Midterm 1 - Amanda Flashcards
Left Ventricle
systemic circulation. Contraction 120 mm Hg and Relaxation 80 mm Hg. Three times thicker than right ventricle. Circular in cross-section to create a pressure pump to maximize pressure.
Right Ventricle
pulmonary circulation. Contracting 24 mm Hg and Relaxation 8 mm Hg. Lower pressure to prevent net loss of fluid into alveoli. Thinner walled than the left ventricle. Crescent shaped cross-section maximizes volume of blood. Volume pump.
Atria
Thin-walled and stretchy to accumulate blood. Is responsible for final 20% of ventricle filling (first part is due to suction when ventricle relaxes)
Veins
thinner walled but larger than corresponding artery. High compliance - stretch easily.
- Superior and Inferior Vena Cava: Return blood to the right atrium
- Pulmonary veins: return blood from lungs to left atrium. Total of 4.
- Coronary sinus: returns blood from the heart muscle into the right atrium
Arteries
Elastin which is much more compliant. Stretchy but springy which is important for blood pressure.
- Pulmonary trunk: carries blood from the right atrium to the lungs
- Aorta: carries blood from the left atrium through systemic circulation
- Coronary arteries: two. Found at the beginning of the aorta and carry blood to the heart muscle.
Atrioventricular Valves
separates atrium and ventricles.
Right side is tricuspid and left is mitral.
Form puckered-lip funnel like structure.
To prevent from blowing backwards are secured to papillary muscle by chordae
Aortic Valve
separates left ventricle from aorta.
three leaflets that meet at thickened edges.
When there is back-flow the leaflets balloon down which allow the edges to push together to prevent opening.
Pulmonary Valve
separates pulmonary trunk and right ventricle.
Functions of valves lying in a plane
First is support of the valves.
Second is to electrically separate the atria and the ventricles.
Echocardiography
ultrasound of heart. Can add doppler to track flow of blood. Transducer placed under the left ventricle so on a echocardiography the transducer is the peak of the pyramid so see heart upside down.
Normal Heart Sounds
S1: AV valves closing as ventricles start to contract. beginning of systole
S2: moment ventricles start relaxing and aortic and pulmonary valves start to close. beginning of diastole
systole: S1 to S2
diastole: S2 to next S1
Split Sound (Heart)
asymmetry in closing of both valves. Occurs on deep inspiration and abnormally with bundle branch block.
S3 Abnormal Heart Sound
Occurs in diastole during the rapid, passive phase of filling. Often heard in kids but more pronounced in elderly persons with an expanded ECF volume and those people with CHF
S4 Abnormal Heart Sound
Occurs in diastole during atrial contraction because of stiff ventricles.
Gallop Heart Sound
Here all four S’s
Laminar Flow
blood is moving straight through vessels as if they were smooth sheets and not changing directions. most efficient movement and does not produce noise. Normal pattern of flow in the cardiovascular system.
Turbulent Flow
pattern of laminar flow breaks down and blood cells swerve around bouncing off walls and causing noise.
Stenosis
generic term meaning narrowing. With a valve it means that a valve can’t open fully and blood flow is narrowed.
AV = diastolic
pulmonary or aortic = systolic
Insufficiency
Also called regurgitation. Valves do not close properly and blood flows backwards.
AV = systolic
aortic or pulmonary = diastolic
Senile Aortic Valve
Occurs in elderly (70s - 80s). stenosis and fibrosis leads to calcification of valves.
Calcification causes left ventricle hypertrophy (thicker) to generate more pressure. High pressures in the left ventricle lead higher pressures in the pulmonary circulation which can cause pulmonary edema and congestive heart failure.
Systolic murmur
Bicuspid Aortic Valve
Form of aortic stenosis caused by a bicuspid valve versus the normal three leaflets. Systolic murmur. Treatment usually involves replacement in middle age.
Rheumatic Heart Disease
Cause is an acute streptococcal infection involving pharyngitis (strep throat). Rheumatic fever develops 2-3 weeks afterwards and carditis causes mitral stenosis. Pressure in the left atrium increases, increasing the pressure in the pulmonary circulation causing pulmonary edema. Common symptom is shortness of breath, dyspnea. Progression leads to congestive heart failure. Diastolic murmur
Infective Endocarditis
Common cause is nosocomial which is medical treatment in a hospital that results in bacteria in the blood. Vegetations form at inflamed valve leaflets. Can lead to aortic or mitral insufficiency (systolic) as well as pulmonary edema.
Artificial Valves
- bi-leaflet: completely artificial valve made out of carbon fibers.
- biological valve: less problematic but shorter duration. Source is pig or cadaver. No immunological problems because endothelium is removed.
- Transcatheter aortic valve replacement: TAVR. only choice where the chest does not have to be cracked open and don’t have to open the heart.
Myogenic Cardiac Cell
cardiac muscle can begin a contraction on its own. Early embryonic heart is always myogenic and normal hearts have specialized cardiac muscle that is myogenic.
Intercalated Disk
interconnect cardiac muscle and allow action potential to conduct over whole heart.
Sinoatrial Node (SA Node): Natural pacemaker of heart which has myogenic properties. Produces action potentials at 100/min with no outside feedback. Parasympathetic nerves innervate SA Node and slow to about 70/min
Atrioventricular Node (AV Node): Inherent rate is 60/min. May act as pacemaker if SA Node is damaged, but isn’t normally because is in a refractory period while SA node initiates action potential.
AV Bundle (of His): Muscle fibers run through the barrier of atrial and ventricular muscle cells (which are physically separated). Muscle fibers are bigger than the SA and AV node. Inherent rate of 30/min.
Right and Left Bundle Branches: Branches from AV bundle and has similar large muscle fibers as AV bundle. Fast conduction.
Purkunje Fibers: conduction is on inner surface of ventricles. Travels downward to bottom of ventricles than up outer walls of ventricles
Cardiac Action Potentials
Ventricles: all are voltage-gated
A: Na+ channel opens causing an upsweep of depolarization. Fast.
B: Ca++ channels slowly open and slowly close causing the action potential to last for an extended period of time (causes plateau).
C: slow K+ channels open causing repolarization.
Cardiac Action Potentials
SA node or any injured or sick cardiac muscle
B: slow Ca++ channels open and slowly close.
C: K+ channels open causing repolarization
Cardiac Action Potentials
Pacemaker Potentials (seen in SA Node action potentials) 1. Parasympathetic Innervation: slow down pacemaker potential (less steep slope) causing longer time between heart beats. Nt is ACh with GPCR which opens the K+ channels.
- Sympathetic Innervation: faster depolarization of pacemaker cells to reach threshold faster to produce faster heart rate. Nt is norepinephrine with GPCR which opens Calcium channels.
- Adenosine: drug that opens potassium channel through GPCR to slow heart rate.
Refractory Period in Cardiac Action Potentials
period of time when ion channels aren’t back to normal state and are incapable of producing an action potential.
Ventricles have to have a refractory period before action potential or else tetanus would occur where there is steady contraction with one action potential after another which wouldn’t allow the blood to pump any blood.
Lidocaine
Blocks opening of voltage-gated ion channels in cardiac ventricular action potentials as well as in skeletal muscle.
Introduction to Electrocardiograms
Lead II: most common
P wave: action potential moving through the atria
QRS wave: action potential moving through the bulk of the ventricles
T wave: repolarization of ventricular tissue.
First Degree AV Block
Conduction velocity is greatly slowed so have a large interval between P and QRS wave.
Often is benign (athlete with good vagal tone). Can be due to heart disease (schema) or a variety of drugs including beta blockers, CCB’s and digoxin.
Second Degree AV block
Some of the action potentials never get to the AV node (see a P with no QRS). P to QRS interval is variable.
Causes can be schema, benign, or drug effect that reduces excitability of the heart including BBs, CCB’s and digoxin.
Third Degree AV Block
Prolonged and misshaped QRS waves. Action potential never gets through the AV node so other specialized tissue (probably bundle branch) is causing the QRS waves.
Causes can be mild MI.
Ectopic focus in ventricles.
Premature Atrial Contraction
extra contraction due to an ectopic focus in atria, causing an extra heartbeat.
Cause: heart disease or benign
Longer pause after premature contraction leads to more filing of ventricles. Person may feel next beat as a little pulsation in the chest.
Premature Ventricular Contraction
ectopic focus in ventricle shows as a prolonged and misshapen QRS wave.
Shape of the QRS wave can be upwards or downwards or both depending (two ectopic focus) on which side of the heart.
Cause: heart disease or benign.
Supraventricular Tachycardia
heart rate over 100/min
Paroxysmal: most typical are episodes that show up maybe due to stress or caffeine.
No changes in blood vessels so ventricles don’t fill properly and usually are pumping less blood than normal. May have syncope.
Most common cause is AV node re-entry. May have a fast and slow pathway in AV node. Fast pathway causes an action potential and then after the refractory period the slow pathway creates the next action potential.
Wolff-Parkinson-White Syndrome
Type of supraventricular tachycardia
Rare cause is an accessory pathway that creates a loop from the normal pathway then after the action potential goes through the ventricles it exits back into the atria through an accessory pathway. Cure is ablation which is to destroy the tissue that holds the accessory pathway.
Ventricular Tachycardia
Ectopic focus in ventricle that is constantly producing an action potential.
Cause can be due to an MI, or may be genetic (abnormal ion channel “myopathy”)
Will lapse into ventricle fibrillation which is death. Treatment is to have a pacemaker/defibrillator combination that blasts an action potential into the heart to wipe the slate clean if an individual goes into ventricular tachycardia.
Atrial Fibrillation
Action potential continues over atria indefinetly and cause the atria to quiver instead of pumping.
Periodiacally the action potential hits the AV node causing contraction
ECG is a random action potential frequency.
May or may not be symptomatic.
Ventricular Fibrillation
lethal arrhythmia
Causes include MI, myopathy leading to ventricular tachycardia.
Treatment: pacemaker with a defibrillator.
Valves and Heart Sounds in the Cardiac Cycle
All occur at the very end of the peak of the QRS wave.
AV Valve: The AV valve is closed. Ventricular pressure increases. Atrial pressure remains low and constant. When ventricular pressure falls below atrial pressure the AV valve opens.
Aortic Valve: Left ventricular pressure increases. When left ventricular pressure is higher than aortic pressure the aortic valve opens. When the left ventricular pressure falls below aortic pressure the aortic valve closes.
Heart Sounds: S1 is heard right at the closing of the AV valve. S2 is heard when both the AV valve opens and the aortic valve closes which occurs simultaneously.
Phase 1 of Cardiac Cycle
Isovolumetric Contraction: Phase 1. Systole. AV valve closes, aortic valve is closed and have S1 heart sound.
Phase 2 of Cardiac Cycle
Ejection: Phase 2. Systole. Aortic valve opens. First half of ventricular pressure and second half is reduced.
Phase 3 of Cardiac Cycle
Isovolumetric Relaxation: Phase 3. Diastole. Aortic Valve closes. Ventricular pressure drops.
Phase 4 of Cardiac Cycle
Passive Filling: Phase 4. Diastole. Aortic pressure falls and atrial pressure starts rising. Split into rapid filling then passive filling.
Phase 5 of Cardiac Cycle
Atrial Contraction: Phase 5. Diastole. AV valve open.
Angiotensin II production in heart failure
Poor renal perfusion appears to kidney as low ECF volume. Kidney releases renin which acts to convert angiotensinogen to angiotensin I. ACE converts angiotensin I to angiotensin II which constricts arterioles (increases afterload) and expands ECF.
Mean arterial pressur
= CO + TPR. Where TPR is determined by the diameter of the smallest arteries, arterioles. Vasoconstriction of arterioles increases TPR and vasodilation decreases TPR
Carotid Baroreceptor Reflex
Reflex that adjusts the mean arterial pressure back to a normal level. Sensors are in the carotid sinus and the integrating center is the medulla.
Atherosclerosis: sequence of events to form a fatty streak
Begins with damage to the endothelium resulting in an inflammatory response. LDL cholesterol and apolipoprotein apoB accumulates in the tunica intima. Macrophages begin to accumulate at the site. Macrophages take up so much cholesterol they are now called foam cells that start to accumulate in the growing plaque. This is seen as a fatty streak in the coronary arteries.
