Cardiac

Question 1

Numbers to know:

CaO₂

DaO₂

VO₂

CvO₂

Answer 1

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

Question 2

Ohm’s law

Answer 2

Flow = ∆Pressure

^{<span><span> Resist</span>ance</span>}

Cardiac Output = ∆Pressure (MAP-CVP)

^{<span><span> Resist</span>ance </span><span>(SVR)</span>}

Question 3

Poiseuille’s law

Answer 3

Q = ˙π * r⁴(P1 - P2)

8 n l

Flow = (pi) x (radius⁴) x (P1-P2)

8 x (viscocity) x (length of tube)

Question 4

Two determinants of Blood Viscocity

Answer 4

1. Hematocrit
2. Temperature

Question 5

Cardiac Output

(Formula + Normal Values)

Answer 5

CO = SV x HR

CO = MAP

SVR

(5-6 L/min)

Question 6

MAP

(Formula + Normal Values)

Answer 6

MAP = (CO x SVR) + CVP

80

MAP = Systolic + 2(Diastolic)

3

(70-105 mmHg)

Question 7

FICKS PRINCIPAL

Answer 7

Cardiac Output = Total Body Oxygen Consumption

(Pulmonary Arterial O₂-Pulmonary Vein O₂)

CO = VO₂

(Ca0₂ - Cv0₂)

Question 8

VENOUS RETURN

Answer 8

VR = PSF(7)- PRA(0)

RVR(1.4)

VR = MEAN SYSTEMIC FILLING PRESSURE

Question 9

REYNOLDS #

Answer 9

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

Viscocity

<2000 = laminar flow

>4000 = turbulent flow

2000-4000 = transitional flow

Question 10

RESISTANCE/PRESSURE AND FLOW

Answer 10

Q = (PIE)(r to the 4th) / 8Ln ) (P1-P2)

Question 11

Resistance in Parallel

Answer 11

1/Rtotal = 1/R1 + 1/R2 + …

Question 12

Capillary Blood Flow

Answer 12

T= Pr

r = radius

Question 13

Factors that effect Pressures (5)

Answer 13

Aortic Distensibility

Stroke Volume

HR P

eripheral Resistance

Ejection Velocity

Question 14

Systemic Vascular Resistance

(Formula + Normal Values)

Answer 14

SVR = (MAP - RAP) x 80

CO

SVR = (MAP - CVP) x 80

CO

800-1500 dynes/sec/cm²

Question 15

Afterload

Answer 15

Tension is proportional to Pressure times radius / wall thickness

Question 16

Stroke Work

Answer 16

Stroke Work = SV x MAP

Question 17

Factors that effect inotropy

Answer 17

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

Question 18

Factors that increase ventricular filling (preload) 5

Answer 18

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

Question 19

Two things that increase CVP

Answer 19

1. Increased thoracic venous volume - total blood volume - Venous return, r/t muscle contraction, respiration and gravity 2. Decreased venous compliance

Question 20

Stroke volume and increased preload

Answer 20

Increased preload = increased SV r/t increased end diastolic volume

Question 21

Stroke volume and increased afterload

Answer 21

Increased afterload = Decreased stroke volume r/t increased end systolic volume

Question 22

Stroke volume and increased isotropy

Answer 22

Increased isotropy = Increased stroke volume r/t decreased end systolic volume

Question 23

Ejection Fraction

Answer 23

EF = SV / EDV SV = EDV- ESV

Question 24

Decreased O2 delivery to tissue

Answer 24

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

Question 25

Cardiac index and Stroke Index

Answer 25

CI = CO / BSA BSA = M2 SI = SV / BSA

Question 26

02 Delivery

Answer 26

O2 Delivery = CBF x CaO2 CBF = Coronary blood flow (mL / Min) Ca02 = Oxygen concentration of arterial blood (mL 02 / mL Blood)

Question 27

Cardiac Work (Formula)

Answer 27

Cardiac Work = SW x HR * How much work being done for a unit of time * Cardiac minute work or Ventricular minute work

Question 28

Cardia Index (Formula + Normal Values)

Answer 28

CI = _CO_ BSA (**2.8/4.2** L/min/m²)

Question 29

Stroke Volume (Formula + Normal Values)

Answer 29

1. **Stroke Volume =** EDV - SEV 2. **Stroke Volume =** CO x _1000_ HR (**50 -110** mL/beat)

Question 30

Stroke Volume Index (Formula + Normal Values)

Answer 30

Stroke Volume Index = _SV_ BSA (**30-65** mL/beat/m²)

Question 31

Ejection Fraction (Formula + Normal Values)

Answer 31

**Ejection Fraction =** _EDV -ESV_ x 100 EDV Remember SV = EDV - ESV (60-70%)

Question 32

Pulse Pressure (Formula + Normal Values)

Answer 32

**SBP - DBP** _Stroke Volume Output_ Arterial Tree Compliance (normal = **40** mmHg)

Question 33

Systemic Vascular Resistance INDEX (Formula + Normal Values)

Answer 33

**SVR =** (_MAP - RAP_) x 80 CI **SVR =** (_MAP - CVP_) x 80 CI **1500-2400** dynes/sec/cm² / m²

Question 34

Pulmonary Vascular Resistance (Formula + Normal Values)

Answer 34

**PVR =** _(MPAP - PAOP_) x 80 CO **150-250** dynes/sec/cm2 / m2

Question 35

Pulmonary Vascular Resistance INDEX (Formula + Normal Values)

Answer 35

**PVR** = (_MPAP - PAOP_) x 80 CI **250-400** dynes/sec/cm² _/ m²

Question 36

Frank Starling Mechanism

Answer 36

INCREASED **ventricular volume** results in HIGHER **cardiac ouput** to a point. (this is based on sarcomere cross bridges)

Question 37

Contractiliy (inotropy) is and INDEPENDENT variable that is UNRELATED to \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_.

Answer 37

Prelaod and Afterload

Question 38

Key **electrolye** in exitation-contraction coupling

Answer 38

**Calcium** | (think calcum induced calcium-release)

Question 39

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

Answer 39

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

Question 40

**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

Answer 40

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

Question 41

The Law of LaPlace

Answer 41

Used to understand myocardial afterload **Wall Stress =** _Intraventricular Pressure x Radius_ Ventricular Thickness

Question 42

Coronary Blood Flow Equation

Answer 42

**Coronary Blood Flow =** _Coronary Perfusion Pressure_ Coronay Vascual Resistance (Ohm's Law)

Question 43

Coronary Perfusion Pressure

Answer 43

**CPP** = Aortic DBP - LVEDP or CPP = DBP - **Pulmonary artery occlusion pressure**

Question 44

Normal Values for Coronary Blood Flow What is the % of Cardiac Output?

Answer 44

Coronary blood flow = **225-250** mL/min This is **4-7%** of Cardiac Cutput

Question 45

Coronary vasculature **autoregulates** between a MAP of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_.

Answer 45

Coronary vasculature **autoregulates** between a MAP of **60-140** mmHg

Question 46

Myocardial oxygen consumtion rate

Answer 46

**8-10** mL/min/100g of tissue

Question 47

Myocardial Oxygen Extraction Ratio

Answer 47

**70%**

Question 48

Coronary Sinus Oxygen Saturation

Answer 48

**30%**

Question 49

Explain myocardial supply and demand

Answer 49

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.**

Question 50

Drug therapy for valvular disease

Answer 50

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

Question 51

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

Answer 51

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

Question 52

Pathophysiology of mitral stenosis

Answer 52

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 cm² (**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

Question 53

What are some complications associated with Left atrial enlargement?

Answer 53

* Left atrial enlargement - Predisposes to **a-fib** * A-fib→**stasis** and development of **thrombi** * **Anticoagulants** are needed

Question 54

Severe MS can lead to

Answer 54

CHF

Question 55

Mitral Stenosis Anesthetic Management **GOALS**

Answer 55

**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 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**)**

Question 56

Induction for MITRAL STENOSIS pharmacologic considerations

Answer 56

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-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** 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

Question 57

Patho of mitral regurgitation

Answer 57

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

Question 58

Appearance of mitral regurgitation: 1. On PCWP tracing 2. x-Ray 3. EKG

Answer 58

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)

Question 59

Mitral regurgitation anesthetic management GOALS

Answer 59

**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**

Question 60

Causes of of aortic stenosis. Associated size and pressure?

Answer 60

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 **2.5-3.5**cm². Significant AS is associated with valve area of **\<1 cm²** and a transvalular gradient of **\>50mmHg.**

Question 61

Explain the **pathology of angina** associated with **aortic stenosis**. What is the classic symptom triad with Aortic Stenosis?

Answer 61

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!)

Question 62

Aortic Stenosis anesthetic management GOALS from class

Answer 62

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**

Question 63

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

Answer 63

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

Question 64

Causes of aortic regurgitation

Answer 64

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

Question 65

Causes and management of Tricuspid Regurgitation

Answer 65

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**

Question 66

How do we treat a-fib with RVR?

Answer 66

BBs, CCBs, amiodarone, or digoxin.

Question 67

Preop eval

Answer 67

Syncope, fainting, compensation? Major end organ disease? Cardiac hypertrophy, increased SNS output for compensation? How bad is the CV disease?

Question 68

One of the single best questions for many CV assesments

Answer 68

Exercise tolerance

Question 69

Common symptoms of CHF with valve disease

Answer 69

Dyspnea, orthopnea, fatigue - **CHF is a common conpanion with valvular disease**

Question 70

what is a common arrythmia associated with valvular disease?

Answer 70

Atrial Fibrilation - due to left atrial enlargement

Question 71

What are the sighns and symptoms associated with Left atrial enlargement?

Answer 71

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

Question 72

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

Answer 72

1. Stress induced tachycardia 2. A-fib - when there is a loss in atrial contraction

Question 73

Induction of anesthesia for Mitral Regurgitaion

Answer 73

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??

Question 74

Mirtal Regurgitation Maintinence and of Anesthesia drug considerations

Answer 74

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

Question 75

Monitor considerations for Mitral Reurgitation **and** Mitral Stenosis.

Answer 75

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)

Question 76

Explain why Normal Sinus Rhythm **MUST** be maintainded in Aortic Stenosis

Answer 76

**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

Question 77

Maintinence of anesthesia in a patient with Aortic Stenosis (key points, drugs and likely complications)

Answer 77

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

Question 78

Intraoperative monitoring for aortic stenosis MUST consist of this

Answer 78

**5 lead EKG** that is capable of detecting myocardial ischemia

Question 79

Explain the basis of the valvular disease that has the highest perioperative risk

Answer 79

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

Question 80

The **magnitude** of aortic regurgitation depends on what two things?

Answer 80

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

Question 81

Explain the peripheral signs of **hyperdynamic circulation**. Where is it evident?

Answer 81

1. Widened pulse pressure 2. Decreased Diasotolic BP 3. Bounding pusles (evidient in disease processes such as aortic regurgitation, liver failure)

Question 82

Aortic Regurgitation Anesthetic Management **GOALS**

Answer 82

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**)

Question 83

Aortic regurgitation **INDUCTION** anesthetic management.

Answer 83

**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) 4.

Question 84

Aortic Regurgitation consiterations for **Maintinence** of Anesthesia

Answer 84

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 replacemen**t of blood loss to maintain LV SV 5. Treat high SBP with **SNP**

Question 85

Formula for **Ventricular Compliance**

Answer 85

**C Ventricular** = _Ventricular Volume_ Ventricular Pressure

Question 86

Beck's Triad

Answer 86

_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

Question 87

Explain **Pulsus Paradoxis**

Answer 87

**SBP** decreases \> **10** mmHg on **inspiration** **(increased venous return** bows ventricular septum toward left heatr leading to decreased **stroke volume, cardiac output** and **SBP)**