AA APEX CARDIAC A&P CONT. Flashcards
Chronotropy is
Heart rate
Inotropy is
Strength of contraction (contractility)
Lusitropy is
Rate of myocardial relaxation (during diastole)
Dromotropy is
Conduction velocity (how fast the action potential travels per time)
What is the function the Na/K ATPAse? .
The sodium-potassium pump maintains the cell’s resting potential. Said another way, it separates charge across the cell membrane keeping the inside of the cell relatively negative and the outside of the cell relatively positive
How it works: Sodium Potassium ATPase
It removes the Na+ that enters the cell during depolarization.It returns K+ that has left the cell during repolarization.
Na and K+ how many ions in and out
For every 3 Na+ ions it removes, it brings 2 K+ ions into the cell.
List the phases 0 of the ventricular action potential, and describe the ionic movement during each phase.
Phase 0: Depolarization → Na+ influx
Phase 1: ion movement
Initial repolarization → K+ efflux & Cl- influx
Phase 2 ion movement
Plateau → Ca+2 influx
Phase 3 ion movement
Repolarization → K+ efflux
Phase 4: ion movement
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)
List the 3 phases of the SA node action potential, and describe the ionic movement during each phase.
Phase 0:
Depolarization → Ca+2 influx
List the 3 phases of the SA node action potential, and describe the ionic movement during each phase. Phase 3:
Repolarization → K+ efflux
List the 3 phases of the SA node action potential,
Phase 4
Phase 0
Phase 3
What process determines the intrinsic heart rate, and what physiologic factors alter it?
Rate of spontaneous phase 4, TP and RMP
Heart rate is determined by the
rate of spontaneous phase 4 depolarization in the SA node.
We can increase HR by manipulating 3 variables:
TP N
RMPN
- 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 becomes less negative what happens?
(shorter distance between RMP and TP).
When TP become more negative
(shorter distance between RMP and TP).
2 ways to make distance between RMP and TP short?
RMP less negative
TP becomes more negative
What is the calculation for mean arterial blood pressure? If given DBP and SBP
MAP = (1/3 x SBP) + (2/3 x DBP)
MAP if CO is given formula
MAP = [(CO x SVR) / 80] + CVP
Normal MAP is
Normal = 70 - 105 mmHg
What is the formula for systemic vascular resistance?
[(MAP - CVP) / CO] x 80
Normal SVR is
Normal = 800 - 1500 dynes/sec/cm^5
What is the formula for pulmonary vascular resistance?
[(MPAP - PAOP) / CO] x 80
Normal PVR
150 - 250 dynes/sec/cm^5
The Frank-Starling relationship describes the relationship between
ventricular volume (preload) and ventricular output (cardiac output):
↑ preload →
↑ myocyte stretch → ↑ ventricular output
↓ preload →
↓ myocyte stretch → ↓ ventricular output
Increasing preload increases To the right of the plateau
ventricular output, but only up to a point.
Increasing preload too much, additional volume does what? Leading to -______and _______PAOP
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.
Filling pressures ( other names for frank starling)
CVP PAD PAOP LAP LVEDP
EDV determinants 2
RVEDV
LVEDV
Ventricular output 4 determinants
CO
SV
LVSW
RVSW
What factors affect myocardial contractility?
Contractility (inotropy) describes the contractile strength of the heart.
Just remember that Chemicals affect
Contractility - particularly Calcium
Contractility factors either
alters the amount of Ca+2 available to bind to the myofilaments or impacts the sensitivity of the myofilaments to Ca+2.
5 things that increase contractility
SNS stimulation Catecholamines Calcium Digitalis PDE
Myocardial ischemia and contractility
Decreases
Hypoxia and contractility
Decreases
Acidosis and contractility
Decreases
Hypercapnia and contractility
Decreases
Propofol and contractility
Decreases
BB and CCBs on contractility
Decreases
HYPERkalemia and contractility
Decreases
Discuss excitation-contraction coupling in the cardiac myocyte.
a) The myocardial cell membrane depolarizes.
b)During the plateau of the ventricular action potential (phase 2), Ca+2 enters the cardiac myocyte through L-type Ca+2 channels in the T-tubules.
c) Ca+2 influx turns on the ryanodine-2 receptor, which releases Ca+2 from the sarcoplasmic reticulum (this is called calcium-induced calcium-release).
d) Ca+2 binds to troponin C (myocardial contraction).
e)Ca+2 unbinds from troponin C (myocardial relaxation).
Most of the Ca+2 is returned to the sarcoplasmic reticulum via the SERCA2 pump.
f)Once inside the sarcoplasmic reticulum, Ca+2 binds to a storage protein called calsequestrin.
The next time the cardiac myocyte depolarizes, the whole process repeats.
Most of the Ca+2 is returned to the sarcoplasmic reticulum via the
SERCA2 pump.
Once inside the sarcoplasmic reticulum, Ca+2 binds to a storage protein called
calsequestrin.
During the plateau of the ventricular action potential (phase 2), Ca+2 enters the cardiac myocyte through
L-type Ca+2 channels in the T-tubules.
Ca+2 binds to troponin
C (myocardial contraction).
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.
we use the systemic vascular resistance as a surrogate for LV afterload.
Normal SVR
800-1500 dynes/sec/cm-5
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
The force that pushes the heart apart
Intraventricular pressure is
The force that holds the heart together (it counterbalances intraventricular pressure)
Wall stress
Wall stress is reduced by:
Decreased intraventricular pressure
Decreased radius
Increased wall thickness
List 3 conditions that set afterload proximal to the systemic circulation. (AHC)
- Aortic stenosis
- Hypertrophic cardiomyopathy
- Coarctation of the aorta
Diastole phases are (4)
Rapid filling
Reduced filling
Atrial kick
Isovolumetric relaxation
Systolic phases are (2)
Isovolumetric contraction
Ejection
The ejection fraction is a. It is Said another way, the
measure of systolic function (contractility)
The percentage of blood that is ejected from the heart during systole.
EF
EF is the stroke volume relative to the
end-diastolic volume.
Normal EF =
60 - 70%
LV dysfunction is present when
EF < 40%
SV is calculated as:
EDV - ESV
Width of the loop
SV =
Right side of the loop at the x-axis
EDV =
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 - LVED
Aortic DBP is the
LVEDP is the
pushing force
resistance to the pushing force
Therefore, CPP can be improved by
increasing AoDBP or decreasing LVEDP (PAOP).
Which region of the heart is most susceptible to myocardial ischemia? Why?
The LV subendocardium is most susceptible to ischemia. . As aortic pressure increases, the LV tissue compresses its own blood supply and reduces blood flow. The high compressive pressure in the LV subendocardium coupled with a decreased coronary artery blood flow during systole increase coronary vascular resistance and predisposes this region to ischemia.
The LV subendocardium is best perfused during
diastole
Factors that increase oxygen demand
HR, BP , stimulation, Wall tension, EDV, Afterload, contractility
Tachycardia HTN SNS stimulation Increased Wall tension Increased EDV Increase afterload Increased contractility
Decrease oxygen delivery are
Decrease coronary flow
Decrease CaO2
Decrease oxygen extraction
Factors leading to decreaed coronary flow?
Tachycardia
Decreased aortic pressure
Decreased vessel diameter
Increase EDP
Factors that lead to decrease CaO2
Hypoxemia
Anemia
Factors leading to Decreased oxygen extraction
left shift dissociation curve
Decreased capillary density
Discuss the nitric oxide pathway of vasodilation.
Nitric oxide is a smooth muscle relaxant that induces vasodilation.
teps 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).
Nitric oxide activates
guanylate cyclase.
Catalyzes the conversion of L-arginine to nitric oxide.
Nitric oxide synthase
Increased cGMP and Calcium
reduces intracellular calcium, leading to smooth muscle relaxation
S1:
Closure of mitral and tricuspid valves
Marks onset of systole
S1
S2
Closure of aortic & pulmonic valves
Marks onset of diastole)
S2
May suggest systolic dysfunction (
S3
Normal in kids and athletes
S3
May suggest diastolic dysfunction
download
May suggest diastolic dysfunction
S4
MV opens and closes where on the loop
bottom of the loop,
AV opens and closes where on the loop
top of the loop.
What are the two primary ways a heart valve can fail?
Stenosis or regurgitation
In 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 in what kind of valve failure?
Stenosis
In Regurgitation:
The valve is incompetent (it’s leaky).
Some blood flows forward and some blood flows backwards during chamber systole, in which type of valve failure.
Regurgitation
Regurgitation main issue
Increase volume
Stenosis main issue
increase pressure
How does the heart compensate for pressure overload?
PCP
Pressure Overloads
Concentric Hypertrophy
sarcomeres added in PARALLEL
How does the heart compensate for Volume overload?
VES
Volume Overload
Eccentric Hypertrophy
sarcomeres added in SERIES
List the hemodynamic goals for the 4 common valvular defects.
Aortic Stenosis - HR, preload, SVR, contract. PVR
HR - Slow normal
Preload increased
SVR 0 to elevated
contractility and PVR 0
List the hemodynamic goals for the 4 common valvular defects. Mitral Stenosis – HR, preload, SVR, contract. PVR
HR - Slow normal
Preload, SVR, Contractility 0
PVR AVOID increased
Avoid SVR increase in 2 valvular defects
Mitral stenosis
Mitral insufficiency or regurg.
List the hemodynamic goals for the 4 common valvular defects. Aortic Insufficiency – HR, preload, SVR, contract. PVR
Heart rate increased
Preload normal or increased
SVR decreased
Contractility and PVR 0
Where do you want preload in aortic regurg?
normal or increased
Where do you want HR in aortic regurg?
INCREASED
You want SVR decreased in 2 valvular defects
Aortic insufficiency
Mitral insufficiency
You want tachycardia in 2 valvular defects
Aortic insufficiency
Mitral insufficiency
Where do you want preload in mitral regurg
0 to increased
Mitral issues you want to avoid
Increased in PVR
What is the most common dysrhythmia associated with mitral stenosis?
Atrial fibrillation
Atrial fibrillation is associated with
mitral stenosis
List 6 risk 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 Diabetes mellitus Serum creatinine > 2 mg/dL
What is the risk of perioperative myocardial infarction in the patient with a previous MI?
General population
0.3%
What is the risk of perioperative myocardial infarction in the patient with a previous MI?
MI if > 6 months =
6%
What is the risk of perioperative myocardial infarction in the patient with a previous MI?MI if 3 - 6 months =
15%
What is the risk of perioperative myocardial infarction in the patient with a previous MI? MI < 3 months =
30%
The highest risk of reinfarction is greatest within
30 days of an acute MI.
High (Risk > ___%)
5%):
High (Risk > 5%): procedures
♥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 procedures %
(Risk = 1-5%):
Intermediate procedures risks
Carotid endarterectomy Head and neck surgery Intrathoracic or intraperitoneal surgery Orthopedic surgery Prostate surgery
Low (Risk :
<1%)
Low (Risk :
<1%)
What is the Modified New York Association Functional Classification of Heart Failure?
Class I: Asymptomatic
Class II: Symptomatic with moderate activity
Class III: Symptomatic with mild activity
Class IV: Symptomatic at rest
Infarcted myocardium releases 3 key biomarkers:
creatine kinase-MB, troponin I, and troponin T.
Cardiac troponins vs CKMB
Cardiac troponins are more sensitive than CK-MB for the diagnosis of myocardial infarction.
Initial elevation of all Cardiac enzymes
3-12 hours
Peak elevation of CKMB
24h
Peak elevation of CK-MB
24h
Peak elevation of Troponin I
24h
Peak elevation of Troponin T
12-48 h
CK-MB return to baseline when
2-3 days
Troponin I return to baseline when
5-10 days
Troponin T return to baseline when
5-14 days
How do you treat intraoperative myocardial ischemia?
Treatment of myocardial ischemia should focus on interventions that make the heart slower, smaller, and better perfused.
Increase O2 demand cause by
Treatment
Increase BP
increase HR
Increase PAOP
Beta blocker to a HR < 80bpm
Increased depth of anesthesia, vasodilator
Nitroglycerin
Decrease O2 supply causes and Treatment.
decrease HR, BP
Increase PAOP
Treatment
Anticholinergic, pacing
Vasoconstrictor, reduce depth of anesthesia
NTG, inotrope
The diastolic pressure-volume relationship is affected by:
Age > 60 years
Ischemia
Pressure overload hypertrophy (aortic stenosis or HTN)
Hypertrophic obstructive cardiomyopathy
Pericardial pressure (increased external pressure)
What is the difference between systolic and diastolic heart failure?
Systolic Heart Failure – The Ventricle Doesn’t Empty Well
Diastolic Heart Failure – The Ventricle Doesn’t Fill Properly
The hallmark of systolic heart failure is a
decreased ejection fraction with an increased end-diastolic volume.
Volume overload commonly causes what kind of dysfunction?
systolic dysfunction.
Diastolic failure occurs when the heart is .
unable to relax and accept the incoming volume, because ventricular compliance is reduced
The defining characteristic of diastolic dysfunction is
symptomatic heart failure with a normal ejection fraction
Systolic HF preload is
HIGH
Diastolic HF volume required to stretch noncompliant ventricle LVEDP does not correlate with
LVEDV (TEE is best)
Why is a left ventricular vent used during CABG surgery?
A left ventricular vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt).
Solubility of a gas is a function of y extension, this affects the pH.
temperature,
As temp decreases, more
CO2 is able to dissolve in the blood.
Alpha-stat
does not correct for the patient’s temperature. This technique aims to keep intracellular charge neutrality across all temperatures. It is associated with better outcomes in adults
pH-stat
corrects for the patient’s temperature. This technique aims to keep a constant pH across all temperatures. It is associated with better outcomes in peds.
This technique aims to keep a constant pH across all temperatures. It is associated with better outcomes in
ph -Stat ; peds.
An aortic cross clamp placed above the artery of 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)
Beck’s triad occurs in the patient with
acute cardiac tamponade.
Signs of Beck’s triad include:
Hypotension (decreased stroke volume)
Jugular venous distension (impaired venous return to right heart)
Muffled heart tones (fluid accumulation in the pericardial space attenuates sound waves)
