Cardiac Physiology Yr1FA23 Flashcards
Each cycle of cardiac contraction and relaxation is initiated by
depolarization of the sinus node.
True/false: The cycle of cardiac contraction and relaxation being initiated by the sinus node is seen on the EKG?
FALSE
The P wave records
atrial depolarization and contraction.
The first part of the P wave reflects
right atrial activity; the second part reflects left atrial activity.
(the PR segment)
There is a brief pause when the electrical current reaches the AV node and the EKG falls silent
ventricular conducting system
(bundle of His, bundle branches, and Purkinje fibers)
The first part of the ventricles to be depolarized
the interventricular septum.
Ventricular depolarization generates what on the EKG
the QRS complex.
The wave of depolarization then spreads along the ventricular conducting system (bundle of His, bundle branches, and Purkinje fibers) and out into the
Ventricular Myocardium
The T wave records
repolarization of the ventricular myocardium
Is Atrial Repolarization seen on the EKG?
NO
the time from the start of atrial depolarization to the start of ventricular depolarization.
The PR interval
the time from the end of atrial depolarization to
the start of ventricular depolarization.
The PR segment
the time from the end of ventricular
depolarization to the start of ventricular repolarization.
The ST segment
the time from the start of ventricular
depolarization to the end of ventricular repolarization.
The QT interval
measures the time of ventricular depolarization.
The QRS interval
Alpha 1 Receptor Site
Vascular Smooth Muscle
Heart
Alpha 1 Receptor Action
Arterial Vasoconstriction
Alpha 2 Receptor Site
Vascular Smith Muscle
Presynaptic Nerve terminal
Alpha 2 Receptor Action
Vasoconstriction of venous capacitance vessels
Local feedback, inhibition of norepi release
Beta 1 Receptor Site
Heart
Beta 1 Receptor Action
Increased inotropic and chronotropic activity
Increased Av node conduction velocity
Beta 2 Receptor Site
Vascular smooth muscle
Bronchial smooth muscle
Beta 2 Receptor Action
Vasodilation of peripheral vasculature
Bronchodilation
D1 Receptor Site
post-synaptic
Vascular smooth muscle
(renal, Splanchnic, cerebral)
Renal Tubules
D2 Receptor Action
Decreased norepi release
D2 Receptor Site
Presynaptic sympathetic nerve terminals
D2 Receptor Action
Decreased norepi release
V1 Receptor Site
Vascular smooth muscle
platelets
Hepatocytes
myometrium
V1 Receptor Action
Vasoconstriction
Platelet aggregation
Glycogenolysis
Myometrial contraction
V2 Receptor Site
Basolateral membrane of collecting duct
Vascular endothelium
Vascular smooth muscle
V2 Receptor Action
INsertion of AQP-2 H2O channels in the apical membrane
induce AQP-2 synthesis
release of vwf and factor VII
vasodilation
V3/V1B Receptor Site
Anterior Pituitary gland
V3/ V1B Receptor Action
Release of ACTH
Prolactin
Endorphins
Norepinephrine Dose
0.02-.2 mg/kg/min
Norepinephrine Receptors
A1>B1& B2
Norepinephrine Inotropy
+
Norepinephrine Chronotropy
+
Norepinephrine SVR effects
+
Norepinephrine PVR Effects
+
Phenylephrine Dose
0.02-0.3 mcg/kg/min
Phenylephrine Receptors
Alpha1
Phenylephrine Inotropy Effects
<->
Phenylephrine Chronotropy effects
-
Phenylephrine SVR Effects
+
Phenylephrine PVR Effects
+
Vasopressin Dose
0.02-0.5 units/kg/hr
Vasopressin Receptors
V1 V2
Vasopressin Inotropy
<->
Vasopressin Chronotropy effects
<->
Vasopressin SVR Effects
+
Vasopressin PVR Effects
+
Nitroprusside Dose
0.2-5 mcg/kg/min
Nitroprusside Receptors
Increase cGMP in vascular myocytes
Nitroprusside Inotropy
<->
Nitroprusside Chronotropy
<->
+
Nitroprusside SVR
-
Nitroprusside PVR
-
Nicardipine Dose
0.5-5 mcg/kg/mni
Nicardipine Receptors
Calcium Channel Blocker
Nicardipine Inotropy
<->
Nicardipine Chronotropy
<->
Nicardipine SVR
-
Nicardipine PVR
-
Nitroglycerin Dose
0.2-10 mcg/kg/min
Nitroglycerin Receptors
Nitroglycerin Inotropy
Nitroglycerin Chronotropy
Nitroglycerin SVR
Nitroglycerin PVR
Epinephrine Dose
0.02-0.2 mcg/kg/min
Epinephrine Receptors
A1A2B1B2
Epinephrine Inotropy
+
Epinephrine Chronotropy
+
Epinephrine SVR
+
Epinephrine PVR
+
Epinephrine high-dose Inotropy
+
Epinephrine high-dose Chronotropy
+
Epinephrine high-dose SVR
<->
Epinephrine High-dose PVR
<->
Dopamine low dose
2-5 mcg/kg/min
Dopamine mid dose
5-10 mcg/kg/min
Dopamine high dose
> 10 mcg/kg/min
Dopamine low dose Receptors
D1, D2
Dopamine mid dose receptors
B1, B2> A1
Dopamine high dose receptors
A1>B1, B2
Dopamine low dose inotropy
same
Dopamine low dose chronotropy
same
Dopamine low dose SVR
same
Reduces
Dopamine low dose PVR
Same,
Reduces
Dopamine mid dose Inotropy
+
Dopamine mid dose chronotropy
+
Dopamine mid dose SVR
Dopamine Mid dose PVR
<->
Dopamine high dose Inotropy
+
Dopamine high dose chronotropy
+
Dopamine high dose SVR
+
Dopamine high dose PVR
+
Milrinone Loading Dose
25-75 mcg/kg
Milrinone Receptors
PDE3 Inhibitor
Increased cAMP
Milrinone infusion dose
0.25-0.75 mcg/kg/min
Milrinone Inotropy
+
Milrinone Chronotropy
+
Milrinone PVR
-
Milrinone SVR
-
Dobutamine Dose
2-20 mcg/kg/min
Dobutamine Receptors
Dobutamine Inotropy
+
Dobutamine Chronotropy
+
Dobutamine SVR
-
Dobutamine PVR
-
Function of Systemic circulation
Delivers oxygen to all body cells and carries away wastes
OXygenated blood is pumped to all body tissues via
The Aorta
Deoxygenated blood is pumped to the lungs via
Pulmonary arteries
Function of Pulmonary arteries
Eliminates CO2 via the lungs and oxygenates the blood
Deoxygenated blood returns to the heart via
Vena Cava
Oxygenated blood returns to the heart via
Pulmonary Veins
General function of the CV system
Transporting nutrients to the body tissues
Transporting waste products away
Transporting hormones from one part of the body to another
Temperature regulation
When valves are open, what is the skeletal muscle doing?
Contracted skeletal muscle
When valves are closed, what is the skeletal muscle doing?
Relaxed skeletal muscle
In cardiac Action potential, Phase 0
fast, voltage-gated Na+ channels open. K+ channels close
In phase 0 of Cardiac AP, is it fast or slow
Fast
In phase 0 of Cardiac AP, what are the Na+ and K+ Channels doing?
Voltage- GatedNa+ channels open
K+ channels close
Describe Phase 1 of Cardiac AP
transient outward rectifier potassium channels (Ito) open briefly
Describe Phase 2 of Cardiac AP
slow L-type Ca2+ channels
open (plateau).
Phase 3 of Cardiac AP
Ca2+ channels close. K+ channels re-open
Phase 4 of Cardiac AP
Resting Membrane Potential is re-established (K+ channels stay open)
RMP of Cardiac AP
-90
Phase 0 Membrane potential (mV)
-90-+20
Phase 1 membrane potential (mV)
+20
Phase 2 Membrane Potential (mV)
+10
Phase 3 Membrane Potential (mV)
-20
Plateau phase
actin / myosin molecules remain activated for 300ms.
Ca2+ enters here
Ca2+ entering during plateau phase helps
activate the muscle for sustained, forceful contraction.
Absolute Refractory Period (Definition)
all inactivation gates are closed no electrical stimulus will elicit another action potential.
Absolute Refractory period runs from
Runs from phase 0 through most of phase 3.
True or False: Heart Muscle can be tetanized
FALSE
Because of the long refractory period, heart muscle cannot be tetanized
Relative Refractory Period
Some inactivation gates are open
An action potential can be elicited but a higher stimulus voltage is required and not all channels participate.
In the SA Node, timing of depolarization to depolarization is
Intrinsic HR
In the SA Node, Pacemaker potential is due to
gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).
Electrical Properties of the SA Node
gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).
The heartbeat originates in
The SA Node
After the SA node, where does the electicity conduct through?
and spreads over the heart by cell to cell conduction through a complex pathway
Why is the SA Node the pacemaker?
because it has the fastest rhythm.
It is the first structure to show electrical activity with each beat.
Order of conductance of electricity through the heart
SA Node
AV Node
AV Bundle
Left and Right Bundle Branches
Purkinje Fibers
Ventricular Myocardium
Atrial Conduction Velocity
1-1.2 m/S
AV Node conduction Velocity
0.02-0.05 m/s
AV Bundle Conduction Velocity
1.2-2.0 m/s
Bundle Branches and Purkinje Fibers’ Conduction Velocity
2.0-4.0 m/s
Ventricular Myocardium Conduction Velocity
0.3-1.0 m/s
SA Node Rate of discharge (B/min)s
60-100 B/min
AV Node Rate of Discharge
40-55 B/min
Bundle Branches/ Purkinje Fibres Rate of Discharge
25-40 B/min
Which tissue has the slowest conduction Velocity?
AV Node
Why is the AV node the slowest in conduction?
It has small diameter cells, few gap junctions and slow phase zero
Which structure conducts the fastest in Cardiac AP?
Purkinje FIbers
Why are the Purkinje Fibers the fastest for conduction?
It has small diameter cells, few gap junctions and FASTphase zero
Atrial , ventricular, and Bundle of His tissue conduct at what velocity
1m/sec
What is the only pathway to the Ventricles in Conduction?
The AV Node
The paucity of gap junctions in the AV node also causes a safety factor
(the amount of current passed to the next cell/the amount of current needed to reach threshold).
AV node is vulnerable to Injury from
disease which can cause loss of conduction to the ventricles.
(Heart block)
Ablation of the fast-conducting tissue below the AV bundle is very serious. Why?
the spontaneous rate for Purkinje fibers is dangerously low
Ablation of the AV node slows the heart rate down to that of
the next highest pacemaker (below the node)
Baroreceptors in_______detect changes in blood
Carotid Sinus and Carotid arch
Rising pressure stretches receptors
Leads to
Parasympathetic Activation
Decreasing pressure leads to
less stretch on receptors ->sympathetic activation
Why can heart muscle not be tetanized?
Because of the long refractory period
In SA Node conduction, is the sharp spike present?
Sharp spike is absent (no fast Na+ channels). Phase 0 from slow Ca++ channels
In SA Node conduction, how does pacemaker potential occur?
Pacemaker potential is due to gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).
In the SA Node conduction, how is depolarization timed?
Timing of depolarization to depolarization is intrinsic HR
Why is the SA Node the pacemaker of the heart?
Because it has the fastest rhythm.
It is the first structure to show electrical activity with each beat.
How is the rate of Cardiac Pacemakers slowed?
-The Vagus nerve secretes Ach (Parasympathetic activation
-Ach increases K+ conductance at KAch channels, which hyperpolarizes the SA Node cells and opposes the Funny Current (Lf)
-CAMP is also decreased
How is the rate of Cardiac Pacemakers increased?
- Sympathetic nerves secrete norepinephrine which acts at beta receptors on SA node leading to increased cAMP
- cAMP opens the hyperpolarization-activated cyclic nucleotide-gated (HCN) sodium channels which increases If (funny current) during phase 4, thus increasing speed of depolarization.
Describe Sympathetic Neural Regulation of the heart:
Sympathetic stimulation :
Increases HR
Decreases AV Node ERP
Decreased PR
Increased Contractility (SV)
How are the Supraventricular and Purkinje Fibers innervated?
Vagal Innervation
How is everywhere bu the supraventricular and Purkinje fibers innervated?
Sympathetic Innervation
Receptors on Sympathetic Ganglia
AcH- NIcotinic
Receptors on Sympathetic nerves
Norepinephrine
Describe Vagal Neural Regulation of the heart:
Decreased HR
Increased AV Node ERP
Increased PR
What is the largest current in the heart?
Sodium Current
What is the status of Sodium channels at RMP?
Na+ Channels are closed at RMP
Has Alpha/Beta Subunits that are sensitive to cAMP-Dependent protein Kinase
Sodium Current
Regenerated spread of the action potential depends largely on what?
The magnitude of the Na+ Current
The depolarization caused by Na+ also activates what?
Lca
Ik
What inactivates the Na+ Channels in the heart
Sodium-Channel Blockers
L-Type Calcium channels are inactivated by
Dihydropyridines
Phenylalkylamines
Benzothiazepines
This current is activated by voltage, Deactivated by time
L-Type Calcium Channels
At RMP, what is the status of L-Type Calcium channels?
Closed at RMP
Why are Cardiac Action Potentials twice as long as skeletal muscle APs?
Because the K+ channels open so slowly
How is the K+ Repolarization current divided?
IKA- Rapid
IK- Slow
Early outward / A-type current
Found in atrial and ventricular muscle. Activated by depolarization and deactivated quickly. Contributes to phase 1
G-protein activated current
Ach to receptor to GIRK K channels resulting in outward K current. Prominent in SA and AV nodal cells
KATP channels in the sinoatrial node contribute to
HR Control
When fully activated, KATP channels can cause cardiac electrical activity to
STOP;
Contractile Failure
KATP channels play a role in
heart rate control, adaptation to hypoxia, and cardiac excitability
Where is the Funny Current found?
SA, AV and Purkinje fibers
How is the Funny Current Mediated?
by a nonspecific anion channel called HCN… Hyperpolarization activated Cyclic Nucleotide Gated channel
Funny Current conducts which currents?
Both Na and K
Does the Funny Current conduct at positive potentials?
No
Does not conduct at positive potentials
The funny current is activated by hyperpolarization during what phase of the Cardiac Action Potential?
phase 4 of the cardiac action potential, which is also known as diastolic depolarization
Where is the SA Node located?
Sits in RA near the junction of SVC
SA Node size in comparison to other atrial muscle fibers:
Smaller than the other atrial muscle fibers
Cardiac muscle differs from skeletal muscle in that
It has Slow L-Type Calcium Channels
Phase 0 in the SA Nodal cells is due to
Slow Calcium channels
The slowest conduction velocity occurs in the :
AV Node
What is true about aortic Arch baroreceptors?
Stretching of the receptors occurs when arterial pressure suddenly rises
All are true about the sympathetic nervous system EXCEPT:
A- Norepi acts on Beta receptors to increase cAMP
B. Activation of the sympathetic nervous system leads to increased heart rate.
C. Increased cAMP leads to Activation of K+ channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during phase 4
D. Increased cAMP and increased opening of hyperpolarization-actiated cyclic nucleotide-gated (HCN) Sodium channels that increase activity of the “Funny Current” during Phase 4
C.
Increased cAMP leads to activation of K+ Channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during Phase 4
All is true about the sympathetic ns Except:
A- Norepi acts on Beta Receptors to increase cAMP
B. Activation of the SNS leads to increased HR
C. Increased cAMP leads to activation of K+channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during phase 4
D. Increased cAMP and increased opening of hyperpolarization-activated cyclic necleotide-gated (HCN) sodium channels that increase activity of the “Funny Current” During Phase 4
C.
Increased cAMP leads to activation of K+channels that hyperpolarize the cell membrane and increase the activity of the “Funny Current” during phase 4
Select the true statement about L-Type Calcium Channels:
A: Present in the heart and vasculature
B. They are activated by voltage and deactivated by time
C. They are open at very negative membrane potential
D. They are inhibited by Beta Blockers
B.
They are activated by voltage and deactivated by time
True or False: Fast Sodium channels open during Phase 0 of the AP in the SA Node
FALSE
The AV Node:
A: Is located near the Mitral Valve
B. Conducts very quickly
C. Gives RIse to Purkinje Fibers
D. Has an intrinsic pacemaker rate of 300 bpm
C. Gives rise to Purkinje fibers
Which leads would you see changes in for a bundle branch block?
Anterior
Anterior leads are leads V1, V2, V3, and V4. For a left bundle branch block you will see a “beach chair” formation in these leads and in a right bundle branch block you will see “bunny ears” in these leads.
Which of the following is an EKG change seen with hyperkalemia?
A. Sine wave
B. U wave
C. Peaked T waves
D. QRS widening
E. P wave flattening
F. A, C, D, E
G. All of the above
F. A, C, D, E
U waves are seen in hypokalemia not hyperkalemia. Changes seen with hyperkalemia are often progressive, starting with peaked t waves. This progresses to QRS widening and p wave flattening with the sine wave (and eventually torsades) following.
what arrhythmia reflects U waves on the EKG?
Hypokalemia
In which of the following scenarios is a pacemaker NOT indicated?
A. Second degree heart block type I
B. Second degree heart block type II
C. Third degree heart block
D. Third degree heart block caused by lyme disease
E. A and B
F. A and D
F. A and D
Third degree heart block caused by lyme disease IS reversible when treated with corticosteroids and antibiotics and may not indicate need for a pacemaker. Second degree heart block type I (wenckebach) rarely progresses to third degree heart block and is usually transient and benign. It also does not indicate need for a pacemaker. Type II second degree heart block on the other hand often progresses to third degree heart block and needs a pacemaker.
What is the fastest conduction system of the heart? What is the slowest?
A: SA node; AV node
B: purkinje fibers; AV node
C: AV node; SA node
D: SA node; purkinje fibers
B: purkinje fibers; AV node
This question is looking at conduction velocity NOT the rate of pacemaker discharge (BPM)
When discussing neural regulation of the heart, the right vagus nerve innervates what structure?
A: purkinje fibers
B: AV node
C: SA node
D: myocardium
C: SA node
The right vagus nerve innervates the SA node and the left vagus nerve innervates the AV node and purkinje fibers. There is sympathetic innervation everywhere in the heart.
What leads do you look at to determine axis?
A: aVR, I
B: aVL, III
C: aVF, I
D:aVF, II
C: aVF, I
If lead I is positive and lead aVF is negative, what is the axis?
A: Left axis deviation
B: Normal axis
C: Right axis deviation
D: Extreme right axis deviation
A: Left axis deviation
- Which of the following is represented by the Q wave?
A. Atrial depolarization
B. Atrial repolarization
C. Ventricular depolarization
D. Septal depolarization
D. Septal depolarization
- Which of the following will carotid massage/vagal maneuver terminate?
A. A flutter
B. A fib
C. PAT
D. AVNRT
D. AVNRT
Carotid massage should not regularly be done, but is theoretically only helpful in terminating SVTs such as AVNRT. It can be useful in determining if a rhythm is atrial flutter as the ratio to atrial/ventricular depolarizations will become longer (i.e. 1:2 to 1:3 or 1:4).
- In which of the following arrhythmias would your patient most likely be on anticoagulation?
A. SVT
B. A flutter
C. A fib
D. V tach
C. A fib
Pretty much all a fib patients will be on anticoagulants as the quivering atria can allow blood to move slowly and form clots.
- Which of the following arrhythmias is defibrillation (NOT synchronized cardioversion) used for?
A. A fib
B. A flutter
C. V tach
D. F fib
E. Asystole
F. Pulseless electrical activity (PEA)
G. A and B
H. C and D
I. A, B, E, F
J. C, D, E, F
K. All of the above
H. C and D
A fib and A flutter require synchronized cardioversion or else this can lead to R on T phenomenon and cause torsades. Asystole and PEA are non-shockable rhythms and you cannot use defibrillation or synchronized cardioversion on these patients.
Non-Shockable Rhythms
PEA
Asystole
Your patient in the ICU is found to have metabolic acidosis (pH< 7.35). Which way is their oxyhemoglobin curve shifted: left or right?
Right
With metabolic acidosis there is an increase in H+ ions which shifts the curve to the right. Anything that “increases” will shift the curve to the right (increased offloading of O2/decreased affinity) and anything that “decreases” will shift the curve to the left (decreased offloading of O2/increased affinity)
The Frank Starling curve relates:
a. Stroke volume and preload
b. Preload and afterload
c. Afterload and force of contraction
a. Stroke volume and preload
The greater the heart muscle is stretch during filling (PRELOAD/ left ventricular end diastolic pressure), the greater the force of contraction and the greater the quantity of blood pumped into the aorta (SV). The greater the preload (up until a certain point), the more the myosin and actin before aligned and the greater the contraction.
At low doses, dopamine acts of what receptors?
a. Alpha 1 receptors
b. Beta 1 receptors
c. Beta 2 receptors
d. Dopamine receptors
d. Dopamine receptors
2-5 mcg/kg/min D1, D1
5-10 mcg/kg/min B1>B2>A1
>10mcg/kg/min A1>B1, B2
- Which of the following drugs would be the most useful in treating ventricular tachycardia?
a. Procainamide
b. Labetalol
c. Verapamil
d. Phenytoin
A- Procainamide
Class I antiarrhythmics are particularly useful in treating ventricular arrhythmias (wide QRS). Amiodarone and sotalol would be appropriate alternatives.
