Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
150 Cards in this Set
- Front
- Back
|
What artery supplies the SA and AV nodes?
|
The right coronary artery RCA
|
|
|
What artery supplies the inferior bottom of the left ventricle in most people?
|
The posterior descending branch of the RCA
|
|
|
What artery supplies the right ventricle?
|
Acute marginal artery branch of the RCA
|
|
|
What artery supplies the anterior interventricular septum?
|
Left Anterior descending LAD
|
|
|
What artery supplies the left atrium?
|
Left circumflex artery
|
|
|
Most posterior part of the heart is:
|
The left atrium
|
|
|
3 structures inside the carotid sheath; post/lat/med?
|
Int Jugula Vein = lateral
Vagus nerve = posterior Common Carotid artery = medial |
|
|
Where do you hear Aortic stenosis and Pulmonic stenosis?
|
Aortic area = right 2nd IC space
|
|
|
Where do you hear Pulmonic stenosis also?
|
Left 2nd IC space
|
|
|
Where do you hear Aortic regurgitation and Pulmonic regurgitation?
|
Left sternal border
|
|
|
What are 2 defects that would cause a PANSYSTOLIC MURMUR in the tricuspid area?
|
-Tricuspid regurgitation
-Ventricular septal defect |
|
|
What 2 defects would cause a DIASTOLIC MURMUR in the tricuspid area?
|
-Tricuspid stenosis
-Atrial septal defect |
|
|
What would be indicated by a murmur in the mitral area during
-systole -diastole |
Systole = mitral regurg
Diastole = mitral stenosis |
|
|
How does Cardiac output change initially during exercise? Why?
|
It increases - because stroke volume increases
|
|
|
How does Cardiac output change after a long PERIOD of exercise? Why?
|
It increases still because of an increase in HEARTRATE
|
|
|
How does Cardiac output change if heart rate is TOO fast?
|
CO decreases because there is not enough time for the VENTRICLES to fill; filling is incomplete.
|
|
|
What is the hallmark situation that causes insufficient diastolic filling of the ventricles?
|
Ventricular tachycardia
|
|
|
What is CO =?
|
CO=SVxHR = (MAP/RAP)/TPR
|
|
|
How can we measure CO based on Fick's principle?
|
CO = Rate of O2 consumption divided by the difference between arterial O2 and veinous O2
|
|
|
How do you calculate MAP based on blood pressure measurements?
|
MAP = 2/3DP + 1/3SP
|
|
|
What is Pulse Pressure? What is it equivalent to?
|
PP = SP - DP; equiv to Stroke Volume
|
|
|
What is Stroke Volume?
|
SV = EDV - ESV
|
|
|
What is Ejection fraction? What is it an index of? What is it normally?
|
EF = SV/EDV; an index of ventricular contractility; normally ~55%
|
|
|
What are the 3 main determinants of Stroke Volume?
|
SV -> CAP
-Contractility -Afterload -Preload |
|
|
What changes in CAP will increase stroke volume?
|
-Increased Contractility
-Increased Preload -Decreased afterload |
|
|
What are 4 things that will INCREASE contractility and thus SV?
|
-Catecholamines
-Increased intracell Calcium -Decreased extracell Sodium -Digoxin/Digitalis |
|
|
How do catecholamines increase contractility?
|
By increasing the activity of the Calcium pump on the SR - increase release of Ca into the cell
|
|
|
How do Cardiac glycosides - Digitalis/Digoxin increase contractility?
|
By increasing INTRAcellular Sodium which inhibits Calcium efflux; keeps it around longer
|
|
|
What are 5 things/conditions that DECREASE cardiac contractility?
|
-B1 blockers
-Cardiac failure -Acidosis -Hypoxia/hypercapnia -Calcium channel Blockers |
|
|
What are 3 physiological conditions in which SV is increased?
|
-Exercise
-Pregnancy -Anxiety |
|
|
What is the increased SV in exercise important for?
|
INITIAL increase in cardiac output; later CO increase is due to increased Heartrate from SNS
|
|
|
What is the stroke volume in a FAILING heart and why?
|
Decreasd - because the failing myocardium has decreased contractility!
|
|
|
What are 4 factors that increase myocardial OXYGEN DEMAND?
|
-Increased AFTERLOAD
-Increased Contractility -Increased Heartrate -Increased Heart SIZE (wall tension) |
|
|
What is Afterload directly proportional to?
|
DIASTOLIC arterial pressure
|
|
|
Why is Afterload determined by DIASTOLIC arterial BP?
|
Because that is the pressure the left ventricle is pumping against at the BEGINNING of systole, at the END Of DIASTOLE
|
|
|
And what is diastolic arterial pressure determined by?
|
Peripheral RESISTANCE - TPR
|
|
|
What is Preload?
|
Ventricular End diastolic volume - the amount of blood filling the ventricles after diastole.
|
|
|
How does increasing PRELOAD affect stroke volume?
|
It increases it!
|
|
|
How does increasing AFTERLOAD affect stroke volume?
|
It decreases it
|
|
|
How do increases in Afterload and Preload affect cardiac WORK?
|
Both INCREASE cardiac work
|
|
|
When would you want the heart to NOT be working harder?
|
In ANGINA
|
|
|
So what drug decreases
-PRELOAD -AFTERLOAD |
Preload decreased by VENOUS dilators - Nitroglycerin
Afterload decreased by ARTERIAL dilators - Hydralazine |
|
|
What are 3 physiologic conditions that increase PRELOAD?
|
-Exercise (somewhat)
-Increased blood volume (transfusions) -Excitement (SNS) |
|
|
How does increased blood volume increase preload?
|
By increasing mean systemic filling pressure
|
|
|
How does SNS increase preload?
|
By constricting the veins which shifts blood to the stressed volume; increases Psf too.
|
|
|
How does SNS activation affect AFTERLOAD and by what mechanism?
|
Increases afterload by vasodilating the arteries which increases TPR - reduces the slope on the VR curve.
|
|
|
What is Ejection fraction? Normal?
|
EF = EDV-ESV/EDV = SV/EDV
Normal is 55% |
|
|
What is Bloodflow equal to?
|
Q = P/R
|
|
|
What is R?
|
Resistance
|
|
|
What is R calculated by?
|
Poiseuille's law:
R=8nl/pi r^4 |
|
|
What 3 things increase blood viscosity, n?
|
-Polycythemia vera
-Multiple myeloma -Hereditary spherocytosis |
|
|
What determines TPR MOST? What does this in turn regulate?
|
Arteriole diameter
-Regulates Capillary flow |
|
|
How are Cardiac output and EDV/Preload changed in congestive heart failure?
|
-CO is low
-EDV is high because the heart can't pump it out enough |
|
|
Why is EDV high in CHF?
|
In an attempt to increase cardiac contractility by the Starling force concept; but the heart is not FUNCTIONING well enough so it just clogs things up
|
|
|
What is used to increase contractility/CO, and decrease EDV in CHF?
|
Digitalis
|
|
|
What can increase CO and decrease EDV in NORMAL people? How?
|
Exercise - by SNS activity
|
|
|
What initially increases CO in exercise and what does it later?
|
Initially = increased SV
Later = increased HR |
|
|
Wo what are the 2 things that increase cardiac contractility and hence increase CO and SV?
|
-Circulating catecholamines (SNS)
-Drugs - Digitalis |
|
|
What are 2 things that DECREASE cardiac contractility?
|
-Drugs - depressants (CCB's)
-Myocardial infarction (necrosis) |
|
|
On the Cardiac Cycle diagram, what is on the Y vs X axis?
|
Y = PRESSURE
X = VOLUME |
|
|
What is Phase I of the Cardiac Cycle?
|
Isovolumetric Contraction of the Left Ventricle
|
|
|
What valve changes occur at the START and END of isovolumetric LV contraction?
|
Start: Mitral valve closes
End: Aortic valve opens |
|
|
What heart sound is Mitral valve closing?
|
S1
|
|
|
What heart sound is Aortic valve closing? When does this occur?
|
S2 - at the end of Systolic Ejection
|
|
|
What is the highest period of oxygen consumption during the cardiac cycle?
|
Isovolumetric contraction! Phase I!!!
|
|
|
What is S3?
|
Isovolumetric Relaxation
|
|
|
What happens at the end of S3 before S4?
|
Mitral valve opening
|
|
|
What are S4/S5?
|
S4 = Rapid diastolic filling
S5 = slow diastolic filling |
|
|
When is S3 heard? What is it a sign of?
|
At the END of Rapid filling - sign of dilated Congestive Heart failure
|
|
|
When is S4 heard and what is it a sign of?
|
During Filling - sign of a stiff ventricle from Hypertrophy - Hypertension
|
|
|
What is S4 also called?
|
Atrial KICK
|
|
|
What is S2 splitting?
|
The normal physiologic closing of the AORTIC valve before PULMONIC upon inspiration
|
|
|
What is Wide splitting associated with?
|
Pulmonic stenosis - it takes too long to shut
|
|
|
What is Fixed splitting associated with?
|
ASD
|
|
|
What is PARADOXICAL splitting and what is it associated with?
|
Aortic shutting AFTER the pulmonic; associated w/ Aortic stenosis (IT takes too long to shut)
|
|
|
What are the 3 points to remember on the jugular venous pulsation curve?
|
A, C, and V
|
|
|
What is A wave on JVP curve? What does it coincide with on the ECG?
|
Atrial contraction - between P and Q waves on ECG
|
|
|
What is the C wave on JVP curve?
What does it coincide with on the ECG? |
Right VENTRICLE contraction - when the Tricuspid valve bulges back into the atrium; coincides with the S-T segment
|
|
|
What is the V wave on JVP curve?What does it coincide with on the ECG?
|
Increase in atrial pressure as it fills against the closed Tricuspid valve; occurs just after the T wave.
|
|
|
What is the major ion that allows for prolonged contraction of Myocardial muscle cells? What is the most important source?
|
Calcium - extracellular
|
|
|
What are 2 things that extracellular calcium achieves for the myocardium?
|
-Prolonged Plateau phase
-Opens Ca-gated Ca channels on the SR to increase calcium even more |
|
|
So the 3 main features that contrast Cardiac muscle to skeletal muscle are:
|
-Plateau via Calcium
-Automaticity - spontaneous depolarization of nodal cells -Electrical coupling by GAP junctions |
|
|
Where do the long AP's with the plateau phase occur? 3 types of cells:
|
-Atrial myocardiocytes
-Ventricular cardiomyocytes -Purkinje fibers |
|
|
What is Phase 0?
|
Rapid upstroke - Na influx through voltage-gated Na channels
|
|
|
What happens to the Myocardial cell's membrane potential during the rapid upstroke phase?
|
It goes from -85 mV to above 0 mV and threshold!
|
|
|
What is Phase I?
|
Initial repolarization due to a brief K+ efflux thru voltage gated potassium channels
|
|
|
What stops Phase I?
|
Calcium v-gated channels open and Calcium influx balances K efflux to maintain stability of the membrane potential
|
|
|
What happens to the Na v-gated channels during phase I?
|
They become refractory and begin the ERP - effective refractory period.
|
|
|
How long does the myocardial cell AP last?
|
100 msec - very long!
|
|
|
What is phsae 2?
|
The plateau phase
|
|
|
What does Calcium do during phase II?
|
-Keeps the long plateau going
-Opens Ca-gated Calcium channels on the SR to allow for more Ca to get into the cell and trigger contraction |
|
|
What is phase III?
|
Rapid Repolarization
|
|
|
What is phase III caused by?
|
Opening of slow voltage-gated K channels, and shutting of Calcium channels
|
|
|
What is Phase 4?
|
Resting potential
|
|
|
What is the resting membrane potential of cardiac myocytes?
|
-85 mV; set by K leak channels
|
|
|
What extrudes Calcium from the myocyte?
|
Ca/Na exchangers
|
|
|
What maintains the gradient for Na to want to flow into the cell in exchange for Ca extrusion out?
|
Na/K ATPase
|
|
|
What inhibits the Na/K ATPase and what is the result?
|
Digitalis - blocks Ca extrusion and prolongs contraction; positive inotropism!
|
|
|
Where do PACEMAKER action potentials occur? 2 cells:
|
-AV node
-SA node |
|
|
What ion is responsible for the upstroke of the AP in nodal cells?
|
CALCIUM
|
|
|
What is NOT seen in the nodal cells?
|
No phase 2 plateau phase
|
|
|
What is the major difference in Phase 4 of nodal cells compared to myocardial cells?
|
It does not rest at -85; it undergoes constant diastolic depolarization
|
|
|
What ion is responsible for the diastolic depolarization of phase 4 in nodal cells? Via what channel?
|
Sodium - via FUNNY Na channels
|
|
|
What are the Na channels that achieve rapid depolarization in the MYOCARDIAL cells?
|
FAST sodium channels; absent in nodal cells!
|
|
|
What is responsible for the repolarization phase 3 between the upstroke and diastolic depolarization in nodal cells?
|
Potassium as usual
|
|
|
What sets the heart rate of nodal cells?
|
The slope of the diastolic depolarization phase.
|
|
|
What increases the slope and what is its affect?
|
SNS - Epi/NE - increase the heart rate
|
|
|
What decreases the slope?
|
ACh/PNS - slows heart rate
|
|
|
On the ECG what is the P wave?
|
Atrial depolarization
|
|
|
On the ECG what is the PR interval? Normal?
|
Delay of depolarization through the AV node - normally <200 msec
|
|
|
What is the QRS complex? How long does this normally take?
|
Ventricle depolarization <120msec
|
|
|
On the ECG what is the QT interval?
|
MECHANICAL contraction of the ventricles
|
|
|
On the ECG what is the T wave?
|
Ventricle REpolarization
|
|
|
How come we can't see the Atrial REPolarization on the ECG?
|
It's masked by the QRS complex
|
|
|
What is the ST segment?
|
The isolectric period in which the ventricle is COMPLETELY DEPOLARIZED
|
|
|
What is a U wave?
|
A pathologic sign of HYPOKALEMIA
|
|
|
What is the QT interval again?
|
Mechanical contraction of the ventricle
|
|
|
What does anything that prolongs the QT interval predispose to?
|
TORSADES DES POINTES
|
|
|
What is Torsades des Pointes?
|
Ventricular tachycardia showing SINUSOIDAL waveforms on ECG
|
|
|
What is Torsades des Pointes a risk for? What is it caused by?
|
-Risk for total Vfib
-Predisposed by anything that prolongs the QT interval |
|
|
What does Vfib look like on ECG?
|
Completely erratic waves with no identifiable waveforms
|
|
|
How is Vfib treated?
|
As an EMERGENCY - needs CPR and fibrillation to survive!
|
|
|
What is Wolff-Parkinson White syndrome?
|
An accessory pathway between atria and ventricles; bypasses the AV node
|
|
|
What is the result of bypassing the AV node?
|
The ventricles depolarize too EARLY
|
|
|
What is the characteristic ECG finding in Wolf-Parkinson-White syndrome?
|
a Delta-wave - early uprising of the QRS complex
|
|
|
What does Wolf-Parkinson-White predispose to?
|
Re-entry circuits leading to Supraventricular tachycardia
|
|
|
What causes an erratic and irregular baseline on the ECG, with no discrete P waves in between irregularly spaced QRS complexes?
|
Atrial fibrillation
|
|
|
What causes a sawtooth pattern on ECG?
|
Atrial flutter
|
|
|
What is the sawtooth pattern?
|
Back to back atrial P waves, like 3 in a row, and THEN a QRS
|
|
|
What causes AV block 1st degree?
|
A prolonged PR interval >200 msec
|
|
|
What types of AV block are usually asymptomatic?
|
1st degree and 2nd degree Mobitz 1
|
|
|
How is Mobitz type I of 2nd degree AV blocks different from 1st degree?
|
The prolonged PR interval gets longer and longer until it skips a beat - a P wave not followed by a QRS wave.
|
|
|
How is Mobitz type I different from Mobitz type II 2nd degree?
|
No prolongation of the PR interval in type II of 2nd degree; beats are just dropped
|
|
|
What is 3rd degree AV block?
|
Complete block; the atria and ventricles beat completely independently of each other.
|
|
|
What do peripheral (carotid and aortic) chemoreceptors respond to? 3 things:
|
-Decreased PO2 - <60 mm Hg
-Increased PCO2 -Decreased pH of blood |
|
|
What do CENTRAL medullary chemoreceptors respond to?
|
-Increased PCO2
-Decreased pH (not to PO2) |
|
|
What are the central chemoreceptors responsible for?
|
The Cushing reaction - response to increased ICP and ischemia
|
|
|
What are the 2 responses of peripheral circulation to the Cushing reaction?
|
-Hypertension (increased SNS)
-Tachycardia (PNS) |
|
|
What organ in the body receives the largest share of systemic CO?
|
Liver
|
|
|
What organ gets the highest bloodflow per gram of tissue?
|
KIDNEY
|
|
|
What organ has the largest AV O2 difference?
|
HEART!
|
|
|
How is increased oxygen demand of the heart met?
|
By increasing coronary BLOODFLOW - NOT by increasing the amount of O2 extracted
|
|
|
What are the 6 organs for which bloodflow is regulated by autoregulation?
|
-Heart
-Brain -Kidneys -Lungs -Skeletal muscle -Skin |
|
|
What organs are autoregulated by Local Metabolites?
|
-Heart
-Brain -Skel muscle (active) |
|
|
What are the 3 most important metabolic factors that regulate HEART bloodflow?
|
-Adenosine
-NO -Oxygen |
|
|
What are the 2 most important metabolic factors that regulate BRAIN bloodflow?
|
-CO2
-pH |
|
|
What metabolites regulate exercising skeletal muscle bloodflow?
|
-K
-Lactic acid -Adenosine |
|
|
What regulates kidney bloodflow?
|
-Myogenic autoregulation
-Tubuloglomerular feedback |
|
|
What regulates bloodflow through the lungs?
|
Hypoxic vasoconstriction!
|
|
|
What regulates SKIN bloodflow?
|
SNS - for regulating TEMPERATURE
|
