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149 Cards in this Set
- Front
- Back
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Coronary artery anatomy
What supplies the right ventricle |
acute marginal artery (from the RCA)
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Coronary artery anatomy
What supplies the posterior septum |
posterior descending/ interventricular artery (off the RCA)
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Coronary artery anatomy
What supplies the Posterior Left ventricle |
Circumflex artery (off LCA)
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Coronary artery anatomy
What supplies the apex and anterior interventricular septum |
Left anterior descending artery (off LCA)
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During which part of the heart cycle do the coronary arteries fill
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diastole
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Where is the left atrium located in relation to the rest of the heart
what does an enlargement of the left atrium cause |
most posterior portion of the heart
enlargement --> dysphagia (compression of esophageal nerve) or hoarseness (compression of recurrent laryngeal nerve, branch of vagus) |
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What is cardiac output?
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CO = stroke volume * heart rate
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Given the rate of oxygen consumption, the arterial oxygen content, and the venous oxygen content, how can you calculate CO?
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Fick principle
rate of O2 consumption / (arterial -venous O2 content) |
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How do you calculate Total peripheral resistance?
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TPR = (mean arterial - mean venous pressure) / CO
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How do you calculate Mean arterial pressure?
1. using CO and peripheral resistance 2. Using diastolic and systolic arterial pressure |
1. MAP = CO * Total peripheral resistance
2. MAP = (2/3) diastolic pressure + 1/3 systolic pressure |
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Pulse pressure =
Pulse pressure is proportional to what? |
systolic pressure - diastolic pressure
Proportional to stroke volume |
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2 ways to calculate stroke volume
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CO/HR
End diastolic volume - end systolic volume |
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4 factors that increase contractility
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1. catecholamines (increases Ca pump in SR)
2. increase in intracellular Ca 3. Decrease in extracellular Na (inhibits Na/Ca exchanger) 4. Digitalis (increases intracellular Na --> increase in Ca) |
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5 factors that decrease contractility (and stroke volume)
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1. beta blockade (decreases cAMP)
2. Heart failure (systolic dysfunction) 3. Acidosis 4. Hypoxia/hypercapnea 5. Non dihydropyridine Ca channel blockers |
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What is preload?
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Ventricular end diastolic volume
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What is afterload?
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mean arterial pressure (proportional to peripheral resistance)
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Venodilators vs. vasodilators
which on affects preload? Afterload? |
Venodilators (nitroglycerin) --> decreased preload
Vasodilators (hydralazine) --> decreased afterload |
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How is preload affected by
a. exercise b. blood volume c. excitement |
a. increases slightly
b. increases c. increases (sympathetic) "preload pumps up the heart" |
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The force of ventricular contraction is proportional to...
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initial length of the cardiac muscle fiber (preload)
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What does the starling curve measure
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CO or stroke volume vs. preload (ventricular end diastolic volume)
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What is ejection fraction and how is it calculated
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EF = index of ventricular contractility
EF = SV/EDV = (EDV - ESV) / EDV |
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What is a normal ejection fraction?
What happens in heart failure |
Normal = >55%
in heart failure, EF goes down |
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How do you calculate the pressure gradient that drives blood flow
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delta P = Q (flow) * R (resistance)
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How do you determine resistance to blood flow?
to what is it directly proportional? Inverse? |
Resistance = pressure/flow = (8*viscosity*length) / (pi*r^4)
directly related to viscosity inversely related to radius^4 |
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How do you calculate the total resistance of vessels in series?
In parallel? What accounts for most of the TPR? |
R1 + R2 + R3
1/R1 + 1/R2 + 1/R3 Mostly, arterioles account for TPR --> regulate capillary flow |
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main factor that determines viscosity of blood?
3 states in which viscosity is increased |
hematocrit
1. polycythemia 2. hyperproteinemic states (multiple myeloma) 3. Hereditary spherocytosis |
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What does the starling curve measure
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CO or stroke volume vs. preload (ventricular end diastolic volume)
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What is ejection fraction and how is it calculated
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EF = index of ventricular contractility
EF = SV/EDV = (EDV - ESV) / EDV |
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What is a normal ejection fraction?
What happens in heart failure |
Normal = >55%
in heart failure, EF goes down |
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How do you calculate the pressure gradient that drives blood flow
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delta P = Q (flow) * R (resistance)
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How do you determine resistance to blood flow?
to what is it directly proportional? Inverse? |
Resistance = pressure/flow = (8*viscosity*length) / (pi*r^4)
directly related to viscosity inversely related to radius^4 |
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How do you calculate the total resistance of vessels in series?
In parallel? What accounts for most of the TPR? |
R1 + R2 + R3
1/R1 + 1/R2 + 1/R3 Mostly, arterioles account for TPR --> regulate capillary flow |
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main factor that determines viscosity of blood?
3 states in which viscosity is increased |
hematocrit
1. polycythemia 2. hyperproteinemic states (multiple myeloma) 3. Hereditary spherocytosis |
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What happens to a CO vs. right atrial pressure curve if
a. heart failure, narcotic overdose b. exercise, AV shunt |
a. negative inotrope --> shift down
b. positive inotrope --> shift up |
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What is the operating point of the heart on a cardiac function curve
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CO = venous return
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what does the x-intercept of a venous return graph signify
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the mean systemic pressure = pressure in the system if the heart were stopped
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what can shift the venous return curve to the left (down)?
Right (up)? |
Decreased blood volume
Increased blood volume |
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What can shift the operating point of the heart down on a cardiac function curve?
up? |
down = increased total peripheral resistance (ex. hemorrhage) --> loss of inotropy and volume
up = decreased TPR (ex. exercise, AV shunt) --> increase in inotropy and volume |
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5 phases of LV contraction
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1. Isovolumetric contraction
2. Systolic ejection 3. Isovolumetric relaxation 4. Rapid filling 5. Reduced filling |
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What is the phase of the LV that has the highest oxygen consumption
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Isovolumetric contraction
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How does increaseing the afterload, aortic pressure, end systolic volume and decreasing the Stroke volume affect the cardiac cycle curve
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ESV increases, EDV decreases
Higher isovolumetric contraction pressure, shorter systolic ejection |
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Heart sounds - what's happening
and where is it loudest S1 |
Mitral and tricuspid closure
loudest at mitral area (5th intercostal space, mid-clavicular) |
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Heart sounds - what's happening
and where is it loudest S2 |
Aortic and Pulmonary valve closure
Loudest at left sternal border (pulmonic valve) |
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Heart sounds - what's happening
and when is it heard a. normally b. pathologically S3 |
In rapid filling phase (early) of diastole, blood shoots into ventricle
a. pregnant women, children b. dilated ventricles |
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Heart sounds - what's happening
and what does it indicate s4 |
heard in late diastole, LA must push against stiff LV wall
indicates high atrial pressure, ventricular hypertrophy |
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What is happening at different peaks on graph measuring JVP
a. a wave b. c wave c. v wave |
a. atrial contraction
b. RV contraction (closed tricusipid --> bulging into atrium) c. increased RA pressure due to filling against a closed tricuspid |
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What is happening to cause a normal S2 split?
In a healthy person, when is this split more pronounced? |
Aortic valve closes before Pulmonary valve
In inspiration, split is more pronounced |
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In listening to a man's heart, you hear an abnormally widely split S2 that splits even farther on inspiration
what are 2 pathological conditions that could cause this |
pulmonic stenosis
RBBB |
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In listening to a woman's heart, you hear a fixed split S2
what is one condition that causes this |
atrial septal defect
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Listening to a person's heart, you hear a split S2 that seems to get less split on inspiration
a. what is this b. 2 conditions that cause this |
a. paradoxical splitting (P2 before A2)
b. aortic stenosis or LBBB |
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What accounts for normal splitting of heart sounds
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Inspiration --> drop in intrathoracic pressure --> more blood enters lungs, less return to left heart -> pulmonic valve opens later, aortic valve earlier
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you hear a sysolic murmur over the aortic area
3 possibilities |
aortic stenosis
flow murmur aortic valve sclerosis |
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You hear a diastolic murmur at the left sternal border
2 possibilities |
aortic regurg
pulmonic regurg |
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You hear a systolic murmur at the left sternal border
1 possibility |
hypertrophic cardiomyopathy
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You hear a systolic ejection murmur at the pulmonic area
2 possibilities |
Pulmonic stenosis
Flow murmur (*ASD) |
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You hear pulmonary flow murmur and a diastolic rumble
what condition does the patient have and what is happening what will happen to these heart sounds over time |
ASD
pulmonic flow murmur --> increased flow across pulmonic valve diastoic rumble --> increased flow across tricuspid valve Over time, you will start to hear a louder diastolic murmur of pulmonic regurg as pulmonary artery dilates |
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You hear a pansystolic murmur over the tricuspid area
2 possibilities |
Tricuspid regurg
VSD |
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You hear a diastolic murmur over the tricuspid area
2 possibilities |
tricuspid stenosis
ASD (increased flow across tricsupid valve) |
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You hear a systolic murmur at the mitral area
dx? |
mitral regurg
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You hear a diastolic murmur at the mitral area
dx? |
mitral stenosis
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Right side vs. Left sided heart sounds
which increase on inspiration? expiration? |
inspiration = right sided
expiration = left sided |
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You hear a high-pitched, blowing, holosystolic murmur at the apex, radiating to the axilla
What are 3 common causes of this condition |
mitral regurgitation
ischemic heart disease, mitral valve prolapse, or LV dilation |
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How is the sound of a mitral regurgitation affected by
a. maneuvers that increase TPR (hand grip, squatting b. maneuvers that increase LA return (expiration) |
a. increase
b. increase |
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You hear a holosystolic murmur that is loudest at the tricuspid area, radiates to the right sternal border
what causes this (2) |
Tricuspid regurgitation
caused by RV dilation or endocarditis (possibly due to rheumatic fever) |
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what maneuvers could you do to increase the sound of a tricuspid regurgitation
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inspiration (increases RA return)
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You hear a crescendo-decrescendo systolic ejection murmur following a click
murmur radiates to carotids/apex on exam, pulses are weak compared to syncope dx? What made the click? what causes this pathology often? |
aortic stenosis
EC is due to abrupt halting of valve leaflets Often caused by age-related calcific aortic stenosis or bicuspid aortic valve |
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Patient has weak pulses compared to heart sounds
what is this called? what can it lead to? when do you see it? |
pulsus parvus et tardus
can lead to syncope often see with aortic stenosis |
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patient has a loud, holosystolic, harsh-sounding murmur at the tricuspid area
dx? |
VSD
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On auscultation, you hear a late systolic crescendo murmur with a midsystolic click
it is loudest at S2 what is the lesion? what causes the click? what maneuvers can you do to confirm? |
Mitral valve prolapse
Click = sudden tensing of chordae tendinae do maneuvers that increase TPR --> louder |
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Patient has a mitral valve prolapse
what are 3 possible causes? what can this condition predispose a person to? |
myxomatous degeneration, rheumatic fever, chordae rupture
infective endocarditis |
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On auscultation, you hear an immediate high-pitched 'blowing' diastolic murmur
you also see bounding pulses and head bobbing, as well as wide pulse pressure dx? 3 causes? what can decrease the intensity of the murmur? |
aortoic regurgitation
aortic root dilation, bicuspid aortic valve, rheumatic fever vasodilators |
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On ausculatation, you hear a diastolic murmur. You hear an opening snap, then a delayed rumbling, late diastolic murmur. During diastole, you measure the LA pressure to be much greater than the LV pressure.
dx? often secondary to what condition? what can you do to make this murmur louder? what happens if it is chronic? |
mitral stenosis
secondary to rheumatic fever increase return to RA (expiration) if chronic, can lead to dilation of RA |
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Patient has a continuous, machine-like murmur that is loudest at S2
dx? causes (2) |
PDA
congenital rubella or prematurity |
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Cardiac vs. skeletal muscle
Which one has an action potential with a plateau and what is this due to? |
Cardiac muscle, due to Ca influx
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Cardiac vs. skeletal muscle
nodal cells spontaneously depolarize -when do they do it? -what does this allow for |
cardiac
deplarize during diastole --> automaticity due to ion channels |
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Cardiac vs. skeletal muscle
cells connected by gap junctions |
cardiac
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5 phases of ventricular Action Potential
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0 = Rapid upstroke, Na in
1 = initial re-polarization, Voltage gated K channels open, Na channels close 2 = plateau - Ca in voltage gated channels --> balances K, stimulates Ca from SR --> myocyte contraction 3= rapid repolarization by K efflux through voltage-gated K channels, closure of Ca channels 4 = Resting potential, high K permeability through K channels |
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3 leaky currents in cardiac myocytes
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K out
Na, Ca in |
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Pacemaker Action potential
How does phase 0 differ from ventricular action potential? |
Ventricular = rapid upstroke mediate by voltage gated Na channels
SA/AV = no Na channels, slow upstroke by voltage gated Ca channels allows AV node to prolong conduction from atria to ventricles |
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Pacemaker Action potential
How does phase 2 differ from ventricular AP? |
Ventricular = plateau caused by Ca influx and K efflux balanced
SA/AV = no plateau |
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Pacemaker Action potential
How does phase 3 differ from ventricular AP? |
Both have K eflux and inactivation of Ca channels
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Pacemaker Action potential
What accounts for the automaticity of the SA/AV nodes? |
In diastole, when the current goes below -40 or -50, the leaky, passive Na current slowly depolarizes the cell through "If" channels
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Pacemaker Action potential
What is the determinant of heart rate? |
The slope of phase 4 in the SA node = the rate of slow depolarization through the leaky Na channels
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How is heart rate affected by ACh/adenosine and why?
catecholamines? |
decrease rate of diastolic depolarization through the leaky "If" channel --> slower heart rate
Increases the chance that If channels are open --> increased HR |
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ECG
What is happening at the P wave |
atrial depolarization
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ECG
What is happening in the PR interval |
conduction through the AV node (normally < 200ms)
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ECG
What is happening during the QRS complex |
Ventricular depolarization (normally < 120ms)
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ECG
What is happening during the QT interval |
mechanical contraction of the ventricles
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ECG
What is happening during the T wave? T wave inversion indicates? |
Ventricular repolarization
Recent MI |
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Why can you not see atrial repolarization on ECG
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masked by the QRS complex
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What is happening during the ST segment on an ECG
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ventricular repolarization, isoelectric
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On ECG you see an inverted U wave.
What are 2 possible causes |
Hypokalemia, bradycardia
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What does the 100ms delay in conduction through the AV node on an ECG allow for
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gives time for ventricles to fill
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Atria, ventricles, AV node, Purkinje
Put in order of fastest electrical conduction to slowest |
Purkinje > atria > ventricle > AV
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AV, Purkinje, SA
Put in order of fastest conduction to slowest |
SA > AV > purkinje/bundle of his/ventricles
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On ECG, you see ventricular tachycardia with sinusoidal waveforms shifting around an isoelectric point
what is this called? what can cause it? what can it lead to? |
Torsades des points
Long QT Can progress to V-fib |
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Patient is a child with severe congenital sensorineural deafness
On ECG, you see torsades des pointes Dx? Path? |
Jervell and Lange-Nielsen Syndrome
Congenital defect in cardiac Na or K channels --> long QT |
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On ECG, you see a small delta wave preceding the QRS.
What is this caused by? what is one possible consequence |
Wolf-Parkinson-White
Caused by accessory pathway from atrium to ventricle (bundle of Kent) that allows for bypassing the AV node --> preexcitation of ventricle Reentry current --> supraventricular tachycardia |
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On ECG you see irregularly irregular baseline with no P waves, with irregularly spaced QRS complexes
dx? what can this cause and how do you prevent it? How do you treat |
atrial fibrillation
atrial stasis --> stroke, treat prophylactically with warfarin to prevent thromboembolism Beta or Ca channel blocker |
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On ECG, you see a rapid succession of identical, back to back atrial depolarization waves, like a sawtooth
dx? treat? |
Atrial flutter
try to convert back to sinus rhythm, use class IA, IC, or III antiarrhythmatics |
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On ECG, you see a PR time >200ms
Dx? symptoms? |
1st degree AV block
asymptomatic |
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On ECG, you see a progressive lengthening of the PR interval, until a beat is 'dropped' (p not followed by QRS)
dx? Symptoms? |
2nd degree (mobitz I, wenchebach)
asymptomatic |
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On ECG, you see a pattern of 2 P waves for every QRS response
-The PR interval is constant dx? How can it progress? |
Mobitz type II (second degree block)
can progress to 3rd degree |
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On ECG, you see a random pattern of P and QRS waves. P and QRS seem to be totally dissociated from each other.
The atrial rate is faster than the ventricular rate. dx? what is happening? treat? |
3rd degree heart block
atria and ventricles beating independently Treat with a pacemaker |
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What type of heart block can Lyme disease cause
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3rd degree
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On ECG, you find a completely erratic rhythm with no identifiable waves
dx? what should you do? |
Ventricular fibrillation
Fatal unless CPR and defibrillation |
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What are 2 mechanisms y which a fall in mean arterial pressure is sensed?
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1. medullary vasomotor center senses decrease in baroreceptor firing --> sympathetic stimulatin
2. Juxtaglomerular apparatus senses decrease --> interprets as decrease in effective circulating volume --> RAAS |
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What are 3 mechanisms by which the sympathetic nervous system can correct for decreased mean arterial pressure?
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activation of sympathetic receptors
b1 --> increase heart rate and contractility --> increase CO a1 --> venoconstriction --> increase in venous return --> increase CO a1 --> arteriolar vasoconstriction --> increase TPR |
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What are two ways in which activation of the RAAS can lead to restoration of mean arterial pressure?
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Ang II --> vasoconstrict --> increases TPR
Aldosterone --> increases blood volume --> increases CO |
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What is the sensor in the heart that responds increased blood volume and atrial pressure
what are its effects |
Atria senses, releases ANP --> generalized vasodilation, efferent renal arterioles constrict, afferent arterioles dilate --> natriuresis (also seen in escape from aldosteronism)
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2 places you see baroreceptors and chemoreceptors and their pathways
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1. aortic arch --> vagus nerve -> medulla (only responds to increased BP)
2. carotid sinus --> CN9 --> solitary nucleus of medulla (responds to increase or decrease in BP) |
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After a hemorrhage, what is the pathway by which HR, contractility, and BP are restored?
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Hemorrhage --> low arterial pressure --> low stretch --> decrease afferent baroreceptor firing --> increases efferent sympathetic, decreases efferent parasympathetic
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What is the effect of a carotid massage on heart rate, and how does this mechanism work
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decreases HR
Increasing pressure on carotid artery --> stretch of baroreceptors --> increase afferent baroreceptor firing --> decrease in HR |
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What do chemoreceptors respond to and where are they found?
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Found in carotid and aortic bodies
Respond to low PO2 (<60), high PCO2, low pH in blood |
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What do central chemoreceptors in the brain respond to?
what do they not respond to? |
respond to pH and PCO2 of CSF, influenced by arterial CO2
Does not respond to pO2 |
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Patient presents to the ER with
-HTN -bradcardia -respiratory depression what is going on? |
Cushing's triad indicates rising ICP
high ICP --> constriction of arterioles --> cerebral ischemia --> sympathetic response --> HTN --> reflex bradycardia |
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Which organ has the
largest share of systemic CO |
Liver
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Which organ has the
Highest blood flow per gram tissue |
Kidney
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Which organ has
100% O2 extraction --> large A-V difference? How does this organ respond to higher O2 demand? |
Heart
increases coronary artery blood flow |
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What are the normal pressures in the...
right atrium |
<5
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What are the normal pressures in the...
Right ventricle |
<25/<5
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What are the normal pressures in the...
Pulmonary artery |
<25/<10
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What are the normal pressures in the...
Left atrium |
<12
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What are the normal pressures in the...
Left ventricle |
<130/10
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What are the normal pressures in the...
aorta |
<130/90
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What can you measure to get a sense of the left atrial pressure?
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Measure pulmonary capillary wedge pressure with a swan-Ganz catheter
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What is a normal pulmonary capillary wedge pressure?
If the PCWP is greater than the LV ventricular pressure, what pathology does this indicate? |
PCWP should be <12
Mitral stenosis --> rise in PCWP |
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What is the definition of autoregulation
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maintaing blood flow to an organ over a wide range of perfusion pressures
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Factors that determine autoregulation...
3 in the heart |
local metabolites - O2, adenosine, NO
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Factors that determine autoregulation...
1 in brain |
local metabolites - CO2 (pH)
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Factors that determine autoregulation...
2 in kidneys |
Myogenic and tubuloglomerular feedback
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Factors that determine autoregulation...
lungs |
hypoxia --> vasoconstriction (so that only well-ventilated areas are perfused)
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Factors that determine autoregulation...
3 in skeletal muscle |
Local metabolites - lactate, adenosine, K
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Factors that determine autoregulation...
Skin |
Sympathetic stimulation -> temperature control
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4 Starling forces that determine net filtration pressure through capillary membranes
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P net = (Pc - Pi) + (Oc - Oi)
Pc = capillary hydrostatic Pi = interstitial hydrostatic Oc = capillary osmotic Oi = interstitial osmotic |
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How do you determine net fluid flow through a capillary
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Net fluid flow = (Pnet)(Kf)
Pnet = net filtration pressure Kf = filtration constant (capillary permeability) |
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4 common causes of edema
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1. increased capillary pressure (heart failure)
2. decreased plasma proteins --> less plasma proteins (nephrotic syndrome, liver failure) 3. Increased capillary permeability (Kf) (toxins, infection, burns) 4. increased interstitial osmotic pressure (lymphatic blockage) |
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Syphilitic heart disease (aortitis)
what happens? |
Inflammation of adventitia --> disrupted vaso vasorum --> ischemia of outer 2/3 of aorta --> dilation of aorta and valve ring --> aneurysm
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Syphilitic heart disease
what would you see a. grossly b. histo |
a. calcification of aortic root, ascending aortic arch
b. tree bark appearance of aorta |
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Syphilitic heart disease
what are 2 conditions that it can cause |
1. aneurysm in ascending aorta or aortic arch
2. aortic valve incompetence |
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What is the most common primary cardiac tumor and what does it produce
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Left atrial myxoma
produces VEGF |
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Patient with multiple syncopal episodes comes into clinic
You see a 'ball valve' obstruction in the LA What kind of tumor is this? |
myxoma
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Where do 90% of myxomas occur
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atria (mostly Left)
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Most frequent primary cardiac tumor in children
what disease is it associated with? |
rhabdomyosarcoma
associated with tuberous sclerosis |
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What is the most common type of heart tumor
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metastases (from melanoma, lymphoma)
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What is kussmaul's sign
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rise in JVP on inspiration
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What is it called when you see dilated, tortuous superficial veins on a person
a. cause? b. predisposes them to...? c. rare but dangerous complication |
a. chronically increased venous pressure
b. predisposes to poor wound healing, varicose ulcers c. thromboembolism |
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In cold temperatures, your patients fingers and toes get cyanoitc
what is this condition? what is happening |
Raynaud's disease
Cold temp/emotional distress --> arteriolar vasospasm --> cyanosis |
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Difference between raynaud's disease and raynaud's phenomenon
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Raynaud's phenomenon was secondary to a mixed CT disease, SLE, or CREST syndrome
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