Apex- Cardiac Pathyophys Flashcards
Which surgical procedure presents the HIGHEST risk of CV morbidity and mortality for the patient with CAD?
A. ORIF femur fracture
B. VATS
C. Open AAA repair
D. Carotid endarterectomy
C.
High risk procedures = emergency surgery (esp in elderly), open aortic surgery, peripheral vascular surgery, long surgical procedures with significant volume shifts and/or blood loss
If a patient had a recent MI, the risk of re-infarction is greatest within ________ days/weeks of the orginal event
30 days
How long should elective surgery be delayed for after an MI?
4-6 weeks
5 patient risk factors that increase risk for cardiac event during surgery
which one confers the greatest risk of periop MI?
- ischemic heart disease
- CHF
- cerebrovascular disease
- DM
- Creat > 2mg/dL
unstable angina = greatest risk
unstable angina → new-onset angina (<2 months), increasings sx (intensity, freq, duration), duration exceeding 30 minutes, sx responding less to medical therapy
Risk of perioperative MI in the general population is ~ ____ %
0.3%
If the patient has ahd a previous MI, than the perioperative risk of reinfarction is:
- if > 6 months ago →
- if 3-6 months ago →
- if < 3 months ago →
- if > 6 months ago → 6 %
- if 3-6 months ago → 15%
- if < 3 months ago → 30%
remember as <3 months ago = 30%, then half it, and half it again
NYHA heart failure classification for someone with symptoms with less than normal activity but no symptoms at rest
3
compared to sx with normal activity + no sx at rest = 2
Which NYHA heart failure classification requires referral to a cardiologist prior to GA
Class 3 - symptoms with less than normal activity (none at rest)
or
Class 4 - symptoms with minimal activity or even at rest
T/F- NYHA heartfailure class 4 patients to undergo MAC anesthesia can proceed without a cardiac referrel as long as the preoperative evaluation reveals stable cardiac disease
True
When should a patient be referred to a cardiologist before surgery?
NYHA classification of 3 or 4 who is scheduled for high- or intermediate-risk surgery
factors that reduce myocardial o2 supply (4)
- tachycardia
- hypoxemia
- anemia
- left shift in oxyhemoglobin curve
Factors that increase myocardial o2 demand (7)
SNS stimulation : increased HR and BP
Increased preload/wall tension
Increased afterload
Increased contractility
Myocardial injury and infarction injure the sarcolemma. Disruption of the sarcolemma allows for what to happen?
intracellular proteins (CK-MB, troponin-I, tropinin-T) to enter systemic circulation
What lead is best for monitoring dysrhythmias?
Lead II
it also can identify inferior wall ischemia (II = inferior ischemia)
Most MIs occur within ______ hours after surgery
48
Treatment of intraoperative myocardial ischemia should focus on itnerventions that do what?
make the heart slower, smaller, and better perfused
Which leads are best for detecting LV ischemia intraoperatively?
AKA: ST changes
V3, V4, V5
*classic teaching says V5 is best (anterior axillary line 5th ICS)
*newer data says V3 & V4 may be superior to V5
*if need to choose- choose V4 - midclavicular line 5th ICS
The combination of what 3 leads has an ischemic detection rate of up to 96%?
II, V4, V5
Do most MI’s occur intraop or postop?
postop - within 48 hrs of surgery
Myocardial ischemia & advanced age
Curve A demonstrates a greater rise in pressure at a given volume → decreased compliance → myocardial ischemia and advanced age
Curve C demonstrates increased compliance → aortic insuffiency and dilated cardiomyopathy
If the patient has diastolic dysfunction, CVP and PAOP will (overestimate/underestimate ventricular filling pressures)
overestimate
pts with diastolic dysfuction require higher filling pressures to prime the ventricle
What describes the ventricular filling pressure that results from a given end-diastolic volume?
Diastolic compliance
Decreased diastolic compliance shifts the curve (up/down) and (left/right)
What does t his mean?
up and left
Theres a higher end diastolic PRESSURE for a given volume
Increased diastolic compliance shifts the curve (up/down) and (left/right)
what does this mean?
down and right
there is a LOWER end-diastolic PRESSURE for a given EDV
What do elevated filling pressures put patients at a higher risk for?
Pulmonary edema
What are 2 conditions that dilate the heart and cause increased diastolic compliance (lower pressure for a given volume)
Dilated cardiomyopathy
Chronic aortic insufficency
What are PAOP and CVP indirect measurements of?
Volume
Identify a compensatory mechanism in the patient with CHF:
A. decreased brain natriuretic peptide
B. Decreased LVEDP
C. Increased renal blood flow
D. Increased sympathetic tone
D. Increased sympathetic tone
To maintain BP, pts with CHF rely on elevated levels of circulating catecholamines (increased SNS tone)
*anesthetic techniques that reduce SNS tone can preceiptate CV collapse - ex) a standard propofol induction dose is not a good idea bc it decreases SNS tone while simultaneously reducing myocardial contractility. Propofol should be slowly titrated at a much lower dose
CHF reduces renal blood flow which is the primary mechanism that activates RAAS
Atrial dilation from CHF increases release of natriuretic peptides
Identify a compensatory mechanism in the patient with CHF:
A. decreased brain natriuretic peptide
B. Decreased LVEDP
C. Increased renal blood flow
D. Increased sympathetic tone
D. Increased sympathetic tone
To maintain BP, pts with CHF rely on elevated levels of circulating catecholamines (increased SNS tone)
*anesthetic techniques that reduce SNS tone can preceiptate CV collapse - ex) a standard propofol induction dose is not a good idea bc it decreases SNS tone while simultaneously reducing myocardial contractility. Propofol should be slowly titrated at a much lower dose
CHF reduces renal blood flow which is the primary mechanism that activates RAAS
Atrial dilation from CHF increases release of natriuretic peptides
Most common cause of right heart failure
left heart failure
3 ways to treat RV failure
- Reverse causes of increased PVR (hypoxia, hypothermia, hypercarbia, acidosis, high PEEP, nitrous oxide)
- Inotropes → milrinone, dobutamine
- Pulmonary vasodilators → inhaled nitric oxide or sildenafil (PDE-5 inhibitor)
Pathophysiolgoic complications r/t chronic systemic HTN include all of the following EXCEPT:
A. LVH
B. increased myocardial o2 concsumption
C. dysrhythmias
D. Decreased diastolic filling time
D. Decreased diastolic filling time
diastolic filling time is determined by the HR, not BP
Systemic HTN increases afterload. The LV must generate a higher amount of wall tension to open the aortic valve → to compensate for this increased afterload: heart undergoes concentric hypertrophy → increased MVO2 → thicker heart = reduced compliance = diastolic dysfunction (decreased lusitropy)
T/F- systemic HTN is almost always caused by an increased SVR
True
SBP &/OR DBP ranges for
Normal, Elevated, Stage 1, 2, and 3 HTN
Normal → <120 & <80
Elevated → 120-129 & <80
Stage 1 HTN → 130-139 or 80-89
Stage 2 HTN → > 140 or > 90
Stage 3 HTN → >180 and/or >120
Stage 3 HTN = hypertensive crisis
primary vs secondary HTN
primary → no identifiable cause (95%)
secondary → + identifiable cause (5%)
Normal cerebral autoregulation occurs at a CPP between what and what?
CPP 50-150
Why is it important to adequately hydrate the chronically hypertensive patient prior to anesthetic induction?
Bc hypertensive patients are volume contracted (even more so if they are on a diuretic)
→ agents that cause myocardial depression and vasodilation will unmask a volume contracted state and these patients will have an exaggerated hypotensive response to anesthetic induction
why shouldn’t a betablocker be started on the day of surgery in a patient who is normally not on a betablocker?
Studies have shown it increases the risk of hypotension, vradycardia, stroke, and death.
Why shouldnt peeps take their ACE/ARBs prior to surgery?
It can produce vasoplegia under anesthesia
*refractory hypotension
ACEi/ARB induced vasoplegia that is unresponsvie to conventional first-line therapies (vasopressors and fluids) should be treated with what? (3)
- vasopressin
- terlipressin
- methylene blue (nitric oxide antagonist)
How does methylene blue tx refractory hypotension?
it inhibits nitric oxide (substance released from the lining of the vessels that results in vasodilation)
@ what systolic/diastolic BP should elective surgery be delayed in favor of optimization?
SBP > 180
DBP > 110
Measuring the BP on the arm (or worse the leg) in the patient in the sitting position will (over/under)estimate the BP in the brain
overestimate (the brain BP is lower)
HTN crisis occurs wehn the BP exceeds what?
When is it deemed a hypertensive EMERGENCY?
180/120
when there is evidence of end-organ damage (otherwise its called HTN urgency)
CNS: encephalopathy, stroke, papilledema
Cardiac: CHF
Renal: HTN-induced acute renal dysfunction
What is the MOST common cause of secondary HTN?
A. PIH
B. Coarctation of the aorta
C. Renal Artery Stenosis
D. Cigarette Smoking
C. Renal artery stenosis
A narrowed renal artery (atherosclerosis or fibromuscular dysplasia) reduces renal blood flow. In attempt to increase GFR, the kidenys activate the RAAS system
What is the definitive treatment of renal artery stenosis?
What shouldn’t these patients be give if B/L stenosis and why
renal artery endarterectomy or nephrectomy
No ACE inhibitors bc they can significantly reduce GFR and preciptate renal failure in pts with B/L renal artery stenosis
Match the HTN drug it its drug class
Drugs: perindopril, terazosin, eprosartan, nisoldipine
perindopril → ACE
terazosin → alpha blocker
eprosartan → ARB
Nisoldipine → CCB
Drug that reduces afterload, preload, vs preload and afterload
hydralazine → afterload reduction
nitroglycerine → preload reduction
Sodium nitroprusside → preload and afterload reduction
What 3 things can be targeted to reduce blood pressure?
ANS → alpha/beta blockers
Myocardium and VSM → CCBs, arteriodilators, venodilators
Kidney → ACEi’s, ARBs, loop diuretics, thiazide diuretics, K sparing diuretics, aldosterone antagonists
suffix “-zosin”
drug class, how they reduce BP
what other 2 drugs fall in this class that dont end in zosin?
Alpha-1 antagonists
→decrease intravascular calcium → vasodilation → decreased SVR (afterload)
Phenoxybenzamine (long acting, non-competitive, selective); phentolamine (short acting, competitive, non-selective)
Selective B1 antagonists and how do they reduce BP
MABE AB
Metoprolol, Atenolol, Bisprolol, Esmolol, Acebutolol, Bextolol
→reduction in: inotropy, chronotropy, dromotropy, & renin release from juxtaglomelular aparatus
non-selective beta blockers
TPPNS
Timolol, Pindolol, Propanolol, Nadolol, Sotalol
*in addition to beta 1 effects, beta 2 blockade results in vasoconstriction in the muscle (not as profound decrease in BP)
Alpha-2 agonists - 2 most common and how do they reduce blood pressure
precedex and clonidine
-reduce sympathetic outflow
-“ipine” - what drug class, what do they target, and how do they reduce BP
CCBs - dihydropyridinines
→ target vasculature → decreases intravascular calcium → vasodilation → decreased SVR (Afterload)
What CCBs are the non-dihydropyridines , what classes are they, and how do they work?
Which produces more myocardial depression?
specific uses for each
Diltazem (Benzothiazepine)
Verapamil (Phenylalkamine)
→targets mycoardium > vessels
→ reduces: inotropy, chornotropy, dromotropy, SVR (afterload)
verapamil (dont use if on beta blockers > can result in CHB)
verapamil - angina, MI, SVT (afib/flutter)
diltazem - chronic HTN, arrhythmia protection (afib/flutter)
How do loop diuretics work?
3 examples
inhibit NA-K-2Cl transporter in the thick ascending loop of henle
→diuresis → reduced venous return (preload)
fureosemide, bumetanide, ethracrynic acid
4 Thiazide diuretics (mneumonic), how do they combat HTN
MICH
Metolazone, Indapamide, Chlorthialidone, HCTZ
inhibits the NA-Cl transporter in the DCT
→diuresis → reduced venous return (decreased preload)
K+ sparing diuretics vs Aldosterone antagonists
-examples of each, where do they work
K sparing = Triameterene & amloride
Aldosterone antagonists = Spironolactone
they inhibit K+ excretion and NA reabsorption by the principle cells in the collecting ducts
→ K sparing diruetics work indepdently of aldosterone
→ aldosteron antagonists also block aldosterone at mineralcorticoid receptors
A patient with a hx of CAD with an EF of 35% develops AFIB with RVR. Which is the BEST treatment for this patient
A. Verapamil
B. Diltaizem
C. Nifedipine
D. Nicardipine
B. Diltaizem
Rank the order in which the following CCBs impair contractility from most to least
→ nifedipine, verapamil, nicardipine, diltazem
Verapamil → nifedipine → diltazem → nicardipine
What is the only CCB proven to reduce the M&M from cerebral vasospasm?
Nimodipine
What are the 3 types of voltage-gated calcium channels; which ones do all clinically used CCBs bind to and what happens?
L type = long-lasting or slow channel
N type = neural
T type = transient
*CCBs bind to the alpha-1 subnit of the L-type calcium channel
→ this prevents calcium from entering the cardiac and VSM cells
Which CCB is useful as a coronary antispasmodic?
Nicardipine
MOA of clevidipine
Arterial vasodilator → reduces SVR without affecting preload
lipid emulsion (EDTA preservative)
How is clevidipine metabolized?
by tissue and plasma esterases
1/2 life = 1 minute (full recovery 5-15 mins after stopping gtt)
Identify the anesthetic considerations for constrictive pericarditis (select 2):
- kussmaul’s sign is usually present
- it is mot commonly caused by a virus
- afterload should be reduced
- bradycardia should be avoided
Kussmaul’s sign is usually present
Bradycardia should be avoided
→constrictive pericarditis limits the hearts ability to move within the pericardial sac → decreased myocardial compliance and limits diastolic filling
acute pericarditis (not constrictive) is usually caused by a virus
Kussmauls sign is a paradoxical rise in CVP and JVD during inspiration resulting from RV filling defect (impared RV compliance)
→ since stroke volume is reduced, the cardiac output is HR dependent ( avoid bradycardia)
→ BP = CO x SVR → if CO is limited, the BP must be maintained by SVR → DO NOT REDUCE AFTERLOAD
Identify the anesthetic considerations for constrictive pericarditis (select 2):
- kussmaul’s sign is usually present
- it is mot commonly caused by a virus
- afterload should be reduced
- bradycardia should be avoided
Kussmaul’s sign is usually present
Bradycardia should be avoided
→constrictive pericarditis limits the hearts ability to move within the pericardial sac → decreased myocardial compliance and limits diastolic filling
acute pericarditis (not constrictive) is usually caused by a virus
Kussmauls sign is a paradoxical rise in CVP and JVD during inspiration resulting from RV filling defect (impared RV compliance)
→ since stroke volume is reduced, the cardiac output is HR dependent ( avoid bradycardia)
→ BP = CO x SVR → if CO is limited, the BP must be maintained by SVR → DO NOT REDUCE AFTERLOAD
T/F- constrictive pericarditis is usually caused by a virus
False- Acute pericarditis is usually caused by a virus
3 conditions that affect the pericardium and limit the hearts ability to move within the pericardial sac
- acute pericarditis
- constrictive pericarditis
- cardaic tamponade
Acute vs constrictive pericarditis
Acute is usually caused by a viral infection/inflammation. It doesn’t reduce diastolic filling unless the inflammation leads to constrictive pericarditis or cardiac tamponade.
→constrictive pericarditis is caused by fibrosis or any condition where the pericardium becomes thicker. it leads to reduced diastrolic filling.
treatment for constrictive pericarditis
pericardiotomy
3 main anesthetic considerations for constrictive pericarditis
- avoid bradycardia → since SV is reduced, CO is dependent on HR (CO= HR x SV)
- preserve contractility
→ ketamine, etomidate, benzos, opioids, pancuronium
→ volatile agents with caution - maintain afterload
*Aggressive PPV can decrease venous return and CO
The pericardium is composed of ____ layers that are seperated by _______mls of clear fluid
2 layers:
Visceral layer → attached to myocardium
Parietal layer → anchored in the mediastinum
Seperated by 10-50mls of clear fluid
What is Kussmauls sign
& what does it indicate
an increase in CVP and JVD during inspiration
due to RV filling defect (impared RV complianc)
→constrictive pericarditis
What is pulsus paradoxus
& what is it indicative of?
Decreased SBP > 10mmHg during inspiration
indicative of impaired diastolic filling
What presents as ST elevation with normal enzymes
what else would be present
acute pericarditis
Acute CP with pleural component → increased CP with inspiration and postural change; releaved by leaning forward or supine
*Pericardial friction rub
*Fever
Treatment of acute pericarditis
usually resolves spontaneously
Drugs to relieve pain → salicylates, oral analgesics, corticosteroids
Why is it important to maintain spontaneous ventilation as long as possible for someone with constrictive pericarditis/tamponade
bc spontaneous respirations = negative pressure inside chest wall to draw in air → also helps blood flow more easily into the RA and supply preload
once positive pressure ventilation takes place- you lose that preload and CO
Is dressler’s syndrome associated with constrictive or acute pericarditis
acute
What are the 3 components of Becks triad
what do they indicate
Muffled heart tones, JVD, hypotension
→pericardial temponade occurs when the pericardium fills with fluid → this restricts the hearts movement and impairs its ability to function as a pump
*fluid accumulation in the pericardial sac → muffled heart tones
*decreased venous return to the heart → JVD
* decreased SV → hypotension
What is a pericardial effusion
accumulation of fluid inside the pericardial sac
it’s not an emergency and seldum requires intervention
Clinical presentation of cardiac tamponade (4):
- Becks triad:
→ muffled heart tones from fluid accumulation in the pericardial sac
→ JVD from decreased venous return to the right heart
→ hypotension from decreased stroke volume - Pulsus paradoxus
→ decrease in SBP > 10mmHg during inspiration d/t impaired diastolic filling - Kussmaul’s sign
→ paradoxical increase in CVP and JVD during inspiration d/t impaired RV compliance (impaired filling) - Reduced EKG voltage (from fluid in the pericardial sac impeding transmission of signals)
How do CVP, PAOP coincide with
CVP = right cardiac diastolic filling pressure?
PAOP = left cardiac disastolic filling pressure?
i think, idk maybe
Describe the pressure-volume loop of cardiac tamponade
Left shift → from decreased LV EDV
Narrower loop → from decreased stroke volume
Higher/steeper slope during ventricular filling → decreased ventricular compliance
What is this and why does it happen
Pulsus paradoxus → decrease in SBP by >10mmHg during inspiration
*negative intrathroacic presssure on inspriation → increased venous return to the RV → bowing of interventricular septum toward the LV → decreased SV → decreased CO → decreased SBP
A patient with blunt chest trauma presents for pericardiocentesis. He exhibits JVD and kussmaul’s sign. What is the BEST induction agent for this patient?
A. Propofol
B. Etomidate
C. Ketamine
D. Midazolam
C. Ketamine
*the patient with pericardial tampone relies on an elevated SNS tone to maintain BP. Most GAs cause myocardial depression and reduced afterload (both of which ontribute to CV collapse)
→local anesthesia is the preferrred technique for pericardiocentesis
if GA is required, ketamine is the best option as it activates the SNS which increases HR, contractility, and afterload
Surgical management of cardiac tamponade (2)
Pericardiocenteisis (needle aspiration) and pericardiostomy
Optimal anesthetic mangement for cardiac tamponade
Local anesthethesia to preserve hemodynamic stability
if GA required, use drugs that preserve myocardia function such as : ketamine, n20, benzos, and opioids
→maintain NSR, preload, afterload, , and contractiltiy
→ spontaneous ventilation is preverred over PPV
Pericardiocentesis vs Pericardiostomy
complications
Pericardiocentesis → needle is used to aspirate pericardial fluid
Pericardiostomy → surgical opening and drainage of the pericardium (subxiphoid, thoracoscopic, or thoracotomy)
PTX, re-accumulation of pericardial fluid, puncture of the coronary vessels or myocardium
A patient presents to the preop clinic with hx of infective endocarditis; which procedure puts this pt at the HIGHEST risk of an adverse outcome:
A. cystoscopy
B. Colonoscopy
C. Dental implant
D. Coronary stent placement
Dental implant
→pts at high risk for developing bacteremia after certain “dirty procedures” should receive antibiotic prophylaxis
What is infective endocarditis
a bacterial infection of the heart valves and endocardium
What patients should receive prophylaxis for infective endocarditis? (3)
Hx IE
Prosthetic heart valve
Congential heart defect
What non-cardiac procedurs are indications for prophylaxis for infective endocarditis (3)
- Dental procedures with gingival manipulation
- certain resp procedures
- biopsies of infected lesions
What cardiac procedures are NOT indications of prophylaxis for infective endocarditis? (3)
- MVR
- CABG
- Coronary stent placement
IV antibiotics for IE prophylaxis (4)
ACCC
Ampicillin
Cefazolin
Ceftriaxone
Clindamycin
What is infective endocardities usually caused by?
Bacteremia
bacteria in the bloodstream
What is infective endocardities usually caused by?
Bacteremia
bacteria in the bloodstream
T/F- unrepaired cardiac valve disease requires prophlyatic antibotics for IE
False
T/F- bronchospy with biopsy requires prophlyactic antibiotic of IE
True
Which intervention is MOST likely to precipitate hemodynamic instablity in the patient with hypertrophic cardiomyopathy
A. Esmolol
B. Nitroglycerine
C. Phenylepherine
D. 500ml Bolus
B. Nitroglycerine
reduces preload → reduction in systolic LV volume → narrowed LVOT → worsens obstruction
- fluid bolus has opposite effect
- slower HR extends LV filling time so esmolol increases LV volume and reduces contractility with helps improve LVOT obstruction
- neo increases aortic pressure which increases transmural pressure , opening the LVOT
Which intervention is MOST likely to precipitate hemodynamic instablity in the patient with hypertrophic cardiomyopathy
A. Esmolol
B. Nitroglycerine
C. Phenylepherine
D. 500ml Bolus
B. Nitroglycerine
reduces preload → reduction in systolic LV volume → narrowed LVOT → worsens obstruction
- fluid bolus has opposite effect
- slower HR extends LV filling time so esmolol increases LV volume and reduces contractility with helps improve LVOT obstruction
- neo increases aortic pressure which increases transmural pressure , opening the LVOT
What 3 things determine blood flow through a LVOT
- Systolic LV volume (preload)
- Force of LV contraction
- Transmural pressure (increased aortic pressure increases transmural pressure, opening the LVOT)
What is the most common cause of sudden cardiac death in young atheletes?
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy leads to what kind of obstruction during systole
2 causes
LV outflow tract (LVOT) obstruction
- congenital hypertrophy of the in interventricular septum
- SAM - systolic anterior motion of the anterior leaflet of the mitral valve
3 conditions that worsen LVOT
4 treatments
- Decreased preload
- Increased contractility
- decreased afterload
Betablockers, CCB, Fluids, Phenylepherine
4 other names for hypertrophic cardiomyopathy
- Obstructive hypertrophic cardiomyopathy (OHCM)
- Hypertrophic obstructive cardiomyopathy (HOCM)
- Asymetric septal hypertrophy (ASH)
- Idiopathic hypertrophic subaortic stenosis (IHSS)
T/F- SAM can occur after mitral valve replacement
False -mitral valve REPAIR
NOT replacement!
In a patient with a bare-metal cardiac stent presenting for bunionectomy, what is the MINIMAL amount of time that the patient should wait before undergoing surgery (answer in days)
30 days
What should patients be on after getting a coronary stent and why?
Dual antiplatelet therapy to prevent stent thrombosis
ASA & thienopyridine (clopidogrel or ticlopidine)
The duration to postpone elective surgery after stent placement for the following:
Angioplasty without stent
Baremetal stent
DES
Angiplasty without stent → 2-4 weeks
BMS → 1-3 months
DES → 6-12 months
- First generation DES = 12 months
- *Current generation DES = 6 months
T/F - for most surgeries aspirin can be continued throughout the perioperative period
When should clopidogrel and ticlopidine be stopped?
True
Clopidogrel → stop 7 days prior
Ticlopidine → stop 14 days prior
Aspirin vs Thienopyridine (clopidogrel/ticlopidine) MOAs
Asprin → irreversible cyclooxygenase inhibitor
Thienopyridine → ADP antagonist
How long to delay elective surgery in someone who had ACS
what about CABG?
ACS → 12 months minimum
CABG → 6 weeks ( 3 months preferred)
How long should ASA be stopped prior to surgery is it is absolutely contraindicated
At least 3 days
Best tx for stent thrombosis
PCI
want blood flow restored in < 90 minutes
Best tx for stent thrombosis
PCI
want blood flow restored in < 90 minutes
Priming the cardiopulmonary bypass machine with a balanced salt solution reduces all of the following except :
A. microvascular flow
B. plasma drug concentration
C. oxygen-carrying capacity
D. blood viscosity
A. Microvascular flow
- because the CPB bypass circuit becomes an extension of hte patient’s circulation, it must be primed with enough volume to de-air the pump. The priming fluid can be a balanced salt solution or blood
-priming with anything other than blood produces hemodultion wich has the following effects:
→ decreased hematocrit, plasma concentration of drugs and plasma proteins, decreased o2 carrying capacity, decreased blood viscosity, increased microvascular flow
3 benefits of the centrifugal pump over the roller pump
- less traumatic to blood cells
→ uses gravity and spins the blood thru a cone - decreased risk of air emboli
→ bc it uses gravity, it cant produce excess negative pressure → decreased risk for air entrainment - Decreased risk of line rupture if arterial inflow line is clamped
→ unable to produce excessively high postive pressure, so if confronted by an excessive afterload, the line wont rupture
What is the preferred type of oxygenator for CBP?
Membrane oxygenator
A bubble oxygenator uses a blood-gas interface with no membrane and increases risk of cerebral air embolism
What is the balanced salt solution comprised of that primes the CBP circuit? (4)
Mannitol
Albumin
Heparin
HCO3-
5 effects of hemodilution during priming of the CBP circuit
- decreased hematocrit
- decreased o2 carrying capacity
- decreased blood viscosity
- decreased plama concentration of drugs and plasma proteins
- increased microvascular flow (due to decreased blood viscosity)
What can happen if air enters the veinous line of hte CPB circuit?
airlock
When is awareness MOST likely to occur during CABG with CPB?
A. Induction of anesthesia
B. Aortic cannulation
C. Rewarming
D. Sternotomy
Sternotomy
due to intense surgical stimulation
An ACT greater than what is adequate heparinization for CBP
> 400
Systolic BP should be what before aortic cannulation?
< 100 mmHg
4 things to think of in the pre-bypass period
- awareness most common during sternotomy
- ACT > 400
- SBP < 100 before aortic cannulation
- Use cell saver or antifibrinolytics to conserve blood loss
What is cardioplegia and what does it do and why?
Potassium-containing solution
→arrests the heart in diastole
→best way to reduce myocardial o2 consumption during CBP
How much protamine to reverse heparin?
1mg protamine for every 100units of heparin given
or just fucking make it simple and say 10mg for every 1,000 units of heparin bc no one is giving < 100units of heparin
3 things to consider post bypass
- Protamine dosing (10mg/1000units)
- Radial artery pressure may be artifically low
- Mycardial depression and heart block by necessitate vasoative meds and cardiac pacing
For CBP, what if hte patient has a allergy or hx of HIT?
alternatives: Bilvalirudin, hirudin, or another factor 10 inhibitors
Why is it important to avoid hypertension during cannulation of the aorta?
goal BP?
bci t can lead to aortic dissection
SBP < 100 (ideal 90-100) or MAP < 70
Re: Cardioplegia:
Potassium (increases/decreases) RMP, which locks what kind of channels in what state?
increases RMP
locks NA+ channels in closed-inactive state
How is the heart “restarted” after cardioplegia?
by infusing cornoary circulation with warm, normokalemic blood
Antegrade vs retrograde cardioplegia
special considerations with antegrade
Antegrade → into aortic root → cornoary arteries
Retrograde → coronary sinus
antegrade- aortic valve must be competent and aorta clamped
Since blood flow is non-pulsatile on pump how do we assess organ perfusion?
MAP
How does protamine work?
it’s a postive base which forms a complex with heparin (negative acid) and neutralizes it
Two side effects of protamine
systemic vasodilation and pulmonary vasoconstriction = side effects
anaphylaxis = allergy
administration over 10-15 mins reduces known side effects
2 antifibrinolytics commonly used during cardiac surgery
aminocaproic acid (amicar)
tranexamic acid (TXA)
Pick the statements that MOST accurately describe intra-aortic balloon pump (select 2)
- increases afterload
- tip of balloon should be positioned 2cm proximal to the brachiocephalic artery
- it inflates during diastole
- it is contraindicated in severe aortic insufficency
- inflates during diastole
- -contraindicated in severe AI
How does an intraaortic balloon pump work?
it inflates during diastole to increase CPP (increases o2 supply)
deflates during systole → redcues after load (decreased o2 demand)
Who is IABP contraindicated in? (Main one + 3 more)
Why?
pt’s with aortic insufficency
→ descending aortic aneuyrsm
→peripheral vascular disease
→sepsis
Ballon inflation would force blood retrograde into the left ventricle (no bueno)
Where should the tip of a balloon of the AIBP be placed
what happens if it is in a more proximal position?
2cm distal to the left subclavian artery
a more proximal position can lead to occlusion of the left common carotid and/or brachiocephalic arteries
indications for IABP (4)
- Cardiogenic shock
- MI
- intractable angina
- Difficult seperation from CPB
Most common complications of IABP (3)
vascular injury
infection @ insertion site
thrombocytopenia
How is a IABP placed?
through the femorlal artery and advanced along the descending aorta
balloon inflation with IAP correlates with what on the arterial waveform?
the diacrotic notch (AV closure, start of diastole)
When does the aortic valve close
at the beginning of diastole
*this is when IABP balloon inflates
When does the IABP balloon deflate and what does it occur with on the EKG?
-just before onset of systole
-R Wave
T/F- timing of IABP is generally unaffected by pacemaker spikes or electrocautery
True
T/F- pts on long term IABP require anticoagulation
true
What do these point correlate with
how is IABP function during these points
R Wave→ Start of Systole → balloon deflates
T Wave → start of diastole → balloon inflates
In the patient with an LVAD, organ perfsion is LEAST dependent on:
-preload
-pump speed
-afterload
-inotropy
Inotropy
LVAD unloads the failing heart by pumping blood from the LV to the aorta, so CO ( thus organ perfusion) are depdendent on → LV preload, pump speed, & pressure gradient across the pump (afterload)
What is an LVAD
A mechanical device that unloads the failing heart by pumping blood from the LV to the aorta.
What 3 things is cardiac output (and thus organ perfusion) depdendent on in someone with an LVAD
- LV preload
- Pump Speed
- Afterload (pressure gradient across the pump)
T/F- with an LVAD, flow can be pulsatile or non-pulsatile
True
If non-pulsatile, then SpO2 and NIBP will be ineffective
→ consider arterial line, serial ABGs, and cerebral ox
Why is regional anesthesia avoided in the patient with an LVAD
bc they are anticoagulated
What is the most common cause of death in the LVAD patient
Sepsis
With an LVAD, the inflow cannula is inserted where?
Where does blood go from there?
inserted into the apex of the LV
from there, blood flows through the LVAD pump and is returned to the aorta through the outflow cannula
When would an LVAD be used (3)
- bridge to recovery
- bridge to transplant
- destination therapy
what 3 conditions would require surgical correction before an LVAD can be placed?
- intracardiac shunt (PFO)
- AI
- TR
What can produce a suction event with an LVAD, what happens
whats the consequences
how to manage it
the combination of a low preload with a relatively high pump speed → LV suck down (part of the LV is sucked into the LV cavity) → occludes teh inflow cannula
tx: fluid administration (to increase preload) & reducing pump speed
consequences → hypotension and ventricular dysrhythmias.
→leftward shift of the interventricular septum alters RV geometry, reducing RV contractility n& compliance
B.
crawford type II d/t mandatory period of stopping blood flow to the renal arteries and some of the radicular arteries that perfuse the anterior spinal cord and possibly the artery of Adamkiewicz.
Acute dissection of hte ascending aorta (what Debakey or standford classifcation) is considered a surgical emergency
what’s something you need to consider in your anesthetic plan
DeBakey 1 or 2
or Stanford A
Aortic valve is often affected, so consider AI in your anesthetic plan
What are aortic aneurysms classified by?
The region of the aorta affected
Aortic Dissection - Standford Type A classification vs Type B
A = involves the Asecnding Aorta
B= does not involve ascending aorta
DeBakey classification system
Type 1 → tear in ascending + dissection along entire aorta
Type 2 → tear in ascending + dissection ONLY in the ascending aorta
Type 3 → Tear in the proximal descending aorta with:
3A: dissection limited to thoracic aorta
3B: dissection along thoracic and abdominal aorta
Acute dissection of the ascending aorta (Debakey ___ or Standford ___) is considered a surgical emergency
what should you consider in the anesthetic plan
Stanford A (involves Ascending aorta)
or
Debakey 1 or 2
(1 = tear in ascending, dissection along entire aorta; 2 = tear in ascending, dissection in the ascending aorta only)
the aortic valve is often affected so treat as if pt has AI
How is dissection of the descending aorta generally handled
medical management (meds for HR, BP, pain)
surgical repair does not always produce a significant benefit
however, these patients often do ultamiely require surgery
Surgical intervention is recommended when the diameter of a AAA is > ____cm or grows more than ____ cm per year
5.5 cm
or grows > 0.6-0.8cm per year
T/F- risk of aneurysmal rupture is best described by Poiseuille’s law
False - law of la place (La Pop!)
what 3 s/s suggest rupture of AAA?
This triad is present in what % of patients
acute onset of back pain, hypotension, and pulsatile abdominal mass
only present in ~ 50% of patients
What is the most common cause of postop death in AAA repair patients?
MI
3 independent risk factors for AAA
What is the incidence of AAA in the US for patients over 50yo?
- Ciggs
- Male gender
- Advanced age
3-10%
T/F- most aneurysms rupture in the right retroperitoneum
false - left retroperitoneum
Why don’t all patients with an aortic aneurysm rupture exsanguinate immediately?
Bc most aneurysms rupture in the left retroperitoneum, allowing for tamponade and clot formation
What is the most common placement for the aortic cross clamp?
Infrarenal
Applying aortic cross-clamp creates ________ by :
→Reducing:
→Shifting:
→Increasing:
A central hypervolemia by:
Reducing → venous capacity
Shifting → more blood proximal to the clamp
Increasing→ venous return
Removing the aortic cross clamp creates _______ by:
- restoring:
- shifting:
- ## decreasing:
creating a….
Central hypovoemia by:
Restoring → venous capacity
Shifting → blood to the lower body
Decreasing → venous return (increased size of tank)
a capillary leak that contributes to loss of intravascular volume
Removing the aortic cross clamp creates _______ by:
- restoring:
- shifting:
- ## decreasing:
creating a….
Central hypovoemia by:
Restoring → venous capacity
Shifting → blood to the lower body
Decreasing → venous return (increased size of tank)
a capillary leak that contributes to loss of intravascular volume
Application of the cross-clamp starves the distal tissues of oxygen → these cells convert to anerobic metabolism, which leads to what 5 changes?
- increased lactic acid production → metabolic acidosis
- prostagladins
- activated complement
- myocardial depressant factors
- hypothermia
T/F- even an infra-renal clamp reduces renal blood flow
true
pt still at risk of AKI
2 things associated with IV contrast dye
- allergic reaction
- renal injujry
When does an endoleak occur with AAA repair?
What do they do if there is one?
when the original graft fails to prevent blood from entering the aortic sac.
Some of them resolve spontaneously (esp early postop leaks), while others may require placement of a second graft or an open repair
Occlusion of hte artery of Adamkiewicz during thoracic aneurysm repair may result in all of hte following EXCEPT:
A. Flaccid paralysis of the lower extremities
B. Bowel and bladder dysfunction
C. Loss of proprioception
D. Loss of temperature and pain sensation
D. Loss of proprioception
An aortic cross-clamp placed above the artery of adamkiewicz can cause ischemia to where?
What syndrome can this result in?
ischemia to the** lower portion of the anterior spinal cord **
Anterior spinal artery syndrome (Beck’s syndrome)
*generally speaking, the anterior cord conttains motor neurons, and the posterior cord sensory neurons
What does anterior spinal artery syndrome result in? (what tracts/fibers/columns contribute to each)
AKA
what’s preserved?
- Flaccid paralysis of the lower extremities → corticospinal tract affected
- Bowel and bladder dysfunction → autonimic nerve fibers affected
- loss of temp and pain sensation → spinalthalmic tract affected
Beck’s syndrome
Touch & proprioception are preserved (dorsal column is spared)
How many posterior vs anterior spinal arteries are there?
Posterior = 2
Anterior = 1
The posterior spinal arteries perfuse what portion of the spinal cord?
the posterior 1/3
The anterior spinal artery perfuses what portion of the spinal cord?
The anterior 2/3
label
Backtrack blood flow from the posterior and anterior spinal arteries coming off the aorta (2 pathways)
Aorta →
Segmental artery → anterior/posterior radicular artery → anterior/posterior spinal artery
&
**subclavian artery → vertebral artery → anterior/posterior spinal arteries **
What does the artery of adamkiewicz perfuse?
the anterior spinal cord in the **thoracolumbar **region
aThe artery of adamkiewicz most comonly originates on the (right/left) side between what what levels in 75% of the population
Where does it arise in the freaky 10% of hte population ?
T8-T12 in 75%
T11-T12
L1-L2 in the freaky 10% of people
What is the radicularis magna ?
The artery of adamkiewicz
*anterior spinal cord in the thoracolumbar region
*T 11-12
*left side
Thoracic aortic cross clamp times > _ minutes pose a significant risk for cord ischemia
> 30 mins
5 spinal cord protective strategies for thoracic aortic surgery
- keep cross-clamp times < 30 mins
- moderate hypothermia (30-32 C) → reduces cord o2 consumption
- CSF drainage
- proximal HTN during cross-clamping → map ~ 100mmHg
- Avoid hyperglycemia
also can do CSF drainage to increase the perfusion pressure gradient
Injury to what spinal tract results in flaccid paralysis of the lower extremities
corticospinal tract
motor (anterior spinal artery)
Injury to what spinal tract results in flaccid paralysis of the lower extremities
corticospinal tract
motor (anterior spinal artery)
Injury to what spinal tract would account for loss of pain and temp sensation?
Spinothalmic trract
(anterior spinal artery)
What is the BEST monitor of neurologic integrity during CEA?
an awake patient
gross
What is the BEST monitor of neurologic integrity during CEA?
an awake patient
gross
What is Amaurosis fugax?
What is it a sign of?
Temporary blindness in one eye
impending stroke
*occurs in 25% of patient s with high grade stenosis
*emboli travel from ICA > opthalmic artery → impaired perfusion of the optic nerve → rentinal dysfunction
Why is it important to know someones blood glucose level prior to taking them to surgery for CEA?
bc hyperglycemia > 200 has been associated with increased risk of stroke and death
*treat with insulin, avoid glucose containing solutions
During cross clamping of the carotid, BP should be elevated; what should BP be after release of cross clamp and why?
<145 to reduce bleeding at the graft site
The 4 significant postop risks associated with CEA?
- hematoma
- labile BP
- RLN injury
- Stroke (embolic most common)
The 4 significant postop risks associated with CEA?
- hematoma
- labile BP
- RLN injury
- Stroke (embolic most common)
What kind of blocks are done for CEA?
what levels
superficial and deep cervical plexus
C2-C4
Why would you avoid regional anesthesia in a COPD patient presenting for CEA ?
risk of ipsilateral phrenic nerve block → dyspea d/t hemidiaphragm paralysis
Cerebral perfusion pressure =
MAP - ICP (or CVP)
whichever is higher *
label
Cerebral oximetry uses what kind of technology to monitor cerebral oxygen in which lobe?
*The patient is at risk when cerebral o2 is reduced how much from baseline?
near-infrared spectroscopy (NIRS)
*Frontal lobe
> /= 25% from baseline
Transcranial Doppler assesses continous blood flow velocity where?
what’s special about this area?
Middle cerebral artery
it’s where most emboli lodge
*it may indicate if a shunt is needed
Where do most emboli lodge in the brain?
in the middle cerebral artery
Carotid stump pressure measures pressure (distal/proximal) to the clamp
What is there a risk of and at what pressure?
What is a low stump pressure an indication for?
Distal
ipsilateral hypoperfusion if < 50mmHg
the need for a shunt to be placed
*most sugeons will avoid shunts a t all costs becuase they increase risk of embolic stroke, but a low stump pressure would be a good indication for a need for one
If doing a CEA and you hear them say they need to place a shunt, what should come to mind?
increased risk for embolic stroke
Why do we want to maintain BP @ patients normal or slightly elevated during carotid cross clamp?
Bc blood vessels in the ischemic area maximally dilate and become pressure depedent (loss of autoregulation)
Besides concerns of bleeding of the new graft, what is another reason to reduce BP < 145 after clamp comes off carotid?
bc HTN → reperfusion injury → cerebral edema
label
What should you do if you end up in PACU and there is a hematoma developing on your CEA patient
remove the sutures to decompress the wound
Which is more common postop CEA - hypertension or hypotension?
why
when does it subside?
HTN
exposing baroreceptors alters their sensitivity
within 24 hours
Main reason agaisnt B/L CEA
carotid body denervation results in decreased ventilatory response to hypoxia
*peripheral chemoreceptors
Goal ACT during carotid artery angioplasty stenting
how much heparin should they get? ex 80kg pt
> 250 sec
50-100units/kg
80kg should get 4,000 - 8,000 units of heparin
What part of carotid artery angioplasty stenting can activate the baroreceptor reflex?
balloon inflation
*pretreat with atropine/glyco
In the patient with RIGHT subclavian steal syndrome, arterial flow is diverted from the:
A. right vertebral artery → right subclavian artery
B. Right subclavian artery → left subclavian artery
C. Left vertebral artery → right subclavian artery
D. Left subvlavian artery → right subvlavian artery
A. Right vertebral artery → right subclavian artery
*Subclavian steal syndrome can reduce cerebral perfusion. If there’s an occlusion of the subclavian or innominate artery proximal to the origin of the ipsilateral artery, then there can be retrograde flow that travels down the vertebral artery (instead of towards the brain).
Subclavian steal occurs when there is an occlusion of what, where?
What does it result in?, tx?
s/s? (5)
occlusion of the subclavian or innominate artery PROXIMAL to the origin of the ipsilateral vertebral artery
BP may be diminished in that arm; tx = subclavian endarderectomy
- syncope
- vertigo
- ataxia
- hemiplegia
- ishemia
label
Subvlavian steal syndrome “steals” blood from which vessel?
The vertebral artery (posterior cerebral circulation)
A Patient with a hx of heart failure with preserved EF is scheduled for a lap chole; the primary anesthetic consideratio includes:
A. Fluid restriction
B. Preventing tachycardia
C. Targeting a MAP of 60mmHg
D. administering a postive chronotrope
B. Preventing tachycardia
HFpEF → heart is less able to accept the incoming volume bc ventricular compliance is reduced
*maximizing coronary blood flow is the highest priorrity for this patient → a slower HR improves O2 supply (increased diastolic time) while simultaneously reducing O2 demand
LV coronary perfusion presssure is AoDBP - LVEDP where optimal = higher AoDBP and lower LVEDP; however, LVEDP does not correlate to LVEDV
*these patients require adequate preload to stretch a non-compliant ventricle
estimate the CPP (coronary)
42mmHg
CPP = Aortic DBP - LVEDP
use PA diastolic pressure as a surrogate for PAOP
Anesthetic considerations for the patient with SYSTOLIC heart failure includes a/an:
A. avoidance of inotropes to reduce myocardial o2 demand
B. increased afterload to perfuse hypertrophied myocardium
C. increased heart rate to maximize cardiac output
D. increased preload to stretch a noncompliant ventricle
C. increased heart rate to maximize CO
*The hallmark of systolic heart failure is a decreased EF with an increased end-diastolic volume (bc the ventricle does not empty well).
→ since the heart cant squeeze well, a greater volume of blood remains in the ventricle after each contraction (decreased SV) - only way to maintain cardiac output is to increase HR.
What is the hallmark of systolic heart failure
Anesthetic considerations for preload/afterload/hr/contractility
a decreased EF with an increased EDV (ventricle doesn’t empty well)
Preload → already high, don’t let it get higher
Afterload → decrease to reduce the LV workload
HR → mintain high/normal range
Contractility → inotropic support as needed
Which of the following are MOST closely associated with diastolic heart failure (select 3):
-dialated CM
-essentail HTN
-TR
-3rd heart sound
-ischemic heart disease
-AS
Aortic Stenosis
Ischemic heart disease
Essential hypertension
diastolic failure is associated with decreased ventricular compliance; the heart is unable to relax to accept the incoming volume → AKA: the ventricle doesn’t fill properly (explains why LVEDP overestimates the EDV
What is the defining characteristic of diastolic dsyfunction?
symptomatic heart failure with a normal EF.
3 most common causes of diastolic heart failure
other conditions it’s associated with (6)
AS, ischemic heart disease, long-standing essential HTN
concentric hypertrophy, old age, valve stenosis, HOCM, cor pulmonale, obesity
Which drugs ahve been proven to reverse LV remodeling in the patient with heart failure (select 2)
-clonidine
-esmolol
-enalapril
-spironolactone
Enalapril & Spironolactone
*ACE inhibitors and aldosterone inhibitors are first line agents in the patient with heart failure
what compliance curve correlates with the condition that produces the ABP waveform
The blue one
that waveform illustrates biferiens pulse and can occur in the patient with AI
Which region of the myocardium receives the LEAST amount of perfusion during systole?
A. RV epicardium
B. RV subendocardium
C. LV epicardium
D. LV subendocardium
D. LV Subendocardium
it’s primarly perfused during diastole (very little to no perusion durin
An elevated CK-MB is MOST consistent with:
A. AS
B. MI
C. Rheumatic fever
D. CHF
B. MI
What are the 3 substances released by the cardiac myocytes wehn they are deprived of o2 and the cell membrane explodes lol
CKMB, Troponin I, Troponin T
Which factors primarily affect myocardial O2 supply (select 2)
-P50
-Inotropy
-Diastolic time
-Wall tension
rank in order from hightest to lowest o2 cx
P50 & Diastolic time
Heart rate & Pressure work > contractility > wall stress > volume work
An increase in which of the following is associated with teh HIGHEST increase in myocardial o2 consumption (select 2)
-wall stress
-HR
-volume work
-pressure work
HR & Pressure work
Which agents reduce myocardial o2 demand? (select 2):
-dobutamine
-metoprolol
-mso4-
-atropine
metoprolol & morphine
Calcium channel blockers produce their CV effects by binding to the:
A. Alpha-1 subunit of the L-type calcium channel
B. alpha-1 subunit of the T-type calcium channel
C. Beta subunit of the L-type calcium channel
D. Beta subunit of the T-type calcium channel
A. Alpha-1 subunit of the L-type calcium channel (long-lasting/slow channel)
N = neural, T = transient
this binding prevents calcium from entering cardiac and vascular smooth muscle cells
A patient presents with diaphroesis, chest pain, and SOB. His BP is 220/110. Select the BEST IV drug for this patient:
A. Nimodipine
B. Nifedipine
C. Nicardipine
D. Verapamil
C. Nicardipine
Nicardipine and nifedipine are potent vasodilators, however only nicardipine is available for IV administration → they are best used to decrease SVR and/or releave angina
*verapamil reduces HR and contractility & also causes mild coronary vasodilating properties. It is primarily used for controlling SVT and/or angina. & causes LITTLE systemic vasodilation
What is the MOST common cause of acute pericarditis?
A. RA
B. Viral infection
C. SLE
D. Radiation
B. Viral infection
*most common cause for constrictive is radiation or previous cardiac surgery
Which abnormality is MOSt likely to occur in the patient with pericardial tamponade?
A. Pulsus alternans
B. Pulsus tardus
C. Pulsus paradoxus
D. Pulsus Parvus
C. Pulsus paradoxus
Normally the systolic BP decreases a little during inspiration (a few mmHg), but in the patient with pulsus paradoxus, the SBP decreases by 10mmHg or more
Antibiotic prophylaxis agaisnt endocarditis may be indicated if a patient has a history of (select 2):
A. MVP
B. unrepaired cyanotic heart disease
C. prostethetic heart valve
D. cardiac stent placement
B & C
unrepaired cyanotic heart disease & prosthetic heart valve
Which of the following are MOST likely to reduce stroke volume in the patient with hypertrophic cardiomyopathy:(3)
-Esmolol
-Neo
-Ephedrine
-Nitroprusside
-Hypervolemia
-Valsalva maneuver
what is your main concern with these patients?
Valsalva, ephedrine, nitroprusside
LVOT obstruction = main concern
-valsalve decreases preload
All of the following diseases cause secondary hypertension EXCEPT:
A. Coarctation of the aorta
B. Conn’s disease
C. Hashiomoto’s disease
D. Cushing’s syndrome
C. Hashimoto’s disease (atoimmune dz resulting in hypothyroid)
Conn’s disease (hyperaldosteronism) → too much aldosterone
Cushing’s syndrome (hyperadrenocorticism) → too much glucocorticoid
