CV pathophysiology Flashcards
high risk procedures for a patient with CAD include (4)
emergency surgery (esp in elderly)
open aortic surgery
peripheral vascular surgery
long surgical procedures with volume shifts and/or blood loss
general risk factors for cardiac risk patients include (6)
high risk surgery
hx of ischemic heart disease (unstable angina confers greatest risk of perioperative MI)
CHF
CVD
DM
serum creatinine >2
risk of reinfarction after MI is:
>6 mo:
3-6 mo:
<3 mo:
> 6 mo: 6%
3-6 mo: 15%
<3 mo: 30%
intermediate risk surgeries include (5)
CEA
head and neck surgery
intrathoracic or inter peritoneal surgery
ortho surgery
prostate surgery
low risk surgeries include (5)
endoscopic procedures
cataract surgery
superficial procedures
breast surgery
ambulatory procedures
NYHA classification, level of impairment, and functional limitation (4 classes)
which classes of NYHA patients should be referred to a cardiologist before surgery
class 3 or 4
unless its a minor procedure under MAC
PAOP is a surrogate for
LVEDP
ex) CPP=DBP-LVEDP but only have PAOP
CKMB initial elevation, peak elevation, return to baseline after MI
initial: 3-12h (same as Troponin I and T)
peak elevation: 24h
return to baseline: 2-3d
Troponin I initial elevation, peak elevation, return to baseline after MI
initial: 3-12h (same as CKMB and troponin T)
peak elevation: 24h
return to baseline: 5-10d
Troponin T initial elevation, peak elevation, return to baseline after MI
initial: 3-12h (same as CKMB and Troponin I)
peak elevation: 12-48h
return to baseline: 5-14d
best leads to use to detect an MI and WHY
leads II, V5.
lead II: aids in ID of inferior wall ischemia. also monitors for dysrhythmias where QRS is narrow and P wave is crucial for dx
V5: classic teaching says this is best for LV ischemia but new data says maybe V3/4 is best,
CHOOSE V4 on NCBRNA***
CVP and PAOP may over estimate LVEDV for any condition that does what?
reduces ventricular compliance
name examples that would shift the compliance curve to the red (highest) (5)
age >60y
ischemia
pressure overload hypertrophy (aortic stenosis or HTN)
hypertrophic obstructive cardiomyopathy
pericardial pressure (increased external pressure)
etiology of HFrEF (systolic failure)
pumping problem
MI
valve insufficiency
dilated cardiomyopathy
etiology of HF with preserved EF (diastolic failure) (7)
filling problem
MI
valve stenosis
HTN
hypertrophic cardiomyopathy
cor pulmonale **
obesity*
compare systolic HF and diastolic HF in terms of
EDV
EDP
ESV
SV
LV mass
LV geometry
which drugs can reverse cardiac remodeling
ACEI’s and spironolactone (aldosterone antagonists)
compare anesthetic management of systolic HF and diastolic HF in terms of
preload
afterload
contractility
HR
most common cause of RV failure
LV failure
tx for RV failure includes
inotropes (milrinone, dobut)
pulmonary vasodilators (inhaled NO or sildenafil, PDE5)
reverse cause of increased PVR
conditions that increase PVR (5)
increased PEEP
N2O
Hothermia
acidosis
hypercarbia
list 4 physiologic adaptations of HF
- SNS activation
- excessive vasoconstriction
- fluid retention
- myocardial remodeling
3 physiologic functions of BNP
- natriuresis
- diuresis
- vasodilation
how does CHF effect beta receptors?
causes down regulation of beta receptors
most common cause of constrictive pericarditis
cardiac surgery
the patient has an aortic balloon pump. which part of this arterial BP waveform corresponds with diastolic augmentation and improvement of coronary BF?
remember balloons inflates during diastole. pressure is higher than unassisted systole. balloon deflates during systole to decrease after load.
which region of the pressure volume loop corresponds to S3 heart sound?
best heard during the middle 1/3 of diastole after S2 (aortic valve closure)
gallop, suggestive of HF but can be a normal finding in children and teens.
with a patient who has an LVAD, CO is highly dependent on
preload
mnemonic for debakey classification of aneurysm: BAD
B: both (type 1)
A: ascending (type 2)
D: descending (type 3)
stage 1 HTN
130-139 SBP OR 80-89 DBP
stage 2 HTN
SBP >140 OR DBP >90
stage 3 HTN (hypertensive crisis)
SBP >180 and/or DBP >120
cerebral auto regulation happens between a CPP of
50-150mmHg
what does chronic HTN do to cerebral auto regulation
SBP and DBP that permit anesthesia delay
SBP >180 and DBP >110
when does a HTN crisis turn into a HTN emergency
evidence of end organ damage ex) encephalopathy, stroke, papilledema, CHF, renal dysfunction
coarctation of aorta clinical findings and diagnostic tests
clinical findings: upper limb BP > lower limb BP, weak femoral pulse, systolic bruit, HTN
dx tests: aortography, echo, CT/MRI
renovascular disease clinical findings (3) and diagnostic tests (4)
clinical findings: HTN, bruit, severe HTN in young patient
dx tests: CT angiography, MRA, aortography, duplex ultrasonography
hyperadrenocorticism (cushings disease) clinical findings and diagnostic tests
clinical findings: HTN*, weight gain (truncal obesity), hyperglycemia, muscle and bone weakness, weakened immunity, hirsutism, moon face
dx: dexamethasone suppression test, glucose tolerance test, urinary cortisol, adrenal CT/MRI
hyperaldosteronism (conns disease) clinical findings and diagnostic tests
clinical findings: HTN*, hypokalemia, alkalosis, fatigue/weakness, parasthesia, nocturnal polyuria/polydipsia
dx: Cp aldosterone, Cp renin, Cp K, urinary potassium
pheochromocytoma clinical findings and diagnostic tests
clinical findings: HA, palpitations, diaphoresis
dx: plasma metanephrines, urinary catecholamines, urinary vanillylmandelic acid (VMA)
pregnancy induced HTN clinical findings (4) and diagnostic tests (4)
clinical findings: peripheral and pulmonary edema, HA, sz, RUQ pain
dx: urinary protein, platelet count, uric acid, CO
how alpha 1 antagonists decrease BP
decrease iCa2+ and decrease SVR
how B1 antagonists decrease BP
decrease inotropy, chronotropy, HR, dromotropy, and renin release from juxtaglomerular apparatus
selective B1 antagonists
acebutolol
atenolol
bisoprolol
esmolol
metoprolol
non selective b1 and b2 antagonists
nadolol
pindolol
propanolol
sotalol
timolol
mixed a1/b1/b2 antagonists
bucindolol, carvedilol, labetalol
how a2 agonists decrease BP
decrease SNS outflow
how CCB’s (dihydropiridines) decrease BP
decrease intravascular calcium and decrease SVR
how CCB’s (non dihydropiridines including verapamil and diltiazem) decrease BP
targets myocardium more than vessels
deceased inotropy, chronotropy, dromotropy, svr
what hydralazine dilates primarily and how it decreases BP
arteriodilator that increases NO and decreases SVR (after load)
what SNP dilates primarily and how it decreases BP
equal arterial and venodilator and increases NO, decreases SVR (after load) and decreases venous return (preload)
what NTG primarily dilates and how it decreases BP
primarily venules, increases NO, decreases venous return (pre load)
MOA of ACEI’s
inhibits ATII mediated vasoconstriction and inhibits aldosterone release
MOA of AT2 receptor blockers
inhibits ATII mediated vasoconstriction and inhibits aldosterone release
MOA of loop diuretics and examples
Inhibits Na/K/2Cl transporter in thick portion of ascending loop of henle. increased diuresis and decreased venous return
ex) furosemide, bumetanide, ethacrynic acid
MOA of thiazide diuretics and examples
inhibits Na/Cl transporter in distal convoluted tubule
diuresis- decreased venous return
ex) HCTZ, metolazone, indapamide, chlorthalidone
MOA of K sparing diuretics and examples
inhibits K excretion and Na reabsorption by principal cells in collecting ducts.
acts independently of aldosterone
ex) triamterene, amiloride
MOA of aldosterone antagonists and examples
inhibits K excretion and Na reabsorption by principal cells in collecting ducts.
blocks aldosterone at mineralocorticoid receptors
ex) spironolactone
compare and contrast dihydropiridines and non dihydropiridines in terms of
target
clinical effects
examples
which CCB impairs contractility the most
verapamil
only CCB shown to reduce M&M from cerebral vasospasm
nimodipine
clevidipine MOA
arterial vasodilator that reduces SVR without affecting preload
contraindications to clevidipine (3)
allergy to eggs, soy, egg products, soy products, severe AS***, impaired lipid metabolism
compare and contrast constrictive and acute pericarditis in terms of
cause
s/sx
tx
anesthetic management
becks triad
JVD (decreased venous return to right heart)
HoTN (decreased SV)
muffled heart tones (fluid accumulation around sac)
does pericardial effusion affect diastolic filling time or ventricular compliance
no because it doesn’t increase pericardial pressure
best method of dx for cardiac tamponade
TEE
what pathophysiological issue is outlined by this pressure volume loop (green part)
cardiac tamponade. decreased LVEDV (loop shifts to left), decreased SV (loop is narrower), decreased ventricular compliance (notice higher slope during ventricular filling)
presentation of cardiac tamponade
becks triad (muffled heart tones, HTN, JVD), pulsus paradoxus, kussmauls sign (increased CVP and JDV during inspiration), reduced EKG voltage, compression of heart, lungs, trachea, esophagus
drugs to avoid and drugs that are safe to use during cardiac tamponade as well as other anesthetic management techniques
maintain SNS since SV is severely decreased and this helps with compensation
maintain spontaneous ventilation- PPV can impair venous return and CO
-local anesthesia is preferred for pericardiocentesis with spontaneous ventilation
hemodynamic goals for cardiac tamponade:
HR
preload
contractility
afterload
HR: maintain. since SV is reduced, CO is dependent on HR
preload: maintain or increase.
contractility: maintain or increase (inotropes)
afterload: maintain. essential to decrease SV and CO
patients at high risk for infective endocarditis that need prophylactic abx (6)
previous infective endocarditis
prosthetic heart valve
unprepared cyanotic congenital heart disease
repaired congenital heart defect if repair is less than 6 months old
repaired congenital heart defect that have residual effects and impaired endothelialization at the graft site
heart transplant with valvuloplasty
abx prophylaxis is not required for patients with a hx of (3)
unrepaired cardiac valve disease including mitral valve prolapse
CABG
coronary stent placement
procedures where abx prophylaxis to protect against endocarditis include
dental procedures with gingival manipulation and/or damage to mucosal lining
resp procedures that perforate mucosal lining with incision or biopsy
biopsy of infective lesions in skin or muscle
IV abx of choice if PCN allergic
clinda 600mg or for peds 20mg/kg
three things that determine BF through LVOT
- systolic LV volume
- force of LV contraction (decreasing contractility decreases obstruction and increases CO)
- transmural pressure
LVOT is caused by
congenital hypertrophy of intraventricular septum
systolic anterior motion of anterior leaflet of mitral valve. occurs during systole!
if the patient has bare metal stent, delay surgery for
30 days
how long to wait for surgery if patient got angioplasty without stent
2-4 weeks
for stable ischemic heart disease, first generation drug eluding stents you should wait ______ months and current generation you can wait ______ months
12 months minimum for first gen
6 months minimum for current gen
for acute coronary syndrome, wait for surgery after insertion of drug eluding stent for
12 months minimum
after a CABG, wait how long until surgery
6 weeks
3 months preferred
stop ASA how many days before surgery if not absolutely contraindicated?
3 days
stop clopidogrel how many days before surgery
7 days
stop ticlodipine how many days before surgery
14 days
best outcome for stent occlusion is if intervention happens in
<90m
key facts of roller pump for CPB
compresses blood tubing that mechanically pumps blood forward
pump flow remains constant regardless of afterload
roller pump is more likely to entrain air if venous reservoir runs dry, which can lead to air embolism
key facts of centrifugal pump for CPB
non occlusive, uses gravity and spins blood through a cone.
less traumatic to blood cells
reduces pressure if increased after load is detected and has less chance of VAE
does have lack of an occlusion point. therefore if theres an excessively high after load, blood backs up towards venous circulation which reduces patients circulating BV.
oxygenator in CPB
point in CPB where gas exchange occurs.
membrane oxygenator uses blood membrane gas interface. safer.
you can prime CPB with
blood or balanced salt solution (mannitol, albumin, heparin, HCO3-)
ACT for CPB
> 400 seconds
where is anterograde cardioplegia introduced
aortic root (where circulation gets to coronary arteries). aortic valve must be competent and the aorta must be clamped.
where is retrograde cardioplegia introduced
coronary sinus
the tip of an aortic balloon pump should be positioned
2cm distal to the left SCA
indications for IABP (4)
cardiogenic shock
MI
intractable angina
difficult separation from CPB
contraindications for IABP (4)
severe AI
descending aortic disease (aneurysm)
severe PVD
sepsis
how to confirm position of IABP (3 tests)
CXR, fluoro, TEE
outline arterial waveform and IABP
inflation correlates with dichrotic notch on aortic pressure wave form
deflation of IABP during systole correlates with what on EKG
R wave
when a patient has an LVAD, CO is dependent upon (3)
- LV preload
- Pump speed
- pressure gradient across the pump (after load)
how LVAD works
pumps blood from LV to aorta
inflow of cannula is inserted into apex of LV. blood is returned to aorta through outflow cannula
with an LVAD, what are some issues the patient cannot have in order to receive it (4)
PFO, AI, tricuspid regurgitation, competent aortic valve
if a patient has an LVAD and the flow is non pulsatile how can you measure SpO2/NIBP (3)
aline, serial ABG’s, cerebral oximetry
describe LV suck down when patient has LVAD
LV preload low, pump speed high. part of LV is sucked into LV cavity-occludes inflow cannula
five IVF and reduce pump speed
outline the crawford classification of aortic aneurysms
Type 1: outlines all or most of descending aorta and only upper part of abdominal aorta
Type 2: outlines all or most of descending aorta and most of of abdominal aorta
Type 3: only lower part of descending thoracic aorta and most of abdominal aorta
Type 4: none of descending thoracic aorta and most of abdominal aorta
classification of aortic dissection: stanford
type A: involves ascending aorta
type B: does not involve ascending aorta
classification of aortic dissection: debakey
BAD mnemonic
type 1: tear in ascending aorta and dissection along entire aorta
type 2: tear in ascending aorta and dissection only in ascending aorta
type 3: tear in proximal descending aorta with
3a: dissection limited to thoracic aorta
3b: dissection along thoracic and abdominal aorta
which crawford type aneurysms are the most difficult to repair
crawford type 2 and 3
which kind of aortic dissections are a surgical emergency
debakey 1 or 2 or stanford a (consider AI as well). this involves acute dissection of ascending aorta
dissection of descending aorta management
medical
how is AAA most commonly detected and what is the triad
pulsatile abdominal mass
HoTN, back pain, pulsatile abdominal mass
most aneurysms rupture in left retroperitoneum
most common cause of postop death after AAA repair
MI
which factors increase following cross clamp removal during AAA repair
PVR and total body O2 consumption increase
applying aortic cross clamp creates central hypervolemia by
reducing venous capacity
shifting greater proportion of blood volume to proximal clamp
increasing venous return
removing aortic cross clamp creates central hypovolemia by
restoring venous capacity
shifting greater proportion of blood to lower body
decreasing venous return
creating capillary leak that contributes to loss of intravascular volume
what is an EVAR
minimally invasive approach for correcting AAA
anesthetic management of EVAR patient
continuously monitor BP with aline
patient will receive IV contrast dye
maintain UOP
describe endoleak
when original graft fails to prevent blood from entering aortic sac. some resolve spontaneously while some need a new graft or open repair
2 posterior spinal arteries
aorta–> segmental a–> posterior radicular a –>posterior spinal artery
aorta –> SCA –> vertebral artery –>posterior spinal artery
what part of SC does posterior spinal arteries perfuse
posterior 1/3 of SC (in green)
what part of SC does anterior spinal artery perfuse
anterior 2/3 of SC (yellow)
where does artery of adamkeweisz most commonly originates from
T11-12
becks syndrome aka anterior spinal artery syndrome sx
flaccid paralysis of LE’s
bowel and bladder dysfunction
loss of temperature and pain sensation
touch and proprioception are preserved
which spinal tracts are perfused via anterior blood supply
corticospinal tract (motor, flaccid paralysis)
autonomic motor fibers (bowel and bladder dysfunction)
spinothalamic (sensory tract, loss of pain and temperature sensation)
spinal cord protection strategies during thoracic cross clamp includes
moderate hypothermia (30-32c)
CSF drainage
proximal HTN during xclamp (MAP 100)
avoidance of hyperglycemia
SSEP/MEP monitoring
partial CPB (LA to femoral artery)
drugs (corticosteroids, CCB’s, and/or mannitol)
what does SSEP monitor
only monitors posterior cord
sign of impending stroke during CEA
amaurosis fugax (blindness in one eye)
emboli travel from ICA to ophthalmic artery
ways to monitor neurological integrity and cerebral perfusion
keep patient awake
EEG
cerebral oximetry
transcranial doppler
SSEP
carotid stump pressure
after aortic cross clamping, reduce aortic BP to <
145mmHg systolic
postop considerations for CEA
hematoma
RLN injury
hemodynamic instability
carotid denervation
carotid artery angioplasty stenting (CAS)
uses percutaneous trans vascular access to pass stent into carotid artery
maintain ACT >250s
balloon inflation can activate baroreceptor reflex, pretx
filter placed beyond angioplasty balloon
embolic CVA treated with recombinant tissue plasminogen activator
in the patient with right subclavian steal syndrome, arterial flow is diverted from the
right vertebral artery to right SCA
describe subclavian steal syndrome
occlusion of sublavian or innominate a. proximal to origin of ipsilateral vertebral artery
-results in reversal of BF where vertebral BF flows toward ipsilateral SCA
s/sx subclavian steal syndrome (think brain and ipsilateral arm)
syncope, vertigo, ataxia, hemiplegia
arm ischemia, weak pulse
3 best EKG leads to monitor for intraop ST changes
V3, V4, V5
most common cause of secondary HTN
renal artery stenosis
dresslers syndrome
acute pericarditis after MI
