Cardiac A&P Flashcards
What is the primary Calcium ion reservoir in the body?
The Sarcoplasmic Reticulum
How does the SA Node stimulate an action potential?
-Changes in automaticity of SA node are due to ANS stimulation
-Spontaneously produces its own action potential
-Depolarizes at 90 bpm
-“Pacemaker” of the heart.
What is Phase 0 of the SA Node Action Potential (Pacemaker Action Potential)?
Rapid depolarization due to Ca and Na influx.
What is Phase 3 of the SA Node Action Potential (Pacemaker Action Potential)?
Repolarization due to K+ efflux
What is Phase 4 of the SA Node Action Potential (Pacemaker Action Potential)?
Spontaneous depolarization from resting membrane potential (-60 mV) to threshold (-30 mV) due to Na influx (slow depolarization)
Why is there a pause at the AV Node?
-To allow for coordinated contraction between Atria and ventricles.
-Allows atria to completely empty (and ventricles to fill) before ventricles contract.
-Atrial conduction is slowed by 0.1-0.13 seconds
Which fibers have the fastest conduction velocity in the heart?
-His-Purkinje fibers depolarize at 20-40 BPM
-Have to create a coordinated ventricular contraction very quickly. So fast that it looks like it’s in unison.
-Lots of branches beneath the endocardium that allow ventricular ctx to happen.
What do anesthetic gasses do to SA node activity & contractility?
-Anesthetic gasses depress SA nodal activity and contractility
-Depress SA nodal automaticity
-Volatiles depress contractility by decreasing entry of Ca+ into cells during depolarization
What is Phase 0 of the Ventricular Action Potential?
Rapid depolarization (Na influx)
What is Phase 1 of the Ventricular Action Potential?
Initial repolarization (Na channels close)
What is Phase 2 of the Ventricular Action Potential?
-Plateau (Ca influx).
-Allows ventricle time to contract, push blood out, and then relax.
-Prevents tetany in ventricular cells.
-Occurs due to increased Ca influx and decreased permeability of K+
-Absolute refractory period.
What is Phase 3 of the Ventricular Action Potential?
Repolarization (K efflux)
What is Phase 4 of the Ventricular Action Potential?
Na-K pump restores resting membrane potential (-90mV) = diastole
What time is sacrificed at high heart rates?
-Systole is relatively fixed in duration
-diastolic time is sacrificed at high heart rates
-Tachycardia not only decreases ventricular filling but also coronary filling (bad for cardiac patients)
What is Excitation-Contraction Coupling?
The conversion of an action potential into a muscle contraction.
-The result of actin and myosin overlapping one another, causing shortening of the myocyte.
What is Calcium-Induced Calcium Release?
-T-Tubules bring extracellular Ca in via voltage-gated receptors (DHP receptor)
-Once in the cell, Ca binds to Ryanodine receptor, causing SR to release more calcium
-As long as Ca is present, actin-myosin will stay crossed.
-When you want to relax, Calcium is pumped via Sarco/endoplasmic reticulum Ca pump (SERCA) back into the SR (uses ATP)
-Also, the Na/Ca pump puts Ca back into the ECF
-Ca release from myosin cross bridges causes heart muscle to relax
Relaxation is ATP and O2 dependent (just like contraction is).
What does End diastolic pressure volume relationship (EDPVR) indicate?
Compliance (Stiffness)
What does End systolic pressure volume relationship (ESPVR) indicate?
Contractility (slope)
How do you calculate Stroke Volume?
SV = EDV-ESV
How do you calculate EF?
EF = SV / EDV
Review PV Loop pictures
Yes
How do you calculate CO?
CO = HR x SV (4-6 L/min)
How do you calculate CI?
CI = CO / BSA (2.5-4.2 .2 L/min/m2)
What is Preload?
-EDV
-Dependent on ventricular filling.
-Venous return is the primary determinant of PL
-75% of blood volume resides in the veins
-When HR is constant, CO is directly proportional to PL to both the R & L heart.
-Inc HR = dec diastole = impaired filling
What is the Bainbridge Reflex?
Increased volume in R atrium cause HR to increase by 10-20%
Why do you want to avoid overfilling?
The point at which further increases in SV are not possible.
-SV diminishes because actin-myosin filaments are pulled so far apart that contraction strength is reduced (sarcomere is overly stretched)
-Will see pressure increase along EDPVR line
What are the components of Afterload?
-Ventricular Wall Tension
-Arterial Impedance to Ejection
-Physical Properties of blood vessels and/or blood (viscosity)
CO and SV are inversely r/t AL
How does Ventricular Wall Tension affect AL?
-Law of LaPlace: T (wall tension) = P (pressure) x R (radius)
-Small radius (vasoconstriction) = increased pressure.
RV > LV in terms of sensitivity to AL changes (LV has larger muscle mass)
How does Arterial Impedance to Ejection affect AL?
-HTN, atherosclerosis. Higher resistance to ejection.
-SVR = 80 x (MAP-CVP/CO). Normal is 900-1500 dynes/cm
-PVR = 80x(pap-lap/co). Normal PVR- 50-150
How do the physical properties of blood vessels/blood affect AL?
Can do autologous blood transfusions and replace with crystalloid to make blood less viscous.
What is the compliance equation?
Compliance = Volume / Pressure
What factors effect Contractility?
-Independent of PL and AL
-Calcium concentration is the most important factor (More Ca = more myosin binding sites = stronger contraction)
-Also affected by Mg, O2, and acidosis
-Slope of the ESPVR line corresponds with contractility
-Dec slope = dec contractility (systolic failure)
Why is the endocardium more vulnerable to ischemia?
Blood flows to endocardium during mainly diastole, making it the most vulnerable to ischemia.
-Blood flows to epicardium during entire cardiac cycle
What is the Coronary Sinus SvO2?
Coronary sinus SVO2 = 35% (i.e. large O2 extraction with little reserve in times of ischemia)
