Term
What is anastomosis and why is it important?
-What are arteries lacking anastomoses? |
|
Definition
Definition: when the ends of arteries fuse to one another
-Important b/c it allows for collateral circulation if one is occluded
-End arteries don't have any anastomoses, i.e renal arteries. |
|
|
Term
1) Another name for visceral pericardium
2) What happens if the pericardial cavity fills with fluid?
3) acute vs. chronic accumulation |
|
Definition
1) Epicardium
2) A Cardiac tamponade results, the heart is compressed
3) If 250 mL accumulate |
|
|
Term
1) Where does the heart sit? What does it span?
2) What parts of the heart lay anterior, posterior, left, and right? |
|
Definition
1) Sits 45˚ant and 45˚left, spans ribs 2-6, from the sternal angle to the xiphoid process
2) Ant: RV; Post: LA; Right margin: RA; Left margin: LV |
|
|
Term
5 features of the right atrium
-similarity w/ left atrium |
|
Definition
1) Auricle appendage
2) Pectinate muscle on anterior wall
3) crista terminalis: crest that separates pectinate and smooth wall
4) Fossa ovalis
5) coronary sinus
-LA has similar general features, but also has 2 left and 2 right pulmonary veins joining up. |
|
|
Term
| 5 Characteristics of the right ventricle |
|
Definition
1) Conus arteriosus: smooth top of the chamber; aortic vestibule in the LV
2) muscular/membranous IV septum
3) Trabeculae carne
4) papillary muscle: prevents backflow, has chordae tendinae
5) Septomarginal trabeculae: ridges between smooth wall and muscle, moderator band is a big one |
|
|
Term
| Where to hear valve sounds |
|
Definition
1) Aortic: between ribs 2/3, right side of sternum
2) Pulmonary: between ribs 2/3, left side of sternum
3) Right AV: between ribs 5/6, left side close to sternum
4) Left AV: same as Right AV, but on mid clavicular line |
|
|
Term
Describe coronary circulation
-What gets the IV septum?
-What gets the nodes? |
|
Definition
-CA come from the aortic sinuses, just above the aortic valve
-Left CA splits into Ant. IV, Circumflex, and left marginal branches. Gets the front of the heart, most of the IV septum
-Right CA gets the posterior third of the IV septum
-Most of the SA/AV nodes are done by the right CA |
|
|
Term
Describe the venous side of coronary circulation.
-What is special about the coronary sinus? |
|
Definition
-Coronary sinus is imbedded in the wall of the heart
-Great cardiac vein: Ant IV, continuation of coronary sinus
-Middle cardiac vein: post IV, joins up w/coronary sinus
-Anterior cardiac veins drain directly into the RA |
|
|
Term
Where does heart sympathetic innervation come from?
-What type of nerves are they?
-Where does parasympathetic heart innervation come from? |
|
Definition
-Comes from the Stellate ganglion at T1, above the heart
-Cardiopulmonary splanchnic nerves
-Parasympathetic comes from the vagus nerve |
|
|
Term
|
Definition
Cardinal (above the heart)-->subcardinal (inf. VC)-->supra cardinal (azygos system)
-vitelline (hepatic portal system) |
|
|
Term
Heart primordium-what gives rise to the heart?
-Where does it start?
-What does the tube contain? |
|
Definition
-Cardiac mesenchyme swells and hollows out
-Heart starts above the head and then swings down
-Starts as two tubes that fuse
-Tube has endocardial tube, cardiac jelly, and myocardial mantle |
|
|
Term
| Segments of the early heart tube |
|
Definition
| Sinus venosus-->atrium-->ventricle-->bulbis cordis-->truncus arteriosus |
|
|
Term
Partitioning the heart tube
-Blood flow |
|
Definition
| The ends are fixed and the middle keeps growing, so it bends in the middle of the ventricles. Blood now flows inferiorly from the atrium, through the LV, to the RV, through the bulbus cordis and out the truncus arteriosus |
|
|
Term
What do endocardial cushions do?
-Where to the septa grow from? |
|
Definition
-Endocardial cushions split the AV canal into left and right
-IV septum comes from the floor
-Septum primum comes from the top and grows down |
|
|
Term
|
Definition
-Primary septa forms. foemen primum appears first and later disappears, foramen secundum forms 2nd and is high up
-Secondary septa forms right of the primary septa. The foramen ovale forms on the lower part of the septum secundum |
|
|
Term
| How atrial septal defects arise |
|
Definition
1) Foramen ovale/foramen secundum are too big and overlap
2) Septum primum fails to fuse w/endocardial cushions
3) holes can form anywhere |
|
|
Term
Ventricular septation
-3 things that have to fuse |
|
Definition
-IV septum can't grow to the endocardial cushions b/c then blood would be trapped in the left ventricle
-Completed by the spiral-septum that forms in the truncus arteriosus
-3: IV septum, spiral septum, and endocardial cushions (this forms the membranous IV septum) |
|
|
Term
1) Fate of the sinus venosus
2) Fare of the bulbus cordis |
|
Definition
1) Smooth part of right atrium and coronary sinus
2) Smooth part of ventricles, the conus arteriosus and the aortic vestibule |
|
|
Term
| What connects the pulmonary trunk to the aortic arch (fetally and in adult? |
|
Definition
Fetal: ductus arteriosus
Adult: ligamentum arteriosum |
|
|
Term
|
Definition
The ductus venosus connects the umbilical vein to the inf vena cava
-Becomes the ligamentum venosum |
|
|
Term
|
Definition
-Defect is a defective spiral septum
Leads to: pulmonary stenosis, IV septal defects, overriding aorta, and RV hypertrophy |
|
|
Term
1) What is responsible for the resting membrane of cardiac cells?
2) What is the simplified version of the Nernst eqtn? |
|
Definition
1) Potassium leaking out and bringing + charge with it
2) E=(61/z)*Log( [Co]/[Ci] ) |
|
|
Term
|
Definition
4=Resting, some K+ leakage
0= Upstroke, Na channels open
1=Notch, slight repolarization, brief outburst of K+
2=plateau, Ca channels slowly open for slow repolarization
3=Repolarization |
|
|
Term
What controls ion flow in depolarization?
-What is key for generating the upstroke? |
|
Definition
-activation and inactivation gates for Na and Ca
-For I-Na: m is activation and h is inactivation
-For I-Ca: d is activation f is inactivation
-The channels must be in their resting state to generate an upstroke |
|
|
Term
| How the m and h channels work |
|
Definition
| It's all voltage dependent. At resting m is closed and h is open. As the cell gets more positive, m starts to open, letting in more Na and making the cell even more positive. This is a positive feedback loop. h is closing all this time and shuts everything off and the gate is in the inactivated state. |
|
|
Term
| How the d and f gates work |
|
Definition
These are for Ca and similar to m and h.
-d opens w/increase of Na and allows Ca to flow in
-This is key b/c Ca triggers release of Ca from the SR to initiate contraction.
-The f gate closes slowly
-These Ca channels are L-type channels |
|
|
Term
| Inward rectification and it's role in plateau |
|
Definition
Part of phase 2 plateau
-K channels are blocked by Mg, K can get in, but it can't leave to repolarize the cell
-The inside of the cell is highly positive and the electromotive force should push K+ out, but these inward rectification K channels prevent this. |
|
|
Term
| What happens if the resting potential is less negative, say -50mV? |
|
Definition
-The h gates will be closed, so even though the m gates might open, an AP cannot be generated.
-This leads Ca to be in charge of carrying the current, which they are not so good at. |
|
|
Term
| What are different K channels? |
|
Definition
I K-1: inward rectifier
I K: delayed rectifier, important for repolarization, split up into Ks, Kr, and Kur
I Ks: slow; I Kr: rapid; Kur: ultrarapid, in atria
I to: outward K+, responsible for the spike at phase 1 |
|
|
Term
| How cardiac cells are like electric cables: |
|
Definition
-Low resistance gap junctions
-Lipid bilayer capacitance
-High capacitance=slow conduction
-High membrane resistance=faster conduction, don't lose it through the membrane |
|
|
Term
| What is the space constant? |
|
Definition
-λ, It describes the rate of voltage decay
-Increased Rm=increased λ
-opposite for Ri |
|
|
Term
How is voltage change propagated along long distances?
-What electrical properties are best for propagation? |
|
Definition
-Via action potentials
-Without AP, voltage propagation is detrimental.
-Low Ri, High Rm, high voltage input |
|
|
Term
| What is special about midmyocardium cells? |
|
Definition
| -M Cells have a prolonged AP and are very vulnerable to drugs and such |
|
|
Term
| What is responsible for sinoatrial node depolarization? |
|
Definition
1) I-f current of inward mostly Na, some K
2) Outward flow of K+
3) Ca channels open and Ca flows in
4) SR rhythmically releases Ca, 1 Ca gets pumped out of cell and 3 K+ come in
1-3 are the membrane voltage clock, 4 is the Sarcolemmal calcium clock |
|
|
Term
| What imaging modality is best for viewing cardiac valves? Coronary arteries? |
|
Definition
Valves=Echocardiogram
Coronary arteries= cardiac CT |
|
|
Term
| QRS labeling designations: |
|
Definition
Q: downward wave, has to be the first one
R: and upward wave
S: downward wave after an R |
|
|
Term
| What happens in the heart during: P wave, PR interval, QRS interval, ST segment, and T wave? |
|
Definition
1) P-wave: 1st part is RA, 2nd part is LA
2) PR interval: AV node
3) QRS: IV septum, ventricles
4) ST: plateau of AP
5) T wave: repolarization of ventricles |
|
|
Term
How much time is a big box on EKG paper? voltage?
-HR estimate ditty |
|
Definition
|
|
Term
| Inferior leads, left lateral leads, right-sided leads, anterior |
|
Definition
Inferior: II, III, aVF
Left lateral: I, aVL, V5, V6
Right-sided: aVR, V1
Anterior: V2, V3, V4 |
|
|
Term
| What's pos/neg in the limb leads? |
|
Definition
I: LA+, RA-
II: LL+, RA-
III: LL+, LA-
aVR: RA+, L limbs -
aVL: LA+, RA/LL-
aVF: LL+, RA/LA - |
|
|
Term
|
Definition
1) aVR
2) aVL
3) I
4) III
5) aVF
6) II |
|
|
Term
| Where are the chest leads placed? |
|
Definition
V1-right of the sternum, 4th IC space
V2-left of the sternum, 4th IC space
V3-between V2 and V4
V4-5th IC space, mid clavicular line
V5-between V4 and V6
V6-5th IC space, mid axillary line |
|
|
Term
| Ways to calculate heart rate from EKG |
|
Definition
-Estimate:-300,150,100,75,60,50
-Actual: 1500/# of boxes, necessary if HR is irregular |
|
|
Term
| Normal durations for: PR interval, QRS interval, QT interval |
|
Definition
-PR interval: .12-.2 sec (3-5 boxes)
-QRS interval: up to .1 sec (2 boxes)
-QT interval: depends on heart rate, about .45 (9 little boxes) |
|
|
Term
| Correcting the QT interval |
|
Definition
-Depends on heart rate so there isn't a standard length
QTc=QT/√(RR)
-RR= length of RR segment preceding the QT, in seconds. |
|
|
Term
| Left/right axis deviation |
|
Definition
| -Left/right from the heart's perspective |
|
|
Term
| One way to systematically view an EKG |
|
Definition
1) PR, QRS, QT interval measurment
2) Look at QRS and T axis
3) Describe rate
4) Describe rhythm
5) Describe abnormalities in P, QRS, ST segment, and T |
|
|
Term
| ST elevation vs. depression |
|
Definition
-ST elevation(≥1mm): an MI, transmural ischemia.
-St depression(≤1mm): in chronic stable angina and non-STEMI, subcardial ischemia
-This is all due simply to the geometry of the dying tissue., current flows from the good tissue to the damaged tissue. |
|
|
Term
| What is the hallmark of infarction? |
|
Definition
-The Q wave
-Must be longer and taller than a small box in leads V2 or V3
-Must also have |
|
|
Term
|
Definition
-Look at the ST segment and T wave
-Hyperacute: tall T-wave, w/or w/out ST elevation
-Acute: elevated ST, very tall T wave, maybe a q-wave
-Long time: T waves invert, ST can be elevated or not. |
|
|
Term
|
Definition
Ant LV: V1-V4
Lateral LV: I, V5-V6
Inf LV: II,III, aVF |
|
|
Term
| Requirements for atrial enlargement |
|
Definition
-Look at lead II or V1, look at the P wave
-RA enlargement: 1st half of p-wave is larger than 2.5 boxes
-LA enlargment: lead II: p-wave wider than 3 boxes; V1: neg portion of p-wave dips down more than 1 box |
|
|
Term
| Ventricular enlargement criteria |
|
Definition
RVH: V1: R wave larger than S, V6: R wave smaller than S
LVH: S in V1+ R in V5 or V6 is ≥ 35mm |
|
|
Term
Definition of bradyarrhythmia
-2 general categories that cause it |
|
Definition
Ventricular heart rate less than 60 bpm
-Sinus node dysfunction or AV blocks |
|
|
Term
Sinus node dysfunction:
-general categories of cause |
|
Definition
1) Sinus bradycardia: normal rhythm, just really slow
2) Chronotropic incompetence: HR doesn't rise w/exercise
3) Tachy-Brady syndrome: fast, long pause, then slow beats
4) Sinus arrest: going normal, then just stops
5) SA exit block: current blocked (by scar or something)
-1st 4 are impulse formation problems, 5th is impulse propagation |
|
|
Term
| AV Blocks and their locations |
|
Definition
1st degree: AV Node
2nd degree Mobitz type I: AV node
2nd degree Mobitz type II: His purkinje system
3rd degree: His purkinje system |
|
|
Term
|
Definition
-1st degree: long PR, no dropped beats
-2nd degree Mobitz type I: Wenckebach, progressive PR delay w/beats dropped
-2nd degree Mobitz type II: fixed PR delay w/beats dropped
-3rd degree: P and QRS function independently |
|
|
Term
Definition of syncope
-characterized by...
-3 categories |
|
Definition
-Transient LOC, due to transient global hypoperfusion
-Characterized by: sudden onset, short duration, spontaneous/complete recovery
-Reflex, CV, Orthostatic Hypotension |
|
|
Term
|
Definition
|
|
Term
Causes of Reflex Syncope
-mechanism |
|
Definition
1) Vasovagal: emotional distress, fear, pain
2) Situational: sneeze, GI, laughing
3) Carotid Sinus Syncope
-Some stimulus leads to venous pooling in the legs, heart picks up, brains senses this and then over compensates with parasympathetic response: BP goes down. |
|
|
Term
| Cardiovascular Syncope causes |
|
Definition
-Arrhythmias: brady or tachy
-Structural disease: valves, ischemia, PE |
|
|
Term
Syncope due to Orthostatic Hypotension
2 forms |
|
Definition
-Autonomic failure: Primary: parkinsons and such, secondary: diabetes, etc; drug induced: alcohol, vasodilators
-Volume depletion: hemorrhage, diarrhea, vomiting |
|
|
Term
| Describe the histological layers of an elastic artery |
|
Definition
1) Tunica intima: endothelium and the internal elastic membrane
2) Tunica media: SM + fenestrated elastic lamellae
3) Adventitia |
|
|
Term
| What's the diameter of an RBC? |
|
Definition
|
|
Term
|
Definition
| An arteriole that bypasses the capillary bed and goes straight to a venule. |
|
|
Term
|
Definition
-Provide mechanical and metabolic support for endothelium in capillaries
-They are also stem cells that can differentiate into SM and endothelial cells in injury |
|
|
Term
| Where does histamine act? |
|
Definition
-On venules
-This is where WBC and fluid can enter the tissue |
|
|
Term
| Endothelial cell characteristics |
|
Definition
-Control import/export
-Secrete molecules to control blood flow/clotting
-Growth factor secretion
-Weibel-Palade bodies: platelet adhesion for injured cells and P-selectin for migrating neutrophils. |
|
|
Term
| Formation of an atherosclerotic plaque |
|
Definition
-Monocytes and SM cells migrate into the tunica intima
-They ingest LDL and become foam cells
-Thickening occurs
-Calcification develop and clots form on the surface |
|
|
Term
3 mechanisms of tachyarrhythmias:
-What categories do those mechanisms fall in? |
|
Definition
1) Re-entry
2) Automaticity
3) Triggered
-Abnormality in pulse formation (focal)=automaticity and triggered;
-Abnormality in pulse propagation (circuit)=re-entry |
|
|
Term
Result of:
1) abnormal automaticity
2) abnormal triggering |
|
Definition
1) increases slope in phase 4 depolarization, decreases threshold
2) Increased Ca++ leads to afterdepolarizations, early EAD in phase 3 or delayed DAD in phase 4 |
|
|
Term
|
Definition
-Inexcitable area due to scar, valve, or differences in depolarization
-This results in a circuit with a slow side and a fast side
-Slow side recovers quickly and fast side recovers slowly
-Normally, by the time a the fast side gets things going the slow side is too late and just dies
-If things are timed right, the slow side current can get things going and it causes a crazy spinning circuit that throws off the heart rate. |
|
|
Term
What is AVRT?
-How does it happen
-What can show up on an EKG |
|
Definition
-Atrioventricular re-entry tachycardia
-Occurs if a person has accessory tracts that bypass the tricuspid or mitral valve
-Can show up on an EKG as a delta wave |
|
|
Term
Orthodromic AVRT vs. antidromic AVRT
What about AVNRT? |
|
Definition
-Ortho is a pathway that goes the normal direction through the AV node
-anti is the pathway going the other way
-AVNRT: N stands for nodal, re-entry circuit within the AV node itself |
|
|
Term
|
Definition
A-fib: Most common arrhythmia, disorganized atrial activity
-irregularly irregular ventricular activity, sometimes originates from the pulmonary veins
A-flutter: fast, but organized and regular |
|
|
Term
Ventricular Tachycardia types
-sustained? |
|
Definition
-Monomorphic: consistent QRS
-Polymorphic: QRS changes beat to beat
-Sustained is greater than 30 seconds |
|
|
Term
|
Definition
| -This is the benign one, most commonly a triggered rhythm. |
|
|
Term
| Three general plans of fixing enhanced automaticity |
|
Definition
1) hyper polarize
2) decrease slope of depolarization
3) increase threshold |
|
|
Term
| General treatment plan for triggered arrhythmias |
|
Definition
EADs: Shorten the AP duration (ie for Torsades)
DADs: reverse the overlying cause (ie digitalis toxicity)
-Addressing the Ca++ directly can cause more problems |
|
|
Term
| Strategies for treating re-entry arr |
|
Definition
1) Increase refractory period of slow conducting
2) slowing conduction
3) suppressing premature beats |
|
|
Term
| Vaughn-Williams Classification of AA drugs |
|
Definition
Class I: Na+ channel blocking
Class II: ß-blocking
Class III: K+channel blocking
Class IV: Ca2+ channel blocking
Non-classified |
|
|
Term
Class I AA mechanism
-subdivisions
-effect on other channels |
|
Definition
-Binds to h gate of Na channel only when in the activated/inactivated state, can't bind during resting state.
-Ia=medium effect, 2a=low effect, 3a=high affect
-Can also have an effect on Ca channels |
|
|
Term
| Class Ia AA w/side-effects |
|
Definition
1) Procainamide: drug-induced lupus, Torsades
2) Quinidine: cinchonism(CNS poisoning), Torsades
3) Disopyramide: anti-muscarinic, Torsades |
|
|
Term
Class IB AA w/indications
-side-effect |
|
Definition
Lidocaine IV: targeted to ischemic tissue b/c it's more depolarized
Mexelitine
-Good for V-tachy, can cause CNS toxicity |
|
|
Term
Class IC AA
-contraindication
-use |
|
Definition
-Flecainide and Propafenone
-Contraindicated for LV systolic dysfunction and heart block
-convert a-fib, maintain sinus rhythm in a-fib |
|
|
Term
Class II AA
-side-effects
-examples
-use |
|
Definition
-These are the ß-blockers, they prolong phase 4 in If channels
-SE: hypotension, bradycardia
-ie Esmolol and metoprolol
-used to: disrupt re-entrant arrhythmias, suppress premature beats |
|
|
Term
Class III AA
-mechanism
-Effectiveness
-examples
-uses |
|
Definition
-These are the K blockers, prolong AP duration, also has similar effects to the other classes as well
-Very effective, but very toxic
-Amiodarone-check liver, thyroid, blue skin
-Sotalol, Dofetilide, Ibutilide
-Suppress V-tachy, convert a-fib and maintain sinus |
|
|
Term
Class IV AA
-mechanism
-example |
|
Definition
-Ca blockers, prolong phase 4
-Verapamil
-control HR in a-fib/flutter |
|
|
Term
Adenosine
-classification, mechanism
-uses |
|
Definition
-Non-classified AA, marked hyperpolarization
-great at diagnosing/terminating SVT |
|
|
Term
Digoxin
-2 main mechanisms
-Pharmacokinetics
-use |
|
Definition
-Direct membrane effects: block Na/K ATPase
-Indirect effects: vagus effects, slow sinus rate
-narrow therapeutic window, can use digoxin Ab
-controls ventricular response in a-fib/flutter |
|
|
Term
| What is Poiseuille's Law? |
|
Definition
Flow is directly related to change in pressure, r^4
Flow is inversely related to viscosity and length of a tube
-Also Flow=Change in Pressure/Resistance |
|
|
Term
| Resistance in vessels: series vs. parallel |
|
Definition
-Series: total R equals sum of individual Rs, i.e. hepatic circulation
-Parallel: total R: 1/R=1/R1+1/R2 etc. i.e. brain, capillaries |
|
|
Term
What causes laminar flow?
-How does this relate to viscosity? |
|
Definition
-Laminar flow is from parallel concentric lamellae flowing in a tube
-Fastest in the center, slowest at the walls of a vessel
-Viscosity is the resistance to slide between adjacent lamellae |
|
|
Term
What is Re? What are the relationships?
How is V related to pressure change for turbulence? |
|
Definition
-Re is a measure of how ∆P varies with flow velocity
-Can predict turbulence
-Directly related to average velocity, inversely related to resistance
-For turbulence V∝√∆P |
|
|
Term
How is the aggregate flow in the aorta, capillaries, and vena cava related?
-how does this relate to air flow in the lung |
|
Definition
-They are all equal.
-The total cross-sectional area of the capillaries is so big that it balances out the high volume and velocity in the aorta
-There is the same flow rate in each airway generation |
|
|
Term
| What does the Starling Resistor model describe? |
|
Definition
-Descibes air/fluid moving through a flaccid tube.
-If the external pressure increases it will collapse the tube |
|
|
Term
1) Is most of the blood in the systemic or pulmonary circulation?
2) What about arterial vs. venous? |
|
Definition
1) 85% in systemic, 15% in pulmonary
2) 20% in arterial, 65% in venous |
|
|
Term
| What are the 3 pressures to consider in the CV? |
|
Definition
1) Hydrostatic: difference in height, resistance plays a role
2) Pressure gradient
3) Transmural: pressure across the wall of a vessel |
|
|
Term
| Bernoulli's Principle in vascular flow |
|
Definition
1) Total fluid energy=potential+kinetic+gravity
2) Potential is from cardiac contraction then stored in the walls of vessels
3) If you increase KE, then PE decreases |
|
|
Term
| Hematocrit, viscosity, and vessel size |
|
Definition
-As the hematocrit increases, so does the viscosity
-However, these effects are less when the vessel size is small |
|
|
Term
| What is axial streaming and plasma skimming |
|
Definition
-Axial streaming: high velocity blood flow causes RBCs to go to the center of the stream
-Plasma skimming: branch vessels get relatively fewer RBCs |
|
|
Term
Where is the largest pressure drop in the circulatory system?
-What is the average capillary pressure |
|
Definition
-The largest drop occurs over the arterioles.
-Avg capillary pressure is 25mmHG |
|
|
Term
| 5 phases of the cardiac cycle |
|
Definition
1) Atrial Systole
2) Ventricular Isovolumic Contraction
3) Ventricular ejection
4) Isovolumetric relaxation
5) Ventricular filling |
|
|
Term
|
Definition
A-mitral valve closes
B-aortic valve closes
C-aortic valve opens
D-Mitral valve opens
1-atrial systole
2-isovolumetric contraction
3-rapid ejection
4-decreased ejection
5-isovolumetric relaxation
6-rapid ventricular filling
7-decreased ventricular filling, diastole |
|
|
Term
|
Definition
Jugular venous pulse
A-a wave, ↑ pressure from atrial contraction
B-c wave, hard to see, ↑ pressure from LA contraction, movement of tricuspid into RA
C-x descent, ↓ atrial pressure from LA ejection
D-v wave, filling of RA against closed tricuspid
E-y descent, opening of tricuspid |
|
|
Term
|
Definition
-atria contract, only add about 5-30% of blood by volume to ventricles
-May cause turbulence and the 4th heart sound S4 |
|
|
Term
What is normal ventricular volume when filled?
-Related values that contribute to preload |
|
Definition
-130 mL
-This is the end diastolic volume (EDV)
-EDP, end diastolic pressure also contributes |
|
|
Term
| Events of ventricular isovolumetric contraction |
|
Definition
-blood moves towards the AV valves and closes them passively
-blood is incompressible and pressure rises while volume remains constant
-NO blood is ejected during this phase
-1st heart sound is heard best at apex when mitral valve closes. This is the lub. |
|
|
Term
Events of ventricular ejection
-Two phases |
|
Definition
1) Rapid ejection: when pressure in the ventricles exceed that in the aorta/pulmonary vessels, the valves passively open. T wave repolarization happens at the peak of this phase
2) Reduced ejection: flow into the aorta/pulmonary vessels continues slowly due to momentum |
|
|
Term
| End of ventricular ejection values |
|
Definition
-Stroke volume (SV): about 75mL
-Cardiac output (CO): 5L/min
-End systolic volume (ESV): 65mL |
|
|
Term
| Isovolumic Relaxation events |
|
Definition
-Ventricular pressure drops and ejection stops
-The A and P valves close causing the 2nd heart sound S2
-Dicrotic notch happens in aortic curve because of elastic recoil of the aorta after ventricular contraction
-All the valves are closed and volume remains that same as the ventricles relax |
|
|
Term
Ventricular Filling events
-Two phases |
|
Definition
-Rapid: when vent. pressure drops below atrial pressure the AV valves open. Blood flows passively, rare 3rd heart sound can be heard S3, aortic/pulmonary pressure drops
-Reduced: vent. volume slowly increases
-This is late vent diastole |
|
|
Term
| What causes the normal splitting of the 2nd heart sound? -What if it doesn't happen? -What if it's split before, but isn't after? |
|
Definition
| -Inspiration causes the RV to increase in size, this leads to the pulmonary valve closing later, rather than with the aortic valve. -If there's fibrosis or thickening this won't happen -If the sound is split before, but then comes together after inspiration this could mean LV block |
|
|
Term
Avg Pressures in: RA, RV-sys/dias, pulmonary artery sys/dias, LA, LV sys/dias, brachial artery
-Cardiac index |
|
Definition
RA: 2
RV-sys/dias: 25/2
Pulmonary artery sys/dias: 25/10
LA: 6
LV sys/dias: 120/6
Brachial: 95
Cardiac index: CO/body SA=3.1 (L/min/m2 |
|
|
Term
| Contractile proteins in cardiac muscle |
|
Definition
-Obviously actin/myosin
-But myosin has two sets of light chains, MLC-1 and MLC-2
-MLC-1: essential, may inhibit contraction
-MLC-2: regulatory, may enhance contraction
-Myosin Binding Protein C is associated with the myosin head and may be involved in cardiomyopathies |
|
|
Term
| What is excitation-contraction coupling in cardiac muscle? |
|
Definition
-Converting an electrical stimulus into a mechanical process
-AP travels down T-tubules, Ca moving into the cell causes the release of more Ca from the SR. Ca then binds to Tropinin C which allows myosin to bind to actin.
-Things break down as Ca is pumped out of the cell and back into the SR. |
|
|
Term
| What's the effect of activation of the ß receptor? |
|
Definition
| -Increased cAMP action-->which leads to increase of Ca uptake and decreased binding of Troponin I to Ca. |
|
|
Term
| A zoom in of what happens at the t-tubule/SR junction |
|
Definition
1) t-tube depolarization causes movement of Ca through the DHP(L-type Ca receptor)
2) Ca binds to the Ryanodine receptor on the SR
3) RyR opens and Ca is released from the SR |
|
|
Term
| Two types of cardiac Ca channels |
|
Definition
-T(transient) channel: opens at more neg voltage, short bursts, no interaction w/Ca antagonists, in atrial tissue, not affected by ß agonists
-L(long-lasting) channel: this is the DHPR, opens at less neg voltage, inactivates slowly, effected by Ca antagonists/ß agonists, found throughout myocardium |
|
|
Term
| Where does Ca go after being involved in a contraction? |
|
Definition
-75% back into the SR via the SERCA-2a pump
-25% from a Na-Ca exchanger in the cell membrane
-1% into mitochondria. Can be a problem in diseased hearts |
|
|
Term
|
Definition
-Phospholamban inhibits uptake. When it's phosphorylated by cAMP related stuff(i.e. epi) Ca can be taken into the SR.
-Ca is stored mainly by calsequestrin |
|
|
Term
| What kind of an effect is ß-activation? |
|
Definition
| -An inotropic effect, increases the contractility. |
|
|
Term
| Describe the effects of different cycle lengths on magnitude of force of a contraction |
|
Definition
1) Treppe Decreased cycle length: more depolarizations/min, more Ca, stronger contraction. ie Sinus Tachy
2) Rest Potentiation: a pause allows Ca stores to return to a more releasable form and the following contraction is augmented. ie bradycardia
3) premature beat causes a small contraction, but the next beat is increased b/c of more Ca. ie PVCs |
|
|
Term
| What are the four determinants of cardiac muscle performance? |
|
Definition
-CHAP
-Contractility, Heart Rate, After-load, Pre-load |
|
|
Term
| What are pericardial inflammation pathogeneses? |
|
Definition
1) Continuous spread: from lung, liver, esophagus, etc
2) Hematogenous spread: septicemia
3) Lymphatic
4) Trauma |
|
|
Term
| Common causes of acute pericarditis: |
|
Definition
TUMOR
T: trauma/tumor
U: uremia
M: myocardial infection/meds
O: other infections, bacterial, fungal, TB
R: rheumatoid, autoimmune disorder, radiation |
|
|
Term
| What virus has a high tropism for the heart? |
|
Definition
| -Coxsackie A and B are the most common viral causes of pericarditis and myocarditis |
|
|
Term
| What is Dressler's syndrome? |
|
Definition
-fever, pleuritis, and pericarditis following MI or open heart surgery.
-treat w/high-dose aspirin |
|
|
Term
|
Definition
3 features of acute cardiac tamponade
-Dec. systemic arterial pressure
-Inc. systemic veinous pressure (JVD)
-small quiet heart |
|
|
Term
|
Definition
-Inflammation of the myocardium with necrosis and degeneration of adjacent myocytes
-Not as much tissue damage as in ischemia
-Can be causes by all microorganisms that affect humans |
|
|
Term
| Big cause of myocarditis throughout the world? |
|
Definition
-Chagas disease
-Trypanosoma cruzi |
|
|
Term
| Definition of a cardiomyopathy: |
|
Definition
| -a disorder of the cardiac muscle that causes abnormal myocardial function not related to disease of other cardiac structures, MI, hypertension, and valvular stenosis/regurgitation |
|
|
Term
| Categories of cardiomyopathy |
|
Definition
1) Primary: dilated, hypertrophic, obliterative(endomyocardial fibrosis)
2) Secondary: have a recognized extrinsic cause (ie drugs) or are part of a systemic process (ie amyloidosis), restrictive falls in here |
|
|
Term
Dilated Cardiomyopathy (DCM)
-pathological finding
-presentation
-why the heart dilates
-potential causes |
|
Definition
-4 chamber dilation
-Most often presents with L heart failure
-Heart dilates due to stress
-Many causes: alcohol, post-partum, inherited is big |
|
|
Term
| Whys is there a systolic murmur and decreased CO in DCM? |
|
Definition
| -The mitral valve is held open and can't function properly. Leads to S3 sounds and decreased CO. |
|
|
Term
Hypertrophic Cardiomyopathy (HCM)
-Cause
-Why it's a problem |
|
Definition
-Typically due to genetic mutations in contractile proteins
-Can block outflow, increased O2 need for cardiac muscle, lower EDV/SV.
-Blocked outflow can cause regurg through mitral valve |
|
|
Term
Restrictive Cardiomyopathies (RCM)
-Causes |
|
Definition
-Rarest kind
-Often secondary to infiltrative processes (amyloidosis) or diseases limited to subendocardial myocardium
-Thick and stiff ventricles |
|
|
Term
Good uses for PA
-Contraindications |
|
Definition
-Good for diagnostic uses, pulmonary edema, shock, pulmonary HT, and RH failure
-Contraindicated for: vascular access issues, LBBB, PE |
|
|
Term
| Take home message for length vs tension in the heart |
|
Definition
| -There is an optimal length that is determined by preload and compliance |
|
|
Term
| Why does tension increase as you increase pre-load? |
|
Definition
| -Troponin C is more sensitive to Ca and more cross-bridges are formed |
|
|
Term
What is contractility?
-what can it be compared to? |
|
Definition
-change in force development independent of change in muscle length (independent of preload)
-Can relate to the amount of Ca influx (ie from a catecholamine) |
|
|
Term
What is afterload in the CV system?
-analogous to what?
-can be related to what in disease? |
|
Definition
-force that opposes shortening/ejection
-analogous to arterial pressure
-can be due to stenotic valves, hypertrophied muscle |
|
|
Term
| How does increasing preload at a constant after load/contractility affect time/shortening/tension? |
|
Definition
-Time to shortening decreases
-Total amount of shortening increases
-Velocity of shortening increases
-Peak tension is unchanged |
|
|
Term
| Increasing afterload independent of preload/contractility has what effect on shortening/tension? |
|
Definition
-Decreases total amount of shortening
-Decreases velocity of shortening
-Increases total tension |
|
|
Term
| Effects of contractility on tension/amount of shortening w/constant pre/after load |
|
Definition
-Increased tension
-Increased amount of shortening |
|
|
Term
| Ejection fraction and normal value |
|
Definition
EF=(SV/EDV) x 100
Normal adult is %60 |
|
|
Term
1) How to tap into the systolic reserve
2) Diastolic? |
|
Definition
1) Increase contractility or dec afterload
2) Increase pre-load |
|
|
Term
| What are the determinants of stroke volume |
|
Definition
1) Preload: pressure gradient, vent filling time, compliance, atrial function
2) Contractility: neurotransmitters, drugs, disease
3) Afterload: aortic pressure, valve flow
4) Ventricular size
5) Hypertrophy |
|
|
Term
What happens to venous pressure if you increase CO?
-What happens to Pv and Pa if the heart stops working? |
|
Definition
-Inc CO will inc Parterial and dec. Pv
-The pressures will equilibrate at 7mmHg, this is the mean systemic filling pressure |
|
|
Term
| What things affect the vascular function curve? |
|
Definition
-This is the relationship between venous return and right atrial pressure
-So blood volume, resistance, constricting the veins would affect it. |
|
|
Term
| Normal cardiac values to know: CO, CI, SV, SVI, SVR, PVR |
|
Definition
CO: 4-8 L/min
CI: 2.5-4 L/min/m2
SV: 50-100 mL
SVI: 25-40 mL/m2
SVR: 800-1200 dynes
PVR: <240 |
|
|
Term
|
Definition
|
|
Term
| How to calculate SVR and PVR |
|
Definition
-Think of Ohm's law: V=IR
SVR=(MAP-CVP)/CO x80
PVR=(mean PAP-PCWP)/CO x80 |
|
|
Term
| Normal pressure values for RA, RV, PA, and PCWP |
|
Definition
Rule of sixes
RA= 6 mmHg
RV=24/6 mmHg
PA=24/12 mmHg
PWCP= 12 mmHg |
|
|
Term
| What parts of an EKG do the Jugular venous pulsations relate to? |
|
Definition
A wave: P-wave
C wave: QRS, closure up tricuspid due to systole
X descent: nothing on EKG
V wave: T wave
Y descent: nothing on EKG |
|
|
Term
| Fick CO vs. Thermodilution CO |
|
Definition
-Fick uses a dye. High dilution of the dye means the dye was around longer to diffuse, so lower CO
-Thermodilution: use cold saline and measure temp |
|
|
Term
|
Definition
-CO (cold/warm): if warm think septic shock
-RA (CVP): decreased in hypovolemic/septic; increased in cardiogenic
-SVR: increased in cardiogenic/hypovolemic; decreased in septic |
|
|
Term
|
Definition
-It's a syndrome, not a single disease
-Results from low CO/can't meet metabolic demands of the body OR
-Can only produce enough CO at the expense of high cardiac filling pressures
-Or both together |
|
|
Term
| What are the classic ways of defining heart failure? |
|
Definition
-Renal problem: sodium/fluid retention
-Forward failing: dec CO; Backward failure: inc LV filling pressures
-Right-sided: venous backup; Left-sided: pulmonary backup
-Systolic: pump problem (contractility/afterload)
-Diastolic: LV stiffness/relaxation (preload) |
|
|
Term
|
Definition
Stage A: HTN, CAD, DM (high-risk)
Stage B: MI, LVH (asymptomatic)
Stage C: HFpEF or HFrEF (symptomatic)
Stage D: HFrEF (end-stage) |
|
|
Term
Systolic dysfunction vs diastolic
HFpEF
HFrEF |
|
Definition
-Systolic dysfunction: a contractile dysfunction, usually dec. EF. With symptoms it is SHF
-Diastolic dysfunction: Filling problem (dec relaxation, non-compliant vent), w/symptoms is DHF. EF is normal
-HFpEF: EF>45-50%
-HFrEF: EF<40-45% |
|
|
Term
| What is the main difference between SHF and DHF? |
|
Definition
-Anatomic structure/function of myocardium and myocytes
-myocyte diameter is decreased in SHF and increased in DHF |
|
|
Term
What are the neurohormonal effects in HF?
-What's the most useful one?
-Why are they bad |
|
Definition
1) Inc. Sympathetic tone
2) Inc renin from kidney-->aldosterone
3) Inc. vasopressin
4) Natiruetic peptides: released in myocardial stress, actually useful (counteract SNS, RAAS, AVP) BNP is diagnostic
-Initially these are helpful, but eventually lead to inc congestion, poor CO, fibrosis. |
|
|
Term
|
Definition
-Two types, both are bad
-Concentric: due to pressure overload, LV dilates to preserve SV, but wall stress increases b/c vent volume increased
-Eccentric: due to volume overload, LV hypertrophies to dec. wall stress and save SV, but this increases the stiffness and results in ischemia |
|
|
Term
| Electrical problems in HF |
|
Definition
3 main problems:
1) Due to large atria, the atria become fibrous and re-entries can occur
2) Scars can form and cause re-entries
3) Vent hypertrophy can lead to dyssynchrony |
|
|
Term
|
Definition
Signs: tachycardia, tachypnea, elevated JVP, rales, S3, hepatomegaly, peripheral edema
Symptoms: dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea (PND), fatigue, abdominal pain/swelling |
|
|
Term
| NYHA Classification of HF |
|
Definition
based on exercise
NYHA I: No limitation
NYHA II: Slight limitation, dyspnea/fatigue w/moderate activity
NYHA III: Marked limitation, dyspnea/fatigue w/minimal activity
NYHA IV: Severe limitation, symptoms present at rest |
|
|
Term
| Precipitating factors that influence HF |
|
Definition
-Increased metabolic demands (fever, infection, hyperthyroidism)
-Increased volume/preload (dietary Na, renal failure)
-Increased afterload (HTN, PE)
-Decreased contractility (EtOH, MI)
-Reduced SV/HR: tachy/brady arrhythmias
-Medication non-compliance: this is a big one |
|
|
Term
1) Treatment strategy for HFrEF
2) for HFpEF |
|
Definition
1) Treat underlying etiology, drugs, devices
2) Drugs not shown to be helpful, control BP, treat comorbidities, |
|
|
Term
| Treatment for Acute Pulmonary Edema |
|
Definition
-Remember LMNOP
L: loop diuretics; M: Morphine; N:Nitrates; O: Oxygen; P: positive pressure ventilation
-Morphine acts as a venodilator for increasing pulmonary venous capacitance |
|
|
Term
|
Definition
1) Diuretics
2) vasodilators
3) vasodilators + inotropics
4) inotropics |
|
|
Term
|
Definition
Cold refers to perfusion, wet refers to congestion
1) 28%, vasodilators 1st, then inotropes. Warm and diurese
2) 67%, diurese and HF meds
3) 5%, End-stage, vasodilators, inotropes, LVAD, transplant
4) reconsider HF diagnosis |
|
|
Term
Diuretics in HF
1) How they get where they need to go |
|
Definition
| 1) Most are secreted into the nephron via PCT, need to increase dose in renal failure patients |
|
|
Term
Loop diuretics
-where they act, 3 examples |
|
Definition
-Act on the loop of Henle
-Furosemide: wide bioavailability
-Torsemide: high bioavailability
-Ethycrinic acid: no sulfa interaction, ototoxicity |
|
|
Term
Thiazide diuretics
-Where they act
-Relationship with loop diuretics
-Examples
-What to watch out for |
|
Definition
-They act on the DCT
-Less potent than Loop Diuretics, but effective in combo
-Hydrochlorothiazide
-Watch for hyponatremia |
|
|
Term
Potassium sparing diuretics
-Where they act
-Example |
|
Definition
-Act on the collecting ducts
-Spironolactone is an aldosterone blocker, shown to improve mortality |
|
|
Term
IV venodilators
-3 of em
-When are they effective? When do you need to be careful? |
|
Definition
-Nitroprusside, nitroglycerin, nesiritide
-Nitroglycerin/nesiritide are OK if warm/wet, not good if patient is cold b/c can worsen hypotension
-Nitroprusside is good if cold, dec. SVR/inc. CO |
|
|
Term
Hydralazine-where it acts
-How it helps |
|
Definition
-This is a pure arterial dilator
-Reduces SVR and increases CO and thus BP |
|
|
Term
|
Definition
| -They are solid ventilators |
|
|
Term
How do ACE inhibitors work?
What are ARBs? |
|
Definition
-Angiotensin Converting Enzyme is used to convert AI to AII, ACE inhibitors prevent this. They increase BK, a dilator that can cause a cough
-ARBs: angiotensin II receptor blockers, get around the cough issue |
|
|
Term
Inotropes-usage guidelines
-types and examples |
|
Definition
-Increase mortality in HF, best if moving to mechanical therapy or transplantation
-ß-agonists: dopamine, dobutamine, norepi
-Phosphodiesterase inhibitors: milrinone, bypasses ß
-Digitalis: increases intracellular Ca by inhibiting Na/K pump, Ca builds up from the Na/Ca exchanger, |
|
|
Term
| Benefit of ß Blockers in HF |
|
Definition
-Improve survival and outcomes in systolic HF
-Combat maladaptive neurohormonal responses in HF |
|
|
Term
|
Definition
-CRT: cardiac resynchronization therapy
-NYHA III or IV.
-persisting symptoms and EF<35% and long QRS |
|
|
Term
| What level of the vasculature has the highest wall to lumen ratio? |
|
Definition
| -That would be the arterioles. There is a lot of resistance in the arterioles, this is where mechanisms that affect diameter have the greatest effect. |
|
|
Term
|
Definition
-Y measures the slope of the strain necessary to stretch something to twice it's original length
-A perfectly elastic substance will have a linear relationship |
|
|
Term
What is compliance?
-How to veins and arteries compare? |
|
Definition
-Compliance is the change in volume caused be a given change in pressure
-Veins are 20x more compliant |
|
|
Term
| What happens to vasculature as a person ages? |
|
Definition
-Their vasculature becomes less compliant, i.e. for a given change in volume it takes more pressure
-Vasculature is composed more of collagen and less elastin as a person ages |
|
|
Term
| What is the Windkessel effect? |
|
Definition
-The elastic nature of the aorta acts as a second pump to keep things going during diastole
-This effect is lost as the arteries become more rigid |
|
|
Term
| What does Laplace's law tell us? |
|
Definition
-The Tension on a cylinder is proportional to the pressure exerted and the radius. Tension on the wall is inversely related to the wall thickness
-This is why the aorta can rupture and why capillaries can withstand high pressures |
|
|
Term
| How does compliance affect pulse pressure? |
|
Definition
| -Low compliance leads to a wider pulse pressure |
|
|
Term
| What happens to an arterial pressure wave form as the wave progresses away from the heart? |
|
Definition
-As you get farther away there is a delay in upstroke and the peak pressure is higher.
-So the femoral artery is a lot taller and happens later than the aorta |
|
|
Term
| How is flow through capillaries regulated? |
|
Definition
-Regulated by pre-capllary sphincters
-PCS are affected by local signals based on metabolism and O2 delivery to local tissues |
|
|
Term
| What is the major determinant of fluid movement in capillaries? |
|
Definition
-The Capillary Hydrostatic pressure (Pc)
-This can be highly affected by small resistance changes. i.e. increasing arterial resistance will decrease Pc |
|
|
Term
| What are the four factors that determine fluid movement in capillaries? |
|
Definition
1) Hydrostatic pressure: pushes fluid out
2) Interstitial fluid pressure: pressures are slightly negative
3) Plasma osmotic pressure: reabsorption into capillary
4) Interstitial fluid osmotic pressure |
|
|
Term
| Starlings Law of fluid movement |
|
Definition
| Fluid movement= (Constant)(Net forces out-net forces in) |
|
|
Term
| 3 factors that can affect smooth muscle contraction |
|
Definition
1) Sympathetic nerve innervation
2) agents produced/secreted by endothelium
3) Circulating hormones, blood gases |
|
|
Term
What is autoregulation?
-3 theories |
|
Definition
-A change in pressure is countered by a change in resistance to keep flow constant
1) myogenic: increase stretch=muscular contraction
2) metabolic: adenosine/O2
3) Tissue pressure: change in perfusion will change the interstitial pressure which will then change the external force on the blood vessel. Really only an issue in encapsulated areas like the brain or kidney |
|
|
Term
|
Definition
-3 have similar effects: NO, prostacyclin, and EDHF. They all relax the muscle all due to Ach, serotonin, thrombin, shear stress (from rapid flow)
-Endothelin I is a potent vasoconstrictor due to thrombin, AII, and epi |
|
|
Term
| Describe sympathetics in cardiac innervation |
|
Definition
1) Pre-ganglionic: come from spinal cord, release Ach
2) Post-ganglionic: release Norepi, target most blood vessels(α1 receptors) and SA/AV nodes and cardiac muscle (β1 receptors). Norepi also affects β2 in some blood vessels and bronchioles |
|
|
Term
| Describe parasympathetics in cardiac innervation |
|
Definition
-Both pre and post ganglions release Ach
-They target the SA/AV nodes
-Nicotinic pre gangion and muscarinic post ganglion |
|
|
Term
How does epi affect peripheral resistance?
What about norepi? |
|
Definition
-It decreases peripheral resistance overall, this is why diastolic BP drops a little with injection
-Norepi doesn't really interact with the ß2R in the vasculature so peripheral resistance will go up |
|
|
Term
| location and actions of the adrenergic receptors |
|
Definition
-α1 and α2 are both in the vasculature and cause constriction
-β1 are in the heart and vasculature and cause dilation, increased HR and increased contractility
-β2 are only in blood vessels and cause dilation |
|
|
Term
| What is accentuated antagonism? |
|
Definition
-The sympathetic and parasympathetic inhibit each other
-Ach and norepi inhibit each other |
|
|
Term
| Basal tone vs. resting sympathetic tone? |
|
Definition
-Basal tone is due to all the factors (vascular filling,etc) except neuronal effects
-Resting sympathetic tone: vascular resistance under resting conditions due to sympathetic activity (inc resistance due to norepi causing constriction). |
|
|
Term
| What's going on in the arterial baroreflex? |
|
Definition
1) Afferent nerves arrive in the brain and then send info back down through the Vagus nerve
2) Pressure receptors in the carotid sinus and aortic arch are affected by stretch. They have less muscle around them
3) Stimulus due to the difference between intravascular pressure and extramural pressure (i.e. carotid massage) |
|
|
Term
| What happens to BP if baroreceptors are lost? |
|
Definition
| -The mean BP doesn't change, but the range of BPs widens |
|
|
Term
| Where else are there BP receptors? |
|
Definition
-The atria (these are stretch): sensitive to filling and relate to pre-load and blood volume
-Anterior LV: pressor, inc HR/TPR
-Posterior LV: depressor, dec HR/TPR |
|
|
Term
| How does the chemoreceptor reflex work? |
|
Definition
-They are located in the carotid bodies and are sensitive to O2 Levels
-Net result is to increase rate and depth of breathing/TPR and decrease heart rate |
|
|
Term
| What happens in a neurocardiogenic response? |
|
Definition
-This is vasovagal syncope
-Inc vagal activity slows down the heart
-Dec sympathetic activity dilates blood vessels
-This all results in dec BP and LOC |
|
|
Term
|
Definition
Due to cold water on the face
-Results in bradycardia, peripheral constriction, coronary dilation
-Magnifies chemo reflex
-Inhibits respiration |
|
|
Term
| How long can CO be maintained in hemorrhage? |
|
Definition
| -Can lose up to 20% of volume and maintain CO |
|
|
Term
| What happens to CO and arterial pressure in hemorrhage? |
|
Definition
-Can lose up to 20% of volume and maintain arterial pressure
-CO drops steadily |
|
|
Term
What has the main effect on cerebral blood flow?
-How much cerebral CO? |
|
Definition
-Metabolites, mostly CO2 a small change in CO2 can have a big effect
-Other stuff like H+, HCO3, K+, O2, adenosine, NO, and CSF pressure
-Brain gets 14% of CO |
|
|
Term
|
Definition
-WIthout the reflex an increased CSF pressure will eventually collapse the blood vessels
-With the reflex as CSF pressure increases MAP will increase to keep flow to the brain |
|
|
Term
Splanchnic Circulation
-How much of the CO?
-Purpose of splanchnic bed |
|
Definition
-Gets 25% of the CO
-Holds a large blood reservoir
-Liver gets most of it's flow venously |
|
|
Term
| How is splanchnic circulation regulated? |
|
Definition
-Local metabolic/hormonal mechanisms: food intake, gastrin-->vasodilation
-Sympathetic activity: vasoconstrictor tone due to norepi
-Mechanical influences: clothes, breathing, size of organs |
|
|
Term
Skeletal Muscle regulation
-How much of the CO? |
|
Definition
-15% of CO
-Flow can vary across a wide range
- |
|
|
Term
|
Definition
-high flow, low resistance, no auto regulation
-hydrostatic plays a role b/c pulmonary pressures are lower |
|
|
Term
| How do you calculate the double product and why is this value helpful? |
|
Definition
-This value is the index of oxygen demand
-HRxpeak systolic BP |
|
|
Term
| What are the 3 compartments of coronary flow? |
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Definition
-R1: resistance is low, this is the conduit
-R2: this is the important one, most of the regulation occurs here, lots of resistance, there is a reserve for dilation, regulated by local factors (mostly adenosine), EDRF (NO released)
-R3: small fraction during systole, gradient through the wall |
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Term
| What is Coronary Flow Reserve? |
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Definition
-CFR is the ratio of flow during max vasodilation to resting flow
-can usually increase 4-5x |
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Term
| Endothelium independent vs. endothelium-dependent parts of flow reserve |
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Definition
-Basically both contribute to decreasing resistance and increasing flow to maintain coronary pressure
-Endo-dependent can be reduced in disease and a loss in control results |
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Term
| How does ∆Ps change with flow in coronary arteries? |
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Definition
| -There is not a linear relationship, so small changes in stenosis narrowing can have big effects on flow |
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Term
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Definition
| -Due to inflowing blood against a distended or incompliant ventricle. (i.e CHF, or exercise), shortly after S2 in early diastole |
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Term
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Definition
-Caused by forceful atrial contraction ejecting blood into a noncompliant ventricle
-heard during late diastole |
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Term
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Definition
I: can’t hear immediately
II: hear immediately when steth goes on chest wall
III: louder than II, subjective
IV: associated w/thrill
V:can hear w/steth partly off the chest wall
VI: can hear w/steth off the chest wall |
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Term
What are the systolic murmurs?
Diastolic?
-descriptions |
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Definition
-Aortic stenosis(crescendo-decrescendo), mitral regurg (holoystolic)
-Aortic regurg(decrescendo), mitral stenosis(low pitched rumbling) |
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Term
| treatment recommendations vs. level of evidence |
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Definition
Treatment: Class I: benefit is definitely greater than risk; Class IIa:benefit is greater than risk; Class IIb: benefit can be equal to risk; Class III: can harm
Evidence: A lots of data, B,C |
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Term
| How to get post test probability from LRs |
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Definition
Prevalence/pre-test prob-->pre-test odds
pre-test odds=(x)/(1-x)
multiply pre-test odds by LR
convert back to post test prob
post test prob=x/(1+x) |
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Term
| Calculating likelyhood ratios |
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Definition
sensitivity is always on top, specificity is on the bottom
there is always a 1-something
for LR- the 1- is on top
LR+=TPR/FPR
LR-=FNR/TNR |
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