Heart Stuff Flashcards
Memorize this shit
mitraL is on…
the Left side
tRicupid is on…
the Right side
Auscultation point for mitraL valve is…
at L 5th/6th ICS on the L side; aka, the apex; below nipple line; sounds can radiate to the axilla from here
Auscultation point for tRicuspid valve is…
at L 4th/5th ICS on the L side; aka, the L lower sternal border (below Erb’s pt.)
Auscultation point for aortic valve is…
at R 2nd ICS on the R side; sounds can radiate to the neck (both carotids) from here
Auscultation point for pulmonic valve is…
at L 2nd ICS on the L side
What is Erb’s point on the chest?
L 3rd ICS on L side - indicates where the mitral and aortic valves are, anatomically
“Mid-systolic crescendo-decrescendo murmur”
Aortic stenosis
“Mid-systolic click”
Mitral valve prolapse
“Late systolic crescendo murmur that gets louder at S2”
Mitral valve prolapse
“Systolic murmur associated with a palpable thrill”
Ventral Septal Defect (VSD)
“Mid-to-late-systolic ejection murmur that radiates to the neck”
Aortic stenosis
“Systolic blowing murmur that’s best heard at the apex”
Mitral regurgitation
“Heard best at L 3rd/4th ICS (aka Erb’s point) and gets louder on hand grip”
Ventral Septal Defect (VSD)
“Wide, fixed, split S2”
Atrial Septal Defect
“Wide, fixed, split S2 with R-BBB + L axis deviation”
Osteum Primum ASD
“Wide, fixed, split S2 with R-BBB + R axis deviation”
Osteum Secundum ASD
“Soft systolic ejection murmur”
Pulmonic stenosis
“Soft systolic blowing murmur that increases on inspiration”
Tricuspid regurgitation
“High-pitched systolic murmur that is louder on the L lower sternal border (aka L 4th ICS/Tricuspid ausc. area); a third heart sound is heard and JVP is slightly elevated.”
Tricuspid regurgitation
S3 heart sounds indicate…
Volume overload problems (“S3 = V”)
S4 heart sounds indicate…
Pressure overload problems
List all the SYSTOLIC MURMURS (there are 7)
- Aortic stenosis (mid-systolic)
- Pulmonic stenosis
- Mitral valve prolapse
- Mitral regurgitation
- Tricuspid regurgitation
- Atrial septal defect
- Ventral septal defect
Also: hypertrophic cardiomyopathy
List all the DIASTOLIC MURMURS (there are 4)
- Aortic regurgitation (early diastole)
- Pulmonic regurgitation
- Mitral stenosis (mid- to late diastole)
- Tricuspid stenosis (late diastole)
“Early diastolic blowing murmur”
Aortic regurgitation
“Early diastolic crescendo murmur best heard at the end of expiration”
Aortic regurgitation
“Opening snap”
Mitral stenosis OR tricuspid stenosis; depends on other clues, but opening snaps are heard IN DIASTOLE
“Late diastolic rumbling murmur”
Tricuspid stenosis OR Mitral stenosis; depends on other clues
“Mid-diastolic opening snap”
Mitral stenosis OR Tricuspid stenosis; depends on other clues
Murmur order during diastole:
Atrial regurgitaiton is early diastole
Mitral stenosis is MID-diastole
Tricuspid stenosis is late diastole
Diastolic murmurs: “AR-MS-TS”
“Rumbling mid- to late-diastolic murmur with opening snap that gets louder on inspiration”
Tricuspid stenosis
“Wide, fixed, split S1”
Tricuspid stenosis
“Late diastolic rumbling”
Mitral stenosis OR Tricuspid stenosis; depends on other clues
“Louder on inspiration with a wide, fixed, split S1”
Tricuspid stenosis
“Continuous, machine-like murmur”
Patent ductus arteriosus (PDA)
“Heart sound heard immediately before S2” (or after S1)
S3 heart sound: indicates a volume overload problem
“Heart sound heard immediately before S1” (or after S2)
S4 heart sound: indicates a pressure overload problem
“Systolic murmur that radiates to the axilla”
Mitral regurgitation
“Murmur that decreases upon administration of amyl nitrate”
Ventral Septal Defect (systolic murmur) Mitral regurgitation (systolic murmur) Aortic regurgitation (diastolic murmur)
All other murmurs get louder with amyl nitrate admin.
blood rushing into a non-compliant and/or stiff ventricle at the end of diastole, or during atrial contraction causes what kind of sound?
an S4 gallop
blood rushing into an overly compliant ventricle, such as that of a dilated cardiomyopathy, and heard immediately before S2, in systole represents what kind of sound?
an S3 gallop
Venous thrombus in the brain indicates what cardiac anomaly?
Patent foramen ovale (PFO)
“Weak pulses, soft S2, holosystolic murmur at apex and late-peaking systolic murmur in R upper sternal border”
Aortic stenosis
What are two major consequences of aortic stenosis?
(1) Decreased cardiac output and (2) increased oxygen demand
“Narrowed pulse pressure”
Aortic stenosis
“Delayed carotid upstroke”
Aortic stenosis
Aortic stenosis causes increased what?
Afterload
Normal aorta has how many cusps?
Three
Patient is in their 40s or 50s and is found to have aortic stenosis. Why?
Probably a bicuspid aortic valve that lead to calcification and then aortic stenosis.
If you decrease preload (Valsalva maneuver) or increase afterload (hand grip), what happens to the murmur of aortic stenosis?
It decreases (because VELOCITY of blood flow decreases across the valve).
If you increase the preload (rapid squatting), what happens to the murmur of aortic stenosis?
It increases/gets louder
Aortic regurgitation causes volume overload in the L ventricle. This leads to sarcomeres within myocytes to add in series, leading to?
Eccentric hypertrophy
Aortic stenosis causes decreased cardiac output, which leads to increased afterload (systemic peripheral resistance will incrase to increase cardiac output). This leads to sarcomeres within myocytes to add in parallel, leading to?
Concentric hypertrophy
Long-standing aortic stenosis can led to left atrial dilation, which compresses the conducting fibers within atrial tissue. This predisposes patients with aortic stenosis to what dangerous complication?
Atrial fibrillation
Because aortic stenosis leads to decreased compliance of the left ventricle, it is a pressure increase problem. That means an S4 sound may be heard along with a mid-systolic crescendo-decrescendo murmur that radiates to both carotids. What complication would muffle or eliminate the S4 sound in aortic stenosis?
Atrial fibrillation
What do transposition of the great vessels, Tetralogy of Fallot, and a persistent truncus arteriosus all have in common?
They are all conotruncal abnormalities associated with failure of neural crest cells to migrate properly.
This is the most posterior part of the heart in anatomical position:
Left atrium
Enlargement of the left atrium can lead to what secondary symptoms (related to its anatomy)?
Dysphagia (compresses the esophagus which is behind it) and hoarseness (compression of the left recurrent laryngeal nerve, a branch of the vagus nerve)
What nerve innervates the pericardium?
Phrenic nerve
Referred pain to the shoulder may be a sign of what heart condition?
Pericarditis
Increased contractility, increased afterload, increased heart rate, and increased diameter of the ventricle (increased wall tension) are all causes of what?
Increased oxygen demand of the heart
Venous dilation affects what cardiac parameter?
Preload - venous vasodilators will decrease preload
Atrial dilation affects what cardiac parameter?
Afterload - arterial vasodilators will decrease afterload
Paradoxical splitting of S2 is a sign of what?
Delay of aortic valve closure, such as in aortic stenosis or left bundle-branch block (L-BBB).
Pediatric patient w/hx of congenital rubella. What may be heard on cardiac auscultation?
Patent ductus arteriosus - continuous machine-like murmur, loudest at S2
Posterior heart infarctions are more associated with arrhythmias because?
90% of people’s AV node is supplied by the posterior descending coronary artery, which branches off of the R-coronary artery. If the patient is L-side dominant, then their AV node will be supplied by the L-coronary artery –> circumflex artery –> posterior IV or descending coronary artery –> AV nodal artery. If the AV node is infarcted, you’ll get AV blocks and arrhythmias.
Which heart chamber is located most posteriorly in the chest?
Left atrium
What anatomic structure sits behind the most posteriorly-located heart chamber in the chest?
The esophagus - it lies behind the left atrium. As such, if the left atrium is hypertrophied, you’ll get dysphagia. Further, transesophageal echochardiogram is better to visualize the left atria and rule out a left atrial thrombus. Transthoracic echo is better for other chambers.
Intraventricular septal infarction may result from the occlusion of either of which two (coronary) arteries?
Either the main Left coronary artery that branches off the root of the ascending aorta, or the anterior descending branch, which, with the circumflex artery, is one of two branches the left main coronary artery splits into. This is because all of its septal branches supply the anterior 2/3 of the interventricular septum. (The posterior descending coronary artery supplies the posterior 1/3 of the interventricular septum)
Which heart chamber is better visualized using a transesophageal echocardiogram?
Left atrium
Two main branches of the left coronary artery are:
Most left: the left circumflex artery (which leads to the posterior descending art)
More medially: the anterior descending branch
Two main branches of the right coronary artery are:
Front: right marginal artery
Back: posterior interventricular, or posterior descending artery
You suspect pulmonic stenosis. Where will you put the stethoscope to listen?
Left side
Second intercostal space
Parasternal/sternal border
Pt. comes in with atrial fibrillation, low blood pressure, but fast heart rate. You wanna slow the heart down to allow for diastolic filling. Despite the fact that they can lower blood pressure further, what drugs are actually useful in THIS particular situation?
Amiodarone
Digoxin
In a patient with low blood pressure and rapid heart rate due to atrial fibrillation, what drugs do you want to AVOID as IV push (because they drop blood pressure even further without benefit of slowing the heart rate)?
Metoprolol (beta-blockers)
Diltiazim
Pt. presents with sudden bilateral pulmonary edema. How do you differentiate between heart failure and Adult Respiratory Distress Syndrome (ARDS)?
Check left atrial pressure with Swann-Ganz. If it’s high, it’s heart failure. If it’s normal, it’s ARDS.
What is considered a “high wedge pressure”?
Anything greater than 18mmHg.
Pulmonary edema plus high wedge pressure equals?
Heart failure
Pulmonary edema plus normal wedge pressure equals?
ARDS, or non-cardiogenic pulmonary edema
50% stenosis of an artery translates to what change in flow rate past the stenosis?
Only 1/16th decrease from original flow rate. Poiseuille’s formula says something something to the 4th power. Change percentages to fractions then multiply it by itself 4 times. 50% is 1/2, so (1/2)(1/2)(1/2)(1/2) = 1/16.
In the cardiac action potential of the ventricular myocytes, sodium influx is represented by which phase?
The depolarization phase, or phase 0 - this is the phase that shoots straight up towards sodium’s preferred membrane potential, which is up in the positives.
In the cardiac action potential of the ventricular myocytes, there is a brief moment of repolarization just before a plateau phase is reached. This is phase 1. Why does it occur?
Because some potassium ions are leaking out of the cell, making the inside slightly more negative, or less positive.
In the cardiac action potential of the ventricular myocytes, the movement of what ion causes the plateau, aka, phase 2?
The inward movement of calcium ions. The balance of the plateau is due to K+ leaving and Ca++ coming in; they are both positive ions.
In the cardiac action potential of the ventricular myocytes, what mediates the repolarization phase, or phase 3?
Phase 3 starts when calcium influx slows down and potassium efflux is unhindered. Potassium’s exit out of the cell is what repolarizes (makes more negative) the cell.
What maintains phase 4, or the resting membrane potential of the myocyte at -90mV in the cardiac action potential of the ventricular myocytes?
The Na+/K+-ATPase pump, which throws three salts out and two bananas in (three sodium ions OUT for two potassium ions IN).
The action potentials of the pacemaker cells (SA node, the AV node, the bundle of HIS cells and Purkinje fiber cells) are different from that of the ventricular myocyte. There are two phases “missing” from pacemaker action potentials. What are they?
Phase 1 and phase 2 (the brief repolarization and the plateau phase).
The depolarization phase of ventricular myocytes is due to rapid influx of sodium, but in pacemaker cells, it is due to influx of what ion?
Calcium
In pacemaker cell action potentials, sodium influx indicates what?
Repolarization, believe it or not.
The slow repolarization phase mediated by sodium influx in pacemaker cells is the reason for what characteristic feature of these cells?
Automaticity
What allows cardiac cells to act as a syncytium?
Gap junctions, which are made of two connexons (themselves made of multiple units of connexin monomers)
During the plateau phase of the ventricular myocyte action potential, calcium influxes from where?
The extracellular fluid
Extracellular fluid influxes into ventricular myocytes during the plateau phase of the action potential, triggering what?
Intracellular calcium release from the sarcoplasmic reticulum.
To start excitation-contraction coupling, intracellular calcium binds to what?
Troponin C
When can you use the Valsalva maneuver or carotid massage on a patient?
When they’re having supraventricular tachycardia; those maneuvers will slow the heart down via baroreceptors
Baroreceptors are found where?
In the aortic arch and carotid sinus.
The aortic arch can sense?
Only increased blood pressure
The carotid sinus receptors can sense?
Both increase and decrease in blood pressure
What happens to angiotensinogen?
Hydrolyzed by renin into Angiotensin I
What happens to angiotensin I?
Cleaved by Angiotensin-Converting Enzyme (ACE) into Angiotensin II
What does angiotensin II do in the kidney?
- Binds its receptors in the efferent arterioles of glomerulus to increase sodium retention in proximal convoluted tubule (PCT), via the sodium-hydrogen exchanger.
- Vasoconstriction by acting on endothelial smooth muscles.
- Increase secretion of aldosterone from adrenal cortex to retain sodium and increase intravascular volume.
Why do stroke (or CVA) patients develop tachycardia and a hypertensive crisis?
It’s mediated by increased PCO2 in the brain (due to necrosis during stroke) which leads to the brain thinking it’s suffocating (it’s more sensitive to increased levels of CO2 rather than hypoxia itself). So, it sends sympathetic info to the heart to pump more blood to the brain.
Chemoreceptors in the carotid bodies and the aortic arch sense what?
PO2 (partial pressure of oxygen in the blood)
How does ADH behave after it’s released from the Posterior Pituitary?
(1) It binds V1 receptors on endothelial cells of vessels to vasoconstrict and raise bp (increases total peripheral resistance: TPR).
(2) It binds V2 receptors on DCT and collecting duct to increase water reabsorption.
Lactate or lactic acid does what to blood vessels?
Dilates them (it’s a vasodilator)
