W1 Anatomy And Physiology Flashcards
Layers of the heart:
which layer contains the conduction system?
Pericardium
Endocardium
Subendocardium
Myocardium
Epicardium
Pericardium — encloses the heart and great vessels. Visceral layer adheres to the heart. Parietal outer fibrous layer attaches to the sternum and medistinum to anchor the heart and maintain it’s position
between the layers is the pericardial fluid that allows the heart to beat in a frictionless manner
Endocardium — single layer endothelial cells
Subendocardium — connects epicardium/visceral pericardium to myocardium, contains conduction system!
Myocardium — thickest muscle layer
Epicardium — or visceral pericardium — it is the outer most layer
Right atrium
Right ventricle
Left atrium
Left ventricle
Interventricular septum
Right atrium
— SVC, IVC and coronary sinus empty deoxygenated blood into this chamber
— separated by left atrium by interatrial septum
— tricuspid valve at the bottom opens into RV
Right ventricle
— contains 3 papillary muscles and chordae tendineae that attach to the edges of the tricuspid valve leaflets
—right ventricular outflow tract is at the apex and that leads to the pulmonic value (3 cusps) that opens into the pulmonary artery
Left atrium
—4 pulmonary veins delivery oxygenated blood to this chamber
— thicker than right
— mitral valve leads to the LV
Left ventricle
—cone shaped, x3 thicker than right ventricle
—contains 2 large papillary muscles and chordae tendineae that distribute to the mitral valve
—leads to aortic valve (3 cusps)
left side is the focus of most of the diagnoses we treat
Interventricular septum
—thick wall between R&L ventricles
Walk through the impulse conducting system — 5 steps
SA node is the pacemaker of the heart. Specialised cells, they have automaticity, they depolarise on their known.
Discuss cardiac innervation
–What does the SNS do? Which NT on which receptor?
–What does the PNS do? Which NT on which receptor?
Innvervated by sympathetic and parasympathetic.
Sympathetic: norepi to increase HR chronotropic (which is the change in heart rate, either + or -) as well as myocardial contraction (inotropic effect)
NE on B1 adrenergic receptors
Parasympathetic (vagus nerve). Slows the conduction causing bradycardia and reduces conduction through the AV node
ACh on the cholinergic receptors
Cardiac vessels of the heart, what is the path?
Coronaries — when do they fill?
Left main (widower maker)
LAD
LCx
RCA
PDA
PLA
Coronary veins
Coronary arteries fill during diastole (not systole!)
— Left aortic root — left MAIN — left ANTERIOR DESCENDING artery — left CIRCUMFLEX
— Right aortic root — right CORONARY artery — POSTERIOR DESCENDING artery — POSTEROLATERAL ARTERY
Electrophysiology
What causes it?
Ions of importance (3)
Movement of ions, through the membrane cause depolarisation, then go through gap junction to the next myocyte
Action potential is dependent on what?
Determined by? 3 (don’t list the three main ions!)
What is the resting membrane potential?
Where is sodium concentration greater? What about K+ ?
Ion movement, which is dependent on
—Concentration gradient — high to low
—Voltage gradient — positive to negative
—Permeability — phospholipid membrane does not simply allow ions to pass. They have to go through gates or channels. Each channel is selective to a specific ion and gated (only open at a certain time)
Cell is a little more positive on the outside
Cell sits at -90mV (starting point) because sodium is being pumped out and potassium freely flowed out, so negative charges are trapped.
Sodium concentration greater outside the cell
Potassium concentration greater inside the cell
Learn phase 0-4 of the depolarisation
When does muscle contraction occur?
-90mV not 85
Phase 0:
—Sodium rushes IN via fast channels
Phase 1:
—Sodium channel closes
—K+ efflux
Phase 2:
—Plateau, slow phase.
—Ca++ influx
—K+ efflux still occurring
—This is where myocytes contract.
Phase 3:
—Ca closed.
—K+ still leaving the cell.
Phase 4:
—Start the process again.
—RMP of the cardiac cell is maintained at -90mV by the Na-K-ATPase pump that keeps a higher intracellular concentration of potassium and a higher Extracellular concentration of sodium
Refractory period:
—any impulse that comes in, cannot accept it.
Pacemaker cells — SA node and AV nodes, and Ischemic atrial/ventricular cells
What is their resting voltage?
What channel do they have?
At what voltage do SA node and AV node fire?
They sit at -60mV (not -90mV)
They don’t have fast sodium channels, they have funny channel — permeable to NA and once it reaches a -40mV threshold, it spontaneously depolarises and influx of Ca occurs. Goes from minus -60 to -40.
Fires on it own.
SA node fires at (60-80)
AV node (40-60 BPM)
Cardiac action potentials:
Refractory period
— how does it differ between atria and ventricles?
—how do AP differ between cardiac muscle and skeletal muscle?
Absolute refractory period
Relative refractory period
Needs chance to fill with blood during diastole. So AP are much longer than nerves and skeletal muscle
Relative refractory: if AP is stronger than normal, it could recharge it to depolarise it again. This is where people have extra heart rates and can set them off into arrhythmia.
Refractory periods of atrial cells is shorter than ventricular muscle cells such that atrial rates exceed ventricular rates
Refractory periods of atrial cells and ventricular muscle cells (important)
Atrial cells is shorter than ventricular muscle cells such that atrial rates exceed ventricular rates
(Remember as you go down the heart, the rate slows, SA node impulses are faster than ventricular foci impulses)
Know the normal sequence of electrophysiology starting with the SA node
Slide 25
—SA node initiates HR
Impulse spreads through atria via intercellular gap junctions
—Impulse spreads through the atria via intercellular gap junctions
—fibrous tissue prevents impulse transmission to ventricles except through the AV node
— AV node slows conduction allowing atrium to contract
—impulse continues to the Bundle of His, onto the Purkinje fibres and finally the ventricular muscle cells
Mechanical contraction
Which proteins are cardiac muscle contractions cells dependent on?
What happens when a myocyte dies? What can you monitor?
What other cardiac marker can you monitor if MI is suspected?
When are these markers elevated?
Actin and Myosin
Tropomyosin & troponin serve regulatory functions
Troponin level: if the myocyte cell died, it will release the troponin into the blood cell
—cardiac troponin rises after 4h and peaks at 24h
—it is elevated for 7-10d
—CK-MB increases after 6-12 hours, peaks at 16-24hr
—CK-MB is useful in diagnosing infarction following an acute MI because levels return to normal after 48h
—but remember Troponin is more specific to MI
Learn the wiggers diagram well
Blank in notability to practice
Start reading from diastole, it is longer, filling up blood.
S1: mitral and tricuspid closing
S2: aortic and pulmonic closing
Isovolumic contraction Pressure building in the left ventricle but blood isn’t going anywhere because it hasn’t overcome the aortic pressure yet, once it does, then the aortic valve opens.
Left atrial kick (contraction) — what is it?
How much extra blood does it give?
What happens at S1 and S2?
Discuss pressure changes in LA and LV with regards to the mitral and aortic valve
—This occurs during late diastole, the LA contracts causing active filling of the LV as well as a small rise in both LA and LV
—Atrial fibrillation patients don’t have atrial kick..
— It gives an extra 10-15% blood
— When the mitral valve closes, this is S1
— S1 coordinates with the pulse!
— When the LV relaxes, the pressure in the LV falls below the aortic pressure and then the aortic valve closes, producing S2.
— When the pressure in the LV falls below the pressure in the LA, the mitral valve opens and the blood floods in
Atrial pressure. Same as mustard coloured line on wiggers diagram
What do A, C and V represent?
A: rise in atrial pressure, contraction, that’s the JVD you’re looking at
C: small rise in atrial pressure as the mitral/tricuspid valves close, bulge and push back into the respective atria
X (descent): passive decline in atrial pressure as the chamber has emptied (vent. Systole)
V: rise in atrial pressure once again as the atrium increase in pressure from the return of blood (M/T valves are closed)
Y (descent): diastole starts
JVP — what does it measure?
How can you ensure you’re on the right vein?
How do you measure?
Good estimate of right atrial pressure
Double upstroke (a and v waves)
No pulsation to palpation (you’re measuring the IJV under the SCM muscle)
Add 5cm to the reading due to the distance from the right atrium to the sternal angle
Is like oil in a car and a dipstick — too much fluid, volume overload. Dehydrated — JVD flat
Extra systolic heart sounds
What are ejection clicks?
Early ejection click
—what is happening
—what is the sound
—when can you hear it?
Mid and late non-ejection click
—what is happening
—where can you hear it?
Early:
—pulmonary/aortic stenosis, stiff valve trying to open
—high-pitched thrill, heard over aortic valve
—heard just after S1
Mid/late:
—occurs in mitral/tricuspid valve prolapse where the valve leaflets bulge abnormally into the atrium during ventricular contraction (regurgitation)
—best heard at apex/PMI
During systole
Extra diastolic heart sounds
Opening snap — what is this?
S3 — aka? What is happening? When do you hear it? Pitch?
S4 — aka? What is happening? When do you hear it? What is going on with the heart?
Pericardial knock — when do you hear it? What’s happening with the heart?
Opening snap:
—Opening valve should be quiet!
—Opening of the mitral/tricuspid valves is audible if they’re stenotic
S3: “ventricular gallop”
—a lot of volume entering ventricles, chordae tendinae to tighten and tense up, really fast entering blood smashing against chordae tendinae.
—Early during rapid inflow of blood.
—Can be normal in kids.
—Heard in early diastole
—Low pitched
—Mitral regurgitation
S4: “atrial gallop”
—volume coming in, but ventricles are stiff, so blood slams against stiff ventricle.
—Caused by the left or right atrium contracting against a stiff ventricle. Heard in late diastole
—Pathological from decreased ventricular compliance from LVH or Ischemic.
Pericardial knock:
—heard in early diastole, after opening snap.
—Caused by abrupt cessation of ventricular filling which is heard in constrictive pericarditis
Learn these murmurs
Learn these murmurs
Listen to murmur videos, how would you describe them?
YouTube Medzcool:
Mitral stenosis
5 important things
—where do you auscultate this murmur?
—when do you hear it
—what is causing these sounds?
—What makes it louder?
—What is the pathology behind this murmur?
—What can it lead to? 2
Mitral stenosis
—heard at the apex
—loud S1 from the rapid closing of the thickened mitral valves
—you also hear an early diastolic snap caused by the valve leaflets “snapping” into the LV (in a vignette: opening snap after S2)
—following the opening snap, you will hear a low pitched descrescendo-crescendo rumbling diastolic murmur that becomes louder after valsalva, exercise
—caused by Rheumatic heart disease
—can lead to pulmonary hypertension, Afib.
Describe this murmur (reference Medzcool YT)
Mitral regurgitation/tricuspid regurgitation
Holosystolic
How would you describe this murmur?
Where do you hear it?
Common causes? 3
—occurs when the mitral/tricuspid should be closed, therefore during systole
—tricuspid: heard at the lower left sternal border but radiates to the right sternal border, since that’s the direction of the regurgitated blood
—mitral: heard at the apex of the heart but regurgitates/radiates to the axilla
—holosystolic high-pitched blowing murmur that starts with S1 and runs until S2
—common cause: mitral valve prolapse, rheumatic fever, infective endocarditis, structural and Ischemic disease
—tricuspid causes: IV drug abuse, Marfan syndrome, pulmonary HTN
—also heard with VSD
Describe this murmur (reference Medzcool YT)
Mitral valve prolapse
Where/when do you hear it?
What does it sound like?
Associated with what?
Caused by what?
What can you do to hear the sound sooner or later?
—best heard at the apex during systole
—MVP is caused by the mitral valve leaflets bulging into the left atrium (mid-systolic click) when the ventricles contract
—sounds like a small whoosh between S1 and S2 (mid-systolic click)
—often associated with regurgitation of blood (which is a longer whooshing sound that runs the distance between S1 and S2
— likely cause is myxomatous degeneration of the mitral valve leaflets
—2% of population, most asymptomatic, if symptomatic, palpitations or chest pain are common
—complications include Arrhythmias, heart failure and endorcarditis
—standing will make the click be heard sooner, squatting later
Describe this murmur (reference Medzcool YT)
Aortic stenosis
Where do you hear it?
What does it sound like?
What pitch pattern?
Radiates where?
What other findings ?
Causes?
—almost sounds like one large whooshing beat, or S1/S2 very close together muffled by a whoosh. Often S2 is diminished or absent in severe aortic stenosis
— heard on the right sternal border @ 2nd IC space
—crescendo-descrendo systolic ejection murmur (think of the aorta as a arch, just like crescendo-decrescendo)
—radiates to the carotids!
—peripheral pulses are often weak and delayed
—common causes: calcified and bicuspid aortic valves
Describe this murmur (reference Medzcool YT)
Aortic regurgitation
What other PE finding might you see with this murmur?
—this occurs when the aortic valve should be closed which is the S2 sound. So you hear this murmur after S2 during diastole
—or best known as early diastolic decrescendo murmur
—heard best at the left parasternal border at the 3rd 4th IC space because remember, the blood is regurgitating back into LV so lower that the aortic valve itself
—can present with bounding pulse or wide pulse pressure
—common causes: bicuspid aortic valve (instead of tricuspid), endocarditis, rheumatic fever, aortic root dilation
