Exam 2 Study Guide Flashcards
Symptoms of ARDS
Arterial hypoxemia
➢ May include tachypnea, bronchospasm, and acute pulmonary hypertension
What is ARDS?
Inflammatory injury to the lung that manifests clinically as acute hypoxemic respiratory failure
Clinical disorders and risk factors associated c/ the development of ARDS include
events that cause direct lung injury as well as those that lead to indirect injury to the lungs in the setting of a systemic process
Sepsis is associated c/ the
highest risk of progression of acute lung injury to ARDS
DIRECT LUNG INJURY
PAPFaNI
- Pneumonia
- Aspiration of gastric contents
- Pulmonary contusion
- Fat emboli
- Near drowning
- Inhalational injury
INDIRECT LUNG INJURY
STMCDA
- Sepsis
- Trauma associated c/ shock
- Multiple blood transfusions
- Cardiopulmonary bypass
- Drug overdose
- Acute pancreatitis
Signs and Symptoms : First sign of ARDS
• Arterial hypoxemia resistant to treatment with supplemental oxygen is usually the first sign
ARDS Death often result of
sepsis or multiple organ failure rather than respiratory failure
Lung volume expansion maneuvers
Incentive spirometry,
Leads to pneumonia to ARDS,
Intraoperative aspiration
ARDS Radiographic signs
may appear before symptoms develop
ARDS Diagnosis 2
- Presentation of acute refractory hypoxemia
* Diffuse infiltrates on chest radiograph consistent c/ pulmonary edema
Resp parameters Ratio in ARDS
Decreased arterial PaO2/FIO2 ratio
Decreased arterial PaO2/FIO2 ratio:
Mild ARDS:
Ratio is 201–300
Decreased arterial PaO2/FIO2 ratio:
Moderate ARDS:
Ratio is 101–200
Decreased arterial PaO2/FIO2 ratio:
Severe ARDS:
Ratio is <101
Treatment of Acute Respiratory Distress Syndrome
POT GOD RICAN
Positive end-expiratory pressure
Oxygen supplementation
Tracheal intubation/Mechanical ventilation
Glucocorticoid therapy (?)
Optimization of intravascular fluid volume
Diuretic therapy
Removal of secretions
Inotropic support
Control of infection
Administration of inhaled β2 -adrenergic agonists
Nutritional support
Anesthesia Considerations for ARDS
Battling ventilation strategies: Protective Ventilation
Vt?
- Protective ventilation
- Prevents ventilator-induced lung injury
- Low Vt (6 mL/kg) = 22% mortality benefit, less inflammatory mediators
ARDS anesthesia considerations what are the 2 types of battling ventilation strategies:
Protective ventilation and OPEN lung ventilation
Anesthesia Considerations for ARDS: Battling ventilation strategies: OPEN Ventilation (PSN)
- PEEP titrated to highest value possible while keeping plateau pressure below 28–30 cm H2O
- Significantly more ventilator-free days and organ failure–free days
- No change in mortality
ARDS Prone positioning
• Exploits gravity and repositioning of heart in thorax to recruit lung units and improve ventilation/perfusion
matching
ARDS additional treatment
Extracorporeal membrane oxygenation (ECMO)
3 features of Asthma (CRB)
- Chronic airway inflammation
- Reversible expiratory airflow obstruction
- Bronchial hyperactivity
What is Status Asthmaticus?
- Life threatening bronchospasm that persists despite treatment.
ASTHMA Characterized by (BHC)
Bronchoconstriction
Hyperactivity
Chronic airway inflammation.
Asthma PREOPERATIVE TESTS
ACE- FA
ABG and Chest Radiography • ECG
FEV:FVC = < 80% AUSCULTATION
Characteristics of Asthma to be EVALUATED preoperatively?
AAA THF CCNS
asthma
Age of onsent Alllergies Anesthetic history Triggering events Hospitalization of asthma Frequency of ED visits Need for intubation and mechanical ventilation Sputum characteristics Cough Current medications
Short acting Bronchodilators used for asthma (SABA) – LAMP
Levalbuterol (xopenex)
Albuterol (Proventil)
Metaproterenol
Pirbuterol (Maxair)
MOA of short acting bronchodilators
B2 Agonist: stimulates beta 2 receptors in tracheobronchial tree
Adverse effects of bronchodilators
TTD hypo
Tachycardia
Tremors
Dysrhythmias
HYPOKALEMIA
Long term treatment of asthma
ILIcLMeMa
- Inhaled Corticosteroids
- Long-Acting Bronchodilators
- ICS and LABA
- Leukotriene Modifiers
- Methylxanthines
- Mast Cell Stabilizers
Asthma INTRAOPERATIVE CONSIDERATIONS INDUCTION
GETA vs LMA vs REGIONAL
2 things to know
- GETA OR LMA VS. REGIONAL
- Airway reflexes must be suppressed to avoid bronchoconstriction in response to mechanical stimulation of hyper-reactive airways
- Stimuli that do not ordinarily evoke airway responses can precipitate life-threatening bronchoconstriction in patients c/ asthma
GETA INDUCTION for asthma
Propofol or Ketamine
• LaryngotrachealAnesthesia (LTA) 4%Lidocaine
• Sevoflurane (BETTER) vs Desflurane
LMA induction for asthma
No GERD or aspiration risk
• Better method of airway management – less
instrumentation
MAINTENANCE of ASTHMA • Opioids = • Neuromuscular blocking agents. • Hydration • Ventilation: • Slow inspiratory flow rate (at least 2 seconds) • Sufficient exhalation time. (I:E) • Humidification/warming of inspired gases
suppress cough reflex vs. histamine release and chest rigidity. Use fentanyl
Ketamine for asthma may cause
Increase in secretion and drooling
Asthmatic patient start bucking and coughin
deepen anesthesia, may get bronchospasm if not deep enough
2 meds help reduce cough reflex for asthma
Sevoflurane and lidocaine
Meds to avoid with asthma as far as NMB
Atracurium and Mivacurium because they are associated with Histamine release
Asthma continue bronchodilators till ______and if they take glucocorticoids?
Day of surgery ; they should receive supplementation during surgery
Asthma induction use
Propofol and fentanyl
Intraoperative bronchospasm shows as
Increase PEAK inspiratory pressure
Delayed rise of the expiratory end tidal CO2
Tx of intraoperative bronchospasdm
Increase concentration of inhaled agent
Administer aerosol bronchodilator
Reduce TV
Increase expiratory time
I: E ratio 10 BPM
60/10 =6
2:4 → 1:2
I: E ratio 8 BPM
60/8 = 7.5 seconds/breath
2:5.5 -> 1:3
I: E ratio 6 BPM
60/6 = 10 sec/breath
Inspiration of at least 2 = Expiration 8
I:E 1:4
I: E ratio of 12 BPM
60/12 = 5 seconds
inspiration of at least 2 exp 3
1:1.5
Asthma Emergence
Deep extubation unless contraindicated.
• IV Lidocaine (again).
AVOID THE FOLLOWING DRUGS PROVOKING
ASTHMA SYMPTOMS:
ABS SAN MS
- ASPIRIN
- BETA ANTAGONISTS (labetalol)
- SOME NSAIDS: KETORALAC (?)
- SULFITES
- Atracurium
- Neostigmine
- Morphine
- Succinylcholine
PERIOPERATIVE COMPLICATIONS
- Laryngospasm
- Bronchopasm
- Status Asthmaticus
Laryngospasm CXR:
** pink frothy sputum = Negative Pressure Pulmonary
Edema
** Coarse breath sounds
Treatment of Laryngospasm
in 24 hrs but mayrequire mechanical vent.___laryngeal edemaTX_ nebulized racemic epinephrineIV corticosteroids
- Increase Fi02
- CPAP/PEEP
- Reintubation
0.5-1 mg/kg Lasix IV
= will self correct c/in 24 hrs but may require mechanical vent.
Treatment of Laryngospasm
ICR L
- Increase Fi02
- CPAP/PEEP
- Reintubation
0.5-1 mg/kg Lasix IV
= will self correct c/in 24 hrs but may require mechanical vent.
***Laryngeal edema TX
- nebulized racemic epinephrine
- IV corticosteroids
TREATMENT of bronchospasm first step
R/O obstruction d/t migration of ETT, secretions, and kinking
Bronchospasm, Most definitive is through
fiberoptic.
Status asthmaticus ANESTHESIA CONSIDERATIONS
• Life-threatening bronchospasm that doesn’t resolve despite treatment
CO2 in status asthmaticus
Hypercarbia (PaCO2 > 50 mm Hg) requires tracheal intubation and mechanical ventilation
Extreme cases of status asthmaticus may need GA c/
Volatile agent to produce bronchodilation
For status asthmaticus Expiratory phase must be
prolonged to allow for complete exhalation and to prevent self generated or intrinsic positive end-expiratory pressure (auto-PEEP, AKA breath stacking)
What are the ACUTE INTRINSICE RESTRICTIVE LUNG DISEASE (PULMONARY EDEMA) AANORUCH
ARDS
Aspiration
Neurogenic Problems
Opioids Overdose
Reexpansion of collapsed lung
Upper airway obstruction (negative pressure)
CHF
High Altitude
What are the CHRONIC INTRINSICE RESTRICTIVE LUNG DISEASE (INTERSTITIAL LUNG DISEASE)
SHEALD
Sarcoidosis Hypersensitivity pneumonitis Eosinophillic granuloma Alveolar proteinosis Lymphangioleiomyoomatosis Drug induced pulmonary fibrosis
DISORDERS OF THE CHEST WALL, PLEURA and MEDIASTINUM
KAF PPP MMNNDD SG
Kyphoscoliosis Ankylosing spondylitis Deformities of the sternum Deformities of the costovertebral skeletal structures Flail chest
Pleural Effusion
Pneumothorax
Pneumomediastinum
Mediastinal mass Muscular dystrophies Neuromuscular disorders Neuromuscular transmission Spinal cord transaction Guillain barre syndrome
Other disorders on chart
OPA
Obesity, Pregnancy, Ascites
Pulmonary Edema Pathophysiology
Vigorous inspiratory efforts against an obstructed upper
airway ➔ post-extubation laryngospasm, epiglottitis,
tumors, obesity, hiccups, or obstructive sleep apnea in
spontaneously breathing patients ➔causes ↑ negative intrapleuralpressure ➔NEGATIVE PRESSURE PULMONARY EDEMA
Pulmonary edema Onset:
minutes to 3 hours
Signs/Symptoms of Pulmonary Edema
- Tachypnea
- Cough
- Failure to maintain oxygen saturation above 95% despite high FiO2
Treatment of Pulmonary Edema (MAO
• Maintenance of a patent upper airway
• Administration of supplemental oxygen
• Occasionally brief Mechanical
ventilation
Acute Intrinsic Restrictive Lung Disease
ARDD results in LAP
• Aspiration
• Aspirated acidic gastric fluid
• Rapidly distributed throughout the lung
• Destruction of surfactant-producing cells
• Damages pulmonary capillary endothelium
Results in:
• Leakage of intravascular fluid into the lungs
• Atelectasis
• Producing capillary permeability pulmonary edema
Clinical picture of Acute Intrinsic Restrictive Lung
Disease is similar to that of ARDS
• Arterial hypoxemia
• May include tachypnea, bronchospasm, and acute pulmonary hypertension
Intraoperative aspiration and pulmonary Edema
Atelectasis➔ Leakage of intravascular fluid into the lungs➔ Producing increased capillary permeability
➔ pulmonary edema
Aspiration = is the
active (vomiting) or passive (regurgitation) passage of
material from the stomach, esophagus, pharynx, mouth, or nose to the trachea
Aspiration AVERAGE HOSPITAL STAY IS
21 DAYS c/ ICU
Aspiration Complications:
bronchospasm, pneumonia to ARDS, lung abscess and
empyema.
Aspiration Mortality is
5%
Causes of Aspiration
• Food or any foreign body
• Fluids (blood, saliva, GI contents = pH <2.5
and content >25 mls)
Instraoperative Aspiration Acidic Aspirates →
AIH
alveolar-capillary breakdown
→ interstitial edema, intra-alveolar hemorrhage, increased airway resistance
→ hypoxia.
Instraoperative Aspiration Acidic Aspirates Non acidic fluid
→ destroys surfactant → alveolar collapse and atelectasis → hypoxia.
Instraoperative Aspiration Acidic Aspirates Particulate/food matter → (PAH)
physical obstruction & later inflammatoryresponse
→ alternating areas of atelectasis and hyper-expansion → hypoxia, hypercapnia.
S/sx of Intraoperative Aspiration and %
- Fever (90%)
- Tachypnea
- Rales in 70% of cases
- Cough, cyanosis & wheezing (30-40%)
INTRAOPERATIVE ASPIRATION Anesthetic considerations Prevention.Preoperative
Recognize risks in preop. (Coexisting, fasting times, preop meds
INTRAOPERATIVE ASPIRATION
Anesthetic considerations DOLP
- Delay elective surgery
- Optimize cardiorespiratory function
- Large pleural effusions need to be drained
- Persistent hypoxemia may require mechanical ventilation and PEEP
INTRAOPERATIVE ASPIRATION
Anesthetic considerations- INDUCTION
RSI. However, ETT does not guarantee that no aspiration will occur.
INTRAOPERATIVE ASPIRATION
Anesthetic considerations- POST OP AFTER THE FACT
Supportive care
• Bronch/Suction asap.
• FiO2 x 100%
• PEEP/CPAP
INTRAOPERATIVE ASPIRATION: Maintenance
Anesthetic considerations: VT use and Why?
Use low Vt (6 mL/kg), compensatory increase in ventilatory rate (14 to 18 breaths per minute) while attempting to keep the end-inspiratory plateau pressure at less than 30 cm H2O ➔ avoid BAROTRAUMA.
Intraoperative aspiration fluids and pulmonary
Monitor fluid and CV status
2 unhelpful interventions for Intraoperative aspiration
- Antibiotics and corticosteroids still controversial
* Lavage trachea c/ sodium bicarbonate = not shown to be helpful.
Pulmonary lavage is done for
obstruction (not c/ aspiration).
INTRAOPERATIVE ASPIRATION:Rigid Bronchoscopy =
only when removing solid particles
COPD- Ventilator –> VENTILATION
- Controlled mechanical ventilation is useful for optimizing oxygenation
- Slow respiratory rates (6 to 10 breaths per minute) provide sufficient time for complete exhalation
COPD and Positive pressure ventilation (adverse effect)
Insufficient expiratory time ➔ air trapping or dynamic
hyperinflation ➔ barotrauma
COPD and Tidal volumes
Tidal volumes of 6 to 8 mL/kg combined c/ slow inspiratory flow rates minimize turbulent airflow and help maintain optimal ventilation/perfusion matching
Ventilation strategies for Asthma (SSH)
- Slow inspiratory flow rate (at least 2 seconds)
- Sufficient exhalation time. (I:E)
- Humidification/warming of inspired gases
Mitral Stenosis Heart Sound
Opening snap at early diastole
Mitral Stenosis Auscultate At
Apex in left axilla
Cause of mitral stenosis
Most common cause is
Rheumatic Heart Disease (most common)
• Stress (tachycardia [fever & sepsis])
Mitral stenosis as a result leads to
➔decrease Stroke Volume, leads to Pulmonary Edema d/t high left atrial pressure
Mitral Stenosis complication leads to those symptoms
DOPR
➔ dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea➔ Right sided heart failure
PREOPERATIVE CONSIDERATIONS for Mitral stenosis
The normal mitral valve orifice area is
4 to 6 cm2
ECG changes seen with Mitral stenosis
Broad and notched P waves (LA enlargement) Atrial Fibrillation (30% of patients) = thromboembolism
ECG changes seen with Mitral stenosis
Broad and notched P waves (LA enlargement)
P-mitrale
Mitral stenosis arrhytmia associated with is and treatment
BCDW , range
Atrial Fibrillation (30% of patients) = thromboembolism Beta Blockers, or Calcium Channel Blockers • Digoxin, Warfarin is administered to a target INR of 2.5-3.0
Mitral stenosis Cardiac Catheterization:
Transvalvular gradient and treatment
Transvalvular pressure Gradient is > 10 mmHg (normal < 5 mmHg) ➔increased left atrial pressures
• Diuretics
INTRAOPERATIVE CONSIDERATIONS ***goals: MITRAL STENOSIS avoid Avoid 4 (AHHHH_
- Avoid A-fib with RVR and/or tachycardia (reduces cardiac output)
- Avoid hypotension (drug induced decreases in SVR)
- Avoid head-down position (increase in central blood volume)
- Avoid hypoxemia & hypercarbia (exacerbates pulmonary hypertension)
INTRAOPERATIVE CONSIDERATIONS
***goals: MITRAL STENOSIS avoid
Avoid 4 (AHHHH)
4Hs A
- Avoid A-fib with RVR and/or tachycardia (reduces cardiac output)
- Avoid hypotension (drug induced decreases in SVR)
- Avoid head-down position (increase in central blood volume)
- Avoid hypoxemia & hypercarbia (exacerbates pulmonary hypertension)
Mitral Stenosis INTRAOPERATIVE CONSIDERATIONS
Regional Anesthesia: acceptable? which one is better?
is acceptable (Epidural > Spinal).
DO NOT use this induction agent for Mitral stenosis and why.
No Ketamine (tachycardia)
Ketamine do not use in this valvular disorder
Mitral stenosis
DO NOT use this volatile agent for Mitral stenosis and why.
Nitrous Oxide ➔ pulmonary hypertension
Mitral Stenosis : What kind of anesthesia (light or deep and why
DEEP BETTER because Light anesthesia ➔ tachycardia & HTN (pulmonary and systemic)
Mitral stenosis and fluid management how and why?
Slowly titrate IV fluids (fluid overload [left atrial enlargement]) ➔ pulmonary edema.
Mitral stenosis and hemodynamic monitoring
Invasive monitoring: A line, PAP (manipulation = rupture)
Mitral stenosis and paralytics
Reverse paralytics slowly
Mitral Stenosis POSTOPERATIVE CONSIDERATIONS
- Avoid pain and hypoventilation (respiratory acidosis and hypoxemia) ➔ increasing HR and PVR
- Decreased pulmonary compliance and increased
work of breathing ➔ mechanical ventilation (major
thoracic or abdominal surgery)
Mitral Regurgitation Heart sounds (murmur)
Pan-systolic murmur
Apex; radiates to the axilla
Mitral regurgitation
Apex; radiates to the LEFT axilla
Mitral stenosis
Mitral Regurgitation Causes: (RIMP)
Rupture of chordae tendinae)
Ischemic Heart Disease
Mitral annular dilation
Papillary muscle dysfunction
Mitral Regurgitation can cause ________
which can be compensated or decompensated
➔Can cause decreased LV SV and CO
Mitral Regurgitation can cause Can cause decreased LV SV and CO : Compensated
➔Compensated: LVH & increased compliance of LA
Mitral Regurgitation can cause Can cause decreased LV SV and CO : DECompensated
Increased LA volume ➔ pulmonary edema AND cardiogenic shock
MITRAL REGURGITATION PREOPERATIVE
CONSIDERATIONS : what is severe MR
Regurgitant fraction > 0.5
Auscultation: Holosystolic Apical Murmur (radiation to the axilla)
Mitral Regurgitation
PAOP mitral Regurgitation
Prominent V wave
Mitral Regurgitation Symptomatic patients:
Ace Inhibitors or Beta- Blockers (Carvedilol) & Biventricular Pacing ➔ improvement.
Tall v wave associated with
Mitral regurgitation
Mitral regurgitation and pulmonary circuit
Increase pressure in the pulmonary circuit and produce pulmonary congestion
Pansystolic murmur
Mitral Regurgitation
Mitral REGURGITATION OVERALL ANESTHESIA CONSIDERATIONS GOALS:
3 things to PREVENT (BIM)
Prevent
Bradycardia
Increases in SVR
Myocardial depression
Mitral Regurgitation and Volatile anesthetics good or bad? why?
Good,
Decrease in SVR
Increases heart rate
Minimal negative inotropic effects).
Mitral Regurgitation: Vent Settings
Sufficient expiratory time (adequate venous return).
Types of Anesthesia for Mitral Regurgitation and why?
Neuraxial Anesthesia (decrease SVR). Invasive monitoring
For MS vs MR LV preload
Both Keep normal to increase
For MS vs MR : Heart rate
MS keep low
MR keep High
For both MS and MR things to maintain (RCA)
Rhythm: NS
Contractility
Avoid increase in PVR
For mitral stenosis how should you keep SVR?
Normal
For mitral regurgitation how should you keep SVR?
Decreased
MVP as a valvular disease
• S/sx: anxiety, orthostatic symptoms,
palpitations, dyspnea, fatigue, and atypical
chest pain.
• Most common form of valvular heart disease (1%-2% of US).
MVP severity CIS DD
Benign but➔ CVA infective endocarditis, severe MR, dysrhythmias (Beta blocker therapy), and death.
MVP: OVERALL ANESTHESIA CONSIDERATIONS
Murmur (MSC LSM)
Auscultation: mid systolic click and a late systolic
murmur
MVP Same anesthesia management as MR
No BHM
No brady, HTN, and myocardial depression) & FAST FORWARD FLOW (FFF)
MVP anesthesia : avoid what?
Regional Anesthesia (avoid decrease in SVR; give fluids).
What are the causes of Aortic Stenosis
ABRI
- Aging
- Bicuspid aorticvalve (30 to 50 yo)
- RHD
- Infective endocarditis
Infective Endocarditis Causes
(Frequent Exposure to Bacteremia) DGG
- Dental
- GI
- Genitourinary Tract procedures
Prophylaxis for Infective Endocarditis
- Maintenance of good oral health & oral hygiene (chewing, brushing, flossing, use of toothpicks, etc.) is better than prophylactic antibiotics.
Major changes in the updated AHA guidelines for infective endocarditis prophylaxis are these:
(1) Antibiotic prophylaxis for infective endocarditis is recommended
only under a very few conditions
For Infective ENDOCARDITIS (4) Antibiotic prophylaxis is NOT RECOMMENDED
genitourinary or gastrointestinal tract procedures
For INFECTIVE ENDOCARDITIS (3) Antibiotic prophylaxis is recommended for (Skin)
invasive procedures (those that involve incision or biopsy of the respiratory tract or infected skin, skin structures, or musculoskeletal tissue)
2) Antibiotic prophylaxis is recommended for dental procedures that involve
manipulation of gingival tissues or the
manifpulation of the periapical regions of the teeth,
or perforation of the oral mucosa
PREOPERATIVE ASSESSMENT
- Normal aortic valve area is 2.5 to 3.5 cm2
Severe AS aortic valve area
(0.8 cm2)
Aortic Stenosis Cardiac Catheterization: Transvalvular
pressure gradients
> 50 mmHg
Aortic Stenosis Hypertrophy type _______leading to
Concentric LVH & compression of subendocardial blood vessels ➔ (SAD) Angina Pectoris, syncope, dyspnea on exertion (CHF like).
Systolic murmur (radiate to neck/mimic carotid bruit).
Aortic stenosis
mimic carotid bruit
Aortic stenosis systolic murmur (think sad neck)
Majority area symptomatic.
Aortic stenosis
AORTIC STENOSIS
PERIOPERATIVE MANAGEMENT
Goal: Avoid (hemodynamics )
hypotension and decreasing cardiac output.
Rhythm to maintain for Aortic stenosis
Maintain Normal Sinus Rhythm
Why 2 situations do we avoid with the HR with Aortic stenosis and why?
a. Avoid Bradycardia ➔ LV overdistention
b. Avoid Tachycardia ➔ reduced Cardiac Output (worse!
Aortic Stenosis SVR and why ?
Maintain or slightly ↑ SVR and Cardiac Output
a. Optimize preload (fluids) for LV filling.
Aortic Stenosis when CPR is performed is it effective?
CPR is not effective.
Regional anesthesia is contraindicated with this valvular disorder ? and why?
Aortic Stenosis (significant hypotension)
Best Induction agents for Aortic stenosis
Etomidate & Benzodiazepines
Intraop Maintenance for aortic stenosis include
a. N20/volatile/opioids combo.
When a patient with Aortic Stenosis is TACHY which agent is preferred?
Phenylephrine > Ephedrine (Tachy)
When a patient with Aortic Stenosis has Junctional Rhythm and Bradycardia, treat with (RAE)
Robinul, Atropine, or Ephedrine
Patients with Aortic Stenosis with Persistent Tachycardia
Beta Blockers: Esmolol
Monitoring Modalities for Aortic Stenosis include :
A line, CVP, PAC, or TEE (dependent on severity of AS &
type of surgery).
AORTIC REGURGITATION
Causes: (ABRID)
Aortic Dissection (Immediate Surgery) Bicuspid Aortic Valve RHD Infective endocarditis Drug-Induced (Phen-Fen)
Leaflets and Aortic Regurgitation (A- DAH)
There is Aortic Leaflet Coaptation Failure leading to
➔Decreased Cardiac Output
➔Acute Volume Overload (LVH)
➔Heart Failure
AORTIC REGURGITATION PREOPERATIVE CONSIDERATIONS Pathophysiology
- Angina Pectoris (reduced coronary blood flow➔ coronary ischemia
- Pulmonary Edema (LVEDV increased➔LV failure).
- Normal EF unless LV dysfunction: dyspnea, orthopnea, fatigue
Aortic Regurgitation Pulse
Widened pulse pressure
decreased diastolic pressure
Bounding pulses.
Aortic Regurgitation Auscultation: murmur type and where?
Diastolic Murmur (Right Sternal Border)
Systolic murmur with crescendo, decrescendo
Aortic Stenosis
Aortic Stenosis is a a SCD murmur heard best at
Right upper sternal border
Mitral Valve Prolapse murmur
Mid-systolic click followed by late systolic murmur
MVP best heard at
Apex
Aortic Regurgitation: INTRAOPERATIVE ANESTHETIC CONSIDERATIONS: Main 3 Goals
- Decreasing systolic HTN and LV wall stress
- Improving LV function (also LV failure)
- Maintain forward LV SV (FFF): Avoid Bradycardia, Increased SVR, and Decreasing myocardial depression.
Aortic Regurgitation, Decreasing systolic HTN and LV wall stress how
a. Long term therapy (with good EF):
i. Nifedipine
ii. Hydralazine
Aortic Regurgitation: LV function (also LV failure)
how?
a. IV infusion:
i. Dobutamine (inotropic drug)
ii. Nitroprusside (vasodilation)
Maintain forward LV SV (FFF): Avoid bradycardia, increased SVR, and decreasing myocardial depression What GETA? and why?
a. Iso/Sevo/Des: Increases HR (HR > 80 bpm), decreases SVR, with minimal myocardial depression.
Aortic Regurgitation: Bradycardia or Junctional Rhythm, Give
IV Atropine
May not need invasive monitoring.
Aortic Regurgitation
Aortic Regurgitation High opioid anesthesia
severe LV dysfunction
Parameters check : AS vs AR → LV Preload
For Aortic stenosis maintain LV preload ↑
For Aortic Regurgitation maintain LV preload NORMAL to ↑
Parameters check : AS vs AR → HR
For Aortic Stenosis maintain HR → normal to slow ↓
For Aortic Regurgitation maintain HR → Modest ↑
Parameters check : For BOTH AS and AR
Maintain those 3(CNP) c no problem
Maintain
Contractility, NSR, PVR
Parameters check : AS vs AR → SVR
For Aortic Stenosis maintain SVR modest ↑
For Aortic Regurgitation maintain SVR ↓
Keep this parameter low with Aortic Regurgitation
SVR
TRICUSPID STENOSIS
How frequent and most common cause
• Rare in adults• RHD: most common cause
TRICUSPID STENOSIS Usually with co-existing (TRMA)
Tricuspid regurgitation and often mitral or aortic valve disease
Tricuspid Stenosis Pathophysiology
Increased RAP and increases the pressure gradient between the right atrium and right ventricle
In Tricuspid Stenosis: Right atrial dimensions
are increased, but the right ventricular dimensions are determined by the degree of volume overload from concomitant tricuspid regurgitation
RV dimensions in tricuspid stenosis depend onfactors
degree of volume overload from concomitant tricuspid regurgitation
Tricuspid stenosis Heart sound
Pre-systolic murmur
Best place to listen for tricuspid stenosis
Left sternal edge at 4th ICS
Pre-systolic murmur
Tricuspid stenosis
TRICUSPID REGURGITATION Causes (functional)
Functional: RV enlargement or pulmonary HTN
TRICUSPID REGURGITATION DISEASES Causes
CIA RET
Carcinoid syndromea Infective endocarditis (IV drug use) AV or MV disease. RHD Ebstein’s anomaly TV prolapse
Disease causing TR lead to
RA volume OVERLOAD
Tricuspid Regurgitation Signs and symptoms (JHAP)
- Jugular venous distention
- Hepatomegaly
- Ascites
- Peripheral Edema
TRICUSPID REGURGITATION PERIOPERATIVE ANESTHESIA CONSIDERATIONS
Goals: FLUIDS
Maintenance of IV fluid volume & CVP in high normal range (facilitate adequate RV preload & LV filling).
Avoid in Tricuspid Regurgitation Maintenance of IV fluid volume & CVP in high normal range (facilitate adequate RV preload & LV filling). by
- Avoid PPV and vasodilating drugs (reduces venous return)
* Avoid hypoxemia and hypercarbia ➔ increased PAP
Tricuspid Regurgitation: venous return and vasodilation
Produce pulmonary vasodilation & maintain venous return
Avoid Nitrous Oxide
Avoid air in IV fluids (systemic air embolism)
Pulmonic stenosis is usually
congenital and detected and corrected in childhood
Pulmonic stenosis : An acquired form can be due to (PRIC)
Previous surgery or other interventions
Rheumatic fever
Infective endocarditis,
Carcinoid syndrome, or
Pulmonic stenosis : Significant obstruction can cause
syncope,angina, right ventricular hypertrophy, and
right ventricular failure
PULMONIC VALVE REGURGITATION
• Pulmonic valve regurgitation results from
pulmonary hypertension with annular dilatation of the pulmonic valve
Pulmonic valve regurgitation causes include
connective tissue diseases, carcinoid syndrome, infective endocarditis, and rheumatic heart disease
Pulmonary regurgitation is
rarely symptomatic
Pulmonic Valve Regurgitation Heart sounds (DDM)
Decrescendo diastolic murmur
Pulmonic Valve Regurgitation Heart sounds BEST HEARD
Left upper sternal border
Pulmonic Stenosis Heart sounds (CDEM)
Crescendo-decrescendo ejection murmur
2 murmurs HEART beast at Left upper sternal border
Tricuspid Regurgitation
Pulmonic stenosis
Aortic Stenosis (SU) Aortic Regurgitation (RS)
Right upper sternal border
Right sternal border
Strove volume loss
Acute Aortic Regurgitation
Post CABG compllications
CAM CVM
Cardiac Dysrhythmias: Vfib, afib a flutter, sinus block
Acute Pericarditis
Mitral Regurgitation (from inferior wall MI or complete rupture of a papillary muscle
Ventricular septal rupture (holosystolic murmur)
Cardiogenic shock
Myocardial rupture
What is the role of IV nitroprusside and/or intraaortic balloon pump?
Decrease LV afterload
Increase Forward flow
Ischemic Heart disease Heart anesthetic management Goals
Prevent ischemia
Monitor for myocardial injury
Treat myocardial ischemia or infaction
Ischemic heart disease shivering on awakening
Abrupt and dramatic increases in myocardial oxygen requirements up to 500% increase
Sub-endocardial ischemia → Lead will show
ST segment depression
T-wave inversion
Coronary Vasospasm ➔Variant angina/Prinzmetal Angina
ST segment elevation
Leads = simplest, most effective (80%)
• II & V5
Post op CABG those things can lead to increase Myocardial oxygen demand
Pain, hypoxemia, hypercarbia, sepsis, hypovolemia, hypotension, and hemorrhage
Six independent predictors of major cardiac complications[1] TIHCMS
- High-risk type of surgery (examples include vascular surgery and any open intraperitoneal or intrathoracic procedures)
- History of ischemic heart disease (history of myocardial infarction or a positive exercise test, current complaint of chest pain considered to be secondary to myocardial ischemia, use of nitrate therapy, or ECG with pathological Q waves; do not count prior coronary revascularization procedure unless one of the other criteria for ischemic heart disease is present)
- History of heart failure
- History of cerebrovascular disease
- Diabetes mellitus requiring treatment with insulin
- Preoperative serum creatinine >2.0 mg/dL (177 micromol/L)
Six independent predictors of major cardiac complications DO NOT DO THIS
do not count prior coronary revascularization procedure unless one of the other criteria for ischemic heart disease is present)
Lead abnormalities in ACS
ST segment elevation, depression or inverted T wave
Lead II, III, AVF
Artery responsible
RCA
Lead II, III, AVF
Area of myocardium that may be involved (RSIA)
RA, RV
SA node
Inferior aspect of LV
AV node
I,avL artery
Circumflex coronary artery
I,avL Area of myocardium that may be involved
Lateral aspect of LV
V3 , V5 Artery
LAD coronary artery