilation that may exacerbate PulmHTN→leading to right ventricualr failure)
Induction for MITRAL STENOSIS pharmacologic considerations
- Etomidate is ideal (if you must use propoflol use it with phenylephrine, also give esmolol prior to DVL)
- Goal = ventricular rate controll!
- USE: ß-blockers, CCB
- AVOID: tachycardia →decreases left ventricualr filling and increases left atrial pressure! a drop in SV
- AVOID things that increase HR→ NO KETAMINE, No anticholinergics (glyco or atropine), histamine releasing drugs
- AVOID things that abruptly decrease SVR→ Better to chose a high opioid techniqe over IAs , Propofol, NTG
- USE: Phenylephrine(pure vasoconstrictor)and Vasopressin (does NOT effect the pulmonary vasculature) to treat/avoid decreased SVR
- Possiblly avoid nitrous → it increases pulmonary vascualar resistance which may potentiate pulmonary edema
- Desflurane → not a good choice it decreases SVR and causes increased HR and BP transiently when increased - ISO = slow ∆ abd time for body to adapt
Patho of mitral regurgitation
- Usually d/t rheumatic fever and is almost always associated with mitral stenosis.
- Causes decreased forward LV Stroke volume and retrograde flow during ventricular contraction - resulting in LA fluid volume overload
- Can be caused by RA, MI, ruptured chordae tendonae, ischemia to the papillary muscles, congenital disorders
Appearance of mitral regurgitation:
- On PCWP tracing
- x-Ray
- EKG
- Reguritant flow = V wave on PCWP tracing
- (Size of the V wave correlates with the magnitude of regurgitant flow)
- X-ray shows cardiomegaly
- (eccentric hypertrophy over time to compensate for decreased CO)
- EKG shows Left atrial and left ventricular hypertrophy
- (Atrial = notched broad P wave)
Mitral regurgitation anesthetic management GOALS
Fast, Full, Forward
Goal = improve LV forward stroke volume and decrease the regurgitant fraction:
-
Fast HR: (80-100 bpm)
- Avoid sudden decreases in HR - Bradycardia cuases severe LV volume overload and allows more time for blood to flow backwards
-
Full tank: Preload remains the same
- Increase = more regurgitaion
- Decrease = Less CO (NTG = bad choice
-
Forward: Decreased/Normal Afterload
- Decreased SVR promotes forward flow
- Nitropruside → decreases afterload and allows for more effective cardiac pumping
- Hydralazine (arterial dialator)
- Regional may be a good choice to decrease SVR
- Avoid: sudden increases in SVR, which would promote backward flow
-
Maintain contractility -
- low MAC - balanced techniques - high opioids,
- inotropes
Causes of of aortic stenosis. Associated size and pressure?
- Calcification developed over time (develops around 60-80 years)
- Bicuspid Aortic Valve instead of a Tricuspid Aortic valve (develops around 30-50 years)
- Congenital abnormality
- Rheumatic heart disease or Endocarditis
- Normal valve area is 2.5-3.5cm2. Significant AS is associated with valve area of <1 cm2 and a transvalular gradient of >50mmHg.
Explain the pathology of angina associated with aortic stenosis.
What is the classic symptom triad with Aortic Stenosis?
- Angina is often present without CAD
- The specific contributers to angina
- LV concentric hypertrophy increases oxygen requirements
- Increased myocardial work to overcome stenosis
- decreased O2 delivery d/t compression of the subendocardial vessels
-
Classic triad = Angina, DOE, Syncope
- (75% who are symptomatic will die w/ in 3 years if they do not have a valve replacement!)
Aortic Stenosis anesthetic management GOALS from class
Prevent hypotension and any hemodynamic change that will decrease cardiac output
-
MUST Maintain NSR: Low/normal (60-90)→avoid sudden decreases in HR (worse) AND tachycardia
- BP is HR dependent, need atrial kick
- Maintain Preload→Optimize intervascular fluid volume to maintain venous return and LV filling
- Maintain Afterload→Avoid sudden decreases in SVR→decreased coronary filling
- Maintain contractility
Induction in a patient with Aortic Stenosis. Method? Drugs?
- GENERAL ANESTHESIA is preferred over regional (becsaue regional causes sympathectomy and drop in SVR)
- Good choice is something that DOES NOT decrease SVR-
- Etomidate is best
- High opioid technique if poor LV function
- Etomidate + Benzos
- Propofol + Phenylephrine??
- AVOID: Ketamine - it casuses tachycardia
Causes of aortic regurgitation
- Acute: Infective endocarditis, Dissection of thoracic aortic aneurysm
- Chronic: Rheumatic fever, Chronic HTN, Marfans, idiopathic aortic root dilation, bicuspid aortic valve
Causes and management of Tricuspid Regurgitation
- Usually due to pulmonary HTN.
- RV becomes dilated (usually a functional problem and well tolerated)
- Leads to RV Volume overload
-
GOALS:
- maintain fluid volume→preload dependent
- avoid a drop in venous return (make sure PPV allows for adequate VR)
-
Avoid increase in PA pressure
- Avoid N2O
- increased PA pressure can cause a right to left shunt if the pt has a PFO
- Tricuspid regurge is common in seasoned atheletes
How do we treat a-fib with RVR?
BBs, CCBs, amiodarone, or digoxin.
Preop eval
Syncope, fainting, compensation? Major end organ disease? Cardiac hypertrophy, increased SNS output for compensation? How bad is the CV disease?
One of the single best questions for many CV assesments
Exercise tolerance
Common symptoms of CHF with valve disease
Dyspnea, orthopnea, fatigue - CHF is a common conpanion with valvular disease
what is a common arrythmia associated with valvular disease?
Atrial Fibrilation - due to left atrial enlargement
What are the sighns and symptoms associated with Left atrial enlargement?
- dispnea on exertion
- orthopnea
- paroxysmal nocturnal dyspnea
with mitral stenosis CO is usually maintained by an increase in atrial pressure - what situations cause CO to drop?
- Stress induced tachycardia
- A-fib - when there is a loss in atrial contraction
Induction of anesthesia for Mitral Regurgitaion
Remember: Fast, Full and Forward - choices should be based on avoiding bradycardia and avoiding an increase in SVR
- Maintain fast HR:
- Pancuronium = stimulates the ganglion and causes tachycardia
- Have Atropine ready, maybe give at induction
- Etomidate = minimal changes in HR, SVR and CO
- Propofol + Ephedrine??
Mirtal Regurgitation Maintinence and of Anesthesia drug considerations
Maint.Determined by the degree of LV dysfunction
- Absence of severe LV dysfunction use Nitrous + volitile
- Use a Lower MAC - VAs attenuate increases in BP and SVR that accompany surgical stimulation
- Opioids → Class = minimizes likelyhood of drug induced myocardial depression (stoelting says to use caution with high doses becasue of the decrease in HR and myocardial depression)
- Isoflurane - decreases SVE and prevents increases in BP d/t surgical stimulation - Sevo and Des do as well, OK choices
- SNP, Hydralazine, (NTG???) intra op to decrease BP - they all decrease afterload
Monitor considerations for Mitral Reurgitation and Mitral Stenosis.
- Invasive monitoring depends on the
- surgical procedure
- extent of phydiologic impairment
- presence end organ dysfunction
- CVP (MR used to monitor V-wave)
- +/- a-line
- +/- swan
- consider TEE if undercoing major fluid shift surgeries (MS may require post op intubation d/t CHF/pulmonary edema - need time to equilibrate)
Explain why Normal Sinus Rhythm MUST be maintainded in Aortic Stenosis
HR determines 3 things
-
Time for ventricualr filling
- (increased HR = decreased LV filling = decreased CO)
- Volume of ejected SV
-
Coronary Profusion→coronaries fill in diastole
- (increased HR = decreased coronary blood flow→ ischemia and further LV deterioration)
They are reliant on atrial kick to have adequate LVEDV
- a junctional rhythm or a-fib = dramatic decrease in SV and BP
- Decreased BP = Decreased coronary blood flow = Ischemia
- Hypotension should be treated with Phenylephrine - b/c it WILL NOT increase HR
AS requires aggressive treatment of hypotension to prevent cardiogenic shock →
- it is hard to get a BP back because the force required to overcome the stenotic valve is too high and adequate SV cannot be attained. For this same reason CPR is ineffective in these patients
Maintinence of anesthesia in a patient with Aortic Stenosis
(key points, drugs and likely complications)
- Anestheisa maintained with N2O + opioids or if they have significant LV dysfunction a High Opioid Technique
-
NMB - w/o CV side effects (Roc, Vec, Cis-atra)
- Bad Choice = Pancuronium - stimualtes Ganglion and increases HR
- Hypotension: treat with an alpha agonist - Phenylephrine (it DOES NOT increase HR)
- Treat Junctional Rhythm/Bradicardia (Glycopyrolate, Atropine, Esmolol) →BP is HR dependent
- SVT - treat promptly with cardioversion
- Aortic Senosis has a propensity to develop ventricualar arrythmias- ALWAYS have Lidocaine, Amioderone and a Defibrilator Availible
Intraoperative monitoring for aortic stenosis MUST consist of this
5 lead EKG that is capable of detecting myocardial ischemia
Explain the basis of the valvular disease that has the highest perioperative risk
- Aortic stenosis has the highest risk of intraoperative cardiac complications, increased mortality and increased risk of perioperative myocardial infarction
- The risk for myocardial ischemia in aortic stenosis is INDEPENDENT of their assoiated risk attributed to CAD
The magnitude of aortic regurgitation depends on what two things?
- Time → determined by HR → increase HR = decreased time for regurgitant flow
- Pressure gradient across the aortic valve → peripheral vasodilation will decrease the pressure gradient and facilitat forward flow
Explain the peripheral signs of hyperdynamic circulation. Where is it evident?
- Widened pulse pressure
- Decreased Diasotolic BP
- Bounding pusles
(evidient in disease processes such as aortic regurgitation, liver failure)
Aortic Regurgitation Anesthetic Management GOALS
Goal: maintain forward LV stroke volume
-
High/normal HR→ 80-100 bpm
- High HR = less regurgitant volume (decreased diasotlic time where refurgitation can occur)
- If HR falls below 80 → volume overload and LV failure
- Have Robinul (glyco) and atropine on hand
- Maintain Preload
-
Decreased/normal Afterload→
- AVOID sudden increases in SVR→it will precipitate LV failure
- Use of a vasodialator to decrease afterload (SNP, hydralazine, nifedipine)
-
Maintain contractility → delicate balance
- minimize drug induced myocardial depression
- lower MAC, use of opioids or high opioid technique
(IF LV failure develops tx with vasodialator to reduce afterlaod and inotropes to increse contractility → ie dobutamine + SNP)
Aortic regurgitation INDUCTION anesthetic management.
Goal: Avoid decreases in HR below 80, maintain forward LV stroke voume.
- DOC is usually Etomidate
- Choose a NMB that does not decrease HR
- Roc, Vec, Cis-Atricurium
- Pancuronium - stimulates ganglion = increases HR
- Have atropine and glyco READY! (treat brady promptly)
4.
Aortic Regurgitation consiterations for Maintinence of Anesthesia
-
In the absence of LV dysfunction:
- N2O + volitile anesthetic
- Ususally Iso(minimal cardiac depression, CO maintained, preservation of baroreceptor reflex
- Des and Sevo ok as well
- N2O + Opioids may unmask myocardial dysfunctction
-
With significant LV dysfunction:
- High opioid technique BUT there is a risk for bradycardia - treat promptly with atropine!
- If hypotension occurs DOC is Ephedrine - increases HR
- Mantain volume status, propmt replacement of blood loss to maintain LV SV
- Treat high SBP with SNP
Formula for Ventricular Compliance
C Ventricular = Ventricular Volume
Ventricular Pressure
Beck’s Triad
Presentation of Cardiac Tamponade
- Muffled Heart Tones - pericardial fluid accumulation
- Jugular Vein distention - impaired venous return to the right heart
- Hypotesion - decreased stroke volume
Explain Pulsus Paradoxis
SBP decreases > 10 mmHg on inspiration
(increased venous return bows ventricular septum toward left heatr leading to decreased stroke volume, cardiac output and SBP)
