1 - Cardiology

Question 1

What is the typical aorta pressure (mean, systolic, diastolic)?

Answer 1

Mean - 100 mmHg Systolic - 120 mHg Diastolic - 80 mmHg

Question 2

What is the typical systemic capillary pressure ?

Answer 2

Mean - 17 mmHg

Question 3

What is the typical pulmonary circulation pressure (mean, systolic, diastolic)?

Answer 3

Mean - 16 mmHg Systolic - 25 mmHg Diastolic - 8 mmHg

Question 4

What is the typical pulmonary capillary pressure ?

Answer 4

Mean - 7 mmHg

Question 5

What is the equation for calculating blood flow?

Answer 5

Ohm’s Law: F = (P2-P1)/R Blood Flow = Change in Pressure/ Vessel Resistance

Question 6

What is the typical Total Peripheral Resistance to blood flow (in PRU)?

Answer 6

1 PRU –> R=P/F –> R = 100 mmHg/100 ml/sec = 1PRU When strongly constricted, the resistance can rise to as much as 4PRU. When greatly dilated, the resistance can fall to as low as 0.2 PRU.

Question 7

What is the typical Total Pulmonary Vascular Resistance to blood flow?

Answer 7

0.14 PRU –> R = P/F –> R = 14 mmHG/100 ml/sec

Question 8

How do you calculate the total resistance for vessels in series? In parallel? How is conductance related to resistance?

Answer 8

Series –> R(total) = R1+R2+R3 Parallel –> 1/R(total) = 1/R1 + 1/R2 + 1/R3 Conductance = 1/Resistance Accordingly, the relationships for series and parallel summation is reversed for conductance.

Question 9

What is the mathematical relationship between blood flow and velocity?

Answer 9

V = F/A Velocity = Flow / Cross-Sectional Area

Question 10

Briefly describe Phases of the cardiac cycle.

Answer 10

Phase 4 - Resting potential in ventricular(V) and arterial(A) muscle and the pacemaker potential in nodal(N) cells. Phase 0 - Rapid depolarization at the start of action potentials. Phase 1 - Brief repolarization of the V action potential(AP) immediately after Phase 0. Not in N AP. Phase 2 - Plateau of the V. Abbreviated in A. Absent in N. Phase 3 - Repolarization that returns to resting potential.

Question 11

Describe (in detail) the ventricular action potential.

Answer 11

Phase 4 - resting potential is due tpo high permeability to K. This is due to voltage-gated K channels (iK1) being open in addition to the K leakage channels. They are open at resting and hyperpolarized potentials. Plugged w/ Mg++ in other Phases. Phase 0 - rapid depolarization due to voltage-gated (fast) sodium channels opening resulting in rapid inward Na+ current Phase 1 - brief repolarization - after peak, with only ~10% Na channels remaining open, another voltage-gated K channel opens briefly to allow K to leave the cell. This partially repolarizes the cell to ~0mV. Phase 2 - plateau is produced by the balancing of Na+, K+ and Ca++ channels. K channels are plugged w/ Mg++ –> less repolarization. Ca channels opens in membrane. These are slower than Na+ channels and contribute to excitation/contraction coupling. Phase 3 - repolarization occurs as the slow Ca channels close and opening of slow K channels (iK). In addition, the iK1 begin to be cleared of Mg++ and open. Once at resting potential, the iK channels close and are at Phase 4

Question 12

Describe (in detail) the nodal action potential.

Answer 12

3 differences from Ventricular AP - 1)resting potential is not constant, but depolarizes automatically, thus creating the pacemaker effect 2)depolarization in Phase 0 is much slower 3)Phase 2 is absent Phase 0 - at threshold, the slow Ca channel (iCa) is opened and depolarizes to +10 to +20mV. No Phase 1 No Phase 2 Phase 3 - iK channels open quickly, thus allowing immediate repolarization Phase 4 - spontaneous depolarization occurs to interaction between Na, K and Ca permeabilities. at ~ -60mV 1)iK channels close, 2) iCaT open, promoting depolarization, 3)a new Na channel opens slowly to depolarize

Question 13

Describe parasympathetic effects on cardiac action potentials.

Answer 13

Vagal stimulation causes the release of ACh. ACh decreases Na and Ca permeability while increasing K permeability. This slows the process of depolarization in Phase 4 (pacemaker) of nodal cells. ACh also increases the threshold toward 0mV, further promoting hyperpolarization.

Question 14

Describe sympathetic effects on cardiac action potentials.

Answer 14

Sympathetic stimulation releases norepinephrine. NE increases the permeability of Na, Ca, and decreases K. All of these promote faster depolarization in Phase 4 (pacemaker).

Question 15

Define the I, II, III lead axis.

Answer 15

Lead I: + on L arm, - on R arm Lead II: + on L leg, - on R arm Lead III: + on L leg, - on L arm

Question 16

Define aVR, aVL, and aVF leads.

Answer 16

augmented unipolar limb lead: two limbs are connected to the negative terminal, the third limb is connected to the positive aVR: + on the R arm (+ at 210 deg) aVL: + on the L arm (+ at -30 deg) aVF: + on L foot (+ at 90 deg)

Question 17

What is the typical mean cardiac vector? How does it change over the cardiac cycle?

Answer 17

Mean Cardiac Vector = 56 deg This is created since the ventricular septum is depolarized first (R start) and repolarized last. This creates a positive vector pointing to the apex of the heart. As the depolarization spreads to the ventricle walls, the vector increases, but remains largely at 60 deg. After more than 50% of ventricles are depolarized, the vector begins to shrink (R peak). The last part to depolarize is the superior left ventricle wall. This shifts the vector to ~ -30deg (S dip). During repolarization the vector changes in size, but remains at ~60 deg (T wave).

Question 18

Describe a left- or right-axis deviation.

Answer 18

When any abnormality in the heart interferes with the conduction pattern, an axis deviation is likely. Hypertrophy causes the axis of the heart to shift towards that side since there is more tissue to excite. A left deviation will exaggerate the +R on Lead I and the -S on Lead III. A right deviation will shift Lead I to a -R and create a +R on Lead III. These can also prolong the QRS complex. Common causes: left - left ventricular hypertrophy (hypertension, aortic valvular stenosis, aortic valvular regurgitation), right ventricular hypertrophy (congenital pulmonary valve stenosis), inter-ventricular septum defect

Question 19

What are the key attributes to analyze on an ECG?

Answer 19

1)Rate 2)Rhythm 3)Axis 4)Interval 5)Morphology

Question 20

How do you determine heart rate from an ECG?

Answer 20

Trick - on standard ECG “count over” from one R peak to another, 1 block = 300bpm, 2 = 150bpm, 3=100, 4=75, 5=60, 6=50 On 10 sec ECG –> count R peaks and multiply by 6 Real way - determine R to R interval and take the inverse (1/interval)

Question 21

What are the standard dimensions of an ECG?

Answer 21

vertical - 10 small blocks = 1mV horizontal - 1 small block = .04 sec –> 1 large = .02 sec Chart speed = 25/sec

Question 22

Define a normal sinus rhythm on an ECG.

Answer 22

Normal Sinus Rhythm 60-100 bpm one P wave per QRS complex normal PR interval upright P wave in I, II and aVF Anything NOT NSR is arrhythmia

Question 23

Define the normal ranges for these intervals: P wave, PR, QRS, QT.

Answer 23

P wave - 0.06-0.10 sec PR - 0.12 - 0.20 sec QRS - 0.06-0.10 sec QT - <0.45 sec

Question 24

Describe (in detail) ventricular pressure during the cardiac cycle.

Answer 24

End Diastole - with the A/V valve open and semilunar valves shut, pressure is at venous return pressure (7 mmHg). Aortic kick (P wave) pushes the last 25% into the ventricle and ends diastole Ventricles begin to contract (QRS wave), closing the AV and rapidly increasing pressure. Until exceeding Aortic Pressure (~80 mmHg), the semilunar valves remain close and the ventricles undergo isovolumetric contraction. Once the Aortic and Pulmonary Valves open, the ventricles rapidly empty (70% in first 1/3) and cause peak systolic pressure (~120 mmHg). In the rest of the stroke, ventricular contraction ceases (T wave) and the ventricular pressure falls below aortic pressure, which causes the semilunar valves to close. Since pressure still exceeds atrial pressure, AV valves remain closed resulting in isovolumetric relaxation. Once below atrial pressure (~7mmHg), the AV valves open and begin rapid ventricular filling (70% in first 1/3). Until the aortic kick, slow ventricular filling continues (~5%).

Question 25

Describe (in detail) arterial blood pressure during the cardiac cycle.

Answer 25

Arterial pressure rapidly increases when the Aortic Valve opens and exposes the great arteries to left ventricular pressure. This causes arterial wall distention and and increase in pressure. Eventually, the kinetic energy of the flow is converted to adequate pressure to exceed the lowering ventricular pressure, and blood is pushed backward through the valves until they are suddenly snapped shut. This creates the dicrotic notch in the arterial pressure. Pressure then slowly lowers until the next cycle.

Question 26

Describe (in detail) atrial pressure during the cardiac cycle.

Answer 26

When stimulated by the P wave, the atria contract (a wave) and raise pressure to ~7 mmHg. A wave ends with the AV valve closure and c wave begins. This is a sharper increase in pressure caused by backward bulging of the AV valves during ventricle contraction. During ventricular emptying, pressure drops quickly (x descent) and then begins to rise slowly during towards the end of ventricular contraction. This is caused by the continued atrial filling with the AV valves closed. This peaks when the AV valves open (v wave) and pressure then drops again as the atrial contents are emptied into the ventricle(y descent)≥

Question 27

Describe changes in venous pressure during the cardiac cycle (and the cardiac events they reflect).

Answer 27

During atrial contraction there is an increase in pressure (a wave) followed by a drop. With ventricular contraction and AV valve back-bulging, there is another wave of pressure (c wave). During systole, when the veins and atria are being filled with the AV valves shut another pressure wave is created (v wave)

Question 28

Describe the anatomical basis of the standard heart sounds.

Answer 28

S1 (lub) - closing of AV valves is slower and softer S2 (dub) - closing of semilunar valves shut, higher pitch snap S3 (i beLIVE) - vibration from filling of ventricles during early diastole S4 (BElieve me) - atrial kick (rarely heard)

Question 29

Define: End Diastolic Volume, End Systolic Volume, Stroke Volume, Ejection Fraction

Answer 29

EDV - ventricular volume at the end of diastole (max) ~ 120ml ESV - ventricular volume at the end of systole (min) ~ 50ml SV = EDV-ESV EF = SV/EDV

Question 30

Describe the construction of cardiac valves.

Answer 30

Semilunar Valves - three thin, concave cusps meeting centrally, when closed. Made of strong fibrous tissue to withstand high pressure gradients and high flow AV Valves - larger and thinner than the Semilunar valves, they are also attached to papillary muscles via chordae tendinae which contact during systole. This helps minimize valve back-bulging into the atria

Question 31

What are the major steps to EC Coupling in cardiac muscle?

Answer 31

•Action potential plateau opens voltage gated (L-type) Ca channel •Ca influx triggers release of Ca from SR (CICR) causing 100 fold increase in intercellular calcium •Ca binding to TnC allows cross-bridge formation •ATP required for power stroke and new cross-bridge formation •Diastolic relaxation requires reduced [Ca2+] –Ca pump into SR (directly ATP-dependent) –Na/Ca exchange (indirectly ATP-dependent via Na/K ATPase)

Question 32

What are the main determinants of cardiac performance?

Answer 32

1) Preload 2) Aferload 3) Contractability 4) Heart rate/rhythm

Question 33

Describe the Frank-Sterling Mechanism.

Answer 33

Cardiac output is largely determined by venous return due to the heart’s internal response to ventricular stretching. As the ventricles fill and are stretched, stroke volume increases due to: 1) increased thin/thick filament overlap –> greater power stroke 2) increasing sarcomere length increases the sensitivity to Ca

Question 34

Define preload.

Answer 34

The tension of cardiac muscle PRIOR to contraction. This is the tension developed due to the End Diastolic Volume within the ventricles. Volume and tension is difficult to measure clinically, so the Diastolic Pressure is used as an index of Preload.

Question 35

Define Afterload.

Answer 35

The tension of the ventricle during contraction. Also thought of as the force against which the ventricle must push. This is measured as the systolic pressure since it is this pressure that is required to overcome the arterial pressure/resistance.

Question 36

Define contractility.

Answer 36

The ability of the ventricle to expel blood. Specifically, it is a reflection of the speed and extent of sarcomere shortening. This is an intrinsic property of the heart and is dependent on intracellular Ca.

Question 37

Define La Place’s Equation. What is it’s significance to the cardiac cycle?

Answer 37

T = (P)(r)/2h Tension = (Pressure)x(radius)/(2 x thickness) During ventricular contraction, the walls thicken and the radius shrinks. This will lower the tension in the ventricle as it contracts.

Question 38

What is the relationship between speed of contraction with changing Preload? Afterload?

Answer 38

As Preload increases the velocity and extent of sarcomere shortening increases. As Afterload increases both decrease.

Question 39

Describe the effect of B agrenergic stimulation on cardiac performance.

Answer 39

B adgregenic stimulation is the most important single mediator of cardiac performance. NE/EPI bind to B1 receptors and cause increase in cAMP. This results in: 1) phosphoralyzation of Protein Kinase A –> increase metabolism 2) increased Ca entry, release from SR, and binding to TnC 3) faster uptake of Ca via SR and faster expulsion via NCX –> shorter relaxation period

Question 40

How does heart rate affect cardiac performance?

Answer 40

Heart rate affects performance by two mechanisms: 1) increasing systolic episodes per minute –> increase CO (until ~200 bpm when there is not enough diastole to allow for adequate filling and CO falls.) 2) increased Ca accumulation in SR leads to increased contractility

Question 41

What are the primary indices of cardiac performance?

Answer 41

Ejection Fraction Stroke Work Contractility

Question 42

What are some major methods of measuring Ejection Fraction clinically?

Answer 42

1) Ultrasound (echocardiogram)*** 2) Cardiac Catheterization 4) MRI 5) CT 6) Nuclear imaging

Question 43

Define Stroke Work.

Answer 43

The amount of energy the heart converts to work in a single cardiac cycle. External Work - work to move blood from venous to arterial circulation (overcome the arterial pressure) (99%) Internal Work - work to accelerate blood to ejection speed (1%)

Question 44

Describe intrinsic regulation of the cardiac cycle.

Answer 44

Adjustments to cardiac function through properties inherent to the muscle. 1) Frank-Sterling Mechanism - greater force of contraction with increasing venous return (myocyte stretching) 2) AV Node stretching - increasing HR (15%)

Question 45

What are the primary factors of End Diastolic Volume?

Answer 45

1) end diastolic pressure - preload 2) filling time - heart rate 3) wall distensibility/compliance

Question 46

Describe external regulation of cardiac cycle.

Answer 46

Adjustment to cardiac function through neural and hormonal signaling. 1) Sympathetic - ACh to muscarinic receptors on heart 2) Parasympathetic - NE/EPI to B1 androgenic receptors primarily at SA and AV nodes

Question 47

Define decremental conduction.

Answer 47

Early stimulation (faster rate) of cells results in slower, smaller action potentials due to less Ca++ channel availability. –> AV nodal conduction slows with faster stimulation.

Question 48

What are the hallmarks of WPW syndrome on EKG?

Answer 48

Short P-R interval (100ms) Presence of Delta wave otherwise normal P wave

Question 49

What are the major types of Tachycardia?

Answer 49

Supraventricular Tachycardia - atrial/nodal cells are essential for maintaining the abnormal rhythm Ventricular Tachycardia - only ventricular cells are essential for maintaining the abnormal rhythm

Question 50

What are the major mechanisms for tachycardia?

Answer 50

1) Reentry - self-perpetuating path of stimulation due to abnormal conduction pathway 2) Triggered - secondary depolarization of a focus “triggered” by the preceding bear 3) Enhanced Automaticity - initiated by spontaneous depolarization of AV node

Question 51

What are the conditions required to produce reentry tachycardia?

Answer 51

1) adjacent tissue with different refractory period 2) unidirectional conduction block 3) slow conduction to allow for refractory tissue to recover and be re-stimulated by adjacent tissue where it was previously blocked

Question 52

Describe the EKGs for the following conditions: 1)Supraventricular Fibrillation 2)Ventricular Fibrillation 3)WPW 4)Atrial Flutter

Answer 52

1) SVT - high rate, but otherwise normal rhythm; normal QRS 2) VT - high rate with elongated QRS and other waves missing - anatomical reentry–> QRS is regular - functional reentry–> QRS is irregular and small(squiggle) 3) WPW - short PR, sloped/wide QRS, shift in vector 4) Flutter - P and QRS not in sync, multiple P for each QRS

Question 53

What are the conditions for 1st degree, 2nd degree and complete AV Block?

Answer 53

1st - one P wave per QRS, PR >200 ms; typically caused by increased vagal tone leading to slow conduction to AV node 2nd - Mobitz 1 –> more P waves than QRS, PR progressively increases until there is a dropped beat. Usually improves with exercise Mobitz 2 –> no change in PR prior to dropped beat and is not responsive to exercise. Can progress to complete heart block. Indicative of more wide spread conduction disease. Complete - atrial rate>ventricular rate, constantly changing PR interval so there is no coordination between chambers. Can quickly become asystole.

Question 54

Describe subsidiary pacemakers.

Answer 54

Primary pacemarker - SA node (60-90bpm) Subsidiary - AV node (45-50bpm) -Pukinje fibers (30-40bpm) These cells spontaneously depolarize when the SA node fails, but they are not as dependable in their rate/rhythm.

Question 55

Describe overdrive suppression.

Answer 55

The SA node is the dominant pacemaker because it has the fastest rate of automaticity. The other cells with automaticity are suppressed from spontaneously depolarizing by overdrive suppression. By producing faster depolarizations, the AV node forces the cellular Na/K exchanger to increase its activity to keep pace. This activity hyperpolarizes the cell and counteracts the cell’s own spontaneous depolarization. In this way there is only one pacemaker active at a time (in normal tissue).

Question 56

Define Poiseuille”s equation. What are the assumptions of this equation?

Answer 56

Q = (k)(r^4)(P-P’)/L Q = flow; k=pi/8n; n=viscosity; r=radius; P-P’=change in pressure; L=length Assumptions: 1) Laminar Flow 2) Flow through smooth, cylindrical, rigid tubes 3) Flow is steady and constant 4) Viscosity is constant

Question 57

What are the dominant components of vascular resistance?

Answer 57

R = 8(L)(n)/(pi)(r^4) Resistance is driven predominantly by radius, but is also affected by length and viscosity.

Question 58

Define pulse pressure.

Answer 58

Pulse pressure = systolic - diastolic pressure

Question 59

What are the major forces affecting capillary flow and diffusion?

Answer 59

capillary and interstitial pressure plasma and interstitial colloid osmotic pressure

Question 60

What factors contribute to edema formation?

Answer 60

1) increased capillary permeability 2) decreased plasma colloid osmotic pressure 3) elevated capillary pressure 4) lymphatic obstruction

Question 61

Define compliance and its function within the CV system.

Answer 61

compliance is the measure of the change in volume for a given change in pressure C = dV/dP This allows both arteries and veins to accommodate for the rapid changes in pressure seen during the cardiac cycle and provide a mostly steady blood flow to the CV system. It also allows the system to respond to rapid drops in volume (hemorrhage) without significantly changing pressure.

Question 62

Define unstressed vascular volume. What factors affect it?

Answer 62

Unstressed Vascular Volume is the amount of blood remaining in the vascular systems at zero pressure. This represents the “vascular reserve” for a given vascular tone. This is driven by sympathetic stimulation, leading to vasoconstriction or dilation.

Question 63

What mechanisms prevent venous pooling?

Answer 63

Venous valves Sympathetic tone of veins Lymphatic drainage Lymphatic valves Muscular compression of veins/lymphatics

Question 64

Define systemic filling pressure.

Answer 64

This is the theoretical pressure driving blood into the right atrium. It can also be thought of as the pressure required to bring venous return to zero.

Question 65

Describe the response of the Baroreceptor Reflex to an increase in atrial pressure.

Answer 65

A decrease in Atrial Pressure will be sensed by the baroreceptors as a decrease in stretch/wall tension within the respective artery. The most sensitive baroreceptors are located at the carotid bodies, but they are also distributed throughout the carotids and aortic arch. The decrease in stretch will cause an decrease in nerve impulse to the vasomotor nuclei in the medulla. This response is sensitive to both the change in stretch and the rate of change. By decreasing the rate of nerve signaling, the baroreceptor will direct an increase in sympathetic tone and an inhibition of parasympathetic tone. This will: increase arterial contraction –> increase arterial resistance - increase venous constriction –> increase means filling pressure and increase venous return - increase sympathetic tone on heart –> increase contractility -decrease parasympathetic tone on heart –> increase heart rate - increase release of NE/EPI from adrenal –> increase vasoconstriction/HR further All of these will combine to increase heart rate and counteract the drop in systemic pressure sensed at the baroreceptor.

Question 66

What is the difference between transient, intermittent, and continuous bacteremia?

Answer 66

Transient - bacteria enters the blood stream, but is readil cleared without a inflammatory response Intermittent - spread of infection from an extra-vascular site (kidney, lung, wound) results in inflammatory response (fever) Continuous - bacteria constantly added to the bloodstream from a site of infection within the circulatory system (endocarditis, vasculitis, infected catheter)

Question 67

What is the difference between acute and subacute bacteremia?

Answer 67

Acute - presents rapidly and severely: fever, chills, heart murmur, stroke, embolic infection (Staph. Aureus = 60%) Subacute - gradual onset of symptoms: fatigue, malaise, fever, night sweats, weight loss, cough, CHF (Strep. mitior, S. bovid, S. mutans, and S. sanguis = 60%)

Question 68

What are significant risk factors for the development of infectious endocarditis?

Answer 68

• IV drug use (#1 behavioral risk) - Mitral Valve prolapse (#1 risk) - congenital defect causing venturi effect - prothetic heart valve - poor oral hygiene - GI/bowel surgery - long term hemodialysis/diabetes - Rheumatic Heart Disease (undeveloped world)

Question 69

Discuss prophylactic use of antibiotics to prevent infectious endocarditis?

Answer 69

Prophylactic antibiotics is recommended by the American Heart Association for: 1) prosthetic heart valve recipients, 2) those with previous endocarditis 3) those with cyanotic congenital heart defects 4) cardiac transplant w/ valvunopathy

Question 70

How is a diagnosis of infectious endocarditis made? What is the treatment?

Answer 70

A combination of lab data (three repeated blood cultures positive for the same microbe) and echocardiogram (transthoracic and transesophageal). Risk factors and symptoms may be enough to start Ab prior to determining cause.

Question 71

What are some common complications of infectious endocarditis?

Answer 71

Intracardiac Damage - valvular damage (prolapse, stenosis), perivavalvular damage, CHF Extracardiac damage from seeding - splenic abcess, meningeal/brain abcess Septic Emboli - stroke, mycotic aneurysm Immune Complex disease - glomerulonephritis

Question 72

How is coronary blood flow regulated?

Answer 72

1) local vasodilation in response to changes in metabolic demand (primarily O2) 2) direct sympathetic(NE/EPI) and parasympathetic(ACh) stimulation lead to vasoconstriction/vasodilation 3) indirect nervous control by changing the activity of the heart - sympathetic stimulation leads to increased rate and contractility, increasing the cardiac O2 demand –> vasodilation **coronary vessels have a preponderance of a>B adrenergic receptors, so in the presence of direct sympathetic stimulation, they tend to constrict – HOWEVER, metabolic demand dominates over nervous control

Question 73

What is the prognosis for myocardial ischemia with increasing time from event?

Answer 73

Acute (10sec - 10min) - fully recoverable with repurfusion Subacute (10min - 10hrs) - can be slowly reversible (stunned myocardium) or irreversible damage (infracted myocardium) Sustained (>10hrs) - very slowly reversible (hibernating myocardium) or irreversible (infarcted myocardium)

Question 74

Describe the redundancies of the cerebral circulation.

Answer 74

Arterial: two carotids and two vertebral (basal artery) join together in the Circle of Willis Venous: multiple anastomoses provide excellent redundancy

Question 75

What are the major mechanisms for autoregulation of cerebral circulation?

Answer 75

1) Mechanical - when cerebral spinal fluid > vessel pressure (Pv of Pa), the vessel will collapse and be occluded 2) Chemical - CO2 –> brain is highly sensitive to changes in CO2 concentration; O2 –> brain becomes much more sensitive to changes in O2 once Hemoglobin saturation falls extracerebral H+ causes cerebral vasodilation; K+ –> secreted by brain tissue causes vasodilation; adenosine –> extracerebral vasodilation 3) Neural - while both sympathetic and parasympathetic innervations are present on vessels in the Circle of Willis and on pial vessels, they appear to have little or no effect on cerebral blood flow

Question 76

What are the major anatomical differences between pulmonary and systemic blood vessels?

Answer 76

Pulmonary arteries and veins are much thinner (weaker) and shorter than most systemic counterparts. However, the capillaries are much more dense, representing more of a “sheet of exchange” as opposed to discreet tubes as in systemic circulation.

Question 77

What are the typical pressures in pulmonary circulation? How do these pressures change during the cardiac cycle?

Answer 77

Pulmonary systolic pressure - 25 mmHg Pulmonary diastolic pressure - 10 mmHg Mean pulmonary pressure - 15 mmHg Arterial pressure > capillaries > veins During systole, the shape of the pressure curve will match that of right ventricular pressure, but when the pulmonic valve closes, pressure will coast down until the start of the next cycle. This is compared to the sharp drop seen in ventricular pressure after systole.

Question 78

How is Pulmonary Vascular Resistance measured/calculated?

Answer 78

PVR = (pressure @ main pulmonary artery - pressure @ left atrium) / pulmonary blood flow Pulmonary blood flow = cardiac output in normal heart (thermodilution catheter) Pulmonary wedge pressure is used for left atrium pressure. Float a balloon catheter into pulmonary circulation until the balloon occludes pulmonary arterial branch. Pressure at tip of catheter is wedge pressure.

Question 79

Define Local Control of Blood Flow.

Answer 79

Property of a tissue to modulate its own blood flow independent of neural influence. This is driven by four mechanisms: 1) Basal Tone 2) Autoregulation 3) Active(Functional) Hyperemia 4) Reactive Hyperemia

Question 80

Define autoregulation with regard to local control of blood flow. What are the proposed mechanisms?

Answer 80

The ability to maintain/restore a constant blood to a tissue after a change in perfusion pressure. (Assume: constant metabolic demand, no neural influence) 1) Myogenic theory - increases in the stretch of the smooth muscles of arteries/arterioles (due to increased pressure) cause increased vascular tone and constriction. This will increase resistance and compensate for increased pressure. 2) Metabolic theory - vasodilators are released from the tissue in response to low O2/nutrient levels. As metabolic demand increases relative to nutrient supply (blood flow) vasodilators will cause dilation and a compensatory increase in flow.

Question 81

Define Active Hyperemia. Define Reactive Hyperemia.

Answer 81

Active Hyperemia - Blood flow is increased in response to an increase in the tissue’s metabolic demand (exercise) Reactive Hyperemia - after a period of restricted blood flow, local control will cause an increase in blood flow to “pay back” the nutrient deficit during the period of low flow (vascular occlusion)

Question 82

What are some notable vasodilator metabolites that are thought to participate in local control of blood flow?

Answer 82

**Adenosine - highly metabolically organs (heart, brain, exercising muscle) O2/Hypoxia K+ - short term dilator H+ (pH) - limited dilation CO2 - most important vasodilator in the brain, but less so elsewhere

Question 83

Define the hydrostatic zones of the lungs.

Answer 83

Zone 1 - alveolar pressure > arterial pressure –> vessel is continuously occluded Zone 2 - systolic arterial pressure > alveolar pressure > diastolic arterial pressure –> blood flow is pulsatile Zone 3 - alveolar pressure < arterial pressure –> blood flow is continuous Normal heart, only zone 2/3, but can have regions of zone 1 at apex.

Question 84

Describe the cause and identifying characteristics of an S3 heart sound.

Answer 84

Follows S2 (120-160ms) Caused by rapid filling of ventricle Normal <30y/o, but can indicate Volume Overload

Question 85

Describe the cause and identifying characteristics of an S4 heart sound.

Answer 85

Precedes S1 during atrial kick Caused by blood hitting stiff, noncompliant ventricle wall –> hypertension, AS, LV hypertrophy Always abnormal Unique from a split S1 because it is a low, subtle freq only heard at apex (direction of flow)

Question 86

Describe the cause and identifying characteristics of ejection sounds.

Answer 86

Ejection sounds are due to vibrations from a non-compliant semilunar valve opening. These are high freq sounds following S1 which are unaffected by RESPIRATION and heard best at the APEX(Aorta) or Pulmonary area (pulmonic).

Question 87

Describe the cause and identifying characteristics of a mitral opening snap?

Answer 87

High freq snap caused by opening a stiff Mitral Valve. Sound unaffected by respiration and is best heard at Aortic area, but radiates widely. May be first sign of MS –> the closer the OS gets to A2, the more severe the stenosis.

Question 88

Describe the cause and identifying characteristics of a Mitral Valve Prolapse?

Answer 88

A mid-systolic click caused by a large or weak mitral leaflet popping up into LA. High freq “click” heard best at apex. Changing posture (preload) can change timing of click.

Question 89

Describe the causes and identifying characteristics of an mid-systolic ejection murmur.

Answer 89

Mid-systolic murmur is caused by turbulent flow out of ventricle with a characteristic high freq, crescendo-decrescendo. It will be localized based on cause. Possible causes: Normal (exercise, fever, pregnancy, anemia) Valve stenosis: Aortic or Pulmonic stenosis Obstruction: hypertrophic cardiomyopathy

Question 90

How do you identify Aortic Stenosis during auscultation? Describe the mechanism that makes this type of sound.

Answer 90

AS can be caused by a narrowing in the LV outflow tract at, below or above the valve. Creates a high freq, crescendo-decrescendo mid-systolic ejection murmur. This is due to the large change in pressure across the stenosis. LV pressure >>>Arterial Pressure Best heard in Aorta area, but will radiate up carotid.

Question 91

What is critical AS?

Answer 91

1) Delayed, small volume carotid upstroke (shuddering) 2) Loss of A2 3) Late peaking murmor

Question 92

How do you differentiate Hypertrophic Cardiomyopathy from other mid-systolic murmurs?

Answer 92

Murmur is heard at lower left sternal border (vice aortic area), has a brisk upstroke, there is no ejection sound (snap), and INCREASES with standing/valsalva.

Question 93

How do you differentiate Pulmonic Stenosis from other mid-systolic murmurs?

Answer 93

Similar to AS, but doesn’t radiate up carotids. It will radiate to left infraclavicular area. Intensity increases with inspiration.

Question 94

Describe the causes and identifying characteristics of an holosystolic murmur.

Answer 94

A harsh, blowing, high freq murmur starting with S1 and ending after S2. Caused by flow from high to low pressure compartments: Mitral Regurg, Tricuspid Regurg, or VSD.

Question 95

What are the major causes for Tricuspid Regurgitation?

Answer 95

Functional/Overload

• Pulmonary Hypertension
• RV dilatation from infarct or myopathy

Structural

• IE (most common in IV drug use)
• Congenital
• acquired

Question 96

What are the auscultatory features of tricuspid regugitation? What mechanism creates these sounds?

Answer 96

Holosystolic murmur at lower left sternal border and 4/5 intercostal space. Varies with respiration.

Question 97

What are the characteristic features of Mitral Stenosis on auscultation?

Answer 97

A rumbling diastolic murmur that can vary from a holodiastolic murmur (severe) to a split decrescendo-crescendo dialstolic murmur (mild). Best heard at apex with patient in left lateral decubitus (side). Exercise/squating (increase volume) makes murmur louder.

Question 98

What are the characteristic findings on auscultation for Aortic Regurgitation?

Answer 98

Early diastolic blowing decrescendo murmur starting with A2. AR is high freq and heard best at apex.