Phys exam 2 Flashcards
(141 cards)
1
Q
what action is responsible for the heart sounds
A
the valves closing makes the sound of the heart
2
Q
which valves are wider and why?
- AV valves
- semilunar valves
A
- AV valves are wider.
- semilunar valves are narrow because they need to shoot out with more pressure.
3
Q
The heart does not contract simultaneously.
- What direction does it contract?
- What timing stays the same?
A
- it contracts from top to bottom
- then bottom to top
- Left & right stay the same, though
4
Q
Define cardiac output
- what’s remains the same
- what may be different
How much does each portion get (%):
- renal
- GI
- muscles
- cerebral
- coronary + skin
A
- cardiac output = volume/minute
- pressure may change
- volume stays the same
- each portion
- renal, GI, muscles = 25%
- cerebral = 15%
- coronary + skin = 5%
5
Q
who discovered that veins have one-way valves
A
william harvey
6
Q
amongst the vessels (artery, arteriole, capillary, vein), which has the highest:
- velocity
- surface area
- volume
- control over BP
A
- velocity = aorta
- surface area = capillaries
- volume = veins
- control over BP = arterioles
Arterioles = greatest site of BP drop off
7
Q
what determines the resistance of an arteriole?
- what medications constrict it?
- what medications dilate it?
A
smooth muscle
- constriction = alpha1 agonists
- dilation = beta2 agonists
- NOTE: arterioles are the only** part of the vasculature that **moves
8
Q
what is the only thing that determines total peripheral resitance?
A
arterioles
9
Q
Capillaries
- are they thin/thick
- are they fast/slow
- how many layers of endothelial cells
- are they muscular/not
A
Capillaries are
- thin
- slow
- 1 layer of endothelial cells
- not muscular
10
Q
what function do the capillaries serve?
- what happens to lipid soluble material
- what happens to water soluble material
A
- capillaries are used for diffusion and picking up substances
- lipid soluble stuff goes THROUGH cells (O2, CO2)
- water soluble goes AROUND cells
11
Q
what controls flow in an arteriole?
A
sphincters control arteriole size
- ex) pre-capillary sphincters
12
Q
how many layers do arteries and veins have?
A
3
- endothelium
- external layer
- smooth muscle layer
13
Q
what moves blood forward in veins?
name 2 differences between veins and arteries
A
surrounding muscles move blood forward in veins
3 differences
- they have more capacity than arteries
- they have one-way valves
14
Q
name 5 arteriole dilators (NNHPP)
name 3 arteriole constrictors (AVN)
A
dilating substances
- NO
- nitroglycerin
- histamine
- prostaglandins
- prostacyclins
constricting substances
- angiotensin 2
- vasopressin
- nor-epi
15
Q
what’s the formula for velocity of blood flow?
A
Q = VA
- Q=flow
- V=velocity
- A=area (diameter)
if you take the same volume through a larger area, flow will be slower (ex: capillaries)
16
Q
what happens to flow if….
- resistance goes up
- resistance goes down
- pressure at beginning goes up
what’s the major way to change flow
A
- high resistance = low flow
- low resistance = high flow
- high pressure = high flow
changing resistance = how to change flow
17
Q
what’s Ohm’s law
A
Q=ΔP/R
- Q = flow
- P = pressure
- R = resistance
18
Q
how does dobutamine work for patients with pulmonary embolism?
A
dobutamine increases pressure, therefore decreasing flow
- Q=ΔP/R
(…is this right?)
19
Q
What is Poiseuille’s equation?
- what happens to resistance with
- higher viscosity
- longer tube
- narrower tube
A
Resistance = (Viscosity x Length) / r^4
- greater viscosity = more resistance
- longer tube = more resistance
- narrower tube = more resistancee
20
Q
Using Pouisseulle’s equation for resistance, explain
- dobutamine vs. congestive failure
- dilating mitral stenosis
- angioplasty
A
- dobutamine increases pressure (force of contraction)
- this decreases TPR
- this increases the flow
- dilating mitral stenosis
- increased diameter (radius)
- -> decreased resistance
- -> increased flow
- increased diameter (radius)
- angioplasty
- use thrombolytics to increase flow
21
Q
with flow, what happens if you…
- double length
- double viscosity
- double pressure
- double radius
A
flow when…
- double length = 1/2 flow
- double viscosity = 1/2 flow
- double pressure = 2x flow
- double radius = 16x flow
Only need 19% increase in radius to double the flow
22
Q
series and parallel resistance
- what happens to total resistance with
- resistors in series
- resistors in parallel
what are all blood vessels in? (series/parallel)
A
- resistance in series ADDs
- resistance in parallel DIVIDEs
All blood vessels are in SERIES
- aorta to arteries to capillaries to veins
- cardiac output goes through them sequentially
- greater resistance in ONE means added resistance to the entire system
23
Q
What blood vessel has the greatest variation in diameter (and thus, resistance)?
Thus, what do most BP medications target?
A
arterioles
- this is why most medications target arteriole diameter
- calcium blockers
- ACE inhibitors
- angiotensin receptor blockers
- beta blockers are hard to understand
- beta2 stimulation dilates
- but then why do beta blockers decrease BP?
- beta blockers decrease HR and lower renin
24
Q
what will more parallel resistors do to the total resistance of a system?
A
more parallel resistors = lower total resistance
- adding a new ORGAN will decrease total resistance
- ex) the liver is a resistor in parallel
it’s like many toll booths
- does not mean slower flow
- does not always mean narrowing
25
what is "laminar flow"?
* is it faster or slower flow
* where within a vessel would you see the fastest flow of blood
* by the walls
* center of the vessel
* laminar flow = faster flow
* smooth layers flow quickly
* quickest flow is in the center, without the turbulence from the walls
26
R\_\_\_\_\_\_'s number measures turbulence
what happens to turbulence as you increase...
* density
* diameter
* velocity
* viscosity
**_Reynold's number = turbulence_**
_HIGH turbulence_
* more dense
* more diameter
* more velocity
_LOW turbulence_
* more viscosity
think NASCAR (wider/faster road, dense traffic = racing)
quicksand = not racing
27
what are "shearing forces"
* **Means “breaking flow into layers”**
* More shear = greater difference in velocity
* If everyone’s the same speed, shear is low
* Shear is huge along the walls of a vessel
* Flow is slowest along the walls of a vessel
28
what is compliance?
compliance = volume / pressure
* "how easy going you are without feeling pressure"
* high compliance = a gallon of liquid goes in and pressure doesn't change
* low compliance = a gallon of liquid goes in and pressure shoots up
29
which are high compliance (fill quickly with no pressure change)?
which are low compliance (fill slowly with pressure change)?
* lungs
* veins
* skull
* old arteries
* lymphatics
* stomach
HIGH compliance
* lungs
* veins
* lymphatics
* stomach
LOW compliance
* old arteries
* skull
30
What are the dangers of LOW compliance?
* blood pressure
* vessels
* which body part is this dangerous for
LOW compliance
* causes hypertension
* causes rupturing of blood vessels
* SKULL = dangerous
* emptying a little bit causes a BIG pressure change
* decompressing skull is dangerous
31
What is good regarding compliance of:
* skull
* arteries
* lung
* compliant skull = BAD
* compliant arteries = GOOD
* don't want small volume changes to make HTN
* **_lungs_**
* too compliant = bad (emphysema)
* too non-compliant = bad (fibrosis)
32
Compliance of blood vessels
* what's more compliant?
* arteries
* veins
* why?
what happens to compliance artery\>capilllaries\>veins
* veins are more compliant
* arteries = non-compliant because they need to be able to **_push_**
* compliance goes **_UP_**, pressure goes **_DOWN_** as you go from artery \> capillary \> vein
33
what happens if compliance decreases in blood vessels?
* high blood pressure
* strokes
* myocardial infarction
34
Interpret the attachment
N/A
35
What kind of vessel is the site of pressure and compliance change?
* aka what kind of vessel controls TPR
* Site of pressure change
* Site of compliance change
* Controls vascular resistance aka TPR
**BP = 90-100 mmHg going *INTO* arterioles**
**BP = 30 mmHg _LEAVING_ arterioles (60-70% drop)**
36
Why is there a big pressure change with blood entering/leaving capillaries?
Pressure
* 30 mmhg entering
* 5 mmhg leaving
BIG percentage change
Because capillaries need to push nutrients out
37
More elasticity = ___________ compliance
* More elasticity
* LESS compliance
* ex) arteries
LESS springy would mean better compliance
38
With blood pressure
* greater pressure = _______ stroke volume
Which phase lasts longer (systolic/diastolic)?
* therefore, the mean BP is closer to which?
What is "pulse pressure"?
* With high compliance, would you see a _large or small_ pulse pressure?
* What's the formula for _mean arterial pressure_?
* greater pressure = greater stroke volume
* diastolic phase lasts longer
* you spend 2x as much time in diastole!
* mean BP is closer to diastolic value
* pulse pressure = difference between sys/dias
* high compliance = small pulse pressure
* MAP = diastole + 1/3 pulse pressure
39
what causes the "dicrotic notch" in a heartbeat?
* Dip down in BP after systole
* The springy aortic valve “rebounds” after closing and pushes up, pushing pressure up.
* Like jumping down and up on a trampoline
Image:
* Closure of aortic valve (A2) makes pressure go down
* Rebounding back UP of aortic valve pushes pressure UP
40
What is the MOST “physiologically accurate” measure of organ perfusion
Mean arterial pressure (MAP)
41
What happens to compliance with _atherosclerosis?_
* what happens to BP/MAP
* Does stroke volume change?
The harder the arteries, the less compliant
Greater pressure from the same original stroke volume
Raises Systolic BP, MAP
42
What's aortic stenosis?
What chamber experiences higher pressure as a result?
* Crunchy, clogged aorta
* Blocks exit of blood from Heart
* **Normal** = NO gradient (no difference) between LV and aorta pressure. Both 120
* **Stenosis** = LV pressure \> aorta pressure
43
Which valve(s) lesions give you
* SOB
* CHF
All valves can
44
What happens to the pulse as a result of **aortic stenosis**?
* What happens to timing of aortic valve closure
* What is the timing in relation to the pulmonary valve closure
* How will this sound on exam?
* Delays the pulse
* Decreases perfusion of the brain
* Can result in syncope
* Results in delayed closure of the aortic valve
* Was supposed to be before the pulmonary valve
* Systolic crescendo-decrescendo = murmur (delayed)
45
A long term smoker comes with increasing swelling of his legs. There is ascites and enlargement of the liver and spleen. Which is most likely to be present?
A.Right ventricular hypertrophy
B.Patent foramen ovale
C.Left ventricular atrophy
D.Pulmonary hypotension
E.Increased cardiac output
A.Right ventricular hypertrophy (fyi, the disease is COPD)
46
What happens to the blood in the heart with aortic regurgitation?
* What happens to pulse pressure
* Which chamber is affected?
* Regurgitation = insufficency
* Blood spills backward
* Heart creates an extra high EF to compensate for spillage
* Greater pulse pressure
* LV gets enlarged (bad)
47
What is compliance of the lungs (high/low)
How about the pulmonary artery?
* Pulmonary Artery = very compliant
* to allow for it to be filled with air volume
* Low pressure
* Lungs are “Soft and Squishy”
48
1Which part of vascular system has the greatest CHANGE in pressure?
a. Aorta
b. Arteries
c. Arterioles
d. Capillaries
e. Veins
c.Arterioles
49
What is the main reason Mean arterial pressure is closer to diastolic pressure?
a. Arteries are less compliant than veins
b. Elasticity of Arterioles
c. Loss of fluids by hydrostatic forces in capillaries
d. Two-thirds of cardiac cycle is in diastole
d.Two-thirds of cardiac cycle is in diastole
50
3. Which is more elastic?
a. Arteries of older persons
b. Capillaries of young people
c. Veins of older persons
d. Lymph channels at any age
a.Arteries of older persons
* **Elasticity opposes compliance**
* **Thick elastic walls = arteries**
51
4. What is the site of action of treatment of Aortic regurgitation?
a. Aorta
b. Pulmonary artery
c. Arterioles
d. Capillaries
e. Veins
**c.Arterioles**
* All of our drugs target arterioles
* Aorta = on LEFT
* Pulmonary artery = on RIGHT
52
What is the most accurate test of aortic stenosis?
a. Electrocardiogram (EKG)
b. Chest Xray
c. Left heart catheterization
d. Right heart catheterization
e. Echocardiogram
**c.Left heart catheterization**
It’s the only way to get the most specific pressure measurements
53
**Why do aortic stenosis and regurgitation cause dyspnea?**
a. Increased hydrostatic pressure in peripheral capillaries
b. Loss of oncotic pressure
c. Pulmonary hypertension
d. Increased pulmonary capillary hydrostatic pressure
e. Increased venous return to right heart
**d.Increased pulmonary capillary hydrostatic pressure**
* Peripheral capillaries are your hands, and you don’t breathe from there
* Oncotic pressure = plasma proteins and that doesn’t deal with this
* D is correct because blood & fluid gets backed up into the lungs, then pushing fluid back into the alveoli, making you SOB
54
A man with shortness of breath that has been happening for months with a systolic murmur going to his neck. What test will you do first to show the diagnosis?
a. Xray
b. Cardiac Catheterization
c. EKG
d. Echocardiogram
d.Echocardiogram
55
Injection drug user with fever and a murmur. Blood cultures grow Staphylococcus. He develops sudden shortness of breath, lung congestion and rales. Murmur worsens. What structure broke?
a. Chordae/Papillary muscle
b. Atrial septum
c. Aorta
d. Pulmonary artery
a. Chordae/Papillary muscle
56
A woman is in intensive care with overwhelming infection and septic shock. Her blood pressure is 70/40 and pulse 120/minute
Which of these will help her?
a. Nitric Oxide
b. Nitroglycerin
c. Histamine
d. Prostaglandins
e. Norepinephrine
e.Norepinephrine
57
54 female, in emergency department with severe hypertensive crisis. Headache. Dyspnea. Confused. BP 210/140mm hg. Drugs affecting which of these vascular structures will lower blood pressure best?
a. Aorta
b. Arteriole
c. Capillaries
d. Vein
b.Arteriole
58
How the heart is special (not a question)
* Nodal tissue that initiates its OWN beating
* Unique conduction system (Bundles and Purkinje fibers and second modulating AV node
59
Which node is the fastest in the heart (SA or AV)?
SA is the fastest
60
What is the sequence of the electrical system in the heart?
* SIABBPM
* SA node
* internodal tracts
* AV node
* bundle of his
* bundle branches
* purkinje fibers
* myocardium (muscle cells)
61
Does nodal tissue need an outside stimulus to depolarize?
What happnens with the presence of an outside stimulus?
What's the first conduction structure that's in the ventricles?
* No outside stimulus needed to depolarize the heart
* however, an outside stimulus can speed/slow the heart
* The first fiber in the ventricles is the bundle of His
62
SA node
* nickname?
* what gives it automaticity?
* what's it's rate per minute
* what structures does it split into
* pacemaker
* is the FASTEST one
* "pacemaker cells" give it automaticity
* rate = 60-100/min
* splits into internodal pathways
63
How many internodal pathways are there and what do they lead to?
* what's their function?
* 3 internodal pathways
* leading to the AV node
* there are 3 because it offers multiple **_detours_** to AV node in case one is compromised
64
Atrial fibrillation
* what is "fibrillation"
* why is it **_atrial_** fibrillation?
* is ventricle filling active or passive?
* how much of CO is done by atrial systole?
* what's the greatest risk factor
* why
* what's the greatest risk of complication
* fibrillation = seizure of the heart
* happens when SA **_and_** internodal pathways aren't working
* **_atrial_** because it stops before it hits the venricles
* ventricle filling is passive
* approx 10% of CO is from atrial systole
* greatest risk factor = HTN
* because it leads to cardiomyopathy
* stretching the heart leads to short circuiting
* greatest complication = stasis \> clots/emboli \> stroke
65
AV node
* is conduction relatively fast or slow?
* what is it responsible for
* what's its rate per minute
* AV conduction is relatively slow
* responsible for regulating rate
* rate is 50-60 per minute
66
SA or AV node?
* which is the site of more treatments?
* which is the site of more dys-rhythmias?
* what's less severe fibrilliaton called?
* name a few drugs (x3)
* AV node is the site of treatments
* AV node is the site of dysrhythmias
* **_atrial flutter_** is treated
* calcium blockers
* beta blockers
* digoxins
67
as you go down the heart, does conduction get faster, slower, or stay the same?
* is a left or right bundle branch block more dangerous?
* signal gets slower as you go down
* LEFT bundle branch block is way more dangerous
* because we LIVE off of the LV
68
what element is **_cardiac resting membrane potential_** tied to?
* why this specific element?
* what equation ties to this
what's the key concept difference between cardiac action potential and nerve/muscle action potential?
* resting membrane potential is tied to **potassium**
* ****because it's **_ungated_**
* nernst equation explains this
* balance of...
* concentration forces vs. electrical forces
Difference between cardiac vs. nerve/muscle
* it's SLOWER. there's a prolonged plateau that allows time to move the blood in the heart
* you don't need time for this in nerve/muscle
69
How long does depolarization take in the SA node versus...
* the purkinje fibers?
* skeletal muscle?
What's the point of longer refractory periods?
* what's junctional rhythm?
What happens during the plateau?
* **_Depolarization times_**
* 150 ms = SA node
* 300 ms = purkinje fibers
* 1 ms = skeletal muscle
* longer refractory period = allows heartbeat to be **sequential**
* otherwise, heart pumps in both directions at the same time (**_junctional rhythm_**)
* the **plateau** = prolonged deporalization
* isovolumetric contraction
* allows blood to move around
* it's **_the_** unique feature of cardiac action potential
70
When you cardiovert someone, do you do it
* before the refractory period
* after the refractory period
* during the refractory period
What's the wrong time and what would happen if you did it at the wrong time?
* you cardiovert any time when you're NOT in the refractory period
* if you did it **_during_** the refractory period, you would cause v-fib or asystole
71
What phase (1,2,3,4) is the plateau?
What occurs during this time?
What's the status of the membrane potential?
Plateau = phase 2
* Time for
* fluids to move out of heart
* Wave of electricity to spread
* Caused by Ca++ going INTO cells
* Positive IN keeps membrane potential UP!
72
In the heartbeat, what happens to ion channels (Na, K, Ca) during...
* Phase 1
* Phase 2
* Phase 3
* Phase 4
* Phase 5
1. Na channels open
2. Na channels close, some K channels are open
3. Ca2+ channel open. Positive charges going in maintain plateau
4. Voltage gated K channels (Big ones!) open
5. Back to resting membrane potential
73
**_Phase 0_**
* what's this called? the \_\_\_\_\_\_\_\_
* what ion gates open?
* what happens to the polarity?
Phase 0 = the **_upstroke_**
* **_aka atrial, ventricular, purkinje_**
Na gates open, shoots up to +20mV
* Na **_inactivation**_ gates close before then, because they're _**pre-timed_**
* EQ potential would be +65mV, but we never reach that
when membrane is most negative, that's when you have the greatest voltage change per time
74
What happens at Phase 1 of the heartbeat?
* what channels close
* what channels open
* what signals the end of phase 1
What happens at Phase 2 of the heartbeat?
* what channels open
* what stops repolariztion
* what ions are L-type channels and what do they do
* name some calcium channel blockers (x3)
* does this slow a sinus heart rate? why?
Phase 1
* Sodium channels have closed
* Un-gated **potassium** channels open
* (K+) OUT, brings the action potential DOWN towards repolarization, until it hits **_plateau_**
Phase 2
* Ca channels open
* **Positive** going IN stops repolarization (the plateau)
* •The “L-type” (or LONG) Ca channels PREVENT repolarization
* They are blocked by calcium channel blocking medications (which allow repolarization)
* (nifedipine, amlodpine, diltiazem)
* They do not SLOW a sinus heart rate because if you're blocking the Ca channel, it repolarizes sooner
75
**What happens during phase 3?**
* which ion gates open/close
* what ion action allows RE-polarization
**What happens during phase 4?**
* what is the final resting membrane potential?
**_Phase 3 repolarization_**
* Voltage gated K+ channels open
* Ca channels CLOSE
* Voltage gated channels are way bigger, more volume
* Positive K+ OUT allows repolarization
**_Phase 4_**
* Back at resting membrane potential (-85 mV)
* Based on Un-gated K+ channels
76
Final summary of heartbeat (phase 0-4)
* Does this happen in nodal or non-nodal tissue only?
* What heart structures does the depolarization travel through?
Final summary
* This is unique to the part of the conduction system in the heart that is NOT NODAL TISSUE (NOT THE SA NODE)
* This is what goes through the atrium, ventricles, and purkinje fibers.
* Plateau is unique. And it is **_not_** automaticity.
77
Learn the attached image
78
Learn the attached image
79
How is the SA node different than the **_other_** neural tissue in the heart?
* Un-stable phase 4
* Phase 4 is constantly depolarizing Na+
* Upstroke (Phase 0) is based on CALCIUM (not sodium)
* No phase 1 or 2
* Automaticity unstable Phase 4
* -65 mV to -45mV
* “Funny sodium channels”
* Funny = Constantly Depolarizing
* Funny channels **shut off** as it rises to **-45mV** to allow calcium to go in
80
Learn the following image **_regarding heart depolarization_**
81
Regarding heart depolarization, what speeds/slows phase 4?
* sympathetic ____ phase 4
* parasympathetic _____ phase 4
* ex) NE/epi = sympathetic
* ex) acetylcholine = parasympathetic
* sympathetic SPEEDS phase 4
* parasympathetic **slows** phase 4
* "vagal stimulation"
82
Effects of parasympathetic (vagal) and sympathetic nerve activation on AV nodal action potentials
* which speeds and which slows?
83
What are latent pacemakers, in general?
* what are the three latent pacemakers
* what are their rates/minute
**Latent** pacemakers = **backup** emergency pacemakers
* AV node: 40-60/minute
* Bundle of His: 40/minute
* Purkinje fibers: 20-30/minute
84
Solve the attached question
Where in the heart is the defect?
a. Internodal Pathways
85
86
87
88
What's the definition of **conduction velocity**?
* what tissue in the heart is the fastest
* **_which is the slowest_**
* why??
* what are the speeds
* how does resistance relate to conduction
What are some types of abnormally FAST conduction (x3)?
* what syndrome is associated with this
* how is it cured
conduction velocity = speed at with AP is propagated (m/sec)
* purkinje fibers = fastest (2-4 m/s)
* AV node = slowest (0.01 m/s)
* lower resistance = faster conduction
AV node **must** be slow to allow ventricles to fill
* prevents contraction of ventricles before the heart gets a chance to fill completely
types of abnormally FAST conduction
* A-fib
* supraventricular tachycardia
* WPW syndrome = pre-excitation syndrome
* sends you into either sVT or VT
* **_cured by ablation_**
89
Propagation of action potential in the heart
* What's the relationship between upstroke and current
* What does this mean for voltage per until of time
* What's the resistance of
* the membrane (high/low)
* internally (high/low)
Velocity is the size of the inward current
* More upstroke = More current=dVoltage/dTime
* High membrane resistance + low internal resistance = SUPER FAST! (keeps it all inside)
* Tunnel wall = high membrane resistance (thick and insulated to take the electricity forward)
* No traffic/all green lights = low internal resistance
* **_Gap junctions_** also speed things up
90
What is excitability in regards to AP in the heart?
* definition
* what ion channels does this relate to
Excitability
* Capacity to generate an action potential
* Amount of current needed to get to threshold
* How easy it is to open sodium activation channels
91
In the heart...
* What's a refractory period?
* What's an absolute refractory period?
* What's a relative refractory period?
**_Refractory period:_** Depolarization will...
1. Open Na activation gates
2. Close inactivation gate (slower)
* Closed inactivation gates make the cell “refractory”
* **Allows one-way flow**. Time delay allows time to push the blood out
**_Absolute refractory period_**
* You can’t depolarize while you’re already depolarized
* Sodium channels closed
* No stimulus can create an action potential
* Includes
* Upstroke (phase 0, 1)
* Plateau (phase 2)
* Most of repolarization (phase 3)
* **ARP ends when it comes below -50 mV**
**_Relative refractory period_**
* Can be depolarized by an extra big stimulus
* Some Na channels have recovered
* In “effective” refractory period, impulse cannot propagate
92
Learn the attached image
* Autonomic cardiac effects
93
Learn the attached image
* Dromotopic effects
* What is "dromo" latin for?
* Which is fast? (sym/parasym)
* Which is slow? (sym/parasym)
* What drug class creates a positive dromotopic effect?
DROMO = RACE
Sympathetic
* Positive **_dromotopic effects_**
* AV fast!
* Beta-1
* Alpha does not touch heart!
Parasympathetic
* Negative **_dromotopic effects_**
* AV slow!
94
Acetylcholine effect on the heart
* What effect does this have on HR?
* What effect does it have on the polarization of the SA node?
* What effect does this have on the special Gk protein?
95
**Electrocardiogram: define...**
* P wave
* PR interval
* QRS
* T wave
* ST wave
* **P Wave** = Atrial depolarization
* **PR interval** = Time for atrial depolarization to hit ventricles (from SA -\> AV node)
* **QRS** = Ventricular depolarization
* **T Wave** = Ventricular repolarization
* **ST wave** = Important for ischemia
* depression implies myocardial ischemia (decreased blood)
* elevation is even worse, implies MI
96
Why are we unable to see the atrial repolarization in the QRS?
What's the QTc?
**Atrial repolarization** is buried in the QRS because the atrium is much smaller in terms of muscle, and we don’t actually see it in the repolarization
**_QTc_** = a QT corrected for the heart rate, tells you who will have a fatal arrhythmia
97
**Heart Rate Calculation**
* What does each box represent?
* How many boxes makes a heart rate of 60 (aka 1bps)?
* Each box is 0.2 seconds
* 5 boxes makes a HR of 60
98
A 37 year old man with a history of testicular cancer comes to the office for a follow up.
EKG shows this. What is it?
* a. Tachycardia
* b. Normal
* c. Bradycardia
c. Bradycardia
* This is a harmless sinus bradycardia because you see a P wave for each QRS.
* No treatment required.
* 7 big boxes apart (5+) is very slow
99
A patient is lightheaded with low blood pressure
What is the treatment?
* a. Atropine
* b. Acetylcholine
* c. Muscarine
* d. Tricyclic antidepressant
a. Atropine (speeds HR. anti-cholinergic)
* Tricyclic antidepressants have mild anti-cholinergic effects, but we can’t use these therapeutically
100
64 year old woman with light headedness.
What is the MECHANISM of the treatment?
a. Faster opening of Voltage gated K+ channel
b. Slowing Na+ channel
c. Speeding/shortening Phase 4
d. Opening Ca++ channels in SA node
Speeding/shortening Phase 4
* atropine is anti-cholinergic
* so, it speeds up phase 4
* you hit threshhold faster by inhibiting Ach on SA and AV nodes
101
A patient has myasthenia gravis. What is the mechanism of adverse effects of treatment on heart?
* a. Closing Na+ channels
* b. Prolonging Phase 2 (plateau) in purkinje fibers
* c. Gk channels hyperpolarize SA node (by increasing extrusion of K)
* d. Beta 1 stimulation
* e. Loneliness
c. Gk channels hyperpolarize SA node
* (by increasing extrusion of K)
* Use pyridostigmine and neostigmine.
* They inhibit Ach-esterase.
102
Where is the location of the defect?
a. Internodal pathways
b. AV node
c. His Bundle
d. Purkinje
a. Internodal pathways
* The R to R is irregularly irregular
103
What is the FASTEST way to fix (convert) this patient to a normal sinus rhythm?
* a.Beta blockers
* b.Calcium Channel Blockers
* c.Digoxin
* d.Warfarin
* e.Electrical
e.Electrical (aka cardioversion)
104
What is the mechanism of the medication for slowing this patient?
* a. Beta ONE blockade
* b. Beta TWO blockade
* c. Potassium channel
* d. Muscarinic receptors
* e. Nicotinic receptors
Beta ONE blockade
* This is another a-fib
* The drugs all slow down the rate, they don’t convert the rhythm
* Atrial Flutter
* R to R intervals are much more regular
105
Where is the this beat originating?
* a. SA node
* b. Internodal pathways
* c. AV node
* d. Bundle of His
* e. Purkinje Fibers
e. Purkinje Fibers
Wide = slow (myocyte to myocyte)
This is ventricular tachycardia
106
Why is this complex wide?
* a. Decrease Phase 4
* b. Increase Potassium release (hyperpolarization)
* c. Slow conduction through myocardial tissue
c. Slow conduction through myocardial tissue
* (how an artificial pacemaker looks)
* Wide = slow
107
Fill in the blanks--what happens at each stage?
108
# Fill in the values
* Stroke volume
* definition, number
* LVEDV
* definition, number
* Ejection fraction
* definition, number
* Cardiac output
* definition, number
* How many mL/min, roughly?
* Stroke volume
* LV diastolic - LV systolic volume
* Usually 70ml
* LVEDV
* LV end diastolic volume
* usually 120 ml
* Ejection fraction
* SV/LVEDV
* usually 55-70%
* Cardiac output
* SV x HR
* usually 70 x 70 = 4900 ml/min
109
If pressure and resistance stay the same...
* does increasing LVEDV change CO?
* what's another word for LVEDV?
* Yes, more LVEDV = more CO
* another word for LVEDV = preload
* more preload
* = more CO
* = more SV
* = more work
* any increase in SV or CO = more work needed!
110
# Define myocardial "work"
\_\_\_\_\_ x _____ = myocardial work
* does more work mean more/less O2 consumed?
SV x aortic pressure = work
SV x afterload = work
* high BP kills you
* afterload reduction saves you
* vasodilation good for CHF
* lower work = less O2 consumed
111
More afterload = (more/less) work?
More pressure = (more/less) work?
More afterload = (more/less) stroke volume?
More afterload = more work
* More work = more oxygen consumed
* more oxygen consumed = more ischemia
* more ischemia = ARRYTHMIA & DEATH
112
* What's harder on the heart?
* Does it take more work to pump volume or pressure?
* What's the #1 symptom of aortic stenosis (greater afterload)?
More pressure = more work required
* greater volume isn't as big of a deal
#1 symptom in afterload increase = chest pain (angina)
113
More pressure = more work
More work = more O2 needed, heart dies
Congestive heart failure
* ACE inhibitors ____ afterload
* ACE inhibitors ____ mortality
* Digoxin ____ afterload
* Digoxin ____ mortality
WHY?
Congestive heart failure
* ACE inhibitors decrease afterload
* ACE inhibitors decrease mortality
* Digoxin doesn't change afterload
* Digoxin doesn't change mortality
WHY?
* digoxin = making a heart work harder. afterload isn't addressed
114
Law of Laplace
* wall tension
* pressure
* radius
* What's the relation?
* How do you lower wall tension?
* Why does a heart thicken with greater tension?
T = Pr
* bigger radius = bigger tension (like a balloon)
* lower wall tension by
* decreasing radius
* by lowering pressure
* heart thickens to spread out the load
* double thickness = half tension
115
FIck principle
* cardiac output
* 1g/dl hgb = 1.33 mL oxygen
* 15g/dl hgb = 20mL oxygen/dL
* = 200 mL O2 /L blood
* but only 50ml is released per L blood
* artery sat = 100%
* vein sat = 75%
If you consume 250mL O2 per minute, what's the CO?
50ml O2 released per L of blood per minute
thus, 5L blood per minute = CO
116
How much of CO does atrial systole contribute?
10-15%
117
What's first? atrial depolarization or ventricular depolarization?
atrial depolarization
118
What's S3?
* rapid ____ filling
* pathologic of _____ & \_\_\_\_\_\_
* treatment is required? (y/n)
What's S4?
* caused by _____ systole into \_\_\_\_\_\_\_
* pathologic of ______ & \_\_\_\_\_\_
* treatment required? (y/n)
S3
* rapid **ventricular** filling
* pathologic of **CHF** **& pulmonary edema**
* treatment **_is_** required
S4
* caused by atrial systole into stiff non-compliant ventricle
* pathologic of H**TN & LV hypertrophy**
* treatment **_not_** required
119
Other names for LVEDV
* does LV depend on body size?
* what's CO adjusted for BMI?
* what's inotropy?
* sarcomere length
* ventricular filling
* preload
* RA pressure
* filling pressure
LV is dependent on body size
* cardiac index = adjusted CO
* inotropy = contractility
120
How does each respond to CHF?
* kidney
* carotid baroreceptors
Why is there even a reaction in the first place?
CHF = they sense less perfusion from less pumping, so they're going to try to increase blood pressure to increase perfusion.
THESE ARE ALL TEMPORARY FIXES. YOU MUST REDUCE AFTERLOAD (otherwise heart will get tired and die if ony preload is increased)
Kidney
* increase renin
* increase angiotensin
* increase aldosterone
Carotids
* increase ADH
121
What does more venous return do to...
* RA pressure
* LV filling
* LVEDV
* Stroke volume
* CO
More venous return
* more RA pressure
* more LV filling
* more LVEDV
* more stroke volume
* more cardiac output
122
If you double the HR, do you double the CO?
* not necessarily
* because if you double the HR, you decrease the filling time
* therefore although HR goes up
* SV goes down
* if you're exercising, you're also changing the pressure
* that's why when you exercise, HR and CO both go up--because you've changed the pressure
123
What's the **_maxiumum_** for the heart
* RA pressure (what happens when exceeded?)
* CO
What's the **_minimum_** for the heart
* vascular blood volume ('unstressed')
Maximum
* RA pressure = 4mmhg
* CO = 9L/min
* after 4mmhg, RA blood will squirt out
Minimum
* 4L of venous volume "unstressed"
* any less than this and you wont have a blood pressure
* "fill the tank before anything goes through the pipes"
124
Arteries/veins
* what is "stressed volume"
* what is "unstressed volume"
* filling the tank before anything goes through the faucet
* 4L is unstressed venous volume
* anything over 4L is arterial "stresssed" volume
Constriction of veins means decreasing vein compliance, which will shift volume from unstressed to stressed (raises BP)
125
What's the most important factor for cardiac output?
* Venous return creates (RA) pressure
* RA pressure creates LV filling
* LV filling becomes LVEDV
* LVEDV = Stroke Volume
* Stroke volume x Heart rate = CO
Therefore! **Venous Return = Cardiac Output**
126
What do you do for a patient in acute pulmonary edema?
* What needs to be addressed immediately?
Patients with acute shortness of breath, rales, edema, S3 gallop need VOLUME removed from lungs FAST!
1. Venous Dilation
2. Increasing “unstressed” volume
3. Diuretics
127
What percent of the body's bood is held in the venous system?
Name some venodilators
60%
* nitrates/nitros/amyl nitrates
* morphine (acute pulmonary edema)
* furosemide
* sildenafil (nitric oxide--Viagra)
* prostacyclin
128
What does venous dilation do to
* unstressed volume
* stressed volume
* vein compliance
* venous return
venous dilation
* greater unstressed volume
* less stressed volume
* greater vein compliance
* lower venous return
129
TPR
* what kind of vessel has greatest impact on TPR?
* what happens to venous return with
* high TPR
* low TPR
* arterioles control TPR
* relaxing the arterioles allows blood to move **_forward_**
* high TPR = low venous return
* low TPR = high venous return
130
Inotropic effects
* What do **positive inotropes** do for...
* Moving blood (backwards or forwards?)
* contractility (up/down)
* stroke volume (up/down)
* RA pressure (up/down)
* cardiac output (up/down)
131
Decreased RA pressure's effect on **volume of venous return to the heart**
* increased/decreased?
Low RA pressure = more venous return
* you're making it easier for blood to re-enter the heart
132
Increased blood volume leads to more/less...
* stressed volume?
* cardiac output
* RA pressure
what change in venous compliance can achieve the same effect?
More blood volume equals
* greater stressed volume
* greater cardiac output
* greater RA pressure
low venous compliance = same as more blood volume
133
what's the most effective way to increase stroke volume?
* increase filling
* increase contractility
what will increase stroke volume
* sympathetic stimulation
* parasympathetic stimulation
increase stroke volume by increasing **contractility** with a **positive inotrope** (which works via **_sympathetic stimulation_**_)_
* _sympathetic stimulation_ **will always increase CO**
134
135
What does increased TPR do to
RA pressure aka LVEDV
CO
136
A
137
D
138
A
139
D
140
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