Cardiovascular Flashcards
Describe the function of the Na/K Pump
-maintains the cell’s RMP by keeping the inside of the cell (-) and the outside of the cell (+)
-Removes 3 Na+, brings in 2 K+
List the five phases of ventricular action potential
Phase 0 = depolarization = Na influx
Phase 1 = initial repolarization = K efflux and Cl influx
Phase 2 = plateau = calcium influx
Phase 3 = repolarization = k+ efflux
Phase 4 = Na+ / K + pump restores RMP
List 3 phases of the SA node action potential
Phase 4 = Spontaneous Depolarization = Leaky to Na+ (Ca+ influx at the end of phase 4)
Phase 0 = Depolarization = Ca 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. It can be increased by:
1. Rate of phase 4 increases (reaches TP faster)
2. TP becomes more negative (shorter distance between RMP and TP)
3. RMP becomes less negative
What is the calculation for mean arterial blood pressure?
(CO x SVR)/80 + CVP
What is the formula for PVR?
(MPAP - PAOP)/CO x 80
normal = 150 - 250 dynes/s/cm-5
Describe the Frank-Starling relationship
The relationship between ventricular volume and ventricular output (CO)
Ventricular volume = CVP, PAD, PAOP, LAP, LVEDP, RVEDV, LVEDV
CO = SV, LVSW, RVSW
What factors affect myocardial contractility?
Chemicals affect contractility, particularly calcium!!
Increased Contractility = Dig, PDEi
Decreased Contractility = HyperK
Discuss the cardiomyocyte contractility steps
- Depol of T-Tubule opens VG L-type calcium channels. calcium enters myocyte. (phase 2 of the AP)
- Calcium influx activates RyR2 receptors.
- Calcium is released from the SR.
- Calcium binds to troponin C. Stimulates CB formation.
- Calcoium unbinds from troponin C.
- Most of the calcium is returned to the SR via SERCA2 pump (ATP dependent). Once inside. Calcium binds to calsequestrin (storage protein)
- Some of the calcium is removed from the myocyte by sodium/calcium exchange pump.
- Na/K ATPase restores RMP.
How to calculate SVR
MAP - CVP / CO X 80
normal = 800 - 1500 dynes/sec/cm2
What law can be applied to afterload?
Law of Laplace
Wall stress = (Intraventricular pressure x radius) / Ventricular thickness
intraventricular pressure = the force that pushes the heart apart
wall stress= the force that holds the heart together
List 3 conditions that set afterload proximal to the systemic circulation
- Aortic Stenosis
- Coarctation of the aorta
- Hypertrophic CM
How to calculate EF?
Stroke Volume / EDV x 100
mild dysfunction = 41 - 49%
mod = 26 - 40%
severe < 25%
What is the best TEE view for diagnosing myocardial ischemia?
Midpapillary muscle level in short axis
What is the equation for CPP?
AoDBP - LVED
What region of the heart is most susceptible to MI? Why?
LV subendocardium d/t high compressive tissue in LV
Steps in the NO pathway
- NO synthase catalyzes the conversion of L-arginine to NO
- NO diffuses from the endothelium to the smooth muscle
- NO activates guanylate cyclase.
- GC converts guanosine triphosphate (GT) to cyclic guanosine monophosphate (cGMP)
- Increased cGMP reduces intracellular calcium
- PDE deactivates cGMP to guanosine monophosphate to turn off NO
What does S3 & S4 suggest
S3 = heart failure, flaccid & inelastic heart. Heard during middle 1/3 of diastole. Gallop rhythm (rumbling)
S4 = decreased ventricular compliance, caused by atrial systole. Heard before S1.
What does S1 mean
-Closure of mitral and tricuspid valves.
-Marks the onset of systole
-End of LV filling and beginning of isovolumetric contraction
What does S2 mean
-Closure of aortic and pulmonic valves
-Marks onset of diastole
-End of LV ejection and beginning of isovolumetric relaxation
Stenosis Valve
Sarcomeres added in parallel
Concentric hypertrophy d/t pressure overload
Regurgitant valve
Sarcomeres added in series
Eccentric hypertrophy
List the hemodynamic goals Aortic Stenosis
- slow/nml HR
- high preload
- high SVR
-nml PVR & contractility
HD Goals for Mitral Stenosis
-slow/nml HR
-avoid an increase in PVR
-keep everything else nml.
AI goals
-HR high
-Preload high
-Low SVR
-nml PVR & contractility
mitral insufficiency goals
-HR high
-Preload high
-Contractility nml
-SVR low
-Avoid an increase in PVR
what is the most common dysrhythmia associated w/mitral stenosis?
a fibb
List 6 risk factors for perioperative cardiac m&m for non-cardiac surgery
-High risk surgery
-Hx of IHD
-Hx of CHF
-Hx of cerebral vascular dx
-DM
-Cr > 2 mg/dL
Risk of periop MI
Gen pop = 0.3%
MI if > 6 mo = 6%
MI if 3 - 6 mo = 15%
MI < 3 mo = 30%
highest risk of reinfarction is wi/i 30 days of an acute MI recommends 4 - 6 weeks
High, medium, low-risk procedures
High (> 5%)
-emergent, open aorta, PVD sx, long
Intermediate (1-5%)
-CEA, head/neck, intrathoracic, ortho, prostate
Low (<1%)
-endoscopic, cataract, superficial, breast, ambulatory
How do you interpret cardiac enzymes in a patient w/suspected ischemic event
-Troponins are more sensitive than CK-MB
-All enzymes initial elevation is w/i 3 - 12 hours
CK MB peaks @ 24 hours, baseline in 3 days
Trop. I peaks @ 24 hours, baseline in 5-10d
Trop. T peaks @12-48h, baseline in 5-14d
How do you treat an intraoperative MI?
make the heart SLOWER, SMALLER, AND BETTER PERFUSED
-BB to keep HR < 80
-Incr. depth of anesthesia, vasodilate (nitro)
-Avoid an increased PAOP
What factors reduce ventricular compliance?
Age > 60
Ischemia
Pressure overload hypertrophy
Hypertrophic obstructive CM
Pericardial pressure
What is the difference btw HFrEF and HFpEF
HFrEF (systolic failure) = decreased EF with increased end-diastolic volume. Volume overload commonly causes systolic dysfunction
HFpEF (diastolic failure) = heart cannot relax and accept the incoming volume because ventricular compliance is reduced. Symptomatic heart failure with a normal EF.
HD goals for HFrEF
Preload = already high
Afterload = decrease (SNP), maintain CPP tho
Contractility = augment with inotropes (dobutamine)
HR = usually high d/t incr’d SNS tone. If EF is low, than a higher HR is needed to preserve EF
HD goals for HFpEF
Preload = volume required to stretch noncompliant ventricle. LVEDP does NOT correlate with LVEDV!!
Afterload = keep elevated to perfuse a thick myocardium
Contractility = normal
HR = slow/normal to increase diastolic time and CPP
NY Heart Failure Classification
Class 1 - no s/s
2 - s/s with moderate activity
3 - s/s with mild activity
4 - s/s at rest
List 6 complications of HTN
LVH
IHD
CHF
Arterial aneurysm
Stroke
End-stage renal dx
Primary vs. secondary hypertension
Primary is more common and has no identifiable cause (95%)
Secondary is caused by some other pathology
Name 7 causes of secondary hypertension
- Coarctation of the aorta
- Renovascular disease
- Cushing’s (adrenocorticism)
- Conn’s (aldosterone)
- Pheo
- Pregnancy-induced hypertension
What are the 2 major classes of CCBs
Dihydropyridines - targets VSM
-Vasodilation
Non-dihydropyridines - targets myocardium
-Decreased heart rate, contractility, conduction, and coronary vascular resistance
Name the non-dihydropyridines
Verapmail = phenylalkylamine
Diltiazem = benzothiazepine
Anesthetic management of constrictive pericarditis
-CO is dependent on HR - avoid bradycardia
-Preserve HR and contractility (Ketamine, Pancuronium, Opioids, benzos, etomidate)
-Maintain afterload
What is Kussmaul’s sign
Impaired RV filling d/t poorly compliant RV or pericardium. Blood backs up. = JVD, and increased CVP … esp during inspiration
What is pulsus paradoxus
Exaggerated drop in SBP during inspiration (> 10 mm Hg) which suggests impaired diastolic filling
*Negative intrathoracic pressure on inspiration = increased venous return to RV = bowing of ventricular septum towards LV = decreased SV
Kussmauls & Pulsus paraadoxus are present with
constrictive pericarditis
pericardial tamponade
Anesthetic considerations for the patient w/acute tamponade
Local anesthesia is preferred
Any drug that depresses the myocardium or reduces afterload will result in CV collapse
-Avoid = IA, propofol, neuraxial
-Safe = ketamine, nitrous, benzos, low-dose opioids
List 7 patient factors that warrent abx prophylaxis for endocarditis
-Hx endocarditis
-Prosthetic heart valve
-Unrepaired cyanotic congenital heart dx
-Repaired congenital heart dx < 6 mo. old
-Impaired endothelialization at the graft site
-Heart tx w/valvuloplasty
3 surgeries that warrent abx prophylaxis against endocarditis
- dental w/gingival manipulation
- resp. with mucosal lining perf
- biopsy of infected lesion
3 key determinants of flow thru LVOT
- systolic LV volume
- force of LV contraction
- transmural pressure gradient
What factors reduce CO with obstructive hypertrophic cardiomyopathy
- low systolic volume (low preload or high HR)
- high contractility
- low transmural pressure (Aortic DBP low)
How long should elective sx be delayed in the patient with a PCI?
12 months for all DES
Angioplasty w/o stent = 2 - 4 weeks
Bare Metal = 30 days
DES w/stable IHD = 1st gen 12 mo, 2nd gen 6 mo
DES w/ACS = 12 mo
CABG = 6 weeks
What is the difference btw alpha stat and pH stat?
Alpha stat - does not take into consideration the patient’s temperature. Better outcomes for adults.
pH stat takes into consideration the patient’s temperature. Better outcomes for peds.
as temp decreases, more CO2 will dissolve in the blood
Why is a LV vent used during CABG?
Removes blood from the LV from thebesian veins and bronchial circulation
How does the IABP work?
Deflates during systole - decreases afterload, correlates w/R wave on EKG
Inflates during diastole - increases coronary perfusion, correlates w/dicrotic notch
4 c/i to IABP
severe AI
descending aortic dx
severe PVD
sepsis
Discuss the Crawford classification
Used to assess aortic aneurysms r/t thoracic and abdominal aorta
I. descending thoracic aorta & upper abd.
II. thoracic & most abdominal
III. lower thoracic & most abd.
IV. abdominal only
2 and 3 are the most difficult to repair
DeBakey and Stanford
Classifies the aortic dissection
Stanford
A - involves ascending aorta
B - does not involve ascending aorta
DeBakey
1. Tear in AA and dissection along entire aorta
2. Tear in AA and dissection in AA
3. Tear in proximal descending aorta
Which law describes aortic diameter & rupture
Law of Laplace
Wall tension = transmural pressure x vessel radius
Mortality increases significantly once AAA reaches 5.5 cm (sx recommended if growing > 0.6 - 0.8 cm / year)
How does the AoX contribute to anterior spinal artery syndrome
If its clamped above the artery of Adamkiewicz ischemia can occur to lower portion of anterior spinal cord.
Beck’s syndrome = anterior spinal artery syndrome
S/S of Beck’s syndrome
Flaccid paralysis of LE
Impaired bowel/bladder function
Loss of temp/pain
preserved touch & propioception
What is amaurosis fugax?
Blindness in one eye = s/s of impending stroke
EEG monitoring for CEA
EEG monitors cortical electrical function
Risk of cerebral hypoperfusion w/ loss of amplitude, decreased beta wave, and/or slow wave
HIGH incidence of false negative d/t increased or decreased frequency
Increased Hz during EEG
-mild hypercarbia
-early hypoxia
-sz or ketamine
-nitrous
-light
Decreased Hz during EEG
-extreme hypercarbia
-hypoxia
-cerebral ischemia
-hypothermia
-anesthetic OD
-opioids
CEA regional
must block C2 - C4
cervical plexus block!!
