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Flashcards in Cardiac Deck (88):

Numbers to know:





  1. CaO2: Arterial oxygen content = 20 mL/O2/dL
  2. DaO2: Oxygen delivery = 1000 mL/min
  3. VO2: Oxygen consumption = 250 mL/min
  4. CvO2:  Venous Oxygen content = 15 mL/dL


Ohm's law


Flow = ∆Pressure



Cardiac Output ∆Pressure (MAP-CVP)

                             Resistance (SVR)


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

  1. Hematocrit
  2. Temperature


Cardiac Output

(Formula + Normal Values)

CO = SV x HR





(5-6 L/min)



(Formula + Normal Values)

MAP = (CO x SVR) + CVP



MAP = Systolic + 2(Diastolic)



(70-105 mmHg)



Cardiac Output =          Total Body Oxygen Consumption

                                              (Pulmonary Arterial O2-Pulmonary Vein O2)


CO     =     VO2 

                            (Ca02 - Cv02)



VR = PSF(7)- PRA(0)






Renyolds Number = (Density) (Diameter) (Mean velocity)




<2000 = laminar flow

>4000 = turbulent flow

2000-4000 = transitional 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


eripheral Resistance

Ejection Velocity


Systemic Vascular Resistance


(Formula + Normal Values)

SVR = (MAP - RAP) x 80




SVR = (MAP - CVP) x 80



800-1500 dynes/sec/cm2



Tension is proportional to Pressure times radius / wall thickness


Stroke Work

Stroke Work = SV x MAP


Factors that effect inotropy

  1. HR Sympathetic activation
  2. Parasympathetic inhibition
  3. Circulating Catchecholamines
  4. Afterload


Factors that increase ventricular filling (preload) 5

  1. Increased atrial contractility
  2. Increased ventricular compliance
  3. Increased CVP
  4. Increased Aortic Pressure - increased after load  decreased stroke volume = increased end systolic volume - Secondary increase in preload
  5. DECREASED Heart Rate


Two things that increase CVP

1. 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



Decreased O2 delivery to tissue

Supply / demand mismatch causes: Adenosine Release Increased Co2 - Especially in Brain ATP &amp; 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




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



(2.8/4.2 L/min/m2)


Stroke Volume



(Formula + Normal Values)

  1. Stroke Volume = EDV - SEV
  2. Stroke Volume = CO x 1000



(50 -110 mL/beat)


Stroke Volume Index


(Formula + Normal Values)

Stroke Volume Index  =    SV




(30-65 mL/beat/m2)



Ejection Fraction


(Formula + Normal Values)

Ejection Fraction = EDV -ESV    x   100




Remember SV = EDV - ESV



Pulse Pressure


(Formula + Normal Values)




Stroke Volume Output

Arterial Tree Compliance


(normal = 40 mmHg)


Systemic Vascular Resistance INDEX


(Formula + Normal Values)

SVR = (MAP - RAP) x 80




SVR = (MAP - CVP) x 80



1500-2400 dynes/sec/cm2 / m2


Pulmonary Vascular Resistance


(Formula + Normal Values)

PVR = (MPAP - PAOP) x 80




150-250 dynes/sec/cm2 / m2


Pulmonary Vascular Resistance INDEX


(Formula + Normal Values)

PVR = (MPAP - PAOP) x 80




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


(think calcum induced calcium-release)


Explain the path of Calcium in myocyte exitation-contraction coupling.

  1. Depolarization of myocyte membrane opens Voltage gated L-type Ca++  channels
    • this is durring PHASE II of the action potential.
  2.  Calcium Induced Calcium Release
    • Influxed Ca activates ryanodine 2 receptor inducing Ca release form the sarcoplasmic retiulum
  3. Ca++ BINDS to Troponin-C causing CONTRACTION
  4. Unbinding of Ca++ causes relaxation
  5. 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


  1. Phosphokinase A Activates MORE L-Type Calcium channels causing MORE calcium to enter the myocyte
  2. More calcium stimulates the Ryanodine receptor to release MORE calcium
  3. 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




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



Coronary Sinus Oxygen Saturation 



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 CaO MUST increase to satify the demand.


Drug therapy for valvular disease

  1.  Digitalis (Digoxin) - Given to increase contractility and slow the ventricular rate in those with a-fib
  2.  Diuretics - May be given for excess intravascular fluid volume, but resultant hypokalemia can place at risk for digitalis toxicity
  3. Prophylactic Antibiotics - Recommended for the protection against the development of sub-acute bacterial endocarditis


Tests for valvular heart disease? what will they tell us?

  1. Doppler Echo
    • valve movement, flow and pressure gradients
  2. Cardiac cath
    • measure the severity of valvular heart disease
    • valve movement, flow and pressure gradients
  3. ABG→decreased PaO2 and V/Q mismatch


Pathophysiology of mitral stenosis

  1. Most common in females
  2. Primary cause = rheumatic fever (slow development over 20-30 years)
  3. Valvular manifestations:
    • fusion of mitral valve leaflets at the commisures
    • calcification of annulus an leaflets
  4. Senosis with a valve <1 cm(normal 4-6cm2) need 25 mmHg to generate adequate cardiac output
  5. 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



Mitral Stenosis Anesthetic Management GOALS

SLOW, TIGHT, and FULL → prevention and treatment of events that decrease CO or cause pulmonary edema 

  1. Slow HR 50-60:  
    • Avoid tachycardia or a-fib with RVR (both decreases CO and cases pulmonary edema d/t increased RA pressure)
  2. Tight controll of blood volume:
    • Tight fluid administration, give blood or colloids.
  3. Full:
    • manitain preloadavoid 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 reflexincreases HR which will generate a LOW CO in this patient! (avoid NTG, and hgh MAC techniquesIAs will drop SVR). 
    • ​​​Manitain full contractility 

(also avoid arterial hypoxemia/hypoventilation that may exacerbate PulmHTNleading to right ventricualr failure)


Induction for MITRAL STENOSIS pharmacologic considerations

  1. Etomidate is ideal (if you must use propoflol use it with phenylephrine, also give esmolol prior to DVL)
  2. Goal = ventricular rate controll!
    • USE: ß-blockersCCB
    • AVOID: tachycardia →decreases left ventricualr filling and increases left atrial pressure! a drop in SV
    • AVOID things that increase HRNO 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 
  3. Possiblly avoid nitrous → it increases pulmonary vascualar resistance which  may potentiate pulmonary edema
  4. 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

  1. Usually d/t rheumatic fever and is almost always associated with mitral stenosis.
  2. Causes decreased forward LV Stroke volume and retrograde flow during ventricular contraction - resulting in LA fluid volume overload
  3. Can be caused by RA, MI, ruptured chordae tendonae, ischemia to the papillary muscles, congenital disorders


Appearance of mitral regurgitation:

  1. On PCWP tracing
  2. x-Ray
  3. EKG

  1. Reguritant flow = V wave on PCWP tracing
    • (Size of the V wave correlates with the magnitude of regurgitant flow)
  2. X-ray shows cardiomegaly
    • (eccentric hypertrophy over time to compensate for decreased CO)
  3. 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:

  1. 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
  2. Full tank: Preload remains the same
    • Increase = more regurgitaion
    • Decrease = Less CO (NTG = bad choice
  3. 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 
  4. Maintain contractility -
    • low MAC - balanced techniques - high opioids,
    • inotropes


Causes of of aortic stenosis. Associated size and pressure?

  1. Calcification developed over time (develops around 60-80 years)
  2. Bicuspid Aortic Valve instead of a Tricuspid Aortic valve (develops around 30-50 years)
  3. Congenital abnormality 
  4. Rheumatic heart disease or Endocarditis
  5.  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?

  1. Angina is often present without CAD
  2. 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
  3. 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

  1. MUST Maintain NSR: Low/normal (60-90)→avoid sudden decreases in HR (worse) AND tachycardia
    • BP is HR dependent, need atrial kick
  2. Maintain Preload→Optimize intervascular fluid volume to maintain venous return and LV filling
  3. Maintain Afterload→Avoid sudden decreases in SVR→decreased coronary filling
  4. Maintain contractility


Induction in a patient with Aortic Stenosis. Method? Drugs?

  1. GENERAL ANESTHESIA is preferred over regional (becsaue regional causes sympathectomy and drop in SVR)
  2. Good choice is something that DOES NOT decrease SVR-
    • Etomidate is best
    • High opioid technique if poor LV function
    • Etomidate + Benzos
    • Propofol + Phenylephrine??
  3. AVOID: Ketamine - it casuses tachycardia 


Causes of aortic regurgitation

  1. Acute: Infective endocarditis, Dissection of thoracic aortic aneurysm
  2. Chronic: Rheumatic fever, Chronic HTN, Marfans, idiopathic aortic root dilation, bicuspid aortic valve


Causes and management of Tricuspid Regurgitation

  1. Usually due to pulmonary HTN.
  2. RV becomes dilated (usually a functional problem and well tolerated) 
  3. Leads to RV Volume overload
  4. GOALS
    1. maintain fluid volume→preload dependent
    2. avoid a drop in venous return (make sure PPV allows for adequate VR)
    3. Avoid increase in PA pressure 
      • Avoid N2O
      • increased PA pressure can cause a right to left shunt if the pt has a PFO
  5. 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?

  1. dispnea on exertion
  2. orthopnea
  3. paroxysmal nocturnal dyspnea


with mitral stenosis CO is usually maintained by an increase in atrial pressure - what situations cause CO to drop?

  1. Stress induced tachycardia
  2. 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

  1. 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

  1. Absence of severe LV dysfunction use Nitrous + volitile
  2. Use a Lower MAC - VAs attenuate increases in BP and SVR that accompany surgical stimulation
  3. 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)
  4. Isoflurane - decreases SVE and prevents increases in BP d/t surgical stimulation - Sevo and Des do as well, OK choices
  5. SNP, Hydralazine, (NTG???) intra op to decrease BP - they all decrease afterload


Monitor considerations for Mitral Reurgitation and Mitral Stenosis.

  1. Invasive monitoring depends on the
    • surgical procedure
    • extent of  phydiologic impairment 
    • presence end organ dysfunction
  2. CVP (MR used to monitor V-wave)
  3. +/- a-line
  4. +/- swan
  5. 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

  1. Time for ventricualr filling
    • (increased HR = decreased LV filling = decreased CO)
  2. Volume of ejected SV
  3. 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)

  1. Anestheisa maintained with N2O + opioids or if they have significant LV dysfunction a High Opioid Technique
  2. NMB - w/o CV side effects (Roc, Vec, Cis-atra
    • Bad Choice = Pancuronium - stimualtes Ganglion and increases HR
  3. Hypotension: treat with an alpha agonist - Phenylephrine (it DOES NOT increase HR)
  4. Treat Junctional Rhythm/Bradicardia (Glycopyrolate, Atropine, Esmolol) →BP is HR dependent
  5. SVT - treat promptly with cardioversion
  6. 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

  1. Aortic stenosis has the highest risk of intraoperative cardiac complications, increased mortality and increased risk of perioperative myocardial infarction
  2. 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?


  1. Time → determined by HR → increase HR = decreased time for regurgitant flow
  2. 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?

  1. Widened pulse pressure
  2. Decreased Diasotolic BP
  3. Bounding pusles

(evidient in disease processes such as aortic regurgitation, liver failure)


Aortic Regurgitation Anesthetic Management GOALS

Goal: maintain forward LV stroke volume

  1. 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
  2. Maintain Preload
  3. Decreased/normal Afterload
    • ​​AVOID sudden increases in SVR→it will precipitate LV failure
    • Use of a vasodialator to decrease afterload (SNP, hydralazine, nifedipine)
  4. 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. 

  1. DOC is usually Etomidate
  2. Choose a NMB that does not decrease HR
    • Roc, Vec, Cis-Atricurium
    • Pancuronium - stimulates ganglion = increases HR
  3. Have atropine and glyco READY! (treat brady promptly)


Aortic Regurgitation consiterations for Maintinence of Anesthesia

  1. 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
  2. With significant LV dysfunction:
    • High opioid technique BUT there is a risk for bradycardia - treat promptly with atropine
  3. If hypotension occurs DOC is Ephedrine - increases HR
  4. Mantain volume status, propmt replacement of blood loss to maintain LV SV
  5. Treat high SBP with SNP


Formula for Ventricular Compliance

C Ventricular  =  Ventricular Volume

                                Ventricular Pressure


Beck's Triad

Presentation of Cardiac Tamponade

  1.  Muffled Heart Tones - pericardial fluid accumulation
  2. Jugular Vein distention - impaired venous return to the right heart
  3. 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)