Unit 3: Cardiovascular Flashcards
Define:
- Chronotropy
- Inotropy
- Dromotropy
- Lusitropy
Chronotropy = Heart Rate
Inotropy = Strength of contraction (Contractility)
Dromotropy = Conduction velocity
Lusitropy = Rate of myocardial relaxation (during diastole)
What is the function of the sodium-potassium pump?
Maintains cell’s resting potential – separates the charge across the cell membrane keeping the inside relatively negative and outside relatively positive
- removes Na+ that enters during depolarization
- returns K+ that left during repolarization
- for 3 Na+ ions removed – 2 K+ ions enter
What are the five phases of ventricular action potential? Describe the ionic movement during each phase
Phase 0: Depolarization –> Na+ influx
Phase 1: Initial Repolarization –> K+ efflux and Cl- influx
Phase 2: Plateau –> Ca2+ influx
Phase 3: Repolarization –> K+ efflux
Phase 4: Na+/K+ pump restores resting membrane potential
What are the three phases of SA node action potential? Describe the ionic movement during each phase
Phase 4: Spontaneous Depolarization –> leaky to Na+ (Ca2+ influx occurs at the very end)
Phase 0: Depolarization –> Ca2+ influx
Phase 3: Repolarization –> K+ efflux
What process determines the intrinsic heart rate? What physiologic factors alter it?
The rate of spontaneous phase 4 depolarization in SA node
Can increase HR by manipulating 3 variables:
-rate of spont 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 is easier for the cell to depolarize
What are the two calculations for MAP? What is normal?
MAP = (1/3 x SBP) + (2/3 x DBP)
MAP = [(CO x SVR) / 80] +CVP
normal = 70-105
What is the formula for SVR? What is normal?
SVR = [(MAP - CVP) / CO] x 80
normal = 800-1500
What is the formula for PVR? What is normal?
PVR = [(MPAP - PAOP) / CO] x 80
normal = 150-250
What is the Frank-Starling relationship?
Describes the relationship between ventricular volume (preload) and ventricular output (CO)
- increased preload –> increased myocyte stretch –> increased CO
- decreased preload –> decreased myocyte stretch –> decreased CO
*increased preload increases CO only up to a point – additional volume overstretches ventricular sarcomeres decreasing # of cross-bridges that can be formed thus reducing CO (contributes to pulm congestion and increases PAOP)
What is on the y-axis and x-axis of the Frank-Starling curve?
Y-Axis = Ventricular Output (CO, SV, LVSW, RVSW)
X-Axis = Filling Pressures (CVP, PAD, PAOP, LAP, LVEDP) or End Diastolic Volume (RVEDV, LVEDV)
What factors increase and decrease myocardial contractility?
Increased Contractility:
- SNS stimulation
- Catecholamines
- Calcium**
- Digitalis
- Phosphodiesterase inhibitors
Decreased Contractility:
- Myocardial ischemia
- Severe hypoxia
- Acidosis
- Hyperkalemia
- Hypocalcemia
- Volatile anesthetics
- Propofol
- Beta-blockers
- Ca2+ channel blockers
*Chemical affect Contractility - particularly Calcium
What are the steps in excitation-contraction coupling in the cardiac myocyte?
- AP is propagated from adjacent cell
- Depolarization of T-tubule opens voltage-gated L-type Ca2+ channel (Ca2+ enters myocyte) – occurs during phase 2 of AP
- Influx of Ca2+ activates ryanodine-2 receptor (RyR2)
- Ca2+ is released from sarcoplasmic reticulum (Ca2+ induced Ca2+ release)
- Ca2+ binds to troponin C – stimulates cross bridge formation and causes myocardial contraction
- Ca2+ unbinds from troponin C – myocardial relaxation
- Calcium is returned to sarcoplasmic reticulum via SERCA2 pump (when inside binds to calsequestrin)
- Some calcium is removed from myocyte by Na/Ca exchange pump
- Na/K-ATPase restores resting membrane potential
What is afterload? How is it measured in the clinical setting?
Afterload = force the ventricle must overcome to eject its stroke volume
SVR = surrogate for LV afterload
What is the equation for SVR and PVR? What is normal?
SVR = [(MAP - CVP) / CO] x 80 normal = 800-1500
PVR = [(MPAP - PAOP) / CO] x 80 normal = 150-250
What law can be used to describe ventricular afterload?
Law of Laplace
-wall stress = (intraventricular pressure x radius) / ventricular thickness
*wall stress is reduced by decreased intraventricular pressure, decreased radius, increased wall thickness
What two conditions set afterload proximal to the systemic circulation?
Aortic Stenosis
Coarctation of the aorta
Describe the Wiggers diagram
Pay attention to:
- 6 stages of cardiac cycle
- 4 pressure waveforms
- How the pressure waveforms match up to the EKG
- How the valve position changes match up to the EKG
What are the six stages of the cardiac cycle? How do they relate to the LV pressure-volume loop?
- Rapid Filling (diastole)
- Reduced Filling (diastole)
- Atrial Kick (diastole)
- Isovolumetric Contraction (systole)
- Ejection (systole)
- Isovolumetric Relaxation (diastole)
What is ejection fraction? How do you calculate it?
Measure of systolic function (contractility) – Percent of blood ejected from heart during systole (SV relative to EDV)
EF = [(EDV - ESV) / EDV] x 100
What are the classifications of ejection fraction dysfunction?
Normal = >50%
Mild Dysfunction = 41-49%
Moderate Dysfunction = 26-40%
Severe Dysfunction = <25%
How can you calculate the stroke volume and/or ejection fraction with a pressure volume loop?
SV = width of the loop
EDV = right side of the loop at the x-axis
What is the best TEE view for diagnosing myocardial ischemia?
Midpapillary muscle level in short axis
What is the equation for coronary perfusion pressure?
CPP = Aortic DBP - LVED
*increasing AoDBP or decreasing LVEDP (PAOP) improves CPP
Which region of the heart is most susceptible to myocardial ischemia? Why?
LV subendocardium = most susceptible to ischemia
- it is best perfused during diastole
- as aortic pressure increases, LV tissue compresses its own blood supply and reduces blood flow
- high compressive pressure in LV subendocardium coupled with decreased coronary artery blood flow during systole increases coronary vascular resistance and predisposes it to ischemia
What factors 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 (Decrease P50)
- decreased capillary density
What factors increase oxygen demand?
- Tachycardia
- Hypertension
- SNS stimulation
- Increased wall tension
- Increased end diastolic volume
- Increased afterload
- Increased contractility
What are the steps in the nitric oxide cGMP pathway?
Nitric Oxide = smooth muscle relaxant that induces vasodilation
- Nitric oxide synthase catalyzes conversion of L-arginine to nitric oxide
- Nitric oxide diffuses from endothelium to smooth muscle
- Nitric oxide activates guanylate cyclase
- Guanylate cyclase converts guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP)
- Increased cGMP reduces intracellular Ca2+, leading to smooth muscle relaxation
- Phosphodiesterase deactivates cGMP to guanosine monophosphate turning off the NO mechanism
Where do the heart sounds match up on the LV pressure volume loop?
S1: closure of mitral & tricuspid valves – bottom right corner of LV PV loop
S2: closure of aortic & pulmonary valves – top left corner of LV PV loop
S3: suggests flaccid/inelastic heart (think HF) – left side of bottom line of LV PV loop
*gallop rhythm (heard during middle 1/3 of diastole - after S2)
S4: caused by atrial systole – right side of bottom line of LV PV loop
*heard before S1
*may suggest decreased ventricular compliance
What are the two primary ways a heart valve can fail?
Stenosis: fixed obstruction to forward flow during chamber systole
- chamber must generate higher than normal pressure to eject blood
- leads to concentric hypertrophy (sarcomeres added in parallel)
Regurgitation: valve is incompetent (leaky)
- some blood flows forward and some flows backward during chamber systole
- leads to eccentric hypertrophy (sarcomeres added in series)
What is the following LV pressure volume loop?
Mitral Stenosis
What is the following LV pressure volume loop?
Aortic Stenosis
What is the following LV pressure volume loop?
Aortic Regurgitation
What is the following LV pressure volume loop?
Mitral Regurgitation
What are the hemodynamic goals for aortic stenosis?
HR, Preload, Contractility, SVR, PVR
HR: slow to normal
Preload: increased
Contractility: no change
SVR: no change or increased
PVR: no change
What are the hemodynamic goals for mitral stenosis?
HR, Preload, Contractility, SVR, PVR
HR: slow to normal
Preload: no change
Contractility: no change
SVR: no change
PVR: AVOID increase
What are the hemodynamic goals for aortic insufficiency?
HR, Preload, Contractility, SVR, PVR
HR: increased
Preload: no change or increased
Contractility: no change
SVR: decreased
PVR: no change
What are the hemodynamic goals for mitral insufficiency?
HR, Preload, Contractility, SVR, PVR
HR: increased
Preload: no change or increased
Contractility: no change
SVR: decreased
PVR: AVOID increase
What is the most common dysrhythmia associated with mitral stenosis?
Atrial Fibrillation
What are the six risk factors for perioperative cardiac morbidity and mortality for non-cardiac surgery?
- High-risk surgery
- Hx of ischemic heart disease (unstable angina confers greatest risk of periop MI)
- Hx of CHF
- Hx of cerebrovascular disease
- DM
- Serum creatinine >2
What is the risk of periop MI in the pt with a pervious MI?
General Population: 0.3%
MI if > 6 months: 6%
MI if 3-6 months: 15%
MI if < 3 months: 30%
*highest risk of reinfarction is greatest within 30 days of an acute MI
*ACC/AHA guidelines recommend a minimum of 4-6 weeks before considering elective surgery
What are considered HIGH risk surgical procedures according to cardiac risk? (4)
- Emergency surgery (especially in elderly)
- Open aortic surgery
- Peripheral vascular surgery
- Long surgical procedures with significant volume shifts and/or blood loss
What are considered INTERMEDIATE risk surgical procedures according to cardiac risk? (5)
- Carotid endarterectomy
- Head and neck surgery
- Intrathoracic or Intraperitoneal surgery
- Orthopedic surgery
- Prostate surgery
What are considered LOW risk surgical procedures according to cardiac risk? (5)
- Endoscopic procedures
- Cataract surgery
- Superficial procedures
- Breast surgery
- Ambulatory procedures
What cardiac enzymes are released during an MI? When do you see elevation in the values?
Infarcted myocardium releases 3 key biomarkers: CK-MB, Troponin I, and Troponin T
-cardiac troponins are more sensitive than CK-MB for diagnosis of MI
CK-MB: initial elevation 3-12 hrs; Peak 24 hrs; Return to baseline 2-3 days
Troponin I: Initial 3-12 hrs; Peak 24 hrs; Return 5-10 days
Troponin T: Initial 3-12 hrs; Peak 12-48 hrs; Return 5-14 days
*these values must be evaluated in the context of the time of the pt’s EKG
How do you treat intraop myocardial ischemia?
Focus on interventions that make the heart slower, smaller, and better perfused
Increased O2 Demand:
- increased HR –> beta blocker
- increased BP –> increased anesthesia depth, vasodilator
- increased PAOP –> nitroglycerin
Decreased O2 Supply:
- decreased HR -> anticholinergic, pacing
- decreased BP –> vasoconstrictor, reduce anesthesia depth
- increased PAOP –> nitroglycerin, inotrope
What factors reduce ventricular compliance?
Diastolic pressure-volume relationship is affected by:
- age >60
- ischemia
- pressure overload hypertrophy (aortic stenosis or HTN)
- hypertrophic obstructive cardiomyopathy
- pericardial pressure (increased external pressure)
*priming the ventricle requires higher filling pressures
What is the difference between HFrEF (systolic) and HFpEF (diastolic) heart failure?
HFrEF – Ventricle doesn’t empty well
*hallmark of systolic HF is a decreased EF w/ an increased EDV (volume overload commonly causes systolic dysfunction)
HFpEF – Ventricle doesn’t fill properly
*occurs when heart can’t relax and accept the incoming volume because ventricular compliance is reduced
*defining characteristic of diastolic dysfunction is symptomatic HF w/ a normal EF
What are the hemodynamic goals in a patient with HFrEF?
preload, afterload, contractility, HR
Preload: already high (diuretics if too high)
Afterload: decreased to reduce myocardial workload; maintain CPP
Contractility: augment w/ inotropes as needed (dobutamine)
HR: usually high d/t increased SNS tone; if EF is low, then a higher HR is needed to preserve CO
What are the hemodynamic goals in a patient with HFpEF?
preload, afterload, contractility, HR
Preload: volume required to stretch noncompliant ventricle; LVEDP doesn’t correlate w/ LVEDV (TEE is best)
Afterload: keep elevated to perfuse a thick myocardium (Neo); maintain CPP
Contractility: usually normal
HR: slow/ normal to increase diastolic time and CPP
What is the Modified New York Association Functional Classification of Heart Failure?
Class 1: asymptomatic
Class 2: symptomatic w/ moderate activity
Class 3: symptomatic w/ mild activity
Class 4: symptomatic at rest
What are six complications of HTN?
- LV hypertrophy
- Ischemic heart disease
- CHF
- Arterial aneurysm (aorta, cerebral circulation)
- Stroke
- End-stage renal disease
*HTN is high afterload that increases myocardial work and an elevated arterial driving pressure damages nearly every organ in the body
How does HTN contribute to CHF?
HTN –> Increased Myocardial Wall Tension –> LVH –> CHF
HTN –> Increased Myocardial Wall Tension –> Increased MVO2 –> Coronary insufficiency –> Infarction dysrhythmias –> CHF
How does hypertension affect cerebral autoregulation?
Chronic HTN shifts cerebral autoregulation curve to the right
-this adaptation helps the brain tolerate a higher range of blood pressures – however, this comes at expense of not tolerative a lower BP
*malignant HTN increases risk of hemorrhagic stroke and cerebral edema
*hypotension increases risk of cerebral hypoperfusion
What’s the difference between primary and secondary hypertension?
Primary (essential) HTN: has no identifiable cause (more common – 95%)
Secondary HTN: caused by some other pathology (5%)
What are the 6 causes of secondary HTN?
- Coarctation of the aorta
- Renovascular disease
- Hyperadrenocorticism (Cushing’s syndrome)
- Hyperaldosteronism (Conn’s disease)
- Pheochromocytoma
- Pregnancy-induced HTN
What are the two major classes of calcium channel blockers? Examples of each
Dihydropyridines: Nifedipine, Nicardipine, Nimodipine, Amlodipine, Clevidipine
- target vascular smooth muscle (mostly)
- vasodilation via decreasing SVR
Non-Dihydropyridines: Verapamil (phenylalkylamine) and Diltiazem (benzothiazepine)
- target myocardium (mostly)
- decrease chronotropy, inotropy, dromotropy, and coronary vascular resistance
What is the pathophysiology of constrictive pericarditis?
Caused by fibrosis or any condition where the pericardium becomes thicker
- during diastole, ventricles can’t fully relax – reduces compliance and limits diastolic filling
- ventricular pressures increase – creates backpressure to peripheral circulation
- ventricles adapt by increasing myocardial mass – over time this impairs systolic function
What is the anesthetic management of constrictive pericarditis?
Avoid Bradycardia (CO is dependent on HR)
Preserve HR and contractility
- ketamine
- pancuronium
- volatile agents w/ caution
- opioids, benzos, and etomidate are ok
Maintain Afterload
Aggressive PPV can decrease venous return and CO
What is the pathophysiology of pericardial tamponade? How is it diagnosed? What is the treatment?
- Occurs when fluid accumulates inside the pericardium – the excess fluid exerts external pressure on the heart (limits ability to fill and function)
- CVP rises in tandem w/ pericardial pressure (as ventricular compliance deteriorates - CVP and PAOP begin to equalize)
*TEE = best method of diagnosis
*Pericardiocentesis or Pericardiostomy = best treatment
What is Kussmaul’s sign?
Indicates impaired right ventricular filling due to a poorly compliant RV or pericardium
-since RV filling is affected, blood “backs up” causing JUGULAR VENOUS DISTENTION and INCREASED CVP
*most pronounced during inspiration
What two conditions are commonly associated with Kussmaul’s sign?
Constrictive Pericarditis and Pericardial Tamponade
*can occur w/ any condition limiting RV filling
What is Pulsus Paradoxus?
Represents and exaggerated decrease in SBP during inspiration (suggests impaired diastolic filling)
- SBP falls by more than 10mmHg during inspiration
- negative intrathoracic pressure on inspiration –> increased venous return to RV –> bowing of ventricular septum toward LV –> decrease SV –> decreased CO –> decrease SBP
What two conditions are commonly associated with pulsus paradoxus?
Constrictive Pericarditis
Pericardial Tamponade
What is Beck’s Triad? What conditions are associated with it?
Occurs in acute cardiac tamponade
S&S:
- Hypotension (decreased SV)
- Jugular venous distension (impaired venous return to the right heart)
- Muffled heart tones (fluid accumulation in pericardial space)
What are the best anesthetic techniques for the pt w/ acute pericardial tamponade undergoing pericardiocentesis?
Local anesthesia is preferred technique – because hemodynamics are minimally affected
If general is required – primary goal is to preserve myocardial function
-severely decreased SV and increased SNS tone (increased contractility/ increased afterload) provide compensation
*any drug that depresses myocardium or reduces afterload can precipitate CV collapse
What drugs should be avoided in a pt w/ acute pericardial tamponade? What drugs are safer to use?
Drugs to Avoid:
- halogenated anesthetics
- propofol
- thiopental
- high dose opioids
- neuraxial anesthesia
Safer to Use:
- ketamine –best choice
- nitrous oxide
- benzos
- opioids
What 6 patient factors warrant antibiotic prophylaxis against infective endocarditis?
- Previous infective endocarditis
- Prosthetic heart valve
- Unrepaired cyanotic congenital heart disease
- Repaired congenital heart defect if the repair is <6 months
- Repaired congenital heart disease w/ residual defects that have impaired endothelialization at the graft site
- Heart transplant w/ vavuloplasty
What are 3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis?
High risk procedures are thought to be “dirty” where risk of transient bacteremia outweighs risk of antibiotic therapy
- Dental procedures involving gingival manipulation and/or damage to mucosa lining
- Respiratory procedures that perforate mucosal lining w/ incision or biopsy
- Biopsy of infective on the skin or muscle
What are the 3 key determinants of flow through the LVOT?
- Systolic LV volume
- Force of LV contraction
- Transmural pressure gradient
What factors reduce cardiac output in the patient w/ obstructive hypertrophic cardiomyopathy?
Things that narrow LVOT = bad for CO
Increased obstruction and Decreased CO
- decreased systolic volume (decreased preload or increased HR)
- increased contractility
- decreased aortic pressure
What factors improve cardiac output in the patient w/ obstructive hypertrophic cardiomyopathy?
Things that distend LVOT = good for CO
Decreased obstruction and Increased CO
- increased systolic volume (increased preload or decreased HR)
- decreased contractility
- increased aortic pressure
How long should elective surgery be delayed in the patient after a percutaneous coronary intervention?
- Angioplasty w/o Stent: 2-4 weeks
- Bare Metal Stent: 30 days (3 months preferred)
- Drug Eluting Stent (stable ischemic heart disease): 1st gen 12 months – Current gen 6 months
- Drug Eluting Stent (acute coronary syndrome): 12 months minimum
- CABG: 6 weeks (3 months preferred)
What is the difference between alpha-stat and pH-stat blood gas measurement during cardiopulmonary bypass?
Alpha-stat – does NOT correct for pt temperature (aims to keep intracellular charge neutrality across all temps)
*associated w/ better outcomes in adults
pH-stat – corrects for pt temperature (aims to keep a constant pH across all temps)
*associated w/ better outcomes in peds
*as temp decreases, more CO2 will dissolve in the blood - by extension this affects pH
Why is a left ventricular vent used during CABG surgery?
A LV 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?
It 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 CO – deflation correlates with R wave on EKG
What are 4 contraindications to the intra-aortic balloon pump?
- Severe aortic insufficiency
- Descending aortic disease
- Severe peripheral vascular disease
- Sepsis
Describe the Crawford classification system of aortic aneurysms.
- Type 1: all or most of descending thoracic aorta / only upper abdominal aorta
- Type 2: all or most of descending thoracic aorta / most abdominal aorta
- Type 3: only lower descending thoracic / most abdominal aorta
- Type 4: no descending thoracic aorta / most abdominal aorta
Describe Stanford classification system of aortic dissection.
Stanford Type A: involves ascending aorta
Stanford Type B: does not involve ascending aorta
Describe DeBakey classification system of aortic dissection.
- Type 1: tear in ascending aorta + dissection along entire aorta
- Type 2: tear in ascending aorta + dissection only in ascending aorta
- Type 3a: tear in proximal descending aorta + dissection is limited to thoracic aorta
- Type 3b: tear in proximal descending aorta + dissection along thoracic and abdominal aorta
Which law describes the relationship between aortic diameter and risk of aortic rupture in a pt w/ an abdominal aortic aneurysm?
Law of Laplace
- wall tension = transmural pressure x vessel radius
- increased diameter –> increased transmural pressure –> increased wall tension
*mortality increases significantly once AAA reaches 5.5cm
*surgical correction is recommended when aneurysm exceeds 5.5 cm or if it grows more than 0.6-0.8cm a year
How does the aortic cross clamp contribute to the risk of anterior spinal artery syndrome?
Aortic cross clamp placed above the artery of Adamkiewicz may cause ischemia to the lower portion of the anterior spinal cord – can result in anterior spinal artery syndrome (Beck’s Syndrome)
How does anterior spinal artery syndrome present?
- Flaccid paralysis of lower extremities
- Bowel and bladder dysfunction
- Loss of temp and pain sensation
- Preserved touch and proprioception
What is amaurosis fugax?
Blindness in one eye –> sign of impending stroke
*emboli travel from internal carotid artery to ophthalmic artery, which impairs perfusion of optic nerve and causes retinal dysfunction
What information does an EEG monitor give you?
- Monitors cortical electrical function (does not detect subcortical problems)
- Risk of cerebral hypoperfusion w/ loss of amplitude, decreased beta-wave activity and/or appearance of slow wave activity
*High incidence of false-negatives
What conditions can lead to false conclusions on a EEG?
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 technique can be used for the patient undergoing carotid endarterectomy? What levels must be blocked?
- Cervical plexus block (superficial or deep)
- Local infiltration
-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 right endarterectomy. Her airway is completely obstructed. What is the best treatment at this time?
Pt requires emergency decompression of the surgical site
-if surgeon isn’t immediately available – you must do it
Cricothyroidotomy may be required
