Cardiovascular Flashcards
Define chronotropy, inotropy, dromotropy and lusitropy
Chronotropy: heart rate
Inotropy: strength of contraction
Dromotropy: conduction velocity
Lusitropy: rate of myocardial relaxation (during diastole)
Describe the function of the sodium-potassium pump.
the sodium-potassium pump maintains the cell’s resting potential. Said another way, it separates the charge across the cell membrane keeping the inside of the cell relatively negative and the outside of the cell relatively positive.
How it works:
* it removes the Na+ that enters the cell during depolarization
* it returns K+ that has left the cell during repolarization
* For every 3 Na+ ions it removes, it brings 2 K+ ions into the cell
List the 5 phases of the ventricular action potential, and describe the ionic movement during each phase
Phase 0: Depolarization -> Na+ influx
Phase 1: Initial repolarization -> K+ efflux & Cl- influx
Phase 2: Plateau -> Ca +2 influx
Phase 3: Repolarization -> K+ efflux
Phase 4: Na+/K+ pump restores resting membrane potential
List the 3 phases of the SA node action potential, and describe the ionic movement during each phase.
Phase 4: Spontaneous depolarization -> leaky to Na+ (Ca+2 influx occurs at the very end of phase 4)
Phase 0: Depolarization -> ca +2 influx
Phase 3: Repolarization -> K+ efflux
What process determines the intrinsic heart rate, and what physiologic factors alter it?
The rate of spontaneous phase 4 depolarization in the SA node determines heart rate.
We can increase HR by manipulating 3 variables:
* the rate of spontaneous phase 4 depolarization increases (reaches TP faster)
* TP becomes more negative (shorter distance between RMP and TP)
* RMP becomes less negative (shorter distance between RMP and TP)
When RMP and TP are close, it’s easier for the cell to depolarize
When RMP and TP are far, it’s harder for the cell to depolarize
MAP calculation
MAP = (2x Diastolic) + systolic/3
or ((COxSVR)/80)+CVP
normal 70-107 mmHg
What is the formula for systemic vascular resistance
((MAP-CVP)/CO)X 80
Normal: 800-1500 dynes/sec/cm-5
like all of these calculations, you’ll see the normal values vary from book to book
What is the equation for pulmonary vascular resistance?
((MPAP-PAOP)/CO)x 80
Normal 150-250 dynes/sec/cm-5
Describe the Frank-Starling relationship
describes the relationship between ventricular volume (preload) and ventricular output (cardiac output)
* Increased preload -> increased myocyte stretch -> ventricular output
* decreased preload-> decreased myocyte stretch -> ventricular output
Increasing preload increases ventricular output, but only up to a point. To the right of the plateau, additional volume overstretches the ventricular sarcomeres, decreasing the number of cross-bridges that can be formed and ultimately reducing cardiac output. This contributes to pulmonary congestion and increases PAOP.
What factors affect myocardial contractility
Contractility (inotropy) describes the contractile strength of the heart.
Just remember that Chemicals affect Contractility-particularly Calcium (C’s)
Most examples in the table either alters the amount of Ca+2 available to bind to the myofilaments or impacts the sensitivity of the myofilaments to Ca+2
increased contractility: SNS stimulation, catecholamines, calcium, digitalis, phosphodiesterase inhibitors
Decreased contractility: myocardial ischemia, severe hypoxia, acidosis, hypercapnia, hyperkalemia, hypocalcemia, volatile anesthetics, propofol, beta-blockers, calcium channel blockers
Discuss excitation-contraction coupling in the cardiac myocyte
- an action potential is propagated from an adjacent cell.
- depolarization of the T-tubule opens voltage-gated L-type Ca channels. Ca enters the myocyte. This occurs during phase 2 of the action potential
- The influx of Ca activates the ryanodine-2 receptor (RyR2)
- Ca+ is released from the sarcoplasmic reticulum. This is called calcium-induced calcium- release
- Ca binds to troponin C . This stimulates cross-bridge formation and causes myocardial contraction
- Ca unbinds from troponin C. this causes myocardial relaxation
- Most of the calcium is returned to the sarcoplasmic reticulum via the SERCA 2 pump (ATP dependent). Once inside, Ca binds to a storage protein called calsequestrin (CSQ)
- Some calcium is removed from the myocyte by the sodium/calcium exchange pump (NCX)
- The Na/K-ATPase restores resting membrane potential
*the duration of contraction is determine by the action potential duration
What is afterload, and how do you measure it in the clinical setting?
Afterload is the force the ventricle must overcome to eject its stroke volume.
In the clinical setting, we use the systemic vascular resistance as a surrogate for LV afterload.
What law can be used to describe ventricular afterload?
We can apply the law of Laplace to better understand ventricular afterload
Wall stress + (intraventricular pressure x radius)/ ventricular thickness
* intraventricular pressure is the force that pushes the heart apart
* wall stress is the force that hold the heart together (it counterbalances intraventricular pressure)
Wall stress is reduced by:
* Decreased intraventricular pressure
* decreased radius
* Increased wall thickness
List 2 conditions that set afterload proximal to the systemic circulation
Aortic stenosis, coarctation of the aorta
Use the wiggers diagram to explain the cardiac cycle
Pay attention to the following:
* where systole and diastole occur
* 6 stages of the cardiac cycle
* 4 pressure waveforms
* how the pressure waveforms match up to the EKG
* how the valve position changes match up to the EKG
Relate the 6 stages of the cardiac cycle to the LV pressure-volume loop
- Rapid filling- Diastole
- Reduced Filling- Diastole
- Atrial kick- Diastole
- Isovolumetric contraction- systole
- Ejection - Systole
- Isovolumetric relaxation - Diastole
you can measure SV, and EDV
How do you calculate ejection fraction
The ejection fraction is a measure of systolic function (contractility). It is the percentage of blood ejected from the heart during systole. Said another way, the EF is the stroke volume relative to end-diastolic volume.
Amount of blood pumped out of the ventricle/total amount of blood in ventricle x 100= EF%
>50% normal
41-49%- mild dysfunction
26-40%- moderate dysfunction
<25% severe dysfunction
(Stroke volume/End-diastolic volume) x 100
- SV is calculated as: EDV-ESV
what is the best TEE view for diagnosing myocardial ischemia?
midpapillary muscle level in short axis.
What is the equation for coronary perfusion pressure?
Coronary perfusion pressure = Aortic DBP- LVEDP
* Aortic DBP is the pushing force
*LVEDP is the resistance to the pushing force
therefore, increasing AoDBP or decreasing LVEDP (PAOP) improves CPP.
Which region of the heart is most susceptible to myocardial ischemia? Why?
The LV subendocardium is most susceptible to ischemia.
The LV subendocardium is best perfused during diastole. As aortic pressure increases, the LV tissue compresses its own blood supply and reduces blood flow. The high compressive pressure in the LV subendocoardium coupled with a decreased coronary artery blood flow during systole increases coronary vascular resistance and predisposes this region to ischemia.
What factors affect myocardial oxygen supply and demand?
Factors that reduce oxygen delivery:
* Decreased coronary flow- tachycardia, decreased aortic pressure, decreased vessel diameter (spasm or hypocapnia), increased end diastolic pressure
* Decreased CaO2- hypoxemia, anemia
* Decreased Oxygen extraction- Left shift of Hgb dissociation curve (decreased P50), decreased capillary density
Factors that increase Oxygen Demand:
Tachycardia, HTN, SNS stimulation, increased wall tension, increased end diastolic volume, increased afterload, increased contractility
discuss the nitric oxide pathway of vasodilation
Nitric oxide is a smooth muscle relaxant that induces vasodilation.
Steps in the nitric oxide cGMP pathway:
* nitric oxide synthase catalyzes the conversion of L-arginine to nitric oxide.
*nitric oxide diffuses from the endothelium to the smooth muscle,
* Nitric oxide activates guanylate cyclase.
*Guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate
* increased cGMP reduces intracellular calcium, leading to smooth muscle relaxation
* Phosphodiesterase deactivates cGMP to guanosine monophosphate (this step turns off the NO mechanism)
Where do the heart sounds match up on the left ventricle pressure volume loop?
S3: May suggest heart failure
S4: May suggest decreased ventricular compliance
Notice the MV opens/closes on the bottom of the loop, and the AV open/closes on the top of the loop
What are the two primary ways a heart valve can fail?
Stenosis:
* there is a fixed obstruction to forward flow during chamber systole
* the chamber must generate a higher than normal pressure to eject the blood
Regurgitation:
* the valve is incompetent (it’s leaky)
* Some blood flows forward, and some blood flows backward during chamber systole
How does the heart compensate for pressure overload? Volume overload?
Aortic valve stenosis (systole)- Pressure overload concentric hypertrophy - sarcomeres added in parallel
Aortic valve regurgitation (Diastole)- Volume overload eccentric hypertrophy- sarcomeres added in series
List the hemodynamic goals for the 4 common valvular defects
Aortic Stenosis-Full, slow, and constricted
Aortic Regurgitation- Full, Fast, and Forward
Mitral Stenosis- Slower, Maintain, maintain
Mitral regurgitation- Full, fast, forward
What is the most common dysrhythmia associated with mitral stenosis?
Atrial fibrillation
List 6 factors for perioperative cardiac morbidity and mortality for non-cardiac surgery.
- High-risk surgery
- History of ischemic heart disease (unstable angina confers the greatest risk of perioperative MI)
- History of CHF
- History of cerebrovascular disease
- DM
- Serum creatinine >2 mg/dL
What is the risk of perioperative myocardial infarction in the patient with a previous MI?
Risk of perioperative MI in the patient with previous MI:
* General population = 0.3%
* MI if >6 months =6%
* MI if 3-6 months= 15%
*MI <3 months = 30%
the highest risk of reinfarction is greatest within 30 days of an acute MI. For this reason, the ACC/AHA guidelines recommend a minimum of 4-6 weeks before considering elective surgery in a patient with a recent MI.
Categorize high, medium, and low risk surgical procedures according to cardiac risk.
AHA/American College of Cardiology Guidelines Based on Surgical Procedure
High (risk >5%):
* emergency surgery (especially in the elderly)
* Open aortic surgery
* Peripheral vascular surgery
* Long surgical procedures with significant volume shifts and/or blood loss
Intermediate (risk 1-5%):
* Carotid endarterectomy
* head and neck surgery
* Intrathoracic or intraperitoneal surgery
* orthopedic surgery
* prostate surgery
Low (risk <1%)
* Endoscopic procedures
* Cataract surgery
*superficial procedures
*breast surgery
* ambulatory procedures
How do you interpret cardiac enzymes in the patient with a suspected ischemic event?
A cell requires oxygen to maintain the integrity of its cell membrane, and a cell deprived of oxygen dies and releases its contents into the systemic circulation
* infarcted myocardium releases 3 key biomarkers: creatine kinase-MB, troponin I, and Troponin T
* Cardiac troponins are more sensitive than CK-MB for the diagnosis of myocardial infarction
* These values must be evaluated in the context of the time of the patient’s EKG
How do you treat intraoperative myocardial ischemia?
Treatment of myocardial ischemia should focus on interventions that make the heart slower, smaller, and better perfused.
What factors reduce ventricular compliance?
The diastolic pressure-volume relationship is affected by:
* Age >60
* Ischemia
* Pressure overload hypertrophy (aortic stenosis or HTN)
* Hypertrophic obstructive cardiomyopathy (familial)
* pericardial pressure (increased external pressure)
The clinical take away is that priming the ventricle requires higher filling pressures
What is the difference between HFrER (systolic) and HFpEF (diastolic) heart failure?
HF with reduced ejection fraction (HFREF)- the Ventricle Doesn’t Empty Well
*the hallmark of systolic heart failure is a decreased ejection fraction with an increased end-diastolic volume. Volume overload commonly causes systolic dysfunction.
HF with preserved ejection fraction (HFpEF) - The Ventricle Doesn’t Fill Properly
* Diastolic failure occurs when the heart cannot relax and accept the incoming volume because ventricular compliance is reduced. The defining characteristic of diastolic dysfunction is symptomatic heart failure with normal ejection fraction
Compare the contrast the hemodynamic goals in the patient with HFrEF vs HFpEF.
What is the modified New York Association Functional Classification of Heart Failure?
Class 1: Asymptomatic
Class 2: Symptomatic with moderate activity
Class 3: Symptomatic with mild activity
Class 4: Symptomatic at rest
List 6 complications of HTN.
The problem with HTN is a high afterload that increases myocardial work and an elevated arterial driving pressure damages nearly every organ in the body.
* Left ventricular hypertrophy
* Ischemic heart disease
* Congestive heart failure
* Arterial aneurysm (aorta, cerebral circulation)
* Stroke
*End-stage renal disease
How does HTN affect cerebral autoregulation?
The cerebral autoregulation curve describes the range of blood pressures where cerebral perfusion pressure remains constant.
Chronic HTN shifts this curve to the right. This adaptation helps the patient’s brain tolerate a higher range of blood pressures; howver, this comes at the expense of not tolerating a lower blood pressure. Remember that BP past the range of autoregulation is pressure dependent.
* Malignant hypertension increases the risk of hemorrhagic stroke and cerebral edema
* HoTN increases the risk of cerebral hypoperfusion
As an aside, the texts would lead to believe that the width of the curve remains the same in the hypertensive patient; there is good evidence that the width of the curve (range of autoregulation) becomes narrower
What’s the difference between primary and secondary HTN?
Primary (essential) HTN is more common and has no identifiable cause (95% of all HTN cases)
Secondary HTN is caused by some other pathology (5% of all HTN cases)
List 7 causes of secondary HTN
- coarctation of the aorta
- renovascular disease
- hyperadrenocorticism (cushing’s disease)
- Hyperaldosteronism (Conn’s disease)
- Pheochromocytoma
- pregnancy-induced HTN
What are the 2 major classes of calcium channel blockers? list examples of each
Describe the pathophysiology of constrictive pericarditis
Constrictive pericarditis is caused by fibrosis or any condition where the pericardium becomes thicker.
During diastole, the ventricles cannot fully relax, and this reduces compliance and limits diastolic filling. Ventricular pressures increase, which creates backpressure to the peripheral circulation. The ventricles adapt by increasing myocardial mass, but over time this impairs systolic function
Describe the anesthetic management of constrictive pericarditis
CO is dependent on HR.
* Avoid bradycardia
Preserve HR and contractility.
*Ketamine
*Pancuronium
* Volatile agents with caution
*Opioids, benzodiazepines, and etomidate are okay
Maintain afterload
Aggressive PPV can decrease venous return and CO
Describe the pathophysiology of pericardial tamponade
Cardiac tamponade occurs when fluid accumulates inside the pericardium. What separates it from a pericardial effusion is that the excess fluid exerts external pressure on the heart, limiting its ability to fill and act as a pump
CVP rises in tandem with pericardial pressure. As ventricular compliance deteriorates, left and right sided cardiac diastolic pressure (CVP and PAOP) begin to equalize. TEE is the best method of diagnosis, and the best treatment is pericardiocentesis or pericardiostomy
What is Kussmaul’s sign
Kussmaul’s sign indicates impaired right ventricular filling due to poorly compliant RV or pericardium. Since RV filling is affected, the blood essentially “backs up”, which causes jugular venous distention and an increased CVP. It is most pronounced during inspiration
List 2 conditions commonly associated with Kussmaul’s sign.
Although it can occur with any condition limiting RV filling, make sure you associate Kussmaul’s sign with constrictive pericarditis and pericardial tamponade
What is pulsus paradoxus?
Pulsus paradoxus represents an exaggerated decrease in SBP during inspiration (SBP falls by more than 10mmHg during inspiration). This finding suggests impaired diastolic filling.
* negative intrathoracic pressure on inspiration -> increased venous return to RV -> bowing of ventricular septum toward LV-> decreased SV-> Decreased CO-> SBP
List 2 conditions commonly associated with pulsus paradoxus
Like kussmaul’s sign, you should also associate pulsus paradoxus with constrictive pericarditis and pericardial tamponade
What is Beck’s triad? what conditions are associated with it?
Beck’s triad occurs in the patient with acute cardiac tamponade.
Signs include:
* HoTN (decreased SV)
*JVD (impaired venous return to the right heart)
* Muffled heart tones (fluid accumulation in the pericardial space attenuates sound waves)
What are the best anesthetic techniques for the patient with acute pericardial tamponade undergoing pericardiocentesis?
Because hemodynamics are minimally affected, local anesthesia is the preferred technique for pericardiocentesis.
If a general anesthetic is required, your primary goal is to preserve myocardial function. Severely decreased SV and increased SNS tone (increased contractility and increased afterload) provide compensation. Any drug that depresses the myocardium or reduces afterload can precipitate a cardiovascular collapse.
Drugs to avoid: Halogenated anesthetics, propofol, thiopental, high dose opioids, neuraxial anesthesia
Drugs that are safer to use: Ketamine (activation of the SNS makes this the best choice), nitrous oxide, benzodiazepines, opioids
List 7 patient factors that warrant antibiotic prophylaxis against infective endocarditis.
The following conditions are associated with the highest risk for developing infective endocarditis:
* previous infective endocarditis
* prosthetic heart valve
* Unrepaired cyanotic heart defect , or if the repair is < 6 months old
* Repaired congenital heart disease with residual defects that have impaired endothelialization at the graft site
* Heart transplant with valvuloplasty
List 3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis.
High-risk procedures are thought to be “dirty” procedures where the risk of transient bacteremia outweighs the risk of antibiotic therapy
* Dental procedures involving gingival manipulation and/or damage to mucosa lining
* respiratory procedures that perforate the mucosal lining with incision or biopsy
* Biopsy of infective lesions on the skin or muscle
What are the 3 key determinants of flow through the left ventricular outflow tract?
Systolic LV volume
Force of LV contraction
Transmural pressure gradient
What factors reduce cardiac output in the patient with obstructive hypertrophic cardiomyopathy?
Things that distend the left ventricular outflow tract (LVOT) are good for cardiac output, while things that narrow the LVOT are bad.
How long should elective surgery be delayed in the patient after a percutaneous coronary intervention?
Previous intervention duration to wait for elective
Angio without stent: 2-4 weeks
Bare metal stent: 30 days (3 months preferred)
Drug eluting stent:
*stable ischemic heart dx -first gen DES= 12 months
- current gen DES= 6 mths
*Acute coronary syndrome 12 months min
CABG 6 weeks (3 months preferred)
This chart reflects the changes for DES included in the 2016 ACC/AHA guidelines. The old guidelines said a minimum of 12 months for all drug-eluting stents
What is the difference between alpha-stat and pH-stat blood gas measurement during cardiopulmonary bypass?
because the solubility of a gas is a function of temperature. it should make sense that hypothermia complicates out interpretation of blood gas results during CPB. As temperature decreases, more CO2 will dissolve in the blood. By extension, this affects the pH. Knowing this poses an interesting question about how best to manage blood pH during CBP with hypothermia. Should the temperature of the sample be correct or not?
- Alpha-set- does not correct the pts temp. This technique aims to keep intracellular charge neutrality across all temperature. It is associated with better outcomes in adults.
- pH-stat- corrects the pts temperature. This technique aims to keep a constant pH across all temperature. It is associated with better outcomes in peds.
Why is left ventricular vent used during CAPB
A left ventricular vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt)
How does the intra-aortic balloon pump function throughout the cardiac cycle? How does it help the patient?
The intra-aortic balloon pump is a counterpulsation device that improves myocardial oxygen supply while reducing myocardial oxygen demand.
Diastole:
* pump inflation augments coronary perfusion
* inflation correlates with the dicrotic notch on the aortic pressure waveform
Systole:
*pump deflation reduces afterload and improves cardiac output.
* deflation correlates with R wave on the EKG
List 4 contraindications to the intra-aortic balloon pump
Severe aortic insufficiency
descending aortic disease
Severe peripheral vascular disease
Sepsis
Which law describes the relationship between aortic diameter and risk of aortic rupture in the patient with an abdominal aortic aneurysm?
Applying of law of Laplace, we know that the diameter of the AAA correlates with the risk of rupture:
* wall tension= transmural pressure x Vessel radius
* Increased diameter-> increased transmural pressure -> increased wall tension
Mortality increases significantly once the AAA reaches 5.5 cm. Surgical correction is recommended when the aneurysm exceeds 5.5cm or if it grows more than 0.6-0.8 cm/year
How does the aortic cross clamp contribute to the risk of anterior spinal artery syndrome?
An aortic cross clap placed above the artery Adamkiewicz may cause ischemia to the lower portion of the anterior spinal cord. This can result in anterior spinal artery syndrome- otherwise known as Beck’s syndrome (different from Beck’s triad)
How does anterior spinal artery syndrome present?
- Flaccid paralysis of the lower extremities
- bowel and bladder dysfunction
- loss of temperature and pain sensation
- Preserved touch and proprioception
What is the amaurosis fugax?
Amaurosis fugax (blindness in one eye) is a sign of impending stroke. Emboli travel from the internal carotid artery to the opthalmic artery, which impairs perfusion of the optic nerve and causes retinal dysfunction.
A patient is undergoing carotid endarterectomy with EEG monitoring. What does this monitor tell you, an what conditions can lead to false conclusions?
EEG-
* monitors cortical electricl function (does not detect subcortical problems)
* risk of cerebral hypoperfusion with loss of amplitude, decreased beta-wave activity, and/or appearance of slow wave activity
* high incidence of false-negative. Possible causes include:
Increased frequency: mild hypercarbia, Early hypoxia, seizure activity, ketamine, N2O, light anesthesia
Decreased frequency: Extreme hypercarbia, hypoxia, cerebral ischemia, hypothermia, anesthetic overdose, opioids
What regional block technique can be used for the patient undergoing carotid endarterectomy? What levels must be blocked?
Techniques for regional anesthesia for the patient undergoing CEA include:
* cervical plexus block (superficial or deep)
* local infiltration
Regional anesthesia must cover C2-C4
What reflex can be activated during carotid endarterectomy or following carotid balloon inflation?
Baroreceptor reflex
A patient in the PACU develops a hematoma following a right endarterectomy. Her airway is completely obstructed. What is the best treatment at this time?
the patient requires emergency decompression of the surgical site. If the surgeon isn’t immediately available, this falls on you. Cricothyroidotomy may be required.
Resting membrane potential is established by what 3 mechanisms?
- Chemical force
- Electrostatic counterforce
- Sodium/potassium ATPase
Define resting membrane potential
Its the electrical potential across a cell membrane at rest
Define threshold potential
It’s the voltage change that must be achieved to initiate depolarization
What three variables can be manipulated to change the sinus node rate?
The rate of spontaneous phase 4 depolarization
Threshold potential
Resting membrane potential
How does SNS stimulation increase the heart rate?
Norepinephrine stimulates the beta-1 receptor, which increases the heart rate by increasing Na+ and Ca2+ conductance
this increases the rate of spontaneous phase 4 depolarization
What happens to the heart rate if the distance between threshold potential and resting potential narrows?
Heart rate will increase because myocardial cells will reach threshold faster
the amount of oxygen dissolved in blood (PaO2) follows what law?
Henry’s Law
Name 5 factors that increase left ventricular contractility
- SNS stimulation
- Catecholamines
- Calcium
- Digitalis
- Phosphodiesterase inhibitors
List 3 ways that Beta-1 receptor stimulation modulates calcium in the myocyte
- Activation of L-type Ca+2 channels
- Stimulation of the ryanodine 2 receptor to release more calcium
- stimulation of the SERCA2 pump to increase Ca+2 uptake
The net effect is a more forceful contraction over a shorter time
What is the equation for law of Laplace as it relates to the LV?
Wall stress= Intraventricular pressure x radius/ ventricular thickness
What is the normal SVR in an adult?
800-1500 dynes x sec x cm to the -5
what 3 responses are responsible for autoregulation of coronary blood flow
- local metabolism
- myogenic response
- autonomic nervous system
Which myocardial arterial bed is most susceptible to ischemia?
Endocardial blood vessels of the myocardium
Phenylephrine stimulates what effector to ultimately cause vasoconstriction?
Phospholipase C
Why is spinal anesthesia avoided with severe aortic stenosis?
Sympathectomy rapidly reduces SVR leading to profound HoTN, reduced coronary perfusion pressure, and cardiovascular collapse.
list 2 causes of acute aortic insufficiency
- Endocarditis (most common)
- Aortic root dissection (aneurysm or trauma)
List 4 causes of chronic aortic insufficiency
- Valvular calcification
- Marfan syndrome
- Ehler-Danlos syndrome
- Ankylosing spondylitis
Why is ephedrine NOT a good choice for hypotension with mitral stenosis?
It will increase heart rate. Better choices include phenylephrine or vasopressin
General risk factors for cardiac risk
- High risk surgery
- History of ischemic heart disease
- history of CHF
- History of cerebrovascular disease
- Diabetes Mellitus
- Serum creatinine >2mg/dL
High risk cardiac risk based on surgical procedures
Cardiac risk >5%
* Emergency surgery (especially in the elderly)
* open aortic surgery
* peripheral vascular surgery
* Long Surgical procedures with significant volume shifts and/or blood loss
Intermediate risk -cardiac risk based surgical procedures
Cardia risk = 1-5%
* Carotid endarterectomy
* head and neck surgery
* intrathoracic or intraperioneal surgery
* orthopedic surgery
* prostate surgery
Low risk - cardiac risk based on surgical procedures
Cardiac risk <1%
* endoscopic procedures
* Cataract surgery
* Superficial procedures
* breast surgery
* ambulatory procedures
What warrants a referral to a cardiologist before surgery?
If a class 3 (symptoms with less than normal activity) or 4 (symptoms at rest) requires general anesthesia for high- or intermediate- risk surgery
List 3 biomarkers that are released from an infarcted myocardial tissue
- Creatine kinase-MB (CK-MB)
- Troponin l
- Troponin T
Which cardiac marker is the least sensitive for MI?
CK-MB
What are the 3 best EKG leads to monitor intraoperative ST changes?
- V3
- V4
- V5
list 4 physiologic adaptations to heart failure
- SNS activation
- excessive vasoconstriction
- Fluid retention
- Myocardial remodeling
List 3 physiologic functions of BNP
- Natriuresis
- Diuresis
- Vasodilation
released due to volume or pressure overload that leads to ventricular wall stress and BNP release
List 6 things that increase pulmonary vascular resistance
- Hypoxia
- Hypercarbia
- Acidosis (both metabolic and respiratory due to H+ concentration)
- Hypothermia
- High PEEP
- Nitrous oxide (constriction of pulmonary vascular smooth muscle)
How does CHF affect beta- receptors?
It causes down-regulation of beta-receptors
Most common cause of right sided heart failure?
Left sided heart failure
what preoperative blood pressure warrants delay in surgery?
SBP >180
DBP >110
how is clevidipine metabolized?
Non-specific tissue esterases
which cardiac valve defect is a contraindication of clevidipine?
Severe aortic stenosis
list two food allergies that are contraindications to celvidipine.
Eggs (egg products)
Soy (soy products)
define pulses paradoxus
SBP decreases >10 mmHg during inspiration
What is a contraindication to antegrade cardioplegia?
Incompetent aortic valve
List 4 contraindications for the IABP
- Severe AI
- Descending aortic disease
- Severe PVD
- Sepsis
The tip of the balloon is positioned distal to which vessel?
Left subclavian artery
During which part of the cardiac cycle does the balloon inflate?
Inflation correlates with the dicrotic notch on the aortic pressure waveform (onset of diastole)
What is the most common cause of death in a patient with an LVAD?
Sepsis
why might the pulse oximeter not work in the patient with an LVAD?
Depending on the native cardiac function, flow may be non-pulsatile.
What is the classic triad of AAA rupture?
- Back pain
- Hypotension
- Pulsatile abdominal mass
What is the most common cause of postoperative death in patients with a ruptured aortic aneurysm?
MI
Why don’t all patients with an aortic aneurysm rupture exsanguinate immediately?
Most aneurysms rupture in the left retroperitoneum allowing for tamponade and clot formation
When is surgical correction of AAA recommended?
When it reaches 5.5 cm or if it grows more than 0.6-0.8 cm per year
Injury to which spinal tract explains flaccid paralysis of lower extremities?
Corticospinal tract
Injury to what spinal tract explains loss of pain and temperature sensation?
Spinothalamic tract
Carotid denervation from CEA is a problem due to?
reduces the ventilatory response to hypoxia- problem for pts with h/o bilateral CEA
Name 6 signs and symptoms of subclavian steal syndrome
- Syncope
- Vertigo
- Ataxia
- Hemiplegia
- arm ischemia
- upper extremity weak pulse
Refers to diversion of blood flow away from its normal target and the arm. Happens due to subclavian artery stenosis located proximal to the origin of the vertebral artery.
Is subclavian steal syndrome more common on the left or the right side?
Left
What is the most potent vasodilator substance released by cardiac myocytes?
Adenosine- most potent local vasodilator
Adenosine is a byproduct of metabolism, so it should make sense that metabolically active tissue produces adenosine to increase local blood flow.
Transection of the right vagus nerve would MOST likely affect:
SA node automaticity
the right vagus n. innervates the SA node, so transection will affect SA node automaticity
The left vagus n. innervates the AV node
Bundle of kent is an abnormal accessory pathway between the atria and the ventricles found in pts with Wolff-parkinson white syndrome
Contractility is dependent on:
Chemical affect Contractility - particularly Calcium.
(not dependent on preload or afterload)
How much does atrial contraction contribute to cardiac output?
20-30%
What is the most common cause of Aortic Stenosis
Bicuspid aortic valve/ calcification
rheumatic fever and endocarditis are both causes of AS but not the most common
What are the hallmark signs of aortic stenosis and the other valve disorders?
Syncope, Angina, and dyspnea
at the onset survival rate is three, five, and two years
SAD mnemonic
mitral stenosis= pulmonary congestion and a fib
chronic mitral regur= Dyspnea on exertion (DOE),
paroxysmal nocturnal dyspnea, and a fib
acute aortic insufficiency= severe pulmonary edema and CHF
What is SAM?
Systolic anterior motion- a complication of mitral valve repair. The left ventricular outflow tract becomes occluded. The risk is increased when the anterior leaflet is longer than that posterior leaflet or when there is a narrow angle between the mitral annulus and aortic annulus
Pharmacologic treatment is the same as hypertrophic cardiomyopathy:
* Vasodilators and inotropes (nitroprusside and dobutamine) make SAM worse
* Vasoconstrictors and volume expansion (phenylephrine and NaCl bolus) tend to make SAM better)
With mitral valve prolapse what are the goals and what meds are okay/not okay?
Smaller ventricle tends to increase MV prolapse. for this reason the primary management goal for MVP is to prevent excessive cardiac emptying.
Avoid:
* SNS stimulation
* Decreased SVR
* Hypovolemia
* Upright posture (reverse tburg and sitting)
Pharm considerations:
* Phenylephrine is useful for HoTN
* No contraindication for regional
* Etomidate provides cardiostability
* Volatile anesthetics +N2O and or opioids help minimize SNS stimulation, but titrated to no significantly decrease SVR
Avoid Ketamine because it activates the SNS, increases myocardial contractility, and augments LV emptying
Valve problems and when/ where they are heard and what kinds of sounds
Mitral stenosis: MSDA: Diastole at the left axilla - opening snap with a low-intensity murmur during diastole
Mitral regurg: MRSA: Systole at the left Axilla- loud swishing sound during systole, holosystolic murmur
Aortic Stenosis: ASSS: Systole at the right Sternal border: Harsh and noisy murmur
Aortic insufficiency: AIDS: Diastole at the right Sternal border: High pitch blowing murmur
An increase in which factor is associated with the HIGHEST increase in myocardial oxygen consumption?
Heart rate and pressure work
heart rate = pressure work> contractility > wall stress> volume work
CCBs produce their cardiovascular effects by binding to the:
Alpha- 1 subunit of the L-type calcium channel
L type= long-lasting or slow channel
Prevents calcium from entering calcium and vascular smooth muscle cells
What is the MOST common cause of acute pericarditis?
Viral infection
most common cause of constrictive pericarditis = radiation or previous cardiac surgery
What conditions increase the risk of LVOT obstruction (hypertrophic cardiomyopathy)
- Decreased Preload
- Decreased afterload
- Increased HR
- increased contractility
Conditions that decrease preload:
* Vasodilators
* Neuraxial anesthesia
* Hypovolemia
* Postural changes (reverse T-burg)
* Valsalva maneuver
Conditions that decrease afterload:
* Vasodilators
* Neuraxial anesthesia
* Oxytocin
Conditions that increase HR:
* Beta-agonists
* Ketamine
* Panucronium
* Des
* Oxytocin
* Light Anesthesia
* Histamine releasing drugs (morphine, meperidine, thiopental, atracurium)
Conditions that increase contractility:
* Beta- agonists
* Digoxin
* Light anesthesia
Heart failure with reduced EF what to do/avoid
The only way to increase the CO is to increase HR because the body is already compensating with SNS activation.
Preload: it’s already high, so don’t let it get higher
Afterload: Decrease to reduce the LV workload
HR: maintain high/normal range
Contractility: inotropic support as needed
What is the highest systolic BP where the aorta can be safely cannulated
100 mmHG or MAP < 70mmHg and should be heparinized
What is the BEST way to preserve spinal cord blood flow during an ascending aortic aneurysm repair?
Cerebrospinal fluid drainage
CSF drainage- CSF shunting from the brain towards the spinal column during clamping can exert excess pressure on the spinal cord. Draining CSF improves spinal cord perfusion.
Potential acute consequence of a thoracic aortic cross-clamp include:
spinothalamic tract impairment
cardiac conduction pathway with its normal conduction time
Internal SA to AV node pathways = 0.03 seconds or 30msec
Atrioventricular node= 0.09 seconds or 90msec
Atrioventricular bundle (bundle of HIS)= 0.04 seconds
Bundle branches to purkinje fibers = 0.06 seconds or 60msec
In total, there is a built in 0.16 second delay before the impulse from the SA node reaches the ventricles
from the beginning of the bundle branches to the completion of purkinje fiber, activation requires another 0.06 seconds
AV node has the longest conduction time. This delay allows the atria to empty their blood prior to ventricular contraction.
Common symptoms of a patent ductus arteriosus in a premature infant
Respiratory failure - increased SVR causes blood to be directed into pulmonary circulation creating pulmonary congestion
Systolic murmur due to the shunt occurring during systole
Widened pulse pressure due to the additional run-off of blood into the pulmonary vasculature during contraction
typically volume overloaded
what are the signs and symptoms of angina pectoris?
Epigastric pain
others: Jaw pain, retrosternal pain/discomfort/pressure, jaw pain, pain radiating down the neck, pain radiating down the arms specifically the ulnar surface of the forearm and hand, and SOB
What features characterize chronic severe mitral regurgitation?
Regurgitant fraction >50% and enlarged left ventricle and left atrium, a regurgitant volume of >60mL/beat
Data that suggests Aortic stenosis
Moderate aortic stenosis is defined by peak velocity of 3-4 meters per second, a mean gradient of 20 - 40 mmHg, and valve area from 1-1.5cm^2
Severe AS, the peak aortic flow velocity is > 4 m/s, the mean gradient is >40mmHg, and aortic valve area is <1 cm^2
Mild AS peak velocity of 2.6-2.9 m/s, a mean gradient of <20 mmHg, and a valve area of 1.5cm^2
Which anatomic features are MOST responsible for the risk of sudden death in a patient with hypertrophic obstructive cardiomyopathy?
Interventricular septal hypertrophy- septum bulges into the left ventricle during systole obstructing LV ejection
Anterior motion of mitral valve during systole- blocking the LV outflow tract
both starve the LV muscle of oxygenated blood, contributing to ischemia, cardiac dysrhythmias, and sudden loss of cardiac output.
What are early indications of pericardial constriction?
Ascites, peripheral edema, JVD
(Right sided HF)
Others include: fatigue, dyspnea, pulsus paradox, and positive Kussmaul sign
Which features of carvedilol contribute to its efficacy for the tx of HF?
Anti-inflammatory action
antioxidant activity
Alpha-1 adrenergic antagonism
it is a nonselective beta-blocker antagonizing B1 B2 and alpha 1 adrenergic receptors (producing vasodilation). This facilitates off-loading the left ventricle, key for HF, and beta-blockade prevents the development of reflex tachycardia. It also scavenges free radicals, suppresses reactive oxygen species (ROS), and reduces the uptake of LDL into coronary endothelium (anti-inflammatory). Drug of choice for HF.
