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 medicationsShort 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
V3, V5 Area of myocardium that may be involved
Anterolateral aspect of LV
Most sensitive for coronary ischemia
TEE
TEE picks up on
New regional Ventricular wall abnormalities
Elective surgery after cardiac revascularization: Recommendation w/ DUAL antiplatelet therapy
1 PCI without STENTING
> 2 weeks
Elective surgery after cardiac revascularization: Recommendation w/ DUAL antiplatelet therapy
Bare Metal stent
> 30 days (ideal 12 weeks)
Elective surgery after cardiac revascularization: Recommendation w/ DUAL antiplatelet therapy Drug-Eluting Stent
> 1 year
Procedure and TIME TO WAIT for ELECTIVE SURGERY :
Angioplasy without stenting
2-4 weeks
Procedure and TIME TO WAIT for ELECTIVE SURGERY :Bare metal stent placement
AT least 30 days; 12 weeks preferable
Procedure and TIME TO WAIT for ELECTIVE SURGERY :CABG
At least 6 weeks; 12 weeks preferable
Procedure and TIME TO WAIT for ELECTIVE SURGERY: Drug ELUTING STENT Placement
At least 12 months
Evaluation and management of high cardiac risk
Recent MI < 60 days or unstable angina
Recent PCI (risk for death, MI, stent thrombosis, need for REPEAT REVASCULARIZATION
Urgent emergency surgery (EVEN if on antiplatelet therapy)
High cardiac risk surgical procedures
The goals of management of a patient c/ IHD includes:
- Determining extent of IHD and any previous interventions
- Assessing severity and stability of disease
- Reviewing medical therapy and identifying any drugs that can increase the risk of surgical bleeding or
contraindicate a particular anesthetic technique
The goals of management of a patient c/ IHD includes →The need of emergency surgery
takes precedence over the need for additional workup
MAJOR clinical risk factors require intensive preoperative management (DUSS)
Decompensated heart failure
Unstable coronary syndrome
Significant dysrhythmias
Severe valvular heart disease
MINOR clinical risk factors do not independently increase cardiac risk and do not need a work up(4 HLNH)
Hypertension
Left bundle branch block
Nonspecific ST-T wave changes
History of stroke
Minor clinical risk factors do not
independently increase cardiac risk and do not need a work up
Ischemic Heart disease anesthetic management medication
Maintain adequate IV volume, Hgb concentration, heart rate, and BP (Labetalol is ok).
Mechanism of perioperative ACS = ischemia (rather than acute coronary or stent thrombosis) • Optimize
O2 delivery, minimize demand
Mechanism of perioperative ACS = ischemia (rather than acute coronary or stent thrombosis)• Hemodynamic goals:
- Low/normal HR (50-80bpm)
- Normal/high normal BP: 20% baseline, MAP 75-95 mmHg, diastolic 65-85 mm Hg
- Severe HTN increases myocardial O2 supply
Mechanism of perioperative ACS• Intraop HoTN defined:
SBP < 90 mmHg for > 10 min
Mechanism of perioperative ACS
LVEDV level and why?
- Normal LVEDV
* Distention = fluid overload = increase wall stress and O2 demand
Mechanism of perioperative ACS Arterial O2 content HGb threshold and temperature
Adequate arterial O2 content and Hgb (threshold < 9 g/dL c/recent MI or UA, otherwise < 8 g/dL)
• Normothermia = favors tissue release of O2
Preop med management Ischemia HD
• Beta blockers
Maintain
• Do NOT withdraw current therapy
• Do NOT initiate new therapy
Preop med management Ischemia HD• Statins
Maintain
Preop med management Ischemia HD• Aspirin
Depends on surgery and if receiving dual antiplatelet therapy
Preop med management Ischemia HD• ACEI/ARB
Continued with heart failure
• Always held with hemodynamic instability, hypovolemia, acute creatinine elevation
Preop med management Ischemia HD• Clonidine
• Continued if chronically administered (rebound HTN)
Preop med management Ischemia HD• Continue other CV meds
• CCB, digoxin, diuretics
Revascularization (CABG/PCI) is indicated when
optimal medical therapy fails to control Angina
Pectoris (AP) or
• Left main stenosis > 50%
• 70% or greater stenosis in a coronary artery
• CAD with EF < 40%
ABG is preferred over PCI in patients with
STP
- significant left main artery disease,
- those c/ three-vessel coronary artery obstruction, and - - patients c/ diabetes who have two- or three-vessel coronary artery disease
ACS PATHOPHYSIOLOGY
Focal disruption of atheromatous (atherosclerotic) plaques ➔plaque rupture➔coagulation cascade is triggered➔ thrombus➔ occluded coronary artery
➔ ACS.
ACS characteristics
- Angina at rest (>20 mins)
- Chronic Angina Pectoris
- New Onset Angina
NSAID lasts
(lasts platelet’s lifespan [7 days]).
• Aspirin 81 mgs vs. 325 mgs
Angina Pectoris, Thienopyridines (CPT)
(lasts platelet’s lifespan) •
Clopidogrel (Plavix) •
Prasugrel (Effient)
• Ticlopidine (Ticlid)
Platelet Glycoprotein IIb/IIIa Inhibitors (TEA)
• Tirofiban • Eptifibatide• Abciximab
ANGINA PECTORIS
Metabolic O2 demand > supply• Myocardial O2
consumption > coronary blood flow➔ Angina Pectoris
➔ CHF, Cardiac Dysrhythmias, & Myocardial Infarction
Angina Pectoris: Stress Test
• Negative stress test does not
exclude CAD.
Angina Pectoris: Exercise (Treadmill)
• 1 mm of horizontal or downsloping ST-segment depression during or c/in 4 minutes of exercise.
Angina Pectoris: Stress test. Nuclear (Adenosine)
• Assesses coronary perfusion & measures LVEF
Angina Pectoris: Chemical stress test, meds and what they assess
(Atropine or Dobutamine)
• Assesses new ventricular wall motion abnormalities, valvular function, and EF.
Angina Pectoris: Gold Standard
Coronary Angiography
Angina Pectoris: Coronary angiography
Significance of left main CAD
• Greater than 50% stenosis of the left main coronary artery is associated c/ a mortality rate of 15% per year•
Angina Pectoris: Coronary angiography →The most dangerous CAD (widow maker)
Left main coronary artery disease is the most dangerous anatomic lesion (widow maker).
Angina Pectoris Preop Optimization
Lifestyle modification
Optimization prior to surgery is key, via:(e.g., smoking cessation & regular aerobic exercise)
Angina Pectoris Preop Optimization ↓ of risk factors
(e.g., diet, weight reduction)
Angina Pectoris Preop Optimization Pharmacologic management
(e.g., anti HTN, anti cholesterol, ASA)
Angina Pectoris Preop Optimization Identification and treatment of
diseases that can precipitate or worsen the ischemia.
Angina Pectoris Preop Optimization Revascularization procedure
(e.g., CABG, Percutaneous Coronary Intervention [PCI], with or without intracoronary stents).
Common causes of acute chest pain cardiac (RAPA)
Angina
Rest or unstable angina
Acute MI
Pericarditis
Common causes of acute chest pain Vascular (APA)
Aortic dissection
PE
Pulmonary HTN
Common causes of acute chest pain: Pulmonary (PTS)
Pleuritis/PNA
Tracheobronchitis
Spontaneous Pneumo
Common causes of acute chest pain:GI
Peptic ulcer
Pancreatitis
Esophageal reflux
Gallbladder disease
Common causes of acute chest pain: Musculoskeletal
Costochondritis
Cervical disk disease
Trauma or strain
Common causes of acute chest pain: Infectious/psych
Herpes zoster
Panic disorder
Thrombolytic Therapy (e.g, tPA):
a. start 30-60 mins of hospital arrival, and
b within 12 hours of symptom onset.
Aka Percutaneous Coronary Angioplasty (PTCA)
• Treatment of choice for _____ and must be done
severe heart failure and/or
pulmonary edema (when tPA is contraindicated)
• Must be done 90 minutes of arrival and c/in 12 hours
of symptom onset
Functional capacity or exercise tolerance can be
expressed in metabolic equivalent of the task
MET) units• O2consumption (O2) of a 70-kg, 40-year-old
man in a resting state is 3.5 mL/kg/min = 1 MET
Perioperative cardiac risk is increased when a
patient is unable to meet a
4-MET demand during normal daily activities
• Bicycling lightly, walking 3mph, calisthenics, sexual
activity, golfing
• Surgery-specific risk of non-cardiac procedures are
graded as High (EAPP)
Emergency major surgery,
Aortic and other major vascular surgery
Peripheral vascular surgery, and prolonged surgery c/ large fluid shifts and/or blood loss)
Surgery-specific risk of non-cardiac procedures are
graded as Medium (CHEPOI)
Carotid endarterectomy Head and neck surgery Endovascular aortic surgery Prostate surgery) Intraperitoneal and intrathoracic surgery Orthopedic surgery
Surgery-specific risk of non-cardiac procedures are
graded as LOW
Endoscopic surgery
Superficial surgery,
Cataract surgery, Breast surgery, and Ambulatory
surgery)
Under-secreting thyroid tumor
Hypothalamus (TSH-RH)
Pituitary (TSH)
Thyroid (TH)
High (b/c few hypothalamus receptors are bound)
High
Low
Over-secreting thyroid tumor
Hypothalamus (TSH-RH)
Pituitary (TSH)
Thyroid (TH)
Low
Low
High
If problem is TSH, we don’t bother injecting TSH, we just give hormone that is lacking:
Thyroid hormone.
Under-secreting pituitary tumor
Hypothalamus (TSH-RH)
Pituitary (TSH)
Thyroid (TH)
High
Low
Low
Over-secreting pituitary tumor
Hypothalamus (TSH-RH)
Pituitary (TSH)
Thyroid (TH)
Low
High
High
Under-secreting hypothalamic tumor
Hypothalamus (TSH-RH)
Pituitary (TSH)
Thyroid (TH)
Low
low
low
Over-secreting hypothalamic tumor
Hypothalamus (TSH-RH)
Pituitary (TSH)
Thyroid (TH)
High
High
High
Cortisol Under-secreting adrenal gland tumor
ACTH-RH
ACTH
Cortisol
High
High
Low
Cortisol Over-secreting adrenal tumor
ACTH-RH
ACTH
Cortisol
Low
Low
High
ACTH Under-secreting pituitary tumor
ACTH-RH
ACTH
Cortisol
High
Low
Low
ACTH Over-secreting pituitary tumor
ACTH-RH
ACTH
Cortisol
Low
High
High
Under-secreting hypothalamic tumor
ACTH-RH
ACTH
Cortisol
Low
Low
Low
Over-secreting hypothalamic tumor
ACTH-RH
ACTH
Cortisol
High
High
High
So when ACTH is elevated, and body cannot make enough cortisol what happens
aldosterone will ↑, and testosterone will be made in females instead, and estrogens will be made in males. High blood glucose and high blood pressure, and
females develop facial hair while males develop
breasts.
ACTH Over-secreting pituitary tumor CUSHING
Low
High
High
ACTH Over-secreting adrenal tumor CUSHING
Low
Low
High
Cortisol Under-secreting adrenal gland tumor
High
High
Low
PRIMARY ADRENAL INSUFFICIENCY
(adrenal gland is problem)
SECONDARY ADRENAL INSUFFICIENCY
(pituitary is problem)
Secondary Adrenal Insufficiency Pituitary ACTH levels are____cortisol is _____ and hypothalamus ACTH-RH is
low, low,high.
Difference between primary and secondary
adrenal insufficiency is
ACTH level
Primary Adrenal Insufficiency Pituitary ACTH levels are____cortisol is _____ and hypothalamus ACTH-RH is
High, low, High
Cushing’s Syndrome
(1° adrenal hyperplasia) Adrenal gland is problem
Thyroid hormone is
permissive for growth hormone (you need thyroid hormone in order for GH to work).
Not enough thyroid hormone →
stunted growth, even if enough growth hormone is
present.
Hormonal Trigger
◦ Endocrine gland releases a hormone that stimulates another endocrine gland to release its hormone.
◦ Hypothalamus releases a hormone that causes pituitary gland to
release TSH, which causes thyroid gland to release thyroid hormone.
Thyroglobin T4 is
◦ T3 gets used first by body cells.
most abundant form, but it is inert (inactive).
T3 has
robust activity in cell.
◦ T4 takes longer
to be ready; one iodine has to drop off.
As T3 is used up, T4 is being converted by
iodinase to more T3.
To make thyroid hormone, you need
iodine in your body. Iodized salt has enough to meet this need.
Iodine is brought into
follicular cells, gene expression occurs, thyroglobulin is made.
Without enough iodine in diet, thyroid hormone cannot be made, no matter how much TSH is present.
Thyroid Gland role in synthesis
Building block of TH = chemically attaching Ito tyrosine.
In plasma, TH needs a “carrier molecule” or it will be cleared from body
Diabetes insipidus main issue
◦ Not enough ADH (anti-diuretic hormone; a diuretic takes out excess fluid from body)
◦ Because they lack ADH, person urinates frequently (polyuria), so they are thirsty and drink a lot of water (polydipsia). Their blood glucose is normal.
Synthetic form of ADH is
vasopressin
• Hypersecretion of GH in children
◦ Gigantism (overall growth)
• Hypersecretion of GH in adults
◦ Acromegaly: enlarged hands and feet, and big chin, nose, and forehead
Hyposecretion of GH
◦ Pituitary dwarfism
◦ Proportions are normal, overall size is small
GH needs thyroid hormone (TH) to be present.
GH stimulates all cells to
↑ protein synthesis,
fat utilization, and gluconeogenesis.
Gigantism vs acromegaly
result of excess GH during pre-puberty and acromegaly is result of excess GH after growth plates closed.
Acromegaly Anesthesia Considerations
Distorted face = hard to mask ventilate Enlarged tongue/epiglottis Overgrowth of mandible Edematous vocal cords = smaller glottic opening ◦ Assess for hoarseness/stridor Skeletal changes associated with acromegaly may make use of regional anesthesia technically difficult or unreliable
Syndrome of Inappropriate Antidiuretic Hormone
Secretion (SIADH)
Too much ADH → hyponatremia from dilution
◦ Water reabsorbed by renal tubules
◦ Ectopic = small cell lung carcinoma, carcinoid tumors
SIADH Can result from
CNS trauma, infections, medications, hypothyroidism, major surgery
S/S of SIADH
N/V, weakness, lethargy, confusion, depressed mental status, seizures
SIADH diagnosis (RHIN)
Reduced serum osmolality (<270 mOsm/L
Hyponatremia (<130 mEq/L),
Inappropriately increased urine osmolality (hypertonic relative to plasma).
Normal or increased urine Na excretion (>20 mEq/L), and
SIADH Fluid restriction
(< 1L/day)
Democlocydine action
Demeclocycline inhibits action of ADH @ distal tubule
Conivaptan is a ______used in the treatment of
vasopressin-2 receptor antagonist, may be effective; SIADH
SIADH Severe hyponatremia
(<115 mEq/L) may require 3% hypertonic saline
NA Rate of correction should be
0.5mEq/L/h until Na+ 125 mEq/L Then proceed more slowly to prevent central
pontine myelinolysis
SIADH Anesthesia management:
◦ Careful monitoring and administration of fluids and
electrolytes
◦ Can have delayed awakening from anesthesia
◦ Can wake up confused after anesthesia
Flluid resuscitation of SIADH
◦ Fluid resuscitation should be done with 0.9%NS
Thyroid hormones All cells respond to thyroid hormone,
increasing their
metabolic rate (heart speeds up, beats c/ greater force, more nutrients are used, etc).
Too much thyroid hormone is hyperthyroidism; these ppl are
people are thin and active.
When levels of TH are too low, it is called
hypothyroidism; these people are
overweight, move slowly, have no energy.
When there is too much TH, they get
muscles tremors and ↑ blood glucose levels (hyperglycemia).
W/ not enough TH, they lose interest, become
sluggish, they get low blood glucose levels
hypoglycemia
Major stimulus for release of thyroid
hormone is
hormonal (TSH from pituitary tells thyroid gland that it needs to make more thyroid hormone).
What happens when TSH is released?
Every step in process of making TH is ↑: Follicular
cells become larger, metabolism ↑: ↑ in O2 use (especially in mitochondria), heat is generated.
TSH causes stimulation of sympathetic (beta)
receptors in heart, causing ↑ force of contraction and ↑ heart rate
Since thyroid hormone is partly made of
iodine, if a person doesn’t eat enough iodine,can’t make thyroid hormone. how does hypothalamus response
can’t make thyroid hormone.
Hypothalamus responds by putting out more
TSH-RH.
Pituitary will respond by releasing TSH. But thyroid can’t respond by releasing TH if it does not have iodine to make hormone, so it size of follicle grows → gland grows → GOITER.
Hyperthyroidism Anesthesia Management for elective cases
Euvolemia for elective cases
Dexamethasone action
2mg IV q6h ↓hormone release and T4→T3 conversion
Hyperthyroidism Anesthesia Management
Consider airway difficulties
Will need more anesthesia to control SNS response
Protect eyes
Hyperthyrodisim Medications to
Avoid things that stimulate SNS (ketamine, pancuronium, atropine, ephedrine, epinephrine)
Vasopressors to use with hyperthyroidism
Use direct acting vasopressors
◦ Indirect can result in an exaggerated response
Hypothyroidism Anesthesia Management
Airway issues:
swollen oral cavity, edematous vocal cords, goiter
Hypothyroidism and Aspiration
↓Gastric emptying = regurgitation/aspiration
Hypothyroidism and CV
Normally have↓ CO, SV, HR, baroreceptor reflex
↓vent response to hypoxia/hypercarbia (enhanced with
anesthesia)
hypothyroidism
Hypoventilate in general, so mechanically ventilate
Hypothyroidism
Hypothermia common with
Hypothyrodism
Hematologic complications with Hypothyroidism
anemia, dysfunctional plt/coag factors (esp. factor VIII), electrolyte imbalances (hyponatremia), hypoglycemia
Hypothyroidism narcotics
Very sensitive to narcotics and anesthetics in general
◦ Can have significant hypotension
Hypotension with hypothyroidism
◦ BEST treated with ephedrine, dopamine, or epi NOT
phenylephrine (opposite of hyperthyroidism)
◦ If unresponsive, give steroids
Hypothyroidism ◦ Beta receptors may be
less numerous and less sensitive
◦ Use phosphodiesterase inhibitor
People c/ hyperthyroidism can take a drug
called______which does what?
PTU (Propylthiouracil), which inhibits TH production by blocking peroxidase enzyme that joins iodine to tyrosine
→results in lower thyroid hormone levels.
HYPERTHYROIDISM
(Most commonly caused by
Graves Disease, which is an autoimmune disease)
Signs include HYPERTHYROIDISM (GRAVE”S)
thinness, eyes that stick out like a bug (exophthalmoses).
◦ Leads to nervousness, weight loss, sweating, and rapid heart rate.
Hyperthyroidism
◦ Graves’ Disease is when
hyperthyroidism is caused by an autoimmune disorder.
You can have thyroid oblated (killed off) by drinking
radioactive iodine
◦ Kills just thyroid tissue.
◦ As metabolic rate slows, gains weight again.
◦ Can’t be around people for 5 days, and they set
off Geiger counters for months afterwards.
◦ Then start on artificial thyroxin, need to figure
out what their set point is for normal.
Another way is to have thyroid gland surgically
removed.
◦ Parathyroid glands are often damaged or removed
during this surgery.
◦ Often intentionally leave some thyroid tissue
behind, in hopes of leaving enough parathyroid
glands there.
◦ If too many of parathyroid glands are removed,
calcium levels go down, can go into cardiac arrest.
◦ Now patient has to have two hormones
replaced.
Hypothyroidism This can be caused by
Hashimoto’s thyroiditis (autoimmune)
Iodine deficiency
Tumor
Defective enzyme in thyroid.
– Hashimoto’s Thyroiditis - adult hypothyroidism
◦ Antibodies attack and destroy thyroid tissue
◦ Low metabolic rate and weight gain are
common symptom
◦ Myxedema:
non-pitting edema associated c/ hypothyroidism
Cretinism –
Hypothyroidism in children
Short, disproportionate body, thick tongue and
mental retardation
Cretinism (diminished mental ability)
This term describes babies whose MOTHER had lack of iodine.
Baby now cannot get iodine, and baby will have reduced growth and intellectual ability.
Once it is born and gets a healthy diet, it still
won’t go back to normal because TH is necessary for proper myelination and synaptic formation.
Congenital hypothyroidism is term for a
baby
◦ Problem is only
whose thyroid gland is not working correctly (not secreting enough TH). c/ baby, not c/ mom.
Congenital hypothyroidism and cretin babies
have similar symptoms.
◦ Child will stay tiny because GH does not work
c/out TH.
Parathyroid hormone is released by a
Humoral mechanism.
◦ If blood calcium levels are low, parathyroid
hormone is released.
◦ If blood calcium levels are high, parathyroid
hormone stops being released.
Hyperparathyroidism
◦ Hypercalcemia
◦
◦ Skeletal muscle weakness, polyuria, ↓GFR, ↑PR interval,
↓ QT interval, HTN, decreased pain sensation
◦
NMB unpredictable
Hypercalcemia
Hypoparathyroidism
◦ Hypocalcemia
Neuronal irritability, skeletal muscle spasms, tetany, and
possibly seizures
◦ Acidosis and calcium
increases serum calcium
Alkalosis and serum calcium.
Decreases serum calcium
Acute hypocalcemia can present with
stridor and apnea
◦ Congestive heart failure, hypotension, and decreased
responsiveness to β-agonists may occur
Hypocalcemia
◦ Prolonged QT interval
Hypocalcemia
Cushing’s syndrome/Disease
◦ Hypersecretion of cortisol ◦ High blood glucose ◦ High blood pressure ◦ Features of opposite sex ◦ Round “moon” face and “buffalo hump”
Addison’s disease
◦ Hyposecretion of cortisol
◦ Low blood glucose
◦ Low blood pressure results
◦ Also get hyperpigmentation
In Cushing’s Syndrome, all adrenal cortical
hormones (
cortisol, androgens, and
aldosterone) are elevated, but ACTH-RH and
ACTH levels are lo
Cushing’s Disease- pituitary tumor
Cushing’s Syndrome
(excess ACTH)
•Ectopic Cushing ACTH producing tumor
(lungs)
•Iatrogenic Cushing
(side-effect of some medical treatment)
Cushing is a
primary hyperadrenalism
•Over-secreting adrenal tumor-, all adrenocortical hormones elevated
Cushing Signs/symptoms:
buffalo hump, moon face, muscle loss/weakness, thin skin c/ striae, hyperglycemia, immune suppression
Cushing Perioperative management of HTN,
hyperglycemia, intravascular fluid volume (usually elevated), and electrolytes (hypokalemia is common) necessary Pneumothorax is possible during adrenal
surgery
Cushing Preoperative diuresis with
spironolactone is helpful
Cushing When bilateral adrenalectomy is performed,
fludrocortisone will be necessary in the postoperative period
Congenital adrenal hyperplasia (CAH) in a
female fetus causes
These babies have a _______________
some enzyme is not expressed which is
required to convert________
Boys are not affected; girls need__________
If presence of ACTH is driving pathway, and
it is blocked at this enzyme, ACTH can only
be used to make androgens
clitoris to enlarge and labia majora fuse into a scrotal sac. mutation in a gene, cholesterol into corticosteroids, so cholesterol is shunted to pathway that is not compromised: androgen production a surgery and cortisol for life, will be fine..
Leads to overstimulation of adrenal androgen pathways.
Congenital Adrenal Hyperplasia (CAH)
Addison’s disease Also called
Primary Adrenal Insufficiency and
hypoadrenalism; low glucose, low blood
pressure, and hyperpigmentation in hands,
fingers, and gums.
Addison’s disease may be caused by anything
that
disturbs production of adrenal hormones (e.g., Tuberculosis).
In Addison’s disease, adrenal cortex
does not respond to pituitary orders. Cortisol levels are low, but pituitary ACTH and
hypothalamus ACTH-RH hormones are high.
Secondary adrenal insufficiency deficiency
◦ Deficiency of ACTH
Primary Adrenal Insufficiency: Addison’s Disease
◦ Primary hypoadrenalism;
entire adrenal gland is destroyed due to atrophy or autoimmunedisorder
◦ Tuberculosis –disease attacks adrenal gland
◦ ACTH is ↑
Adrenal Gland deficiencies Signs/symptoms:
Water/salt imbalance,
plasma volume depletion, low blood glucose,
pigmentation, Addisonian crisis (low blood
pressure, low blood glucose, need to go to
hospital)
Addison’s Disease Anesthesia Considerations
Treat cause, give _______
replace _________________________
Administer glucocorticoids,
water/Na+ deficits (can be up to 3L)
Addisons’ electrolyte imbalance
Metabolic acidosis and hyperkalemia usually
resolve with fluid and steroid administration
Addison’s and Etomidate
Etomidate transiently inhibits Cortisol synthesis and should be avoided in this patient population
Addison and Anesthetics
Minimal doses of anesthetic agents and drugs are recommended, since myocardial
depression and skeletal muscle weakness are
frequently part of the clinical presentation.
Conn’s syndrome (hyperaldosteronism)
Too much aldosterone is secreted.
Too much salt and water is reabsorbed, person
develops high blood pressure.
Cortisone levels are not effected, so they do not
have elevated blood glucose.
High incidence of ischemic heart disease
Conn’s syndrome
Anesthesia considerations Conn’s syndrome:
Anesthesia considerations:
◦ Preoperative restoration of intravascular
volume, electrolyte levels (K+ supplementation), renal function, and control of hypertension
◦ Na+ restrictions
◦ Spironolactone
◦ Preop echo if hx chronic HTN
DIABETES INSIPIDUS
◦ Pituitary gland does not secrete antidiuretic hormone, or kidney does not respond to hormone.
◦ It can be caused by damage to pituitary or kidney
DIABETES MELLITUS
◦ Hereditary lack of
insulin secretion in pancreas, or resistance to insulin by body’s cells.
◦ Type I diabetes(insulin dependent, develops in children)
◦ Destruction of pancreatic islets by autoimmune
disorders.
◦ Need insulin injections daily throughout life.
◦ Type II diabetes (not insulin dependent, develops in
adults)
◦ Consequence of obesity: cells are less sensitive to insulin.
◦ Initially treated c/ diet and exercise.
◦ Oral medicines or injected insulin may be need
DI Goal: plasma
osmolality is less than 290 mOsm/L◦ Isotonic fluids should be used for volume resuscitation.
DI Anesthesia management Preoperative dose of
DDAVP
desmopressin intranasally or an IV bolus of 100 mU (0.1 unit) of aqueous vasopressin followed by a continuous infusion of 100–200 mU/h (0.1–0.2 units/h)
DI ◦ If plasma osmolality exceeds 290 mOsm/L,
hypotonic fluid should be used for resuscitation
and the vasopressin infusion should be
increased above 200 mU/h.
DI tx since Since vasopressin causes
vasoconstriction of arteriolar beds, close monitoring for myocardial ischemia is recommended
DM
needs to be worked up (silent)________
◦ Gastroparesis = at risk for 2 things
◦ MI
aspiration
Autonomic neuropathy → dysrhythmias, hypotension
DM Anesthesia Insulin
◦ Night before surgery, 1/3 NPH dose
DM Pump rate decreased by
30% overnight, can run basal rate during surgery
Oral hypoglycemics =
hold 24-48 hrs
DM Avoid in entire periop period ; why?
Sulfonylureas block myocardial ATP channels responsible forischemia/anesthesia-induced preconditioning
Intraoperative glycemic control
120- 180 mg/dL
BG > 200 =
glycosuria, dehydration, inhibited wound healing
1 unit of insulin
↓ glucose approximately 25- 30 mg/dL
BG Best sample =
venous, cap + art come out 7% higher, and whole blood is 15% lower than serum values
• Hypoglycemia treatment
treat c/50 mL 50% dextrose in water
• ↑BG 100mg/dL or 2mg/dL/mL
Postop control
- Critically ill = 140-180 mg/dL
* Initiate insulin therapy if > 180 mg/dL
Rigid bronchoscopy
To examine the lung airways
Diagnostic, therapeutic, interventional
Flex vs rigid Thinner and longer
Diagnostic and therapeutic procedures
Flexible
Flex vs rigid Access to lower airways such as third order bronchioles
Flexible
Disadvantage: Foreign object or thick mucus cannot be removed through the lumen
Flexible
Flex vs rigid Topical anesthesia and/or sedation
Flexible
Flex vs rigid Proximal airways
Interventional procedures
Rigid and larger
General Anesthesia
Rigid
Flex vs rigid
Disadvantage Potential soft tissue damage & inability to visualize deeper bronchioles
Rigid
Instruments of choice for Bronchoscopy: RIGID
FEMVS
Foreign bodies Massive Hemoptysis Vascular tumors Small children Enbobronchial resections
Fiberoptic Flexible
Mechanical problem of neck Upper lobe and peripheral lesions Limited hemoptysis PNA for culture DLT posiion Difficult intubation checking position of ET bronchial blockade
Anesthesia for Flexible bronchoscopy Local Anesthesia/MAC
For patient who is awake, cooperative, and breathing spontaneously
Glycopyrrolate 0.2mg to 0.3 mg IV 15-20 minutes prior
Sedatives for patient comfort
Lidocaine & Tetracaine – commonly used
Nebulizer spray – oropharynx and base of the tongue
Anesthesia for Flexible bronchoscopy Block Superior Laryngeal Nerve Internal Branch
Tongue held forward, pledgets in each piriform fossa using Krause forceps
Transtracheal Anesthesia by
Transtracheal injection of local anesthetics
Spraying vocal cords and trachea under direct vision with laryngoscope
Anesthesia for Flexible bronchoscopy Alternative to depress gag reflex
Superior laryngeal nerve block by external approach
Glossopharyngeal block
These blocks depresses airway reflexes, patient to remain NPO for several hours
Anesthesia for Flexible bronchoscopy Transnasal Approach
4% Cocaine topically applied to nasal mucosa or viscous lidocaine
Phenylephrine or Afrin spray can be mixed with lidocaine for vasoconstriction
Most widely used mode of ventilation for rigid bronchoscopy
Jet ventilator
Rigid Bronchoscope
Place
Suction
Reverse with
Patient may cough violently to clear secretions and blood
_______________ decrease airway reactivity
Place ETT or LMA
Suction
Reverse with Neostigmine and Glycopyrrolate and fully before extubation
Patient may cough violently to clear secretions and blood
Lidocaine 1mg/kg to decrease airway reactivity
Wake up from remifentanil tends to be smoother
Postop O2 supplementation preferably humidified
Rigid Bronchoscope Wake up from tends to be smoother
remifentanil
Rigid Bronchoscope Post op O2 supplementation preferably
humidified
POST OP RIGID BRONCHOSCOPOY
CXR – in PACU to check for atelectasis, pneumothorax, and mediastinal emphysema
Rigid Bronchoscope Induction
Maintenance
Preoxygenate well
Consider short-acting paralytics
Succinylcholine 1mg/kg or rocuronium 0.3-0.6 mg/kg
Minimal Opioids use, consider remifentanil 1mcg/kg to avoid postop respiratory depressiong
Rigid Bronchoscope Maintenance
Sevoflurane or Isoflurane and 100% O2 TIVA alternative – (no gas leaks) Propofol 50-150 mcg/kg/min Remifentanil 0.1-0.3 mcg/kg/min Paralytics Short acting NDNMB (atracurium or rocuronium)
Rigid bronchoscope Jet Ventilation –
allows for uninterrupted ventilation and may shorten the length of the procedure (fewer interruptions)
Variable FiO2 secondary to entrainment of air
No EtCO2 available – difficult to determine adequacy of ventilation
Intermittent ABG for prolonged procedure or use of transcutaneous CO2 monitor
Restrict IV fluids to avoid fluid overload
Rigid Bronchoscope complications
Mechanical trauma to the teeth Hemorrhage Bronchospasm Bronchial or tracheal perforation Subglottic edema Barotrauma Airway obstruction Pneumothorax *Note: To avoid some of these complications, it is advised to intubate with an ETT after bronchoscopy under general anesthesia
Rigid Bronchoscope *Note: To avoid some of these complications, it is advised to
intubate with an ETT after bronchoscopy under general anesthesia
Advantages of Bronchial Blockers
Disadvantages:
Can be dislodge and become life threatening
May be difficult to place
Cost more than double lumen tubes
Double Lumen Tubes
Allows a single lumen tube to be placed
Ideal for long cases because of no tube exchange post-operatively, and expected post-operative mechanical ventilation
Can be used to isolate individual lobes
Post op care rigid
A single chest tube usually is placed at the end of case and connected to a sealed drainage unit for postop chest drainage
Pain management:
IV, IM, continuous IV, PCA
Epidural, intercostal blocks, NSAID
When the surgeon says to reinflate the operative lung,
unclamp the lumen and manually ventilate until the lung is inflated. Then change the ventilator settings back to the original, 2 lung ventilation settings to a PRESSURE control setting, be sure to limit peak pressures to < 40 cm H20. When using a smaller Tv, a higher rate will be needed.
Blocks for Bronchoscope
Epidural, Intercostal block, paraveterbral block and/or intrapleural local anesthetic intercostal nerve blocks are performed when other regional techniques are contraindicated
Coming off Post-bypass low cardiac output
Low pulmonary artery pressure:
give volume, increase preload
Coming off Post-bypass low cardiac output
Low ejection fraction:
increase contractility with inotropes
Coming off Post-bypass High afterload (SVR > 1200):
decrease afterload, can use sodium nitroprusside
Coming off Post-bypass Low heart rate:
increase heart rate, program pacemaker
Coming off Post-bypass Arrythmias
Atrial/ventricular pacing, intra-aortic balloon pump set at 1:1
Coming off Bypass Post-bypass hypotension : assess
Assess LV volume and function
Check CVP, PAD, CO/CI, and TEE for wall movement abnormalities
Coming off Post-bypass HYPOTENSION Treat with
volume, calcium, vasopressors, or inotropes as needed
Alpha agonists may be needed
A ventricular assist device may be needed for the right or left ventricle, or both ventricles
Coming off BYPASS Post-bypass hypertension
Assess if the anesthesia level is deep enough
Treat with narcotics and volatile agents as necessary
Some patients may need vasodilators
Off pump CABG
What should be available?
Coronary artery bypass grafting may be done without cardiopulmonary bypass
Patient should be prepped and draped to go on bypass at any time
Best candidate for OFF PUMP BYPASS
Best for hemodynamically stable patients with coronary arteries that can be stabilized on the anterior wall of the heart
Promoted in patients at increased risk for stroke, severe lung disease, severe vascular disease, and renal dysfunction
POST BYPASS PERIOD Protamine
1.3-1.5 mg/100 units of heparin given can be administered once
Hemostasis is controlled
The aortic and vena cava cannulas have been removed
Hemodynamic stability is achieved
Give protamine slowly to prevent hypotension or pulmonary hypertension
POST BYPASS PERIOD ACT
Check ACT 3 minutes after giving protamine – it should be the same or less than baseline
POST BYPASS Anaphylaxis risk
is increased for patients with diabetes who have received NPH insulin and/or vasectomized males
Epinephrine 10 mcg/ml to treat reactions
POST BYPASS Uncontrolled bleeding may be caused by
Inadequate surgical control of bleeding Inadequate heparin reversal Thrombocytopenia Platelet dysfunction Hypothermia if the patient's body temperature is < 35 c Newly acquired coagulopathy
Treatment of Post BYPASS BLEEDING
More protamine FFP Platelets DDAVP Factor VII
POST bypass bleeding Do this before cell saver?
Finish giving protamine before starting to give cell-saver blood, then give blood products
Total neck dissection Thyroidectomy pre-op
Hypertension must be controlled pre-op • Extra risk of exaggerated hemodynamic responses post -op d/t dissection near carotid body and vagus nerve
Intraop total neck dissection BP control
• Gases should be humidified to avoid mucus plugs in this population
Deliberative relative hypotension is desirable for these
surgeries, with aggressive treatment of increased BP
• MAP of 60–70 mmHg, use of remifentanyl
• Laryngeal edema may occur
Total neck dissection intraop important to Avoid administering _____why?
paralytics until after large mandibular nerve and CN XI have been identified
Total neck dissection why do you get bradycardia •
transient bradycardia
Neck dissection Decrease in HR and BP treatment:
stop surgery, lidocaine infiltration of carotid sinus by surgeon, atropine
POST op BP and HR
• Facial nerve injury: facial droop • Recurrent laryngeal nerve injury
Increased Secondary to carotid sinus
denervation • Aggressive pharmacological intervention
Thyroidectomy Thyroid Storm = life threatening!
•
- Hyperthermia
- Tachycardia
- Widened pulse pressure
- Anxiety
- Neuro changes
• Tx thyroid storm :
• ↑FiO2, fluids, e- replacement, cooling blanket, etc.
Thryroid storm CAN BE MISTAKEN FOR
MALIGNANT HYPERTHERMIA!
• When in doubt –> dantrolene
• Can be beneficial for bot
Thyroidectomy – Anesthesia Considerations
• Local anesthetic
with epinephrine injection into neck
• Monitor EKG changes (increased HR, ST-segment changes)
• May want to avoid LA with epi in those patients
hyperthyroid patients
• If hyperthyroidism, have these available
ave beta blockers available
• HTN, tachycardia, or SNS response
Thyroidectomy - Indications
Performed to correct either a benign or malignant process affecting the thyroid gland
• Hyperthyroidism (Graves disease, goiter, toxic adenoma)
• Thyroid cancerDissection near carotid body and vagus nerve may result in
• Noncancerous enlargement of thyroid (goiter)
• Benign or suspicious
nodules
Hyperthyroidism Cause: May be commonly secondary to
Graves’ disease, toxic multinodular goiter, thyroid
adenomas, TSH-secreting tumor (rare), or overdose of thyroid hormone
Hyperthyroidism Common sx:
• Hypermetabolism & SNS overstimulation
• Fatigue, sweating, intolerance to heat, weight
loss or gain
• Thyroid goiter, exophthalmos
• Increased appetite, HR, BP, pulse pressure,
and temperature
• Tremor, anxiety, nervousness
• CHF and Atrial Fibrillation are common in these
patients
Hyperthyroidism
Untreated hyperthyroidism leads to
Thyroid storm
Review
- Hypothyroid
• Cause:
iatrogenic or autoimmune thyroiditis
Common sx Hypothyroidism
Cold, metabolism, cardiac resp function, HR, CO, DTR
Intolerance to cold • Decreased metabolism • Depressed cardiac and respiratoryfunction
• Bradycardia, decreased CO, pulse pressure, temp, mental reflexes, and DTR
• Lethargy, anorexia, weight gain or loss, constipation
• Decreased ventilatory response to hypoxia and hypercarbia
hypothyroidism
These patients are dehydrated
• need volume repletion
• Hyperthyroid:
hypermetabolism, sweating, diarrhea
• Hypothyroid:
adrenal insufficiency (untreated)
Thyroidectomy – Anesthetic Concerns
Hyperthyroid
- Increased:
- HR
- Atrial fibrillation
- Palpitations
- CHF
- Caution using beta blockers
Hypothyroid CV CHAnge
- Bradydysrhythmias,
- Diastolic HTN or dysfunction
- Pericardial effusions
- ECG changes
- ST and QT changes, TdP
• Caution w/ volume expansion with LV dysfunction
Hypothyroidism
Complications of Thyroidectomy• Injury to recurrent laryngeal nerves (RLN) • Bilateral: • Unilateral:
- Will require reintubation
- experience hoarseness.
Thyroidectomy – Anesthesia
• Check with surgeon if needing:
• Muscle relaxant
Thyroidectomy – Anesthesia Avoid
histamine releasing paralytics
Atracurium , Mivacurium
IONM Line up electrodes to
vocal cords
IONM vocal cords aligned with The electrodes, connected to a monitor, sense
EMG (electromyographic) activity from the thyroarytenoid
muscles
Thyroidecomty no _______ why?
• NO muscle relaxants or topical laryngeal
anesthesia!
• to obtain appropriate signals during surgery
Increasing your body weight by 10% causes how much of an increase in OSA risk?
10%
Pickwickian syndrome is named after a character in what famous author’s book?
Charles Dickens
Which of the following is not an adverse effect of Albuterol
Hyponatremia
If you are ventilating at rate of 10, what should your I:E be?
1:2
If you are ventilating at rate of 8, what should be your I:E be?
1:3
If you are ventilating at rate of 6, what should be your I:E be?
1:4
Which commonly used anesthetic agent can exacerbate asthma?
Neostigmine
Which intervention may help with negative pressure pulmonary edema?
Add 8cm H2O PEEP
Which lung volume is not significantly affected by breathing irregularities?
Tidal volume
What is an average hospital stay for patient who aspirate?
21 days
What is the gold standard for assessing angina related to CAD?
Coronary angiography
What type of medication is abciximab?
Glycoproteins IIb/IIIa inhibitor
What might you hear with CHF?
S3 sound
When does thrombolytic therapy need to be administered by for ACS?
12 hours
Which papillary muscle of the mitral valve has the highest chance of rupturing?
Posteromedial
When is CABG preferred over a PCI?
Three vessel coronary artery obstruction
How much heparin would you give for a CABG about to go on bypass?
400units/kg
Upon arriving to the hospital, how long do you have to do a PCI?
90 min
What is the O2 consumption at 2 METS?
7ml/kg/min (3.5ml/kg/min at 1 METS)
What is the highest level serum glucose can rise to during cardiac surgery?
180mg/dL
After a radial neck dissection, a patient is restless in PACU. What might be occurring?
Hypercarbia
Which hormone is released via a neuronal trigger?
ADH
The release of thyroid hormone is a result of what kind of trigger?
Hormonal
What is the highest pressure you can deliver during jet ventilation via cricothyrotomy?
50PSI
Which hormone is released via humoral trigger?
Glucagon
Growth hormone requires which other hormone to function?
Thyroid hormone
Excessive testosterone production in the adrenal cortex will has what affect on males?
Nothing
How long can a keep a cricothyrotomy in for?
5 days
What hormone is released from the neurohypophysis?
ADH
What is necessary to diagnose SIADH?
Concentrated Urine
When should you initiate 3% NS in a patient with SIADH? 115mEq/L (when will you hold surgery?
Less than 125)
What enzyme facilitates iodination of tyrosine?
Peroxidase
What breakdowns T4 to T3
Iodinase
Subglottic stenosis may result from what surgical procedure?
Cricothyrotomy
What medication can decrease the conversion of T4 to T3?
Dexamethasone
What is the largest pure endocrine gland?
Thyroid
If you have an over-secreting pituitary tumor, which body part will reduce its signaling?
Hypothalamus
Decreased TSH-RH, decreased TSH, and increased TH indicates what?
Over-secretion by thyroid
Which childhood disease is a result of hypothyroidism when in the womb?
Cretinism
What antagonizes calcitonin?
Parathyroid hormone
Where is aldosterone produced?
Zona Glomerulosa
Humoral Trigger
Blood is being monitored. When level of substance is too low, it stimulates release of hormone.
Neuronal Trigger
A neuron directly stimulates gland to cause secretion of hormone.
Hormonal Trigger
Endocrine gland releases a hormone that stimulates another endocrinegland to release its hormone.
Humoral triggers Examples are
Parathyroid Insulin, Glucagon Aldosterone Hormone
ACS AVOID
tachycardia, systolic hypertension, sympathetic nervous system stimulation, arterial hypoxemia, and hypotension (c/in 20% of the normal awake patient)
SAD-P
Syndrome Adrenal
Disease Pituitary
Valvular associated with PVC
MVP
P mitrale is associated with
Mitral stenosis
High Peak pressure
May be needed to deliver TV of bronchospasm
Fiberoptic bronchoscopy
• Principal contraindication to pleural biopsy is
coagulopathy
Maintenance volatile for CABG , gas and MAC
Iso, Sevo or des, titrated to 0.5 MAC
Avoid nitrous oxide
Fentanyl and bypass
May be given throughout the case
50 -100mcg if good EF
<50 if bad EF
CABG induction agent if CO is less than 35%
Etomidate 0.2-0.3mg/kg
CABG induction agent if CO is MORE than 35%
Sodium thiopental 2-4mg/kg
Induction meds
Succ , give roc defasciculating dose
Midazolam
COPd and volume
RV gets larger closing capacity
Add peep
For negative pulmonary edema
OPCAB can be used
To Perform multi-vessel bypass
To Carry out redo CABG
In patients with Aortic disease when cannulation of the aorta poses significant embolic risk
OPCABG is best for patients where the side effects of cardiopulmonary bypass are
especially undesirable
OPCABG The major difficulties for this surgery include
hemodynamic alterations with cardiac manipulation and tilting and intraoperative myocardial ischemia.
Off pump better for
ASLVR
- hemodynamically stable patients with coronary arteries that can be stabilized on the anterior wall of the heart
Promoted in patients at increased risk for stroke, severe lung disease, severe vascular disease, and renal dysfunction (SLVR)
Bad for regurgitation
Hypercarbia
Status asthmaticus give
8% sevo
Decrease TV
Lidocaine
PPV
• EKG and MVP change
PVCs, repolarization abnormalities, and prolonged QT interval.
S/sx of MVP:
Palpitation Anxiety Dyspnea Atypical chest pain. Fatigue, Orthostatic symptoms
Regurgitant valve wanted hemodynamics
AB-DA-IPNIC
Stenotic valves wanted hemodynamics
MS-AT-IA-NIP-NIC-minpU
Holodiastolic descrecendo murmur
Mitral stenosis
