Cardiac - Pt 3 Flashcards
1
Q
Cardiac Output =
A
Heart Rate x Stroke Volume
2
Q
Ejection Fraction =
A
(EDV - ESV)/EDV
3
Q
The [] is the percentage of blood in the ventricle that is ejected each beat. Its roughly ~65-70%.
A
Ejection Fraction
4
Q
Stroke Volume =
A
EDV - ESV
5
Q
[] [] [] is the amount of blood remaining in the ventricle after contraction…
A
End Systolic Volume
6
Q
What are the 3 main factors that regulate Stroke Volume
A
Preload
Contractility
Afterload
7
Q
What is “Preload” in terms of stroke volume regulation?
What is the main indicator for the preload?
A
- It is the degree of stretching in the cardiac muscles before contraction.
- You could call it EDV.
- Frank-Starling
8
Q
At rest, cardiac muscles are [] than optimal length…
A
shorter
9
Q
T/F
Ventricle stretching directly relates to a stronger cardiac muscle contraction.
A
FALSE
The contractility of cardiac muscles is directly dependent upon the availability of Ca2+ in the sarcoplasm.
10
Q
T/F
An increase in EDV will lead to an increase in systolic force, to a degree?
A
True
Frank Starling
11
Q
Contractile strength at a given muscle length is independent of [] and [] ?
A
Muscle stretch and EDV
12
Q
What are positive effectors of muscle contactility?
A
- Norepinephrine/Epinephrine
- Glucagon
- Thyroxine
- Digitalis
13
Q
What are negative effectors of muscle contractility?
A
Acidosis
Increased Extracellular K+
Calcium Channel Blockers
14
Q
Describe the effect of the following muscle contractility effectors?
- Norepinephrine
- Glucagon
- Extracellular K+ increase
- Digitalis
A
- Norepinephrine
- increased contractility by stimulating the B1 Adrenergic receptors
- Glucagon
- increased contractility by stimulating the cadiac Ca2+ current by activation of adenylyl cyclase and inhibition of phosphodiesterase
- Extracellular K+ Increase
- Decreased contractility by throwing off the seperation of charge seen in normal cells. This will throw off signal conduction/action potentials and can lead to death.
- Digitalis
- increased contractility dont know why yet.
15
Q
Describe the effect of the following muscle contractility effectors?
- Thyroxine
- Acidosis
- Calcium Channel Blockers
A
- Thyroxine
- Increased Contractility -increases transcription of contractile proteins
- Acidosis
- Decreased Contractility by the competitive inhibition of the slow calcium current by hydrogen ions.
- Calcium Channel Blockers
- Decreased Contractility because duh.
16
Q
What is “Afterload?”
A
- The pressure that must be overcome for the ventricles to eject blood into the major arteries
17
Q
As afterload increases, stroke volume []
A
decreases
18
Q
In which of the following scenarios would Stroke Volume Increase?
- Increase Afterload
- Increase Preload
- Decreased Contractility
A
- Increase preload would lead to a higher stroke volume
19
Q
In which of the following scenarios would stroke volume decrease?
- Increased Preload
- Increased Contractility
- Increased Aortic Pressure
A
- 3, if you increased aortic pressure, the stroke volume would decrease.
- Because the ventricle would not have as much time to eject blood, therefore ejecting a smaller amount.
20
Q
Extrinsic Control of the heart is mediated by the [] [] []
A
Autonomic Nervous System
21
Q
The effects of the autonomic dnervous system on heart rate are called [] …
A
Chronotropic Effects
22
Q
What does Sympathetic innervation do to HR and contractility?
What does Parasympathetic innervation do to HR and contractility?
A
- Increases
- Decreases
23
Q
What section of the central nervous system is in charge of heart beat/contractility regulation?
A
The MEDULLA OBLONGATA
24
Q
During resting condition, what autonomic branch is effecting heart beat?
A
The parasympathetic System
25
1. What part of the Medulla Oblongata controls sympathetic inputs to the heart?
2. What part of the Medulla Oblongata controls parasympathetic inputs to the heart?
1. Cardioacceleratory Center
2. Cardioinhibitory Center
26
Sympathetic Innervation of the Heart:
1. Neurotransmitter used:
2. Sympathetic cardiac nerve attaches to the [] and [] node as well as [] muscle.
3. NTs bind to the [] [] receptors and illicit a [] chronotropic effect
1. Norepinephrine
2. SA and AV node; myocardium muscle
3. B1 Adrenergic Receptors; positive chronotropic effect.
27
Parasympathetic Innervation of the Heart:
1. Neurotransmitter:
2. Nerves project to the [] and [] node via the [] nerve
3. [] chronotropic effects are decreases in heart rate
1. Acetylcholine
2. SA and AV node; Vagus Nerve
3. Negative
28
In the parasympathetic nervous system, Acetylcholine is released and binds to [] receptors on the heart.
1. What effect does this have on the heart?
2. What are the 2 mechanisms that these receptors use to illicit a response from the heart?
* muscarinic
1. Decreases heart rate and contractility.
2. Mechanisms
1. Inhibits adenylyl cyclase
2. Directly increases the conductance of K+ in K+-ACh channels which hyperpolarizes the membrane...making it even harder to illicit action potentials.
29
T/F
On the heart, acetylcholine binds to nicotinic cholinergic receptors?
FALSE
It uses muscarinic cholinergic receptors in its parasympathetic response.
30
[] recording of the electrical activity of the heart
Electrocardiogram
31
Generation of ECG waves caused by the [] electrical activity of the heart
CUMULATIVE
32
Describe both of the axis of EKG paper....
* X-axis: Time (s)
* 1 small box is .04s
* 1 big box is .2s
* Y-axis: Voltage (mV)
* 1 small box 0.1 mV
* 1 big box 0.5 mV
33
1. If a depolarization wave is heading **towards** a (+) electrode, the deflection will be [] on EKG Paper?
2. If a depolarization wave is heading **away from** a (+) electrode, the deflection will be [] on EKG Paper?
1. Positive
2. Negative
34
A flat line on the EKG corresponds to an [] activity in the heart...
isoelectric
35
How do you get a bi-phasic deflection on EKG paper work?
The (+) electrode has to be in the "middle" of the depolarization's wave line.
36
1. A repolarization wave heading toward a (+) electrode will have a [] deflection on EKG paper?
2. A repolarization wave heading away from a (+) electrdoe will ahve a [] deflection on EKG paper?
1. Negative
2. Positive
37
What are the 6 limb leads?
* Lead 1
* Lead 2
* Lead 3
* aVR
* aVL
* aVF
38
The precordial leads record forces moving [] and [].
How many precordial leads are there?
* Anteriorly to posteriorly
* 6 precordial Leads
39
T/F
Each EKG electrode records only the average current flow at any given moment.
True!
40
What causes the slight negative dip of the Q wave on an EKG?
The fact that the left ventricle will depolarize slightly sooner thatn the right ventricle.
41
The P-Q interval represents [] []
Atrial Depolarization to the start of ventricular depolarization
42
The QRS complex represents [] [] ?
Ventricular Depolarization
43
The T Wave represents [] []?
Why is this wave positive??
* Ventricular Repolarization
* Because the heart is Repolarizing "away" from the Normal lead II - which would be a positive deflection.
44
What does the ST segment represent on an EKG?
The time from the end of ventricular depolarization to the start of ventricular repolarization.
45
1. The P Wave Represents []
2. The electrical activity of these elements... immediately follow the P wave, but do not show up on an EKG?
1. Atrial Depolarization
2. SA Node, AV Node, Bundle of HIS, Bundle Branches, Purkinje Fiber
46
1. The QRS Duration represents...
2. The QT interval represents...
1. Ventricular Depolarization
2. Ventricular Depolarization all the way to Ventrciular Repolarization
47
What does the R-R interval represents on an EKG?
The time between ventricular contractions/or depolarizations
48
T/F
If the MEA changes, then the heart has normally changed shape?
True
49
What 3 things can happen to an EKG wave when a chamber hypertrophies or enlarges?
1. EKG wave could increase in duration
2. EKG wave could increase in amplitude
3. The MEA may shift.
50
What are the 3 steps of Ischemia to Infarction?
1. In the first few minutes, **Peaked T-waves, transitioning into inverted T-Waves**
1. Early sign of ischemia
2. Still reversible
2. In the following minutes to hours, **ST-Segment elevation**
1. Approaching permanent damage
3. After Infarction, **Inverted Q-wave/new q-wave**
1. ****Permanent damage is done.
51
Arrhythmias:
1. Any alteration to normal [], [], [], or [] of the heart beat
2. Not all are [], some are fatal
3. Symptoms are usually [] and/or sudden [] - []
1. rhytm, regularity, origin, or conduction
2. dangerous
3. Palpitations, light-headedness
52
What are 2 forms of SA node Arrhythmias? Which one is more worrying?
1. Sinus Bradycardia - rate **under** 60 bpm, everything else is the same
2. Sinus Tachycardia - rate **over** 100 bpm, everything else is the same
53
What are 2 forms of Atrial Arrhythmias?
1. Atrial Flutter
1. **rapid, regular, atrial depolatizations**
2. **Has a saw tooth pattern**
2. Atrial Fibrillation
1. No coordination of atrial depolarization
2. Not necessarily lift threatening becuase 90% of ventricular filling is passive.
3. Can be fixed with a **cardioversion.**
54
What is a conduction Block?
What are the 3 tpyes of conduction blocks?
1. Depolarizations are not conducted properly from atria to ventricle
2. 3 degrees
1. 1st Degree - prolonged PR intervals (\>.2s)
1. due to increased AV node delay
2. 2nd Degree - Not all p-waves are conducted via AV node = **dropped beats**
3. 3rd Degree - No conduction via AV node between atria and ventricle
1. P and QRS are regular but **NOT IN SYNC**
55
The 1st degree of conduction blockage involves a prolonged [] interval.
What type of "delay" is this arrhythmia associated with?
1. PR Interval
2. Av Node Delay
56
What are the 2 types of 2nd degree Conduction Blockage?
1. Mobitz Type I - Wenckebach
1. PR interval gets pregressively longer until a beat is dropped
2. Mobitz Type II
1. PR interbal is set, but a beat (QRS) is still randomly dropped.
57
[] arrhythmias can be very deadly, quickly...
Ventricular
58
What 2 types of ventricular arrhythmia did we cover?
1. **Ventricular Tachycardia**
1. Fast depolarization
2. Ischemic event
3. Can lead to fibrillation
2. **Ventricular Fibrillation**
1. uncoordinated depolarization
2. Rapid Death
59
Digitalis
1. [] contractility, but [] HR
2. Inhibits []/[] ATPase
1. leads to [] intracellular Na+
3. This leads to [] gradient for Na+/Ca2+ exchanged
4. Which leads to [] Ca2+ inside the cell
1. **increase** contractility, but **decrease** HR
2. Inhibits **Na**/**K** ATPase
1. leads to **decreased** intracellular Na+
3. This leads to **decreased** gradient for Na+/Ca2+ exchanged
4. Which leads to **increased** Ca2+ inside the cell
