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127 Cards in this Set

  • Front
  • Back
What is contained in the Carotid Sheath and what is the orientation of the stuff?
1. Internal Jugular Vein (lateral)
2. Common Carotid Artery (medial)
3. Vagus Nerve (posterior)

vein
artery
nerve
(VAN)
Most of the time, what are the brances of the Right Coronary Artery? what do they supply?
Acute Marginal Artery: RV
PDA: posterior IV septum
What's the kicker with the PDA?
It can be a branch of the RCA or LCA, Depending on which CA it comes off determines if the heart is a "right" or "left" dominant heart.

80% are right dominant
20% are left dominant
What are the normal branches off the LCA? supply?
LAD: apex and ant. IV septum
Circumflex Artery: post. LV
Most common artery occluding in coronary artery disease?
LAD
When do coronary arteries fill?
Diastole
What is the most posterior part of the heart? clinical significance?
Left Atrium
If it gets enlarged it can compress the esophagus--->dysphagia
or
compress the recurrent laryngeal leading to hoarsness
What can you auscultate at the upper right sternal border? what abnormalities can be detected here?
Aortic Valve

Systolic Murmur:
aortic stenosis
flow murmur
aortic valve sclerosis
What can you auscultate at the upper left sternal border? what abnormalities can be detected here?
Pulmonary Valve

Systolic Ejection Murmur
pulmonic stenosis
flow murmur from ASD
What can you auscultate at the lower left sternal border? what abnormalities can be detected here?
Tricuspid Area

Pansystolic Murmur
tricuspid regurge
VSD

Diastolic Murmur
tricuspid stenosis
ASD
What can you auscultate at the Apex? what abnormalities can be detected here?
Mitral Valve

Systolic Murmur
mitral regurge

Diastolic Murmur
mitral stenosis
Cardiac Output = ??
Stroke Volume * Heart Rate
What is the Fick Principle?
CO = rate of O2 consumption / (arterial O2 - venous O2)
in terms of not other blood pressures, what does Mean Arterial Pressure = ?
CO * TPR
In terms of other BP's what does MAP = ?
MAP = 2/3Diastolic + 1/3Systolic
What does Pulse Pressure equal?
systolic - diastolic
What does Stroke Volume = ?
2 equations
SV=CO/HR

SV=EDV-ESV
Three things that affect Stroke Volume?
Contractility
Afterload
Preload
How can those three things Inc SV?
Inc Contractility
Inc Preload
Dec Afterload
What are 4 ways to increase Contractility (and thus SV)?
1. Catecholamines (stimulate Ca pump in SR)
2. Inc Intracellular Ca
3. Dec extracellular Na
4. Digitalis (inc intracellular Na, resulting in inc Ca)
What are 5 ways to decrease contractility (and thus SV)?
1. Beta1 blockade
2. Heart Failure
3. Acidosis
4. Hypoxia/hypercapnea
5. Non-dihydropyridine CCB's
4 ways to increase Myocardial O2 demand?
Inc Afterload
Inc Contractility
Inc HR
Inc Heart Size (inc wall tension)
what is preload?
VENTRICULAR EDV
what is afterload = ?
MAP
How do venodilators and vasodilators affect preload and afterload?
Venodilators (e.g. NO) dec preload

Vasodilators (e.g. hydralazine) dec afterload
What does Ejection Fraction = ?
SV/EDV = (EDV-ESV)/EDV
What is Ejection Fraction normal at?
> or = 55%
In terms of viscosity and radius, what is Resistance = ?
[8(viscosity) * length]/pie*radius^4)
How do you calculate resistance in series vs parallel?
Total resistance in series = R1 + R2 + R3...

In Parallel = 1/R1 + 1/R2 + 1/R3...
In us, what does viscosity mostly depend on?
Hematocrit
Three "states" we can be in that will increase our viscosity?
1. Polycythemia
2. Hyperproteinemic states (e.g. multiple myeloma)
3. Hereditary Spherocytosis
What causes the S1 sound? where's it loudest?
Mitral and Tricuspid closure

loudest at mitral area
What causes S2? where's it loudest
aortic and pulmonary valve closure

loudest at LSB
What causes S3 and when do you hear it?
Heard early in diastole during rapid ventricular filling

associated w/ inc filling pressure
more common in dilated ventricles
normal in kids
When do you hear an S4 and what causes it?
late diastole
High Atrial Pressue
Associated w/ Ventricular Hypertrophy; LA must push against stiff LV wall
What are the waves of a Jugular Venous Pulse? what do they represent?
"a" wave = atrial contraction
"c" wave = RV contraction (causes tricuspid to bulge into RA)
"v" wave = inc atrial pressure due to filling against closed tricuspid valve
What is S2 splitting and what increases it?
When the aortic valve closes before the pulmonic

Inspiration increases this difference
What is Wide Splitting? when does it occur?
Wide: means aortic and pulmonic valve closure is wider than normal and inspiration just makes it worse

happens w/ pulmonic stenosis
What is Fixed Splitting? when does it occur?
When aortic and pulmonic closure are wider than normal and inspiration has no effect on them.

associated w/ ASD's
What is Paradoxical Splitting? when does it occur?
When inspiration actually lessens the splitting between aortic and pulmonic closures

associated w/ aortic stenosis
Why does Inspiration cause splitting?
Inspiration---> drop in intrathoracic pressure---> inc capacity of pulm. circulation--->pulmonic valve closes later to accomodate more blood entering lungs
AND
aortic valve closes earlier b/c of decreased return to left heart
Why does Pulomonic Stenosis create wide splitting?
RV emptying is delayed---> delayed pulomonic sound
Why do ASD's lead to Fixed Splitting?
ASD's cause a Left to Right shunt---> inc flow through the pulmonic valve--->delayed closure
What does Aortic Stenosis cause paradoxical splitting?
It delays LV emptying.
Normal order of valve closure is reversed, so P2 occurs before a delayed A2
With inspiration, the later P2 and earlier A2 move closer together
What does a Holocystolic, High Pitched "Blowing" Murmur indicate?
Mitral or Tricuspid Regurgitation
Where should you auscultate for Mitral Regurgitation?
Loudest at Apex and radiates towards axilla
Where should you auscultate for Tricuspid Regurgitation?
Loudest at tricuspid area (lower LSB)
Radiates towards right sternal border
What can cause Mitral Regurgitation?
Ischemic Heart disease
Mitral Valve Prolapse
LV Dilation
What can cause Tricuspid Regurgitation?
RV Dilation
Endocardititis
What can cause Mitral/Tricuspid Regurgitation?
Rheumatic Fever
What does Aortic Stenosis sound like?
Crescendo-Decrescendo Systolic Ejection Murmur following an Ejection Click

Radiates to carotids/apex
what is aortic stenosis most commonly due to?
age-related calcific stenosis
What does a VSD sound like? where best to hear it?
Holosystolic, Harsh Sounding Murmur

Loudest at Tricuspid area
What does a Mitral Valve Prolapse sound like?
Late Systolic murmur w/ midsystolic click
What can Mitral Prolapse predispose you to?
Infective Endocarditis
What does Aortic Regurgitation sound like?
Immediate High Pitched "blowing" diastolic murmur
Typical causes of Aortic Regurgitation?
Aortic Root Dilation
Bicuspid Aortic Valve
Rheumatic Fever
What does Mitral Stenosis sound like?
Opening Snap
then
Delayed rumbling late diastolic murmur
Common cause of Mitral Stenosis?
Rheumatic Fever
What does a PDA sound like?
Continuous machine-like murmur
Where is it best to hear a PDA?
at time of S2
How can inspiration and expiration affect valvular defects?
Inspiration increases the intensity if the defect is on the right side of the heart (more blood into RA)

Expiration increases the intensity of defects on the left side of the heart because more blood flows into LA
What are 3 physiological differences between Cardiac Myocytes and skeletal muscle?
1 Cardiac action potentials have a plateau, due to Ca influx
2. Cardiac nodal cells spontaneously depolarize (due to If channels?)
3. Cardiac myocytes are electrically coupled to each other via gap junctions
What is cardiac muscle contraction dependent on?
Extracellular Ca
it enters during the plateau--->release of other Ca from SR
How many phases are there to Ventricular Action Potential?
5

0-4
What does Phase 0 represent?
Rapid upstroke

voltage gated Na channels open
What does Phase 1 represent?
initial repolarization

inactivation of voltage-gated Na channels
Voltage-gated K channels begin to open
What does Phase 2 represent?
Plateau

Ca influx through voltage-gated Ca channels balances K efflux.
Ca influx triggers Ca release from SR and myocyte contraction
What does Phase 3 represent?
Rapid Repolization

massive K efflux due to voltage-gated slow K channels and closure of voltage gated Ca channels
What does Phase 4 represent?
Resting Potential

high K permeability through K channels
How is Phase 0 of Pacemaker Action Potentials different from Ventricular AP's?
Phase 0

Lacks voltage-gated Na channels

Uses voltage-gated Ca channels

this is slower, so there is a slow conduction velocity
How is Phase 1 of Pacemaker Action Potentials different from Ventricular AP's?
There is no Phase 1 for pacemakers
How is Phase 2 of Pacemaker Action Potentials different from Ventricular AP's?
There is no Plateau
How is Phase 3 of Pacemaker Action Potentials different from Ventricular AP's?
There is an inactivation of the Ca channels and increased activation of K channels--->increased K efflux
How is Phase 4 of Pacemaker Action Potentials different from Ventricular AP's?
Slow Diastolic Depolarization

membrane potential spontaneously depolarizes as Na conductance increases.

This accounts for automaticity of the SA and AV nodes

The slope of Phase 4 = HR
Effects of ACh and Catecholamines on Pacemaker Action Potentials?
ACh decreased rate of depolarization and thus dec HR

Catecholamines inc depolarization and thus inc HR
ELECTROCARDIOGRAM
what does the P wave represent?
Atrial Depolarization
ELECTROCARDIOGRAM
what does the PR interval represent?
conduction delay through AV node
ELECTROCARDIOGRAM
what does the QRS complex represent?
Ventricular Depolarization
ELECTROCARDIOGRAM
what does the QT interval represent?
mechanical contraction of ventricles
ELECTROCARDIOGRAM
what does the T wave represent?
ventricular repolarization
ELECTROCARDIOGRAM
what does the ST segment represent?
Isoelectric
Ventricles depolarized
ELECTROCARDIOGRAM
what does the U wave represent?
caused by Hypokalemia or Bradycardia
ELECTROCARDIOGRAM
what wave or segment illustrates Atrial Repolarization?
Nothing
It's masked by the QRS complex
What is Torsades de Pointes?
Ventricular Tachycardia characterized by shifting sinusoidal waveforms on ECG
Can progress to V-fib
What can cause Torsades de Pointes?
Anything that prolongs QT interval
What is Wolff-Parkinson-White Syndrome? sign of it?
Accessory conduction pathway from atria-->ventricle bypassing AV node.
Ventricles begin to depolarize early--->delta wave on ECG
Can lead to a reentry current--->supraventricular tachycardia
Characteristic ECG findings w/ Atrial Fibrillation?
Irregularly Irregular baseline
No discrete P waves
Irregularly spaced QRS complexes
Complications seen w/ A-fib? rx?
atrial stasis--->stroke

Rx w/ warfarin
Characteristic findings w/ Atrial Flutter?
Rapid succession of Identical, back-to-back atrial depolarization waves
Sawtooth appearance
Rx for Atrial Flutter?
Convert to Sinus Rhythm

Use Class IA, IC, or III Antiarrhythmics
ECG for 1st degree AV Block?
PR interval is prolonged (> 200msec)

Asymptomatic
Types of 2nd Degree AV Block?
Mobitz Type 1 (wenckebach)

Mobitz Type 2
Characteristics of Mobitz Type I, 2nd Degree AV Block?
Progressive lengthening of PR interval till a beat is dropped (P wave with no QRS following it)

usually asymptomatic
What is Mobitz Type 2 like?
Dropped beats NOT preceeded by lengthening PR intervals

This results is pathologic.
Often a 2:1 block w/ 2 P's for every 1 QRS
May progress to 3rd degree
What is up with 3rd Degree AV block?
Atria and Ventricles beat independently from each other.
P's and QRS's are present, but NOT RELATED
Atrial rate is faster than Ventricular Rate
Possible cause of 3rd Degree AV Block?
Lyme Disease
Rx for 3rd degree AV Block?
Pacemaker
ECG for V-fib? Px? Rx?
Completely erratic rhythm--->death unless Rx'd w/ CPR and defib
2 pathways that react to a decrease in MAP?
1. Baroreceptor
2. Juxtaglomerular Apparatus
What happens with the JGA when MAP decreases?
Triggers Renin-Angiotensin Systemt
Ang II ---> vasocontriction--->Inc TPR
Aldosterone-->inc blood volume--->inc CO

all ---> Inc MAP
What happens with the baroreceptors when MAP decreases?
Baroreceptors decrease firing
Triggers Medullary Vasomotor center---> Inc Sympathetic Activity--->
Beta 1's--->inc HR, inc contractility--->inc CO
Alpha1's ---> venoconstriction--->inc CO
Alpha1's ---> art. vasoconstriction---> inc TPR


all---> MAP
When does ANP get released? actions?
Atrial Natriuretic Peptide
Relased from atria in respone to inc blood volume and atrial pressure

Causes generalized vascular relaxation
Constricts efferent renal arterioles
Dilates Afferent renal arterioles
Where are baro and chemo-receptors located?
Baroreceptors = Aortic baroreceptors in aortic arch and Carotid baro's in Carotid Sinus

Chemoreceptors:
In aortic arch
The carotid body
How do the baroreceptors in the Aortic Arch relay info? in response to?
Via the Vagus Nerve to the Medulla

Only respond to INC BP
How do the receptors in the Carotid Sinus relay info? in response to?
Via Glossopharyngeal nerve (IX) to the Medulla

in response to inc or dec in BP
What is the cascade of events when the Baroreceptors sense Hypotension?
1. Dec Arterial pressure
2. Dec stretch
3. Dec Afferent Bara firing
4. Inc Efferent Sympathetic firing and Dec efferent parasympathetic firing
5. Vasoconstriction, Inc HR, Inc Contractility

INC BLOOD PRESSURE!!!
What is up with Carotid Massage?
Inc Pressure on Carotid
Inc Stretch
inc Afferent Baro Firing
Dec HR
So who are the Peripheral Chemoreceptors vs Central?
Peripheral = carotid and aortic bodies

Central = in the brain
What do peripheral chemoreceptors respond to?
Dec PO2, Inc Pco2, Dec pH of blood
What do Central Chemoreceptors respond to?
Changes in pH brain interstitial fluid (which are influence by arterial CO2, not arterial pH cause H+ can cross the BBB but CO2 can)
Doesn't directly respond to PO2
What Reaction are Central Chemoreceptors responsible for? mechanism?
CUSHING REACTION

Inc ICP constricts arterioles--->cerebral ischemia (inc Pco2)--->HTN--->reflex bradycardia
So what does Cushing's Triad = ?
HTN
Bradycardia
Respiratory Depression
Who gets the largest share of systemic CO?
Liver
Who gets the highest blood flow per gram of tissue?
Kidney
How does the Heart meet an increased O2 demand?
Inc coronary blood flow

NOT by inc extraction of O2
What is the pressure in the:
SVC/IVC?
RV?
Pulmonary Trunk
LA?
LV?
Aorta?
SVC/IVC < 5

RV <25/<5

Pulm Trunk: <25/10

LA: (via Swan-ganz reading of PCWP) < 12

LV: < 130/10

Aorta: < 130/90
What are the factors determining autoregulation of blood flow to the HEART?
Local metabolites =
O2
adenosine
NO
What are the factors determining autoregulation of blood flow to the BRAIN?
Local metabolites =
CO2 (pH)
What are the factors determining autoregulation of blood flow to the KIDNEYS?
Myogenic and Tubuloglomerular Feedback
What are the factors determining autoregulation of blood flow to the LUNGS
Hypoxia causes vasoconstriction

this happens so only well-ventilated areas are perfused

in other organs, hypoxia--->vasodilation
What are the factors determining autoregulation of blood flow to the SKELETAL MUSCLE?
Local Metabolites:
lactate
adenosine
K+
What are the factors determining autoregulation of blood flow to the SKIN?
Sympathetic Stimulation---> temperature control
4 forces responsible for determining fluid movement into and out of capillaries?
1. Pc = capillary hydrostatic pressure (pushes stuff out)
2. Pi = interstitial fluid hydrostatic pressure (pushes stuff into caps)
3. Plasma colloid osmotic pressure (pulls fluid into cap)
4. Interstitial osmotic pressure (pulls fluid out)
So net filtration pressure = ?
(Cap hydrostatic - interstitial hydrostatic) - (plasma osmotic - interstitial osmotic) = Net filtration Pressure (Pnet)
What is the Net Fluid Flow = ?
Net Filtration Pressure (Pnet) * Kf

Kf = filtration constant (capillary permeability)
So what causes Edema? examples?
Inc Capillary hydrostatic pressure (heart failure)

Dec Plasma Proteins (dec plasma osmotic pressure; e.g. nephrotic syndrome, liver failur)

Inc capillary permeability (inc Kf; toxins, infections, burns)

Inc interstitial fluid colloid osmotic pressure (lymphatic blockage)