UNIT 3 Cardiovascular Flashcards
define: chronotropy, inotropy, dromotropy, & lusitropy
chronotropy: HR
inotropy: contractility
dromotropy: conduction velocity
lusitropy: rate of myocardial relaxation
describe the function of the Na+ K+ pump
maintains the cell’s resting potential; separates charge across the cell membrane keeping the inside of teh cell relatively negative & the outside relatively positive
list the 5 phases of the ventricular AP & describe the ionic movement during each phase
0 = depolarization (Na+ influx) 1 = initial repol (K+ efflux & Cl- influx) 2 = plateau (Ca++ influx) 3 = repol (K+ influx) 4 = restoration of resting membrane potential (Na+/K+ pump)
list the 3 phases of the SA node AP & describe the ionic movement during each phase
4 = spontaneous depol (leaky to Na+) 0 = depol (Ca++ influx) 3 = repol (K+ efflux)
what process determines the intrinsic HR, and what physiologic factors alter it?
HR is determined by the rate of spontaneous phase 4 depol in the SA node
increase HR by manipulating 3 variables:
- rate of spont phase 4 depolarization
- threshold becoming more negative
- resting membrane potential becoming less negative
what is the calculation for MAP?
SBP/3 + 2DBP/3
OR
[(COxSVR)/80] + CVP
what is the formula for SVR?
[(MAP-CVP)/CO]x80
normal 800-1500 dynes/sec/cm^5
what is the formula for PVR?
[(MPAP-PAOP)/CO]x80
normal 150-250dynes/sec/cm^5
describe the frank-starling releationship
relationship b/n preload (ventricular volume) & CO (ventricular output)
- increased preload –> increased myocyte stretch –> increased ventricular output
the increase in output d/t increased preload only occurs to a point
- after this point, overstretch occurs to the ventricular sarcomeres –> decrease in # of cross bridges that can be formed –> decreased CO
what factors affect myocardial contractility?
increased:
- SNS stimulation, catecholamines
- calcium
- digitalis
- PDE inhibitors
decreased
- myocardial ischemia
- severe hypoxia
- acidosis
- hypercapnia
- hyperkalemia
- hypocalcemia
- IA, propofol
- BB, CCB
discuss excitation-contraction coupling in the cardiac myocyte
myocardial cell membrane depolarizes
- during phase 2: Ca++ enters via L-type Ca++ channels in T tubules
- Ca++ influx turns on ryanodine 2 receptor, which releases Ca++ from sarcoplasmic reticulum
- Ca++ binds troponin C (myocardial contraction)
- Ca++ unbinds troponin C (myocardial relaxation)
- most of Ca++ is returned to sarcoplasmic reticulum via SERCA2 pump
- Ca++ binds a storage protein (calsequesterin) inside the sarcoplasmic reticulum
what is afterload & how do you measure it in the clinical setting?
afterload = the force the ventricle must overcome to eject it’s SV
we can use SVR/PVR
SVR = [(MAP-CVP)/CO]x80 PVR = [(mPAP-PAOP)/CO]x80
what law can be used to describe ventricular afterload?
Laplace
wall stress = PR/thickness
- intraventricular pressure is the force that pushes teh heart apart
- wall stress is the force that holds the heart together
wall stress is reduced by
- decreased intraventricular pressure
- decreased radius
- increased wall thickness
list 3 conditions that set afterload proximal to the systemic circulation
- aortic stenosis
- hypertrophic cardiomyopathy
- coarctation of the aorta
use the wiggers diagram to explain the cardiac cycle
pay attention to the following:
- where systole & 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 (L lower baseline)
- reduced filling (later baseline)
- atrial kick (L lower corner)
- isovolumic contraction (R pressure increase)
- ejection (top slope)
- isovolumic relaxation (L pressure decrease)
how do you calculate ejection fraction?
measure of systolic function (contractility). % of blood that is ejected from the heart during systole
SV/EDV x100
normal 60-70%
LV dysfunction when EF <40%
SV = EDV-ESV
can you calculate the SV and/or EF with a pressure volume loop?
yes
SV = width of loop EDV = righ side of loop at X axis
what is the best TEE view for diagnosing myocardial ischemia?
midpapillary muscle level in short axis
what is the equation for CPP?
CPP = aortic DBP - LVEDP
what region of the heart is most susceptible to myocardial ischemia? Why?
LV subendocardium
- best perfused during diastole
- as aortic pressure increases, LV tissue compresses its own blood supply & reduces BF (this area has high compressive pressure)
what factors affect myocardial oxygen supply & demand?
decreased supply:
- decreased coronary flow (tachycardia, decreased aortic pressure, decreased vessel diameter, increased end diastolic pressure)
- decreased CaO2 (hypoxemia, anemia)
- decreased O2 extraction (L shift of HgB dissociation curve, decreased capillary density)
increased demand
- tachycardia
- HTN
- SNS stimulation
- increased wall tension
- increased end diastolic volume
- increased afterload
- increased contractility
discuss the NO pathway of vasodilation
NO = smooth m relaxant –> vasodilation
NO synthase catalyzes conversion of L-arginine to NO
- NO diffuses from endothelium to smooth m
- NO activates guanylate cyclase
- guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate
- increased cGMP decreases intracellular Ca++ –> smooth m relaxation
- phosphodiesterase deactivates cGMP to guanosine monophosphate (deactivates NO mechanism)
where do the heart sounds match up on the LV pressure volume loop?
S1 = closure of MV & TV (right lower corner) S2 = closure of AV & PV (left upper corner) S3 = may suggest systolic dysfunction (L bottom baseline) S4 = may suggest diastolic dysfunction (R bottom baseline)
what are the two primary ways a heart valve can fail
stenosis:
- 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: leaky
- some blood flows forward & some blood flows backward during chamber systole
how can the heart compensate for pressure overload? volume overload?
volume overload:
- eccentric hypertrophy
- sarcomeres are added in series
pressure overload
- concentric hypertrophy
- sarcomeres are added in parallel
describe pressure volume loops for the following pathophysiologies:
- mitral stenosis
- aortic stenosis
- mitral regurg (acute & chronic)
- aortic regurg (acute & chronic)
mitral stenosis:
- short, L shifted
aortic stenosis:
- tall, R shifted
aortic regurg
- acute: R shifted, decreased pressure, and diagonal isovolumetric relaxation
- chronic: enlarged volume, no change in pressure, diagonal isovolumetric relaxation
mitral regurg:
- acute: R shifted, decreased pressure, diagonal isovolumetric contraction
- chronic: enlarged volume, decreased pressure, diagonal isovolumetric contraction
list the hemodynamic goals for the 4 common valvular defects.
aortic stenosis: slow HR, high preload, high/normal afterload, SR
aortic regurg: high HR, high/normal preload, low SVR
mitral regurg: high HR, high preload, low SVR, avoid increased PVR
mitral stenosis: slow/normal HR, avoid increased PVR
what is the most common dysrhythmia associated w/ mitral stenosis?
afib
list 6 risk factors for perioperative cardiac M&M for noncardiac surgery.
high risk surgery hx of ischemic heart disease (unstable angina = greatest risk of peri-op MI) hx of CHF hx of CVA DM Cr>2
what is the risk of perioperative MI in the patient w/ previous MI
general pop = 0.3%
MI >6mo = 6%
MI 3-6mo = 15%
MI <3 mo = 30%
highest risk of reinfarcation is w/in 30 days of an acute MI
- ACC/AHA recommends at least 4-6 weeks before elective surgery
categorize high, medium, and low risk surgical procedures according to cardiac risk
high (>5%):
- emergency (esp in elderly)
- open aortic surgery
- peripheral vascular surgery
- long surgical procedures w/ significant volume shifts/blood loss
intermediate (1-5%):
- carotid endarterectomy
- head & neck surgery
- intrathoracic/intraperitoneal surgery
- orthopedic surgery
- prostate surgery
low (<1%):
- endoscopic procedures
- cataract surgery
- superficial procedures
- breast surgery
- ambulatory procedures
what is the modified new york association functional classification of heart failure?
class I: asymptomatic class II: symptomatic w/ moderate activity class III: symptomatic w/ mild activity class IV: symptomatic at rest
how do you interpret cardiac enzymes in the patient w/ a suspected ischemic event?
a cell requires O2 to maintain integrity of it’s cell membrane, and when deprived of O2, it dies & releases it’s contents into the systemic circulation
- myocardium releases creatine kinase-MB, troponin I, and troponin T
- troponins are more sensitive than CK-MB for MI diagnosis
- values must be evaluated in the context of the patient’s EKG
CK-MB: elevation 3-12hrs, peaks in 24hrs, returns to baseline in 2-3 days
troponin I: elevation 3-12hrs, peaks 24hrs, returns to baseline in 5-10 days
troponin T: elevation in 3-12hrs, peaks 12-48hrs, returns to baseline in 5-14days
how do you treat intraoperative MI?
goals: make the heart slower, smaller, and better perfused (improve supply, decreased demand):
- slow/normal HR (use BB or pacing, anticholinergic)
- optimize BP (increase IA, vasodilator/vasoconstrictor)
- decrease PAOP w/ NTG or inotrope
what factors reduce ventricular compliance?
age >60yrs ischemia pressure overload hypertrophy (i.e. aortic stenosis/HTN) IHHS pericardial pressure (external)
take away point: higher filling pressures are required to prime the ventricle
what is the difference b/n systolic & diastolic heart failure?
systolic: the ventricle doesn’t empty well
- hallmark = decreased EF w/ an increased end diastolic volume. Volume overload commonly causes systolic dysfunction
diastolic: the ventricle doesn’t fill well
- when the heart is unable to relax and accept the incoming volume b/c compliance is reduced. defining characteristic = symptomatic heart failure w/ normal EF
compare and contrast the hemodynamic goals in the patient w/ systolic vs. diastolic HF
systolic:
- preload is already high (can use diuretics if too high)
- decreased afterload to reduce workload (SNP), but maintain CPP
- augment contractility as needed
- HR is usually high d/t increased SNS (& CO is HR dependent)
diastolic
- preload required to stretch noncompliant (LVEDP doesn’t correlate w/ LVEDV)
- keep high afterload to perfuse thick myocardium
- normal contractility
- slow/normal HR to increase diastolic time
list 6 complications of HTN
LVH ischemic heart disease CHF arterial aneurysm stroke ESRD
how does HTN contribute to CHF?
HTN –> increased myocardial wall tension –> LVH –> myocardium O2 extraction –> coronary insufficiency –> CHF, infarctions, dysrhythmias
(all patho leads to one another)
how does HTN affect cerebral autoregulation?
chronic HTN shifts the curve to the R, allowing the patient’s brain to tolerate a higher range of blood pressures. The pt is then not able to tolerate a lower blood pressure.
What’s the difference b/n primary & secondary HTN?
primary (essential) - more common (95%) & no identifiable cause
secondary - caused by some other pathology (5%)
list 7 causes of secondary HTN.
coarctation of the aorta renovascular disease hyperadrenocorticism (Cushing's) hyperaldosteronism (Conn's) pheochromocytoma pregnancy-induced HTN
What are the 2 major classes of calcium channel blockers? List examples of each.
dihydropyridines (mostly vascular smooth muscle vasodilation & decrease in SVR)
- nifedipine
- nicardipine
- nimodipine
- amlodipine
non-dihydropyridines (mostly myocardium: decrease in HR, contractility, conduction velocity, coronary vascular resistance)
- verapamil
- diltiazem
describe the pathophysiology of constrictive pericarditis
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 a 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 HR dependent: avoid bradycardia!
preserve HR & contractility
- ketamine
- pancuronium
- IA w/ caution
- opioids, benzos, etomidate OK
maintain afterload
aggressive PPV can decrease venous return & 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 an external pressure on the heart, limiting it’s ability to fill & act like a pump.
CVP rises in tandem w/ pericardial pressure. As ventricular compliance deteriorates, L & R diastolic pressure (CVP & PAOP) begin to equalize. LV pressure increases & volume decreases –> decreased coronary perfusion, decreased SV, decreased CO –> increased contractility, HR, RAAS activation
TEE is the best method of diagnosis
TX : pericardiocentesis or pericardiostomy
What is Kussmaul’s sign?
JVD or an increased CVP (most pronounced during inspiration). indicates impaired RV filling d/t a poorly compliant RV or pericardium.
List two conditions commonly associated w/ Kussmaul’s sign
can occur w/ any condition that limits RV filling.
make sure you associate Kussmaul’s sign w/ constrictive pericarditis & pericardial tamponade
What is pulsus paradoxus?
an exaggerated decrease in SBP during inspiration (SBP falls by >10mmHg). Suggests impaired diastolic filling
negative intrathoracic pressure on inspiration –> increased venous return to RV –> bowing of ventricular septum toward LV –> decreased SV –> decreased CO –> decreased SBP
List 2 conditions commonly associated w/ pulsus paradoxus
Like Kussmaul’s sign, you should also associate pulsus paradoxus w/ constrictive pericarditis & pericardial tamponade
What is Beck’s triad? What conditions are associated w/ it?
occurs in those w/ acute cardiac tamponade.
- hypotension (decreased SV)
- JVD (impaired venous return to RV)
- muffled heart tones (fluid accumulation in pericardial space attenuating sound waves)
what are the best anesthetic techniques for the patient w/ acute pericardial tamponade undergoing pericardiocentesis?
because hemodynamics are minimally affected, local anesthesia is preferred.
If GA is required, your primary goal is to preserve myocardial function. SV is severely decreased & increased SNS tone provide compensation.
avoid drugs that depress myocardium or decrease afterload (can precipitate CV collapse)
- IA
- propofol
- TPL
- high dose opioids
- neuraxial
better to use: ketamine, N2O, benzos, opioids
list 7 patient factors that 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 <6mo old
- repaired congenital heart defect w/ residual defects that have impaired endothelialization at the graft site
- heart transplant w/ valvuloplasty
list 3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis
high risk procedures that 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 the mucosa lining
- respiratory procedures that perforate the mucosal lining w/ incision or biopsy
- biopsy of infective lesions on the skin or muscle
What are the 3 key determinants of flow through the LV outflow tract?
systolic LV volume
force of LV contraction
transmural pressure gradient
What factors tend to reduce cardiac output in the patient w/ obstructive hypertrophic cardiomyopathy?
things that distend the LVOT are good for CO, while things that narrow the LVOT are bad.
- systolic LV volume (distended by increased preload, HR, narrowed by decreased preload, HR)
- force of LV contraction (distended by decreased contractility, narrowed by increased contractility)
- transmural pressure gradient - pressure distends the LVOT (distended by increased Ao pressure, narrowed by decreased Ao pressure)
What hemodynamic conditions reduce CO in the patient w/ hypertrophic cardiomyopathy?
increased HR (tx w/ BB, CCB) increased contractility (tx w/ BB or CCB) decreased preload (tx volume) decreased afterload (tx phenylephrine)
How long should elective surgery be delayed in the patient w/:
- bare metal stent
- drug eluting stent
- s/p angioplasty
- s/p CABG
bare metal: 30 days (3 mo preferred)
drug eluting: 6-12mo (6 mo for newer generation, 12 for older)
s/p angioplasty: 2-4 weeks
s/p CABG: 6 weeks (3mo preferred)
What is the difference b/n alpha-stat and pH-stat blood gas measurements during CPB?
because the solubility of a gas is a function of temperature, it should make sense that hypothermia complicates interpretation of blood gas results during CPB. As temp decreases, more CO2 is able to dissolve in the blood. By extension, this affects the pH
alpha-stat: does not correct for patient’s temperature. Aims to keep intracellular charge neutrality across all temperatures. It is associated w/ better outcomes in adults
pH-stat: corrects for the patient’s temperature. Aims to keep a constant pH across all temperatures. It is associated w/ better outcomes in peds.
Why is an LV vent used during CABG surgery?
Removes blood from LV. This blood usually comes from the Thebesian veins & bronchial circulation (anatomical shunt)
How does the intraaortic balloon pump function throughout the cardiac cycle? How does it help the patient?
counter pulsation device that improves myocardial O2 supply while reducing myocardial O2 demand
diastole:
- pump inflation augments coronary perfusion
- inflation correlates w/ dicrotic notch on aortic pressure waveform
systole:
- pump deflation reduces afterload & improves CO
- deflation correlates w/ R wave on EKG
List 4 contraindications to intra-aortic balloon pump.
- severe aortic insufficiency
- descending aortic dz
- severe PVD
- sepsis
Describe the Crawford classification system of aortic aneurysms.
of thoracoabdominal aneurysms
type 1: all or most of descending thoracic aorta & only upper abdominal aorta
type 2: all or most of descending thoracic aorta & most of abdominal aorta
type 3: only the lower descending thoracic aorta & most of abdominal aorta
type 4: none of the descending thoracic aorta but most of the abdominal aorta
Describe the Debakey & Stanford classification systems of aortic dissection.
Stanford:
- A = involves ascending aorta
- B = doesn’t involve ascending aorta
DeBakey:
- Type 1 = tear in ascending + dissection along entire aorta
- Type 2 = tear in ascending + dissection only in ascending aorta
- Type 3 = tear in proximal descending aorta w/:
3a = dissection limited to thoracic aorta
3b = dissection along thoracic & abdominal aorta
Which law describes the relationship b/n aortic diameter & risk of aortic rupture in the patient w/ a AAA
LaPlace
wall tension = transmural pressure * vessel radius
T=PR
increased diameter –> increased transmural pressure –> increased wall tension
mortality increases significantly once AAA reaches 5.5cm; surgical correction is recommended at this time or if it’s growing >0.6-0.8cm/yr
How does the aortic cross clamp contribute to the risk of anterior spinal artery syndrome?
placed above the artery of Adamkiewicz may cause ischemia to the lower portion of the anterior SC. This can result in anterior spinal artery syndrome (aka Beck’s syndrome).
How does anterior spinal artery syndrome present?
flaccid paralysis of LE
bowel/bladder dysfunction
loss of temp/pain sensation
preserved touch & proprioception
What is amaurosis fugax?
blindness in one eye, a sign of impending stroke
emboli travel from the ICA to the opthalmic artery, which impairs perfusion of the optic nerve & causes retinal dysfunction
A patient is undergoing CEA w/ EEG monitoring. What does this monitor tell you, and what conditions can lead to false conclusions?
monitors cortical electrical function (doesn’t detect subcortical problems)
- risk of cerebral hypoperfusion w/ loss of amplitude, decreased beta wave activity, and/or slow wave activity
- high incidence of false negatives (hypercarbia, hypoxia, seizures, hypothermia, ketamine, N2O, light or too heavy anesthesia, opioids)
What regional technique can be used for the patient undergoing a CEA? What levels must be blocked?
cervical plexus block (superficial or deep)
local infiltration
regional must cover C2-C4
What reflex can be activated during CEA or following carotid balloon inflation?
baroreceptor
A pt in the PACU develops a hematoma following R CEA. Her airway is completely obstructed. What is the best treatment at this time?
The pt requires emergency decompression of the surgical site. If the surgeon isn’t readily available, this falls on you. Cricothyroidotomy may be required.
