Physio Exam 2

Antithrombotic properties of endothelial cells can be classified as: 1.Platelet inhibitory effects: ???????????? 2.Anticoagulant effects: •Endothelium shields coagulation factors from tissue factor in the vessel wall •Inactivates and alters activity of thrombin 3. Fibrinolytic effects: Source of t-PA

1. Platelet inhibitory effects: •Endothelium acts as a barrier between vWF and collagen •Secretes platelet inhibitors: Prostacyclin (PGI2), nitric oxide (NO), and adenosine diphosphatase

1.Activation due to shape change mediated by: 2a. 2b.

1.Activation due to shape change mediated by: 2a (collagen). Binding of vessel wall collagen to platelet collagen receptor 2b (thrombin). Binding of thrombin (generated by action of tissue factor on prothrombin) to thrombin receptor

Intrinsic Pathway

1.Activation of factor XII: Trauma to blood or exposure to vessel collagen or glass surface causes: •Conformational change and activation of factor XII to XIIa •Release of procoagulating phospholipids and factor III from platelets 2.Activation of factor XI: Factor XIIa activates factor XI (XIa) in the presence of high-molecular-weight kininogen and is accelerated by prekallikrein 3.Activation of factor IX: Factor XIa enzymatically forms factor IXa 4.Activation of Factor X: Factor IXa, acting in concert with activated factor VIII and with the platelet phospholipids and factor III from the traumatized platelets, activates Factor X ● 5.Factor Xa has the same role as previously described in the slide for extrinsic pathway

Each coagulation reaction involes: (3) §Components assembled on a ____________ charged phospholipid surface provided by _______________

1.An enzyme: An activated coagulation factor 2.A substrate: An inactive pro-enzyme form of a coagulation factor 3.A co-factor: That accelerates the reaction •Calcium •Vitamin K (antagonized by warfarin) §Components assembled on a negatively charged phospholipid surface provided by platelets

Antithrombotic properties of endothelial cells can be classified as: 1. Platelet inhibitory effects: •Endothelium acts as a barrier between vWF and collagen •Secretes platelet inhibitors: Prostacyclin (PGI2), nitric oxide (NO), and adenosine diphosphatase 2. Anticoagulant effects: Inactivates and alters activity of: 3. Fibrinolytic effects: Source of t-PA

1.Anticoagulant effects: •Endothelium shields coagulation factors from tissue factor in the vessel wall •Inactivates and alters activity of thrombin

Left Ventricular Pressure Volume Loop One loop represents one cardiac cycle

1.Atrial systole (begins) (mitral valve closes) 2.Isovolumic ventricular contraction 3.Rapid ventricular ejection 4.Reduced ventricular ejection 5.Isovolumic ventricular relaxation 6.Rapid ventricular filling (mitral valve opens) 7.Reduced ventricular filling *Diastole begins at top left (highest) dot Aortic valve opens at the diastolic arterial blood pressure dot

Determinants of Systolic BP (3) More compliance = ________ peak pressure Increase in SV = _________ in peak pressure

1.Left ventricular stroke volume 2.Diastolic arterial blood pressure 3.Vessel wall compliance *More compliance = lower peak pressure *More stiff = higher pressure Increase in SV = increase in peak pressure Higher pulse = higher pressure

Extrinsic Pathway

1.Release of tissue factor: Traumatized tissue releases a complex of factors called tissue factor •Tissue factor composed of membrane phospholipids of the tissue and lipoprotein complex that acts as a proteolytic enzyme 2.Activation of factor X: Lipoprotein complex of tissue factor forms a complex with factor VIIa and Ca2+ that activates factor X to factor Xa 3.Factor Xa forms prothrombin activator complex (PAC): Factor Xa combines with factor V and tissue/platelet phospholipids to form the prothrombin activator complex (PAC) 4.PAC converts prothrombin to thrombin in the presence of Ca2+ 5.Thrombin converts fibrinogen into fibrin 6.Thrombin also activates factor V within the PAC to further accelerate the process (clot expansion)

120. A 40-year-old woman has been diagnosed with a heart murmur. A " blowing" murmur of relatively high pitch is heard maximally over the left ventricle. The chest radiograph shows an enlarged heart. Arterial pressure in the aorta is 140/40 mm Hg. What is the diagnosis? A) Aortic valve stenosis B) Aortic valve regurgitation C) Pulmonary valve stenosis D) Mitral valve stenosis E) Tricuspid valve regurgitation 122. Which heart murmur is heard during systole? A) Aortic valve regurgitation B) Pulmonary valve regurgitation C) Tricuspid valve stenosis D) Mitral valve stenosis E) Patent ductus arteriosus

120. Over left ventricle has to be aortic *Blowing murmor Aortic valve regurgitation typically has high pulse pressure, which is the systolic - diastolic pressure (100 mm Hg). Also notice that the diastolic pressure decreases to very low values of 40 mm Hg as the blood leaks back into the left ventricle. 122. E During diastole, aortic and pulmonary valve regurgitation occur through the insufficient valves causing the heart murmur at this time. Tricuspid and mitral stenosis are diastolic murmurs because blood flows through the restricted valves during the diastolic period.

124. A 50-year-old woman at a local hospital has been diagnosed with a heart murmur. A murmur of relatively low pitch is heard maximally over the second intercostal space to the right of the sternum. The chest radiograph shows an enlarged heart. The mean QRS axis of the ECG is −45 degrees. What is the diagnosis? A) Mitral valve stenosis B) Aortic valve stenosis C) Pulmonary valve stenosis D) Tricuspid valve stenosis E) Tricuspid valve regurgitation

124. B) This patient has a QRS axis of −45 degrees, indicating a leftward axis shift. In other words, the left side of the heart is enlarged -> extra tension left ventricular walls must exert to expel blood out the aorta. Therefore, these symptoms fit with a patient with aortic stenosis.

13. Which condition will result in a dilated, flaccid heart? A) Excess calcium ions in the blood B) Excess potassium ions in the blood C) Excess sodium ions in the blood D) Increased sympathetic stimulation

13 B) Having excess potassium ions in the blood and extracellular fluid causes the heart to become dilated and flaccid and slows the heart. Lots of Ca2+ surrounding the cardiac myofibrils, becuase extracellular fluid calcium ion concentration increases too much. An excess potassium concentration in the extracellular fluids causes the heart to become dilated because of the decrease in resting membrane potential of the cardiac muscle fibers.

152. What is correct about interpretation of left ventricular pressure-volume loops in valve disease? A) Aortic stenosis shows a taller P-V loop with reduced preload. B) Isovolumetric systolic period is lost in aortic regurgitation but preserved in mitral regurgitation C) Aortic stenosis and regurgitation show a significantly increased afterload. D) Mitral stenosis and regurgitation show a significantly increased afterload.

152. C) Abnormalities of the aortic valve (outflow tract of the left ventricle) associates with significant increases in LV pressure and as such, increases in afterload (which does not occur in mitral stenosis/regurgitation). Preload is unchanged in aortic stenosis. Isovolumetric systolic period is lost in aortic and in mitral regurgitation. Tricuspid stenosis does not associate with loss of left ventricular isovolumetric diastolic period.

17. What is the normal total delay of the cardiac impulse in the A-V node + bundle? A) 0.22 second B) 0.18 second C) 0.16 second D) 0.13 second E) 0.09 second

160 total milliseconds total (30 msec from SA to AV, 90 msec delay through AVm 40 msec to penetrate bundle fibers p = 30ms (to reach, the rest is 130 for a grand total of 160 milliseconds D. 0.13

Constriction of the carotid artery would cause increase or decrease in: HR Parasympathetic Nerve activity Total Peripheral Resistance

17. D) Constriction of the carotid artery decreases blood pressure at the level of the carotid sinus. A decrease in carotid sinus pressure leads to a decrease in carotid sinus nerve impulses to the vasomotor center, which in turn leads to enhanced sympathetic nervous activity and decreased parasympathetic nerve activity. The increase in sympathetic nerve activity results in peripheral vasoconstriction and an increase in total peripheral resistance and heart rate. The decreased parasympathetic nerve activity to the heart would also contribute to the increase in heart rate.

Aortic Valve stenosis (narrowing of aortic valves) would cause increase or decrease in: Pulse pressure Stroke volume Systolic pressure

18. E) Pulse pressure is the difference between systolic pressure and diastolic pressure. The two major factors that affect pulse pressure are the stroke volume output of the heart and the compliance of the arterial tree. An increase in stroke volume increases systolic and pulse pressure, whereas an increase in compliance of the arterial tree decreases pulse pressure. Moderate aortic valve stenosis results in a decrease in stroke volume, which leads to a decrease in systolic pressure and pulse pressure. Diastolic decreases because there is less blood on the aortic side (it went back in to the ventricle)

Athersclerosis would cause increase or decrease in: Pulse Pressure Arterial Compliance Systolic Pressure Constriction of carotid artery would cause increase or decrease in: Sympatheric Nerve activity Renal blood flow Total peripheral resistance

19. B) A person with atherosclerosis would be expected to have decreased arterial compliance. compliance. The decrease in arterial compliance would lead to an increase in systolic pressure and pulse pressure. 20. B) Sympatheric Nerve activity: Increase Renal blood flow: decrease Total peripheral resistance: increase Constriction of carotid artery reduces BP at carotid bifurcation where arterial baroreceptors are located. Decreased arterial pressure activates baroreceptors => increase in sympathetic activity / decrease in parasympathetic activity (or vagal tone). Enhanced sympathetic activity => constriction of peripheral blood vessels, including the kidneys. *increase in total peripheral resistance and decrease in renal blood flow.

Arterio Venous Oxygen Difference How are heart and skeletal muscle different in regards to getting more O2 when they need it? Cardiac muscle oxygen supply altered by:

2 ways to alter Oxygen Supply: Changing amount of O2 extraced from blood or changing amount of blood supplied to tissues *Harder working = consume more O2 *Increase HR, afterload and preload (wall stress) , contractility (costs ATP), all increase O2 demand Skeletal muscle increases both extraction and blood flow for more O2, but heart is already extracting like 80% , so it can only increase blood flow (increase amount of blood supplied to heart)

What changes occur when going from supine to standing? Sympathetic Nerve Activity Increases or decreases Cardiac Contractility Increases or decreases HR Increase or decrease

2. All increase: acute fall in arterial pressure sensed by baroreceptors located in the carotid bifurcation and aortic arch. Activation of the arterial baroreceptors leads to an increase in sympathetic outflow to the heart and peripheral vasculature and a decrease in parasympathetic outflow to the heart. The increase in sympathetic activity to peripheral vessels results in an increase in total peripheral resistance. The increase in sympathetic activity to the heart results in an increase in heart rate and strength of contraction.

Clot contraction further compresses ________ meshwork into a smaller mass _______________ and ______ aid in this process

2.Clot contraction further compresses fibrin meshwork into a smaller mass •Thrombin and Ca2+ aid in this process As the clot contracts - it pulls the broken edges of the blood vessel together Once clot forms, it can either be invaded by fibroblasts and heal (makes small hole in vessel, later replaced by fibrous tissue) or clot dissolves

21. Which one of the following would tend to increase capillary filtration rate? A) Decreased capillary hydrostatic pressure B) Decreased plasma colloid osmotic pressure C) Decreased interstitial colloid osmotic pressure D) Decreased capillary water permeability E) Increased arteriolar resistance

21. B) Decreased plasma colloid osmotic pressure = less proteins for water to follow = less reabsorption Increasing filtration rate either means increasing filtration or decreasing reabsorption (keep them seperated) Decreased capillary hydrostatic pressure = less filtration (wrong) Decreased interstitial colloid osmotic pressure = less protein in institium = more protein in plasma = increase reabsorption (wrong) Decreased permeability = decreased filtration (wrong) Increased arterial resistance = Decreased filtration (wrong)

25. A decrease in which of the following would tend to increase lymph flow? A) Hydraulic conductivity of the capillary wall B) Plasma colloid osmotic pressure C) Capillary hydrostatic pressure D) Vascular conductance E) B and D

25. B) The two main factors that increase lymph flow are an increase in capillary filtration rate and an increase in lymphatic pump activity. A decrease in plasma colloid osmotic pressure increases capillary filtration rate => increase in interstitial volume and hydrostatic pressure, and lymph flow. In contrast, an increase in hydraulic conductivity of the capillary wall and capillary hydrostatic pressure increase capillary filtration rate, interstitial volume and pressure, and lymph flow. An increase in arteriole resistance would decrease vascular conductance, capillary hydrostatic pressure, capillary filtration rate, interstitial volume and pressure, and lymph flow.

13. A 52-year-old female undergoes cardiac catheterization to assess function of her right heart. All pressures appear normal. Her right atrial pressure is between 2 and 6 mmHg over 24 hours. Pulmonary artery pressure is 24/8 mmHg. Which of the following values is expected for her right ventricular pressure? 30/10 mmHg 25/2 mmHg 25/10 mmHg 20/10 mmHg 20/2 mmHg

25/2 mmHg Atrial systole occurs during ventricular diastole (when ventricle fills). For blood to move from atrium to ventricle, ventricular diastolic pressure has to be less than atrial systolic pressure Since atrial systolic pressure is 6 mmHg, then pressure in the ventricle must be lower. During ventricular systole, right ventricular pressure must be higher than pulmonary arterial systolic pressure, which is 24 mmHg.

12 lead ECG

3 bipolar leads (I, II, III) = 6 V1-V6 = 6 6+6 = 12

Adenosine Hypthesis 3 things that increase adenosine release: Insufficient coronary blood flow, _____________ (increase or decrease) in metabolic activity, Myocardial PO2

3 things that increase adenosine release: Insufficient coronary blood flow, increase in metabolic activity, decrease Myocardial PO2 (amount of oxygen in it)

Platelet Plug 1. vWF 2. Collagen and thrombin 3. Conformational change in: 4. ______ release from _________ granules

3. Conformational change in GPIIb/IIIa glycoprotein complex that starts binding to fibrinogen •One fibrinogen cross-link to two GPIIb/IIIa complexes = platelet aggregation 4. ADP release from dense granules (δ) : bind to ADP receptors of dormant platelets (activates)

What is the extent of diastole in the ventricular pressure-volume relationship?

3. D) Diastole includes the isovolumetric relaxation period (D to A) and ventricular filling (A-AV valve opening- to B -AV valve closure-). Thus, the diastole extends from point D to point B. (Imagine D where 3 is and B where 1 is)

30. Which of the following is correct about ECG? A) The mean vector of depolarization moves from negative to positive, from front to back, from left to right B) The P wave represents atrial depolarization and repolarization C) The Q-T interval approximates the time of ventricular contraction D) The P-R interval includes ventricular repolarization E) The T wave always opposes QRS polarity

30. C) The QRS complex represents ventricular depolarization, and the T wave represents ventricular repolarization. The Q-T interval is the time that the ventricle takes to depolarize-repolarize and represents the ven tricular contraction, as observed in the Wiggers' diagram.

Man lost a lot of blood, low BP. What would you expect in response to hemorrhage in the man? Increase or decrease in: HR Parasympathetic Nerve activity Plasma Renin Activity

30. Increase HR and plasma renin activity, decrease parasympathetic nerve activity Arterial baroreceptors are activated in response to a fall in pressure. During hemorrhage, the fall in arterial pressure at the level of the baroreceptors results in enhanced sympathetic outflow from the vasomotor center and a decrease in parasympathetic nerve activity. The increase in sympathetic nerve activity leads to constriction of peripheral blood vessels, increased total peripheral resistance, and plasma renin activity, angiotensin II and a return of blood pressure toward normal. The decrease in parasympathetic nerve activity and sympathetic outflow would result in an increase in heart rate.

________ boxes per minute /beats per minute

300 boxes/beats per minute

31. A healthy 28-year-old woman stands up from a supine position. Moving from a supine to a standing position results in a transient decrease in arterial pressure that is detected by arterial baroreceptors located in the aortic arch and carotid sinuses. Which set of cardiovascular changes is most likely to occur in response to activation of the baroreceptors? Increase or decrease in mean circulatory filling pressure, strength of cardiac contraction, sympathetic nerve activity

31. A) Activation of the baroreceptors leads to an increase in sympathetic activity, which in turn increases heart rate, strength of cardiac contraction, and constriction of arterioles and veins. The increase in venous constriction results in an increase in mean circulatory filling pressure, venous return, and cardiac output.

32. An ACE inhibitor is administered to a 65-year-old man with a 20-year history of hypertension. The drug lowered his arterial pressure and increased his plasma levels of renin. Which mechanism would best explain the decrease in arterial pressure? A) Inhibition of angiotensin I B) Decreased conversion of angiotensinogen toangiotensin I C) Decreased plasma levels of bradykinin D) Decreased plasma levels of prostacyclin E) Decreased formation of angiotensin II

32. E) The conversion of angiotensin I to angiotensin II is catalyzed by a converting enzyme that is present in the endothelium of the lung vessels and in the kidneys. The converting enzyme also serves as a kininase that degrades bradykinin. Thus, a converting enzyme inhibitor not only decreases the formation of angiotensin II but also inhibits kininases and the breakdown of bradykinin. Angiotensin II is a vasoconstrictor and a powerful sodium-retaining hormone. While plasma bradykinin increases, the major cause for the decrease in arterial pressure in response to an ACE inhibitor is the decrease in formation of angiotensin II.

36. What is the normal QT interval? A) 0.03 second B) 0.13 second C) 0.16 second D) 0.20 second E) 0.35 second

36. E) The contraction of the ventricles lasts almost from the beginning of the Q wave and continues to the end of the T wave. This interval is called the Q-T interval and ordinarily lasts about 0.35 second.

What point in the diagram on the left represents the second heart sound?

5

63. What is his diagnosis? A) Normal ECG B) Atrial flutter C) A high A-V junctional pacemaker D) A middle A-V junctional pacemaker E) A low A-V junctional pacemaker

63. B) This patient has atrial flutter, which is characterized by several P waves for each QRS complex. This ECG has two P waves for every QRS. Notice the rapid heart rate, which is characteristic of atrial flutter.

8. Histamine is infused into the brachial artery. Which set of microcirculatory changes would be expected in the infused arm? Increase or decrease in: Capillary water permeability Capillary hydrostatic pressure Interstitial hydrostatic pressure

8. A) Histamine = vasodilator = decrease arteriolar resistance and increase water permeability of capillary wall. The decrease in arteriolar resistance would also increase capillary hydrostatic pressure. The increase in capillary hydrostatic pressure and water permeability leads to an increase in capillary filtration rate, interstitial volume and interstitial hydrostatic pressure.

The cardiac cycle and murmur of a patient in the cardiac cath lab is shown in the figure. What type of valvular dysfunction does this patient have? A.Aortic regurgitation B.Aortic stenosis C.Mitral regurgitation D.Mitral stenosis

A

Sinus Arrhythmia

A sinus rhythm in which the rate varies with respiration, causing an irregular rhythm. (HR increases when you breathe in)

5. A 35-year-old woman visits her family practitioner for an examination. She has a blood pressure of 160/75 mm Hg and a heart rate of 74 beats/min. Further tests by a cardiologist reveal that the patient has moderate aortic regurgitation. Which set of changes would be expected in this patient? Increase or decrease in: Pulse Pressure (systolic- diastolic) Systolic Pressure Stroke Volume

A) The difference between systolic pressure and diastolic pressure is the pulse pressure. The two major factors that affect pulse pressure are the stroke volume output of the heart and the compliance of the arterial arterial tree. In patients with moderate aortic regurgitation (due to incomplete closure of aortic valve), the blood that is pumped into the aorta immediately flows back into the left ventricle. The backflow of blood into the left ventricle increases stroke volume and systolic pressure.The rapid backflow of blood also results in a decrease in diastolic pressure. Thus, patients with moderate aortic regurgitation have high systolic pressure, low diastolic pressure, and high pulse pressure.

ECG changes in STEMI over time:

A. Very early (may only last few minutes) B. Most commonly seen during acute phase C. Late stage (Age indeterminate)

6. A mouse model of ventricular dysfunction is developed wherein the cardiac sarcoendoplasmic reticulum Ca2+-ATPase is mutated causing a reduction of its normal function. The expected impairment in cardiac function is increased end-diastolic pressure decreased heart rate increased ventricular compliance decreased vascular resistance

A. increased end-diastolic pressure Impairments in SERCA function mean that less Ca2+ is removed from the cytosol. The amount of Ca2+ determines how myosin and actin interact. Less Ca2+ = fewer cross bridges (i.e., muscle is more relaxed) and more Ca2+ = more cross bridges. Thus, if more Ca2+ is present in cytosol during diastole, then end-diastolic pressure is higher.

31. When recording lead aVL on an ECG, which is the positive electrode? A) Left arm B) Left leg C) Right leg D) Left arm + left leg E) Right arm + left leg

A. left arm is the positive electrode for lead aVL of an ECG. By convention, the left leg is the positive electrode for lead II of an ECG.

An increase in which of the following tends to increase capillary filtration rate? A.Capillary permeability B.Arteriolar resistance C.Plasma colloid osmotic pressure D.Interstitial hydrostatic pressure E.Plasma sodium concentration

A.Capillary permeability

A beta-adrenergic-receptor blocker is prescribed for a patient with chronic-stable ("effort-induced") angina, and the incidence and severity of anginal attacks are reduced. Which of the following best explains the pharmacologic action by which the beta blocker does this? A.Decreases myocardial oxygen demand B.Dilates the coronary vasculature C.Exerts antiplatelet/antithrombotic effects D.Reduces total peripheral resistance Increases AV nodal conduction velocity

A.Decreases myocardial oxygen demand

A 52-year-old man presents with black tarry stools and hypotension. An endoscopy is ordered and reveals a bleeding ulcer in the antrum of the stomach. Baroreflex-induced compensation for the mild hemorrhage will cause which of the following values to be lower than it was before the hemorrhage? A.Venous compliance B.Ventricular contractility C.Total peripheral resistance D.Heart rate

A.Venous compliance (veins more stiff = increase BP and CO *we want to raise BP

Extrinsic Pathway for Initiating Blood Coagulation

Absence of Ca2+ can impair clotting Extrinsic pathway faster All the steps up to thrombin require calcium

Metabolic Theory

Active Hyperemia: increased blood flow through a tissue associated with increased metabolic activity(Increased O2 demand or decreased supply = increased vasodilator metabolites)More metabolism more metabolites (like adenosine, PO4-, lactate, CO2, K+. H+) = decreased arteriolar resistance = increased blood flow/ vasodilation

Relating Length-Tension Relationship to PV Loops Active and passive tension

Active: Using ATP to get muscle fibers to shorten Stroke volume impacted by cardiac filling

Actual contraction occurs at the : Depolarization of atrial muscle: Depolarization of ventricular muscle Repolarization of ventricular muscle

Actual contraction occurs at ST segment Depolarization of atrial muscle = P wave Depolarization of ventricular muscle = QRS complex Repolarization of ventricular muscle = T wave

Ejection At the end of isovolumetric relaxation:

After isovolumic contraction, pressure in ventricle exceeds aorta pressure and muscle fibers shorten At the instant the aortic valve opens (4), ejection begins, and ventricular volume begins to decrease. (blood from LV into aorta) Initial ejection = rapid (80-85%) of stroke volume ejected (5) Ventricle volume falls during this phase (during latter third of systole, ejection slows (6) -> relaxes *T wave precedes relaxation *Once calcium is removed, heart can relax Pressure in aorta exceeds pressure in ventricle, but ejection continues due to momentum During ventricular systole (mitral valve closes), atrial volume and pressure increasing (atria in diastole, blood returning from veins) Pressure increase = v wave At the end of isovolumetric relaxation, the mitral valve opens

3. In an experimental study, administration of a drug decreases the diameter of arterioles in the muscle bed of an animal subject. Which set of physiological changes would be expected to occur in response to the decrease in diameter? Increase or decrease in Vascular conductance Capillary Filtration Blood Flow

All three decrease Decreases the diameter of arterioles in a muscle bed increases the vascular resistance. The increased vascular resistance decreases vascular conductance and blood flow. The reduction in arteriolar diameter also leads to a decrease in capillary hydrostatic

Phenylephrine _______________________adrenergic agonsit (alpha or beta 1 or 2) Effect on HR, TPR, BP

Alpha -1 adrenergic agonist => Increases intracellular calcium = constriction *increase in total peripheral resistance *increase in resistance = increase in pressure Heart rate decreases, more blood on arterial side (stuck there) *arterial pressure activates baroreceptors = decrease in heart rate caused by vagal activation and sympathetic withdrawal.

Afterload Impacts Frank-Starling Mechanism An increase in afterload shifts curve ___________ At a given preload, an increase in afterload ________ stroke volume. A decrease in afterload would shift curve _____________ resulting in _____________- SV at same preload

An increase in afterload shifts curve downward. At a given preload, an increase in afterload decreases stroke volume. A decrease in afterload would shift curve upward resulting in increase SV at same preload

A 70-year-old female is seen in the clinic for shortness of breath over the last 12-months. She reports no chest pain, nor is there any lower-extremity swelling. Patient history is significant for hypertension over that past two decades, and has not always been adherent to her medical regimen. Blood pressure is 160/95 mmHg, and an S4 is heard on auscultation. Echocardiogram reveals left atrial enlargement, moderate concentric left ventricular hypertrophy and a left ventricular ejection fraction of 70%. Which of the following sets of changes are expected in this patient? Left ventricular comliance increase or decrease Plasma angiotensin II increase or decreas

Angiotensin II induced hypertension and cardiac hypertrophy Decrease in left ventricular compliance, increase in plasma angiotensin II: increases blood pressure by stimulating kidneys to reabsorb more water and by releasing aldosterone

Shear Stress High velocity = ____________ shear stress

"rubbing force" Highest near vessel wall •High velocity → High shear stress •Low velocity → Low shear stress stimulates release of paracrine substances from endothelial cells Areas of low shear stress or turbulent flow show enhanced atherosclerosis small change in the radius of a vessel will have a large effect on wall shear stress Arteries enlarge in response to shear stress

Vasoconstriction and Venoconstriction Increase SNS Activity

*Vein diameter doesn't get much smaller like artery, but it becomes more rigid Vasoconstriction (artery): decrease radius, increase pressure and resistence, decrease flow (smaller diameter = more resistence) Venoconstriction (vein) : lumen becomes rounded, decrease compliance (more rigid) but increase pressure, INCREASE flow (veins have valves)

Normal electrical axis is between:

-30 to 90 = normal axis range

Factors that increase Inotropy (contractility) Decrease? Changes caused by cellular mechanisms that regulate interaction b/n actin and myosin INDEPENDENT of myocyte length Do -Beta adrengeric antagonists-Calcium channel blockers decrease or increase?

-Catecholamines •Cardiac sympathetic nerves •Adrenal catecholamines *Increased ESPVR -Positive ionotropic agents (digoxin) Decrease Inotropy: -Beta adrengeric antagonists -Calcium channel blockers

Clinical Relevance: Impaired Baroreflex Buffering of Blood Pressure

-Clinical causes of baroreceptor denervation: •Neck trauma •Neck radiation •Heart transplant -Increased blood pressure lability contributes to end-organ damage

Reflected wave In younger people, the reflected wave occurs during _________ In older people, the reflected wave occurs during __________

In younger people, the reflected wave occurs during diastole (aortic valve closed) In older people, the reflected wave occurs during systole (aortic valve open) Doesnt snap back as quick Elevated systolic results from decreased arterial compliance Increased forward wave and reflected wave velocity for older person b/c of higher systolic

Cardiac Output and Exercise: CO = SV X HR SV = End diastolic - end systolic

Increase CO with exercise = Increased contractility, Increased sympathetic nerve activity -> release more norepi = Increase in PkA = More calcium phosphoorylated (calcium eneters, stimulates SR to release more ca2+) = More rapid, stronger contraction Exercise: Increased vascular conductance, blood flow, CO2 concentration, arteriolar diameter

Active vs passive heat loss (non-apical skin) Which sympathetic nerve does which? most efficient heat transfer with the environment is when blood is shunted through these surface capillaries

Increase body temp -> Relief of tonic sympathetic control of nonapical skin -> passive vasodilation -> heat loss -> if core temp still high then -> Increase symp. outflow of ach releasing nerves of skin -> active vasodilation -> more heat loss AcH = Active Heat loss (dilation)

Decreased Stroke Volume = _______ contracility (inotropy) Increased sympathetic stimulation/ decreased parasympathetic stimulation = __________ contractility

Increase calcium = increased contractility (Inotropy) End diastolic volume (EDV)(Preload)(Volume at the end of filling) increased filling = stretch Decrease SV = Decrease contractilitly

Central Command

Increase in activity before exercise even starts autonomic changes that anticipate and accompany exercise Baroreceptor reflex fine tunes arterial pressure during exercise, but reflex does not adjust pressures to its resting value, it adjusts them to new higher level proportional to exercise intensity

A 45-year-old woman was referred to a nephrologist for persistent, refractory hypertension over the past 12 months. Physical examination reveals that her blood pressure is 178/105. Subsequent renal angiography reveals narrowing of her left renal artery. Which of the following sets of findings would be expected? Increase or decrease in Plasma Renin activity Plasma aldosterone

Increase in both Renin and aldosterone Pressure in this patient's left renal artery distal to the narrowing is decreased (there is always a pressure drop across a resistance). This decrease in pressure is sensed by the juxtaglomerular cells in the afferent arteriole, which then secrete renin. The increased renin converts angiotensinogen to angiotensin I, and the ACE converts angiotensin I to angiotensin II, which then circulates through the blood and stimulates the adrenal glands to secrete aldosterone

8. A 16-year-old female twisted her ankle while cross-country skiing. Her ski instructor advised her to not remove her ski boot until she arrived at the hospital. Keeping the ski- boot on would be expected to reduce or limit the swelling by most directly impacting which Starling force? Capillary hydrostatic pressure Interstitial hydrostatic pressure Capillary oncotic pressure Interstitial oncotic pressure

Increase interstitial hydrostatic pressure opposes the movement of fluid from capillaries Swelling/edema = fluid going from capillaries (higher pressure) into interstial space (lower pressure). If we increase interstitial hydrostatic pressure than less fluid will leave capillaries

Baroreceptors (carotid sinus and aortic arch)

Increase pressure = More stretch = more action potentials Afferent signal to the brain Arteriole/venule (most important 2 for BP regulation) dont have PNS innervation, all we can do is take foot off the gas (release less norepi) *Veins impact how much blood is coming back to heart The baroreflex is ALWAYS active unless blood pressure equals zero

Inotropy Graphs

Increase slope = increase inotropy (Contractility) Contractility: the ability of cardiac muscle to develop force, independent of preload or afterload Clinical assessment of contractility? •Rate of rise of LVP during isovolumic contraction •Doppler estimates myocardial shortening velocity •Doppler estimates blood ejection velocity through aortic valve

Increase in radius = _________ in wall stress and _________ afterload

Increase wall stress = increase radius = increased afterload Afterload can be defined as ventricular wall stress during systole

A 37-year old woman undergoes a CT scan of the abdomen, which reveals a large peritoneal mass. A subsequent magnetic resonance angiography study showed that the abdominal aorta was constricted to one-half its resting diameter. As a result, resistance to blood flow through the vessel would be which of the following? A.Decreased in half B.Decreased 16-fold C.Increased by 50% D.Doubled E.Increased 16-fold

Increased 16-fold Diameter divided by 2 = resistance to the 4th Q = change in pressure X radius^4/ LXV Just know resistance to blood flow varies in to 4th power of radius (small change in diameter = big changes in relative flow) Change in pressure = 1/ r^4 1/(.5^4) = 16

Increased afterload = ___________ stroke volume

Increased afterload = decreased stroke volume stroke volume is the volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction. The afterload (Just before aortic valve opens) is the amount of pressure that the heart needs to exert to eject the blood during ventricular contraction = DIASTOLIC More pressure opposing blood leaving (afterload) = less blood gets pumped out

Sympathetics Increase nerve activity to: Vein = __ compliance -> ____ pressure -> _______blood flow to heart Artery= ______blood flow -> ______ resistence

Increased nerve activity to vein = decreased compliance, increased pressure, more blood back to heart Nerve activity to artery increased = decreased blood flow = increased resistence Sympathetic innervation of arterioles modulates blood flow Sympathetic innervation of veins is less dense than arteries and modulates blood volume

A 19-year-old male agrees to participate in a study that is investigating cardiovascular responses to exercise in healthy subjects. Of the following hemodynamic or cardiac variables, which change occurs in response to increasing exercise intensity? Impaired Ca2+ uptake into the sarcoplasmic reticulum Increased rate of ventricular relaxation Decreased rate of SA nodal action potentials Decreased diameter of skeletal muscle arterioles Increased venous compliance

Increased rate of ventricular relaxation

Frank-Starling Mechanism Preload: Greater myocyte stretch = __________ Stroke volume

Increasing venous return and ventricular preload leads to an increased stroke volume Preload: Amount sarcomere stretched prior to contraction (determiend by venous pressure, ventricular compliance, HR, and atrial contraction) Greater myocyte stretch = greater stroke volume Stroke Volume effected by Preload, afterload, and contractility

Extrinisic factors on conduction velocity

Increasing: •Sympathetic Stimulation •Muscarinic receptor Antagonists •Beta Adrenergic Agonists •Circulation Catecholamines •Hyperthyroidism Decreasing: •Parasympathetic Stimulation •Muscarinic receptor Agonists •Beta Blockers •Ischemia/Hypoxia •Na and Ca Channel Blockers

Jugular Venous Pressure (JVP) Indirect measure of: *Normal Right atrial pressure = 2-6 mmHG

Indirect measure of R atrial Pressure Increase in R atrial pressure = increase in JVP (similar numbers) No valve b/n right atrium and vena cava

Respiration and Venous Return Inhale = ________ pressure on vena cava

Inhale = less pressure on vena cava (diameter increases) Diaphragm descends, Diameter increases = Decrease pressure = more blood goes through = increase venous return to heart (S2 splitting on inspiration) *takes longer for pulmonic valve to close because it has more blood to pump

Antithrombin (heparin factor) Target and effects:

Inhibits intrinsic pathway mainly (most of the active components on that side except for 12)

Intervals vs Segments in ECG Ischemia vs Infarct Ischemia will _____________ J point (Elevate or depress) Infarct will _________ J point J Point: Where do we look for Ischemia/infarct

Intervals include waves, segments don't (segments part of an interval?) Segments (part of an interval) normally isoelectric/ FLAT: No activity, been depolarized We look for ischemia/infarct at the ST segment J point: QRS complex and the ST segment on the electrocardiogram (ECG), marking the end of depolarization and beginning of repolarization Ischemia = blood flow has decreased -> Infarction -> blood flow has been completely cut off, resulting in necrosis, or cellular death *Not all ischemia = infarct, but all infarct encompasses ischemia

________tropy and _________tropy controlled by Sympathetics What node controls HR

Ionotropy (contraction) and Luisotropy (relaxation) controlled by sympathetics SA controls HR

Aortic Regurgitation Increase or decrease Diastolic pressure: Pulse presure:

LV filling when aortic valve closed (not close all the way) Diastolic decrescendo murmor ØVentricular and aortic peak systolic pressure increase due to large SV-> pulse pressure increased Rapid runoff: Diastolic pressure drops quicker b/c blood can go 2 direction (back to ventricle or down aorta) **aortic regurg = low diastolic because not as much blood is hanging out in the artery Normally, aortic valve closes and left ventricular pressure goes down (isovolumeic ventricular relaxation) Left ventricle: Increase volume (coming from two direction) Increased SV but decreased effective forward aortic flow: SV is just volume of blood ejected from heart, doesnt matter where it goes, some goes back to LV Can lead to pulmonary edema eventually •Ventricular dilation •No true isovolumetric phases (requires aorta to be fully closed) • Increased LV filling pressure, LA and pulmonary vascular pressures

Mitral Regurgitation Large _ wave _____________________ murmor Ventricular systolic and aortic pressure : (increase or decrease) (increase or decrease) LA and pulmonary vascular pressures __________ (increase or decrease) LV filling pressure (increase or decrease) SV but (increase or decrease) effective forward aortic flow

Large V wave becuase as LV contracting, blood back into LA Delta LVP remains large / constant during ejection = holosystolic murmur LA pressure rises as flow moves back across incompetent valve Ventricular systolic and aortic pressure decrease (b/c net ejection of blood into aorta decreased) Increase pulmonary capillary pressure eventually could lead to pulmonary edema •Increase LA and pulmonary vascular pressures • Increase LV filling pressure •Ventricular dilation •Increase SV but decrease effective forward aortic flow •No true isovolumetric phases

Einthoven's Triangle for standard limb leads Lead I: Lead II: Lead III: Axial reference system: Isosceles Triangle (60 degrees each)

Lead I: R arm to L arm Lead II: R arm to L leg Lead III: L arm to L leg Normal axis range = from -30 to +90

Where is the MI? Lead II, III, and aVF = V1 and V2: V3 and V4 = V5 and V6: I and aVL:

Lead II, III, and aVF = inferior /posterior V1 and V2: Septum (some anterior) V3 and V4 = Anterior V5 and V6: Lateral I and aVL: Lateral Wall

Factors That Alter Blood Supply: Reactive Hyperemia Total coronary flow determined by O2 needs of myocardium Peak left coronary flow occurs early in ____________, while peak right coronary flow occurs during ____________

Left coronary flow greater than right coronary flow due to mass and work output of left ventricle (greater than right) Peak left coronary flow occurs early in diastole, while peak right coronary flow occurs during systole -> since left flow greater, total coronary flow greater in diastole Reactive hyperemia:If blood supply cut off then restored, flow increases above normal*comes from completely restricted blood flow

Heart failure with reduced ejection fraction (HFrEF), / systolic failure:

Left ventricle cant contract normally. The heart can't pump with enough force to push enough blood into circulation.

A 47-year-old male has had severe aortic valve regurgitation for one year that has not yet progressed to ventricular failure. An increase in which of the following cardiac hemodynamic variables would be expected? Aortic diastolic pressure Effective net aortic blood flow Left ventricular afterload Left ventricular end-diastolic pressure

Left ventricular end-diastolic pressure

Edema formation during heart failure from increased capillary hydrostatic pressure *The biggest cause of right sided heart failure is left sided heart failure Right vs Left sided ventricular failure:

Left ventricular failure: 1.Blood backs up into left atria and pulmonary cap. 2. Increase (pressure) Pc in pulmonary capillaries 3.Pulmonary edema Right ventricular Heart failure; 1.Blood backs up into systemic veins 2. Increase Pc in lower extremities and abdominal viscera 3.Ascites, Systemic edema

Postural Hypotension Resulting From Autonomic Failure The patient's blood pressure while lying down was 130/70 mm Hg. When standing, BP decreased to 60/30 mm Hg, and the patient felt dizzy. Pulse rate was 75 per minute regardless of position. 1. What was Johnny's initial pulse pressure while lying down? 2. What was the mean blood pressure likely to be under these conditions? 3. What was Johnny's pulse pressure while standing? 4. What was the mean blood pressure likely to be under these conditions? 5. What happened to stroke volume when Johnny stood up? 6. Why would stroke volume decrease when he stood up? 7. When the patient stood up, Pa fell but HR did not increase. Why? 8. What changes would one expect in autonomic activity upon standing? With the patient supine again, an intravenous infusion of norepinephrine caused blood pressure to increase to 180/100 mm Hg and heart rate to increase to 120 per minute. 9. Is Johnny's heart unresponsive to sympathetic stimuli? 10. Did norepinephrine cause the Johnny's heart to move outward along the same ventricular function curve or to shift to a new function curve? 11. How would the brain arterioles respond to the decreased arterial pressure with standing?

Answers: 1. Pulse pressure = 130 - 70 = 60 mm Hg 2. Mean Pa = 70 + 60/3 = 70 + 20 = 90 mm Hg 3. Pulse pressure = 60 - 30 = 30 mm Hg 4. Mean Pa = 30 + 30/3 = 30 + 10 = 40 mm Hg 5. It decreased, as indicated by the reduced pulse pressure. 6. Blood pools in the leg veins, so central blood volume is reduced. Reduced filling of the heart leads to reduced SV. 7. The baroreceptor and cardiopulmonary reflexes are not operating properly because of destruction of autonomic nerves. 8. Increased sympathetic activity and decreased parasympathetic activity. 9. No, because norepinephrine increased Pa and HR. 10. Shift to a new, higher curve. Contractility increased, so stroke volume would be elevated even at the same preload. 11. Metabolic control mechanisms would cause the arterioles to dilate ... this is an example of autoregulation.

A 32-year-old woman is diagnosed with severe aortic stenosis. Which of the following hemodynamic variables is consistent with that diagnosis? A decreased left ventricular end-diastolic pressure A decreased systolic arterial pressure An increased ejection fraction An increased stroke volume An increased left ventricular end systolic volume

Aorta valve opening is very small, accompanied by concentric hypertrophy, which impairs ventricular filling. -Decreased stroke volume -> Decreased systolic arterial blood pressure. Reduced ejection fraction and SV (less blood to eject) Option E: Impaired ventricular filling without sign of systolic dysfunction, LV end-systolic volume may be unchanged or possibly decreased, but cannot be increased.

Systole or Diastole? Sound for each? Aortic Regurgitation Aortic Stenosis Mitral Regurgitation Mitral Stenosis

Aortic Regurgitation: Diastolic Decrescendo Aortic Stenosis: Systolic Crescendo-decrescendo Mitral Regurgitation: Systolic: Holosystolic Mitral Stenosis: Diastolic: Rumbling

Pressure ALWAYS drops across a resistance Pressure prior to resistance ALWAYS higher Aortic Stenosis *As pressure builds it gets louder (depends on pressure gradient) The cause for dizziness when standing is due to an impaired ability to reflexively increase what cardiovascular variable? CO

Aortic stenosis: Less volume makes it through = pressure drop ØVentricular pressure is very high to overcome the high afterload (stenotic valve)(Large pressure gradient ) Delta P = LV pressure - aortic pressure Delta P increase then decreases = crescendo-decrescendo systolic murmor *Decrease pulse pressure and SV, ventricular hypertrophy (decreased compliance), Increased LV filling and LA and pulmonary vascular pressures Renal artery stenosis: Higher pressure before stenosis *lower pressure after stenosis tells kindey to increase renin to make more angiotensin II

Arterial vs Venous Circulation *different routes for different organs *__________ of the arterial walls propels blood forward during diastole

Arterial: High resistance, low compliance (arterial less stretchy, more stiff), high pressure PRESSURE reservoir (95% of energy stored in aorta during systole as potential energy) *Elastic recoil of the arterial walls propels blood forward during diastole Venous: Low resistance, high compliance, low pressure, Volume Reservoir (60% of total blood in venous system)

During exercise, does the following increase or decrease in skeletal muscle? Arteriole Resistance Tissue pH Tissue CO2 Concentration In normal conditions, blood flow to skeletal muscles is determined by:

Arteriole Resistance: decrease Tissue pH: decrease Tissue CO2 Concentration: increase 6. F) The increase in local metabolism during exercise increases carbon dioxide production and decreases tissue oxygen concentration and tissue pH. The decrease in tissue oxygen concentration, tissue pH, and increase in carbon dioxide production increase arteriolar diameter (decrease arteriole resistance) and increase vascular conductance and blood flow to skeletal muscles. Although sympathetic nerves, angiotensin II, and vasopressin are powerful vasoconstrictors, blood flow to skeletal muscles is usually determined by loval metabolic factors

Site of greatest amount of vascular resistance?

Arterioles Vasoactive, respond to stuff, react/contract to hormones, neurotransmitters, most smooth muscle by % Smooth muscle dilates = lumen gets bigger cost of overcoming resistance is the dissipation of pressure, and where resistance is highest, the pressure loss will be greatest = arterioles are resistence vessels b/c greatest pressure drop occurs there

Skeletal Muscle At rest, comprises 50% of body weight but recieves only __% of total Cardiac output During exercise, still 50% of weight but may use up to ____ of cardiac output 2 ways to alter Oxygen Supply: During exercise, flow control shifts from _______________________ to __________________

At rest, gets only 17% of CO (Only releases 5-7% volume of O2 to tissus) *Exercise: up to 80% (30L/min)(meanwhile, blood flow to viscera decreases) *As VO2 max/ATP usage/workload increases, % of CO going to skeletal muscle increases 2 ways to alter Oxygen Supply: Changing amount of O2 extraced from blood or changing amount of blood supplied to tissues Activity increase = more O2 stolen from blood, so less blood comes from venous side During exercise, control of flow shifts to local level metabolic factors that override the high level of sympathetic nerve activity (controls resting muscle flow) *BUT symp. activity (vasoconstriction) still limits vasodilation so BP doesnt fall

At rest, skeletal muscles are relaxed and veins are _________ (open or closed)

At rest, veins are open -High capactiance = blood can pool When muscle contracts, veins compressed -> expelling blood forwad One way valves = no backflow Muscle activity promotes venous return and helps maintain central venous pressure and venous return, and lower venous and capillary pressures in lower limbs.

A 42-year-old woman with lightheadedness and recurrent syncope is taken to the emergency department where she is given atropine. Her symptoms are relieved by an increase in which of the following? A. Heart rate B. PR interval C. Stroke volume D. Venous compliance

Atropine increases HR competitively blocks the effects of acetylcholine

Intrinsic Control: Autoregulation of blood flow 3 circulations with "flat" curves

Autoregulation is the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure. *The autoregulatory range is the range of pressure over which there is little if any change in blood flow As pressure decreases, resistance drops (diameters gets bigger) -> So even though we have less pressure flow stays same *if pressure drops, less stretch, less ca2+, less resistance *increase Pressure => icnrease ca2+ => Increase resistance Flat curves: Cerebral, renal, coronary

A 62-year-old man with congestive heart failure (CHF) develops increasing shortness of breath in the recumbent position. A chest x-ray reveals cardiomegaly, horizontal lines perpendicular to the lateral lung surface indicative of increased opacity in the pulmonary septa, and lung consolidation. Pulmonary edema in CHF is promoted by which of the following? A.Decreased pulmonary interstitial oncotic pressure B.Increased pulmonary capillary hydrostatic pressure C.Increased pulmonary capillary oncotic pressure D.Increased pulmonary interstitial hydrostatic pressure E.Decreased pulmonary capillary permeability

B

1. Listed below are the hydrostatic and oncotic pressures within a microcirculatory bed. Plasma colloid osmotic pressure = 25 mm Hg Capillary hydrostatic pressure = 25 mm Hg Venous hydrostatic pressure = 5 mm Hg Arterial pressure = 80 mm Hg Interstitial fluid hydrostatic pressure = −5 mm Hg Interstitial colloid osmotic pressure = 10 mm Hg Capillary filtration rate = 150 ml/min What is the capillary filtration coefficient (in ml/min/mm Hg) for this capillary wall? A) 5 B) 10 C) 15 D) 20 E) 25

B) Net filtration = filtration coefficient x [(capillary hydrostatic P - interstitial hydrostatic P) - (plasma colloid osmotic P - interstitial colloid osmotic P)] (25--5) - (25-10) = 30-15 = 15 150/15 = 10

46. An increase in which of the following tends to decrease capillary filtration rate? A) Capillary hydrostatic pressure B) Plasma colloid osmotic pressure C) Interstitial colloid osmotic pressure D) Venous hydrostatic pressure E) Arteriolar diameter

B) Plasma colloid osmotic pressure

Myocardial Ischemia Treatment (3)

B-1 receptor blockers inhibit the sympathetic effects on the heart and are very helpful. ACE inhibition prevents the production of angiotensin II and thus decreases the afterload effect on the heart. Nitroglycerin causes nitric oxide release, resulting in coronary vasodilation.

A 57-year-old woman is undergoing a femoral popliteal bypass for her peripheral vascular disease. The vascular surgeon wishes to induce a localized arteriolar constriction to help control hemostasis. An increase in the local concentration of which of the following agents will cause systemic vasoconstriction? A.Nitric oxide B.Angiotensin II C.Atrial natriuretic peptide D.A beta2-adrenergic agonist

B.Angiotensin II Neprilysin breaks down natriuretic peptides (BNP and ANP: increased with reduced ejection fraction. heart failure) ANP and BNP release promoted by atria strech and ventricules becuase of increased CO Favor release of sodium in urine by dilating arterioles -Inhibit renin and reduce angiotensin Breaking down ANP and BNP in kidney with Neprilysin => if we inhibit this, we increase natriuretic peptides, but this also activvates renin-angiotensin system Can cause hypotension, use with angiotensin II inhibitors Summary: ANP and BNP increase sodium exretion, inhibit renin angiotensin system If we inhibit breaking down ANP and BNP, it can help with heart failure

A 52-year-old male is referred to a cardiologist with chief complaints of fatigue, chest pain and difficulty breathing when lying down. Blood pressure is 160/55 mmHg and auscultation detects a diastolic murmur. Echocardiography detects left ventricular dilatation. What type of valvular disease is consistent with these findings? A.Aortic stenosis B.Aortic regurgitation C.Mitral stenosis D.Mitral regurgitation

B.Aortic regurgitation *aortic regurg = low diastolic because not as much blood is hanging out in the artery

A decrease in which of the following tends to increase lymph flow? A.Capillary hydrostatic pressure B.Plasma colloid osmotic pressure C.Lymphatic pump activity D.Arteriolar diameter 48. Which of the following would tend to increase lymph flow? A) Increase capillary hydrostatic pressure B) Increased plasma colloid osmotic pressure C) Increased interstitial volume D) Decreased arteriolar diameter E) Both A and C

B.Plasma colloid osmotic pressure decrease = less trying to come back in = more in interstitium) E. Both A and C So, a decrease in plasma colloid osmotic pressure or an increase in capillary hydrostatic pressure/increased intersitial volume will icnrease lymph flow

Sympathoadrenal System Epinephrine also releases FFA's into the blood. Why is this important? Albuterol = ________ agonist Norepi binds _____

B2: BRONCHIOLES *ALBUTEROL = B2 AGONSIT FFA's = increase in blood, increase in energy for fight or flight Norepi binds Alpha 1

A 47-year-old woman has experienced dizziness for the past 3 months when getting out of bed in the morning and when standing up. Her arterial pressure is 128/92 mmHg lying down and 93/58 sitting. Which of the following sets of physiological changes are expected when moving from a supine to an upright position? Increase or decrease in: Baroreceptor afferent nerve activity Venous Compliance Plasma renin activity

Baroreceptor afferent nerve activity: Decrease Venous Compliance: Decrease Plasma renin activity: Increase Standing decreases venous return to heart BP drops: Less stretch We want to increase BP: brainstem increases sympathetic nerve activity, which decreases venous complianc and increases plasma renin activity

Vasomotion

Basis for coronary reserve Precapillary sphincters comprised of smooth muscle cells: at rest, only a few open/relaxed Max exercise = all open = coronary blood flow rise to max levels *Coronary blood flow increases in proportion to increased total work: CAD = reduced ability to vasodilate (can't increase flow as much) As workload increase more sphincters open: Increase in CO = increase in workload

Phenylephrine

Binds Alpha 1 but NOT beta 1 Constricts the heck out of everything Increases Resistance and BP

During Heat stress: (increase or decrease) Blood volume in skin veins: HR and CO: Renal and splanchnic blood flow:

Blood volume in skin veins increase HR and CO increase Renal and splanchnic blood flow decrease Divert more blood to skin so we dont overheat

64. Which pressure is normally negative in a muscle capillary bed in the lower extremities? A) Plasma colloid osmotic pressure B) Capillary hydrostatic pressure C) Interstitial hydrostatic pressure D) Interstitial colloid osmotic pressure E) Venous hydrostatic pressure

C

A 65-year-old man had the above ECG tracing recorded at his annual physical examination. What is the likely diagnosis? A) Atrial paroxysmal tachycardia B) First-degree A-V block C) Second-degree A-V block D) Third-degree A-V block E) Atrial flutter

C 68. C) Notice in this ECG that a P wave precedes each of the first four QRS complexes. After that we see a P wave but a dropped QRS wave, which is characteristic of second-degree A-V block.

9. An increase in shear stress in a blood vessel results in which change? A) Decreased endothelin production B) Decreased cyclic guanosine monophosphate production C) Increased nitric oxide release D) Increased renin production E) Decreased prostacyclin production

C C) An increase in shear stress in blood vessels is one of the major stimuli for the release of nitric oxide by endothelial cells. Nitric oxide increases blood flow by increasing cyclic guanosine monophosphate.

Activated Protein C Target and effects:

C inhibits V and V3 (rhymes)

39. A 2-fold increase in which of the following would result in the greatest increase in the transport of oxygen across the capillary wall? A) Capillary hydrostatic pressure B) Intercellular clefts in the capillary wall C) Oxygen concentration gradient D) Plasma colloid osmotic pressure E) Capillary wall hydraulic permeability

C) Oxygen concentration gradient

6. A 47-year-old man has an ejection fraction of 0.32 and an end-diastolic volume of 160 ml. What is (approximately) the value of end-systolic volume? A) 48 ml B) 83 ml C) 109 ml D) 51 ml E) 170 ml

C. 109 Ejection fraction (EF)= End diastolic - (End systolic volume or stroke volume (SV)/end-diastolic volume (EDV)) multiplied by 100 and expressed in percent. 160 X 0.32 = (approximately 109 ml)

We administer a dose of epinephrine and observe (among other responses) a direct increase of cardiac rate, contractility, and conduction velocity. Which of the following adrenergic receptors was responsible for these direct cardiac effects? A.a1 B.a2 C.b1 D.b2 E.b3

C. B1

An athlete training for a marathon is suspected to have received illegal erythropoietin injections to increase his red blood cell count. If true, which of the following hemodynamic parameters is expected to decrease? A. Blood pressure B. Blood vessel length C. Capillary blood flow velocity D. Radius of capacitance vessels

C. Capillary blood flow velocity More RBCs = more viscous = reduction in velocity BP would either be unchanged or increased (TPR increase => diastolic BP increase)

An otherwise healthy 21-year-old male presents to the Emergency Department with a 2 hour history of vomiting blood. On exam, his blood pressure is 100/75 and his pulse rate is 100/minute. A hemoglobin is noted to be 12.3 g/dL (normal 13-16). Which of the following hemodynamic variables would be LESS in this patient than it was in his normal state before the hemorrhage? A.Heart rate B.Total peripheral resistance C.Venous compliance D.Ventricular contractility

C.Venous compliance

Cardiac Output = ___________ X ___________

CO = HR X stroke volume

Thoracic Blood Volume Changes During Transition from Supine -> Standing *Most BV shift occurs in veins Orthostatic Hypotension

CVP decreases when standing becuase gravity pulls blood down to legs *decreases right ventricular filling pressure (preload) = decrease SV Left ventricular SV also falls b/c of reduced pulmonary venous return/decreased left ventricular preload = Decreased CO and MAP When stand, barorecptor reflexs restore arterial pressure, needs increased systemic vascular resistance (sympathetic mediated), decreased venous compliance (due to sympathetic activation of veins), decreased stroke volume (due to decreased preload), and increased heart rate (baroreceptor-mediated tachycardia). Problems with this system = orthostatic hypotension = edema in legs Lying down: Increase preload, SV, CO (more even blood distribution to heart)

Refractory periods in cardiac cycle

Calcium cause contraction after QRS Calcium entry at phase 2 T wave = phase 3

Carotid Sinus Nerve Stimulation as Treatment for Refractory Hypertension

Carotid sinus nerve stimulation can stimulate HTN = more APs, stimulates vagal, inhibits SNS to decrease BP (increase baroreflex stimulation = decrease BP) : Treatment for refractory hypertension -Clinical causes of baroreceptor denervation: •Neck trauma•Neck radiation•Heart transplant-Increased blood pressure lability contributes to end-organ damage

Autonomic Regulation During Exercise 1. Central Command 2. Peripheral Sensors 3. Integration of sensory/ Central signals and coordinated response

Central Command: Anticipatory, feed-forward response wherein there are increases in cardiorespiratory function immediately before the onset of exercise. Peripheral Sensors: Monitor changes in the periphery and convey this to the central nervous system: •Baroreceptors (monitor arterial pressure and venous volume) •Chemoreceptors (monitor blood PCO2 and H+ levels) •Skeletal muscle afferent sensors (Exercise-pressor reflex) ‒Class III- Thinly myelinated nerve endings that are mechano-sensitive Class IV- Unmyelinated nerve endings that are chemo-sensitive 3. Goal: GOAL: During exercise, autonomic systems redistribute blood flow among various vascular beds to maintain arterial pressure at levels that ensure adequate flow and oxygen delivery to the active muscle.

Ohm's Law and BP Diameter smaller = ____________ volume, _____________ velocity, _______________ resistance, ____________ turbulence

Change in pressure = flow X resistance Diameter smaller = decreased volume, increased velocity, increased resistance, increased turbulence Arteries are higher resistence, requires more pressure to move blood through Pressure needed to drive flow

Compliance

Change in volume/Change in pressure *ability to stretch and accommodate a volume of blood Higher compliance = more stretchy, less stiff Lower compliance = less stretchy Decreased compliance in veins = Increased SV and CO Steeper slope = less compliant (venous compliance up to 20X greater than artery, but compliance similar at higher pressures) Increase in Sympathetic nerve activity (norepi) on veins = less compliance = decreased slope = smaller volume at higher pressure, drives more blood back to heart = increase in Stroke volume

Central Venous Pressure (CVP)/ Central venous volume What causes it to change? (4 things) Where is atrial caval junction

Changes in: Total blood volume (hemorrhage, etc) Ventricular compliance (stiff ventricle = blood backup in veins = Increase CVP) Venous compliance: -At Atrial caval junction (b/n right atrium and thoracic vena cava), Decrease = more blood to R side of heart = Increase pressure Shifts in venous volume toward/away from central circulation

Which of the following contributes to 1st heart sound during systole? Closure of semilunar valves Contraction of ventricles Contraction of atria Closure of AV valves Flow of blood from atria

Closure of AV valves (tricuspid and bicuspid) Second heart sound = Closure of aortic and the pulmonary valves (semilunar)

Which of the following contributes to 2nd heart sound? Contraction of atria Closure of aortic and the pulmonary valves Contraction of ventricles Flow of blood from atria Closure of AV valves

Closure of aortic and the pulmonary valves (semilunar)

Trauma of the blood vessel or the blood itself causes coagulants to over-ride anti-coagulants Clotting initiated with ____________ activators 2 pathways: Extrinisic begins with: Intrinsic begins in: How does calcium citrate prevent coagulation

Clotting initiated with prothrombin activators Initiates coagulation in 2 ways: 1.By the extrinsic pathway: Begins with trauma to vascular wall and surrounding tissues 2.By the intrinsic pathway:Begins in the blood Calcium Citrate chelates calcium

Effect of Ventricular Compliance on Preload ???????

Compliance is a measure of stiffness: Change in volume / change in pressure Slope of normal compliance curve increased by decrease in ventricular compliance (ventricular hypertrophy), whereas slope of the compliance curve is reduced by an increase in ventricular compliance (ventricular dilation). Decreased compliance increases the end-diastolic pressure (EDP) at a given end-diastolic volume (EDV), whereas increased compliance decreases EDP at a given EDV. LV, left ventricle. Compliance can be reduced by ischemia, infarction or hypertrophy

Purkinje Fibers Connect to: Conduction velocity

Connect to ventricular Myocytes (endocardium to epicardium: N before P) Conduction velocity = 4 m/sec Permits Rapid, synchronous depolarization of ventricles (from myocyte to myocyte)

Intercalated Discs Contain: (2)

Contain desmosomes and gap junctions Cell to cell propagation of APs: Depolarization through Gap junctions

Iontropy

Contractility Intrinsic ability of myocytes to develop independent of myocyte length at given preload Changes caused by cellular mechanisms that regulate interaction b/n actin and myosin INDEPENDENT of myocyte length

Nitroglycerin for Heart

Converted within endothelial cells to nitric oxide, which has potent vasodilatory effects. Reducing myocardial oxygen demand secondary to venous dilation (decreasing preload) and arteriolar dilation (reducing afterload). Much greater effect on reducing preload than afterload -> dilates veins more than arteries. In any case, decreasing preload and afterload which reduces ventricular wall stress and oxygen demand by the heart, thereby enhancing the oxygen supply/demand ratio. A reduction in preload (reduced diastolic wall stress) also helps to improve subendocardial blood flow, which is often compromised in coronary artery disease. * vasodilation of the coronary arteries and relief of coronary artery spasm.

Coronary Circulation: •Entire myocardial blood supply is derived from the rt and lt coronary arteries. Originate at: Coronary veins empty into ________ ________ via coronary sinus Heart only 0.5 % of body weight and under resting conditions receives about 5 % of the cardiac output.

Coronary arteries originate at aortic root Heart fibers small in diameter Coronary veins empty into R atrium via coronary sinus

85. Which of the following sets of changes would tend to increase coronary blood flow? Increase or decrease in: Coronary arteriole Resistance Cardiac adenosine concentration Coronary vascular conductance Cardiac Workload

Coronary arteriole Resistance: Decrease Cardiac adenosine concentration: Increase Coronary vascular conductance: Increase Cardiac Workload: Increase

Summary of Control of Coronary Blood Flow Coronary blood flow is primarily regulated by changes in :

Coronary blood flow is primarily regulated by changes in tissue metabolism.

13. Under control conditions, flow through a blood vessel is 100 ml/min with a pressure gradient of 50 mm Hg. What would be the approximate flow through the vessel after increasing the vessel diameter by 100%, assuming that the pressure gradient is maintained at 50 mm Hg? A) 200 ml/min B) 400 ml/min C) 800 ml/min D) 1600 ml/min E) 700 ml/min

D 13. D) Blood flow in a vessel is directly proportional to the fourth power of the vessel radius. Increasing vessel diameter (or radius) by 100% (2 × control) would increase blood flow 2 to the fourth power × normal blood flow (100 ml/min). Thus, blood flow would increase to 100 ml/min × 16, or approximately 1600 ml/min.

18. Sympathetic stimulation of the heart does which of the following? A) Releases acetylcholine at the sympathetic endings B) Decreases sinus nodal discharge rate C) Decreases excitability of the heart D) Releases norepinephrine at the sympathetic endings E) Decreases cardiac contractility

D) Increased sympathetic stimulation of the heart increases heart rate, atrial contractility, and ventricular contractility and increases norepinephrine release at the ventricular sympathetic nerve endings. It does not release acetylcholine. It does cause an increased sodium permeability of the A-V node, which increases the rate of upward drift of the membrane potential to the threshold level for self-excitation, thus increasing the heart rate.

45. A ventricular depolarization wave, when traveling 60 degrees in the frontal plane, will cause a large positive deflection in which of the following leads? A) aVR B) aVL C) Lead I D) Lead II E) aVF

D) Lead II

A 56-year-old female is seen in the clinic with a chief complaint of becoming dizzy when she stands for the past two-weeks. Her physician asks her to perform a sustained Valsalva maneuver to test the integrity of her autonomic nervous system. Which of the following sets of hemodynamic variables occurs with a sustained Valsalva maneuver?

D. Increase intrapleural pressure, increase CVP, decrease Preload Valsalva: exhale against closed epiglottis, increase pressure on vena cava) due to external compression of the thoracic vena cava as intrapleural pressure rises. Mechanical compression -> reduces the compliance of VC (less blood making it back to heart decreases preload)

Venous return to the right atrium is A.Decreased with skeletal muscle contraction of the legs during exercise B.Decreased by sympathetic activation of the veins C.Increases by forced expiration against a closed glottis D.Increased during inspiration

D.Increased during inspiration

A 38-year-old man has a murmur that ceases with the onset of the second heart sound. The second heart sound occurs at the onset of which phase of the cardiac cycle? Closure of the aortic valve occurs at the onset of which phase of the cardiac cycle? A.Isovolumetric contraction B.Rapid ejection C.Systole D.Isovolumetric relaxation E.Rapid ventricular filling

D.Isovolumetric relaxation S2: Marks beginning of diastole

14. In a given blood vessel, the pressure is held constant and the radius is decreased, which results in a change in blood flow. The resultant change in blood flow could also be accomplished by keeping pressure and radius constant and changing which of the following hemodynamic parameters? Decreasing compliance Decreasing blood vessel length Decreasing vascular resistance Increasing viscosity

D: Increasing viscosity Holding pressure constant and decreasing vessel radius (i.e., increasing resistance) will cause blood flow to decrease. If pressure and radius were held constant, and viscosity (thickness of the blood) increased, blood flow would also decrease.

Arterial Chemoreceptor Reflex

Decrease breathing = decrease pH from Increase in CO2 -> stimulates chemoreflex If blood pressure is within its normal range, the chemoreflex does not evoke a powerful cardiovascular response because of the predominant effect of the inhibitory arterial baroreflex. However, if blood pressure is low, generally below 80 mmHg, activation of the chemoreflex potentiates the vasoconstriction evoked by the baroreflex and helps to restore blood pressure to normal.

Decrease venous compliance: Increased volume = ___________ pressure Decreased volume = _____________ pressure

Decrease venous compliance sends more blood back to heart Increased volume = decreased pressure Decreased volume = increased pressure

Depolarization spreads from _______cardium to ________ardium Repolarization spreads from ________ardium to _________cardium

Depolarization spreads from Endocardium to Epicardium Repolarization spreads from Epicardium to Endocardium

Compliance and Venous Function Sympathetic nerve activity (vasoconstriction)(smooth muscle contraction, vein walls stiffer) results _____ venous return, _____ end diatolic volume, _______ stroke volume

Diameter of veins doesnt change much, but Sympathetic constriction of veins is an important mechanism to decrease tissue blood volume More blood to heart = more stretch = more venous return = increase end diastolic volume/preload -> Increase stroke volume (via Frank Starling mechanism) Vasoconstriction = increase in sympathetic nerve discharge (More APs)

Factors that limit Coagulation Plasminogen activated to plasmin by: (3)

Dilution due to blood flow Activation of coagulaton cascade also activates fibrinolytic cascade: Plasminogen activated to plasmin by factor XII, t-PA, u-PA => mediates fibrinolysis *plasmin regulated by a2-plasmin inhibitor

Blood Pressure vs Work Load During Exercise: Systolic Pressure: Diastolic Pressure: Mean pressure is determined by:

During exercise, systolic goes up and diastolic goes down slightly Mean increases slightly (causd by rise in CO) Pulse pressure: Pressure in arteries: Systolic - diastolic Systolic increases b/c increased stroke volume (more contraction force) Diastolic decreases b/c TPR decreases due to vasodilation in exercising muscle: Rapdi "run-off" of blood from aorta and large arteries b/n cardiac ejections

During exercise, venous return __________ because of an ____________ in the activity of the muscle venous pump. Consequently, end-diastolic volume _______________ and causes a _______________ contraction of the ventricle, in accordance with the Frank-Starling law. During exercise, cardiac sympathetic efferent activity ____________ Stroke volume __________ during exercise Finally, stroke volume can ___________ slightly because of the effect of circulating catecholamines activating beta 1-adrenergic receptors on the myocardium

During exercise, venous return increases because of an increase in the activity of the muscle venous pump. Consequently, end-diastolic volume increases and causes a stronger contraction of the ventricle Cardiac sympathetic efferent activity also increases. Stroke volume increases during exercise, reaching a maximum at 40-45% of the oxygen uptake at maximum exercise (VO2max). Finally, stroke volume can also increase slightly because of the effect of circulating catecholamines activating beta 1-adrenergic receptors on the myocardium Catecholamines cause contraction, requires ATP/energy = increase metabolism/ oxygen extraction

High Yield: During heat stress, cutaneous vasodilation leads to significant (increase or decrease) in TPR and CVP

During heat stress, cutaneous vasodilation leads to significant decreases in TPR and CVP (central venous pressure: pressure at Atrial caval junction) and cardiac preload *Decrease in systemic vascular resistance *arterial pressure decreases *Decrease central blood volume, preload, cardiac filling, stroke volume, High heat: blood to skin can reach 8 liters/minute Dilation of skin arterioles causes up to 500 mL (10% of the blood volume) to pool in the skin veins Sweating leads to dehydration and lower blood volume, which lowers central blood volume.

Impact of static vs. dynamic exercise on cardiac workload

Dynamic: We can use frank starling mechanism, preload Static: Only afterload/ increased resistance (heart works harder) So, for someone with Coronary artery disease, recommend more isometric or dynamic exercise During exercise, venous return increases because of an increase in the activity of the muscle venous pump. Consequently, end-diastolic volume increases and causes a stronger contraction of the ventricleCardiac sympathetic efferent activity also increases. Stroke volume increases during exercise, reaching a maximum at 40-45% of the oxygen uptake at maximum exercise (VO2max). Finally, stroke volume can also increase slightly because of the effect of circulating catecholamines activating beta 1-adrenergic receptors on the myocardiumCatecholamines cause contraction, requires ATP/energy = increase metabolism/ oxygen extraction

26. In control conditions, flow through a blood vessel is 100 ml/min under a pressure gradient of 50 mm Hg. What would be the approximate flow through the vessel after increasing the vessel diameter to four times normal, assuming that the pressure gradient was maintained at 50 mm Hg? A) 300 ml/min B) 1600 ml/min C) 1000 ml/min D) 16,000 ml/min E) 25,600 ml/min

E According to Poiseuille's law, flow through a vessel increases in proportion to the fourth power of the radius. A 4-fold increase in vessel diameter (or radius) would increase 4 to the fourth power, or 256 times normal. Thus, flow through the vessel after increasing the vessel 4 times normal would increase from 100 to 25,600 ml/min.

11. The diameter of a precapillary arteriole is decreased in a muscle vascular bed. An increase in which of the following would be expected? A) Capillary filtration rate B) Vascular conductance C) Capillary blood flow D) Capillary hydrostatic pressure E) Arteriolar resistance As tissue metabolism increases -> Increased Metabolite production => __________________ arteriolar resistance => ________________ blood flow

E) Arteriolar resistance 11. E) A decrease in the diameter of a precapillary arteriole would increase arteriolar resistance. The increase in arteriolar resistance would lead to a decrease in vascular conductance, capillary blood flow, hydrostatic pressure, and filtration rate.

Which of the following is most likely to cause the heart to go into spastic contraction? A) Increased body temperature B) Increased sympathetic activity C) Decreased extracellular fluid potassium ions D) Excess extracellular fluid potassium ions E) Excess extracellular fluid calcium ions

E) Excess extracellular fluid calcium ions Lots of Ca2+ surrounding the cardiac myofibrils, becuase extracellular fluid calcium ion concentration increases too much. An excess potassium concentration in the extracellular fluids causes the heart to become dilated because of the decrease in resting membrane potential of the cardiac muscle fibers.

15. Which phase of the cardiac cycle follows immediately after the beginning of the QRS wave? A) Isovolumic relaxation B) Ventricular ejection C) Atrial systole D) Diastasis E) Isovolumic contraction

E) Isovolumic contraction (followed by ventricular ejection) Right after QRS wave, ventricles begin to contract -> Isovolumic contraction occurs before the ejection phase and increases the ventricular pressure enough to mechanically open the aortic and pulmonary valves.

Which of the following capillaries has the lowest capillary permeability to plasma molecules? A.Glomerular B.Liver C.Muscle D.Intestinal E.Brain 50. Which of the following capillaries has the highest capillary permeability to plasma albumin? A) Glomerular B) Liver C) Muscle D) Intestinal E) Brain

E. Brain Skin or fat tissue has high tissue compliance while brain has low tissue compliance cause its surrounded by hard cranium. 50. Which of the following capillaries has the highest capillary permeability to plasma albumin? Liver * Albumin has slowest rate of net movement across capillary wall

An investigator is conducting a study of hypertension in an experimental animal model, wherein one renal artery is constricted with a clip to reduce blood flow to that kidney. The other kidney is untouched. Which of the following best explains the contribution of the clipped kidney to the hypertension in this experimental model? A. Aldosterone-induced sodium and water excretion B. Angiotensin II-induced renal vein constriction C. Angiotensin I-induced vasoconstriction D. Increased expression of angiotensin-converting enzyme E. Increased renin secretion

E. Increased renin secretion *most sodium moved across capillary by diffusion

A 19-year-old man severs an artery in a motorcycle accident. A bystander applies a tourniquet to stop the bleeding. When the paramedics arrive, the blood pressure of the injured man was only slightly hypotensive and his pupils were reactive. The greatest percentage of the redistributed blood volume came from which of the following? A. Aorta B. Arteries and arterioles C. Capillaries D. Heart E. Venules and veins

E. Venules and veins Veins = greatest compliance

A 24-year-old woman undergoes an annual physical examination for participation on the varsity track team at her college. While auscultating her heart sounds, the sports medicine physician instructs the woman to take in a deep inspiration. During this maneuver, he detects splitting of the second heart sound. Which of the following is the mechanism underlying this finding? A.A decrease in heart rate B.An increased left ventricular stroke volume C.Delayed closing of the aortic valve D.Delayed opening of the mitral valve E.Delayed closing of the pulmonic valve

E.Delayed closing of the pulmonic valve

ECG Changes in STEMI over time

ECG changes in STEMI over time: A. Very early (may only last few minutes) B. Most commonly seen during acute phase C. Late stage (Age indeterminate) Wider Q wave = pathologic

Ventricular Diastole

End of ejection, ventricle at minimum and fibers relax Ventricular repolarization occurs (T waves) = end of contraction and beginning of relaxation Linear velocity of blood in aorta falls (Pressure in aorta exceeds pressure in ventricle) Pressure gradient revered: Blood returns to ventricle (Pressure increased in aorta) Aortic valve closes (7): Momentum of blood causes aortic valve to bulge into ventricle, then return to normal -> Oscillation causes incusura or dicrotic notch Ventricular pressure falls rapidly, volume doesn't change (#8) b/c no valves are open = isovolumic relaxation (end marked by opening of mitral valve (9) Max atrial pressure /volume achieved, causing V wave (Exceeds ventricular pressure) AV valve opens, blood rapidly enters relaxing ventricles (rapid filling phase) Pressure in atrium falls (Y descent) but still above ventricle until ventricular contraction occurs Followed by period of reduced filling (#10) and period of further reduced filling (diastasis; 11) *At rest, 80% of ventricular filling occurs passively Exercise = more dependent on atrial filling

ESPVR

End systolic pressure volume relationship

Hemostasis: Primary Hemostasis (Platelet Plug) Enodthelium disruption exposes blood to : Activation of platelets makes them release 2 granules:

Enodthelium disruption exposes blood to von Willebrand factor (vWF) and collagen localized under endothelial layer -> Aggregation/activation of platelets: Make them sticky, shape change, release secretory granules (ADP, TXA2) = platelet recruitment/aggregation Plug crucial for micro-bleedings

Summary Slide

Essential factors regulating HR (i.e. autonomic nervous system), stroke volume (i.e. ventricular contractility and afterload), and peripheral vascular tone (e.g., locally-produced vasoactive substances, vascular wall stress, angiotensin II, the sympathetic nervous system via type a1 adrenoceptors) have to be collectively considered.

12. World class athletes such as Michael Phelps have a tremendous exercise capacity. See the stroke volume responses to exercise in four different subjects in the attached figure. The primary reason that the athlete has such a difference in stroke volume compared to the other three subjects, is that the athlete has a/an decreased afterload increased cardiac sympathetic nerve activity increased heart rate increased preload

Explanation: Athletes have a strong left ventricle and a high stroke volume. What is ejected by the LV ultimately comes back to the heart in the form of venous return. Thus a high volume of blood returning to the heart provides a high preload.Option A: Athletes typically have normal or slightly lower blood pressures, which could reduce afterload, but this is not the primary reason that stroke volume is high.Option B: Athletes typically have lower levels of sympathetic nerve activity.

Oncotic pressure (colloid osmotic pressure) vs Hydrostatic

Less albumin in blood = less ability of blood to reabsorb fluid form interstitium = build up of fluid in interstitium = edema The primary force driving fluid transport between the capillaries and tissues is hydrostatic pressure, = pressure of any fluid enclosed in a space. Pressure exerted by blood against the wall of a capillary = capillary hydrostatic pressure (CHP) (drives fluid out of capillaries and into the tissues) Fluid exits capillary -> moves into tissues, hydrostatic pressure in interstitial fluid correspondingly rises. This opposing hydrostatic pressure is called the interstitial fluid hydrostatic pressure (IFHP). Generally, the CHP originating from the arterial pathways is considerably higher than the IFHP, because lymphatic vessels are continually absorbing excess fluid from the tissues. Thus, fluid generally moves out of the capillary and into the interstitial fluid. This process is called filtration. Osmotic Pressure The net pressure that drives reabsorption—the movement of fluid from the interstitial fluid back into the capillaries—is called osmotic pressure (sometimes referred to as oncotic pressure). Whereas hydrostatic pressure forces fluid out of the capillary, osmotic pressure draws fluid back in

There are many causes of impaired cardiac function in the setting of coronary ischemia: Oxygen demand more than oxygen supply = MI

Less blood flow, Means less oxygen delivery, Means less ATP production *Decrease ATP: •Impaired dissociation of actin/myosin •Impaired Ca2+ removal from cytoplasm •Alterations in membrane potential (arrhythmia's) Acidosis: •Impairs protein conformation changes •Proton compete with Ca2+ for binding sites

49. A 70-year-old woman came to a hospital emergency department because she was experiencing chest pain. Based on the ECG shown above, what is the likely diagnosis? A) Acute anterior infarction in the left ventricle of the heart B) Acute anterior infarction in the right ventricle of the heart C) Acute posterior infarction in the left ventricle of the heart D) Acute posterior infarction in the right ventricle of the heart E) Right ventricular hypertrophy

Limb leads: R and L Chest leads: Anterior posterior Saw in V2, know its anterior A) This patient has an acute anterior infarction in the left ventricle of the heart. Pick the lead with the st elevation. In general, st elevation takes precedence in diagnosing ecgs. So, V2 is over the septal/ anterior left ventricle so the diagnosis would be acute St elevated myocardial infarction of the left ventricle. GK

____________(local or systemic) Control: Nitric Oxide

Local Control (flow mediated) Increase in flow increases dilation Increased coronary blood flow -> Increase Shear stress -> Increase NO => Vasodilation *Its like a cycle, because dilation makes the artery bigger which means even MORE sheer stress, and so on

Loss of plasma without proportional loss of red blood cells cause hematocrit to ___________ Increasing viscosity _________ velocity

Loss of plasma without proportional loss of red blood cells cause hematocrit to Increase Increasing red cell hematocrit increases relative viscosity and decreases velocity Viscosity inversely related to reynolds number More thin blood = more turbulent

17. A 26-year-old man is brought to the emergency department by ambulance 30 minutes after being shot in the leg. He is unconscious and appears markedly pale. His pulse is 120/min, respirations are 16/min, and blood pressure is 80/60 mm Hg. Compared with a healthy adult, which of the following changes would be expected in this patient? Increase or decrease in Arterial barorecptor firing rate/ Baroreceptor afferent activity Left ventricular end diastolic volume CO Venous Return

Low BP = less stretch = less firing of baroreceptors Rapid pulse and low BP: Decreased LV end diastolic volume (Preload) b/c less blood coming in to heart -> Cardiac output would decrease (HR X SV) Significant blood loss in this subject would be accompanied by a decrease in LV end-diastolic volume and cardiac output. *Baroreceptor reflex fine tunes arterial pressure during exercise, but reflex does not adjust pressures to its resting value, it adjusts them to new higher level proportional to exercise intensity

Lymph circulates to LN through ________ (afferent or efferent) vessels *Lymph fluid contains plasma, water, amino acids, protein, cellular debris, hormones, bacteria, cancer cells...

Lymph circulates to the lymph node via afferent lymphatic vessels Filtration = movement from capillary into interstitial space We want to keep most fluid in capillarues Build up in interstitial space = edema Usually very little protein/albumin in interstitial space -Water follow proteins (proteins draws water out) *ALWAYS PRESSURE DROP ACROSS RESISTENCE *leakage of protein into interstitial fluid = interstitial fluid accumulation = increase in interstitial hydrostatic pressure *When the net flow of fluid into the interstitial space exceeds lymph flow, the interstitial space swells up = edema Higher capillary pressure = more filtration

Total Peripheral Resistance ___ = __ X ___ What happens with hypertension? In exercise: CO ____________(increases or decreases) and TPR _____________

Mean Arterial Pressure (MAP ) = CO X Total Peripheral Resistance (TPR) CO stays same with HTN, so peripheral resistance must be increased Resistance is the opposition to flow

Resistance Exercise:

Mean pressure increases due to an increase in CO. Mean pressure increase proportional to muscle mass and % of maximal force TPR may actually increase because, during strong, isometric contractions, the contracting muscles squeeze down on their own blood vessels, increasing resistance! More importantly, metabolites accumulate in the muscle and activate muscle afferents that increase sympathetic activity. Baroreflex reset / regulate arterial pressure at higher level during static exercise than dynamic exercise. Higher pressure needed during static exercise to force blood flow through the compressed blood vessels.

Frontal Leads measure:

Measure frontal place: Up -> down, left -> right Everything from - to +

Metabolic factors that enhance cerebral blood flow (decrease cerebral resistance) include__________________ in carbon dioxide, hydrogen ion (decreased pH), and adenosine.

Metabolic factors that enhance cerebral blood flow (decrease cerebral resistance) include increases in carbon dioxide, hydrogen ion (decreased pH), and adenosine. Adenosine = most important controller of increasing coronary blood flow Increased plasma adenosine concentration causes arteriolar vasodilation during exercise

Rewatch: How does modifying precapillary or postcapillary resistance impact capillary pressure? Compare the "dotted" vessel to baseline and determine if capillary pressure increased or decreased? (slide 46, lecture 19)

Middle Increased Bottom: Decrease

11. What happens at the end of ventricular isovolumic relaxation? A) The A-V valves close B) The aortic valve opens C) The aortic valve closes D) The mitral valve opens E) The pulmonary valve closes

Mitral valve open 11. D) At the end of isovolumic relaxation, the mitral and tricuspid valves open, which is followed by the period of diastolic filling. Aortic valve closed, now we are dumping fluid into ventricles

Mitral Stenosis *Note: all L sided disease will back up into lungs if left untreated

Mitral valve supposed to be open during diastole -> lets blood across opening = decreased preload -> Decreased SV *Impaired LV filling Increased LA and pul. pressures Diastolic rumble with a presystolic accentuation (just before A wave) Murmur intensity depends on pressure gradient across mitral valve: Delta P = LA pressure - LV pressure During exercise, patient can't increase increase CO much at all, so they cant increase SV much (cant get blood to left ventricle) *Olympic athletes have MASSIVE stroke volume

Function of veins: Effects of Venoconstriction (4) Increase or decrease: Mobilization Capacity Transit Time Resistance

Mobilization: Increase Capacity: Decrease capacitance (more rigid) Transit Time: Decrease (goes faster) (= more pressure )(More blood back to heart = increased preload) Resistance: Increase Veins get less compliant, need to provide more O2 to be oxygenated

Splanchnic renal blood flow athlete vs non-athlete

More fit you are, the longer it takes for you to dip in to the splanchnic renal blood flow (you dont need to pull blood from non-critical organs) *Weaker heart = sooner you pull blood from noncritical organs *Workload at which sympathetic activation and vasoconstriction in non-critical organs was "activated".

Capillaries and Nutrient Exchange The vessels open and close = vasomotion: Due to cyclic contraction and relaxation of precapillary sphincters of arterioles Pinocytosis: large proteins Diffusion and bulk flow account for most capillary exchange Fenestrations = space b/n enodthelial cells

More metabolites produced with exercise = more capillary beds opened (recruit more) = greater dilation of sphincters = more blood/oxygen to skeletal muscle Exercise = increase in metabolites, decrease in closed sphincters If vein gets bigger, more fluid can leave = decrease in hydrostatic pressure

Normal vs Abnormal P-waves

More muscle = higher amplitude Mitral stenosis: second half (hump) of P wave enlarges (L atrium enlarged (LAE)) Hypertrophy of right atrium (enlargement: (RAE) = initial depolarization of p wave gets larger (greater amplitude)

Internodal tracts

More rapid conduction of depolarization (1meter/sec) Anterior interatrial band: Bachman's bundle -> heads to L atrium 3 small bands (anterior lateral, posterior) curve through R atrial walls, terminate in AV node

Early Systole: Mid Systole Early Diastole: Late Diastole: Most myocardial blood flow occurs during:

Most myocardial blood flow occurs in early diastole Coronaries in walls of LV During Systole, the walls are contracting, squeezing blood flow in walls to 0

Conduction velocity over hearts conduction system Fastest: Slowest:

Fastest: Purkinje fibers (4 m/s) Slowest: AV node, atrial muscles, ventricular muscles (0.5 m/s)

Filtration vs Absorption Which is stronger: Capillary osmotic or hydrostatic pressure

Filtration -> out of capillary into interstium Absorption à out of interstium into capillary Kf: Constat, filtration coefficient- measure of membranes permeability to water. Capillary osmotic is not as strong as capillary hydrostatic

Determine Ventricular axis

Find most isoelectric point, go 90 degrees from there (90 degrees from 0 is 90)

Coronary Blood Flow Cycle Flow lower during : (systole or diastole) Flow maximal in: Blood flow to R heart side highest in _________

Flow lower during systole because of mechanical compression of intramuscular coronary vessels. Flow maximal early in diastole as the heart is relaxing, and then it falls as aortic pressure declines. R side pressure not as high = not as loud At * (third circle): Aortic valve closes (shortly after dicrotic notch): Isovolumetric ventricle relaxation: begins diastole: Loosens pressure on L coronary artery Blood flow to R heart side highest during systole, but coronary blood flow highest in diastole Blood leaves LV into aorta into aorta

PR Interval __ msec to reach AV node •Delay through node of __ msec •Penetration through fibrous skeleton in His bundle takes __ msec •Total of ___ msec delay from SA nodal exit before excitatory signal gets to ventricular muscle *Note: Atria =Low voltage b/c not much muscle tissue

From beginning of atrial depolarization to beginning of ventricular depolarization (0.12-0.2 seconds) •30 msec to reach AV node •Delay through node of 90 msec •Penetration through fibrous skeleton in His bundle takes 40 msec •Total of 160 msec delay from SA nodal exit before excitatory signal gets to ventricular muscle

Greater volume = __________ pressure Smaller volume = __________ pressure

Greater volume = decreased pressure Smaller volume = increased pressure *Diaphragm pulled down on inhalation = increase in volume = decrease in pressure

Determinants of Diastolic Arterial Blood Pressure (2)

HR (HR increase = increase inflow, decrease outflow) Peripheral resistance *Decrease in volume = decrease in pressure *A compliant vessel does not resist stretch

Junctional (Escape) Rhythm ECG: Whats missing?

HR of 50 (No P Waves and Normal QRS morphology) No p-wave, normal QRS SA node not firing AV node taking over

The administration of atropine to a healthy subject would cause their resting heart rate to resemble the resting heart rate of which subject in the figure?

Heart transplant: These patients have no parasympathetic activity Atropine blocks Acetylcholine from binding = increase HR

Horizontal (chest) and frontal (limb) plane leads Limbs leads: electrical vector of ventricular depolarization

Horizontal Depolarization first goes towards V1 -> positive deflection Then depolarization turns towards left atrium (away from V1) -> small negative deflection in V1 (not always seen) V5 detects depolarization traveling towards it = positive P waves Frontal Plane: Atrial vector pointed down and left (60 degrees) -> towards lead II *P wave always + in lead II (in sinus rhythm) *P wave also usually positive in aVL, -aVR, aVF, I, V4, V5, V6

Cushing's Reflex Dead w/o treatment

Hypotensive shock (BP <60 mmHg) or cerebral occlusion (stroke, head trauma, tumor) leads to decreased brain perfusion Decreased O2/ hypoxia (and increased CO2 (which dilates, so we want to constrict)) to pons and medulla powerfully activates sympathetic autonomic control centers -> severe rise in blood pressure (>200 mmHg) -> last ditch effort by body to restore cerebral blood flow -> increases microvasculature pressure. (blood flow improves, but increased hydrostatic pressure exacerbates cerebral edema and increases intracranial pressure (ICP)). HTN Bradycardia Irregular breathing

Effect of Intracranial Pressure on Cerebral Blood flow ICP: Increased by: Effect of increased ICP ___ = ____ - CPP CPP = ___ - ___

ICP = intracranial pressure: Pressure in fluid filled space b/n cranium and brain Increased ICP decreases transmural pressure (inside minus outside pressure) of blood vessels (particularly veins), which can cause vascular collapse, increased resistance, and decreased blood flow. Therefore, the effective cerebral perfusion pressure (CPP) is mean arterial pressure (MAP) minus ICP. CVP, central venous pressure.

Core temp increase = Cutaneous Blood vessels (dilate or constrict), contributing to __________ (increased or decreased ) TPR and ____________ volume of blood in skin veins

If core temperature increases, cutaneous blood vessels dilate, contributing to decreased TPR and also increasing volume of blood in skin veins. Heat stress = loss of body fluid -> decreases blood volume. *hotter you get = more dilated skin arterioles get = lower BP gets *Passive vasodilation = Releases less norepi: normally causes constriction, but now we have less

26. If the Purkinje fibers, situated distal to the A-V junction, become the pacemaker of the heart, what is the expected heart rate? A) 30/min B) 50/min C) 60/min D) 70/min E) 80/min

If the Purkinje fibers are the pacemaker of the heart, the heart rate ranges between 15 and 40 beats/min. .

Increased Capillary wall permeability: Immune response leading to inflammation

Immune reactions that cause release of histamine and other immune products Toxins Bacterial infections Vitamin deficiency, especially vitamin C Prolonged ischemia Burns Inflammation = release of vasodilators, like histamine and cytokines

Edema Formation During Elephantiasis Cause:

Impaired Lymphatic Drainage •Parasitic tropical disease •Transmitted by black flies and mosquitos •Elephantiasis is a condition of extreme edema that occurs when lymph vessels become blocked by filarial worms.

Effect of Lymph Node removal Sprained ankle example

Impaired lymphatic drainage can't remove fluid from interstitium Therapies = massage, Compression = Pressure increases interstitial hydrostatic pressure, which opposes the movement of fluid from the capillaries Sparined ankle and starling forces: Elevate: less fluid coming down into leg = decreasing hydrostatic pressure Ice = contraction of arterioles Wrap it: Increase interstitial hydrostatic pressure

In exercise, we ___________ CO but TPR _____________

In exercise, we increase CO but TPR decreases Increased workload: O2 consumption increases, but peripheral resistance drops (resistance of ALL of our arterioles, but only our arterioles to our skeletal muscles are getting bigger, other arterioles are getting smaller. We are looking at the overall) (because its the skeletal muscles getting bigger) -Rise in CO causes BP and HR to increase SV decreases because there is less time to fill If you can't increase cardiac output (Heart disease) then you can't fill dilated arterioles as well = exercise intolerance due to BP drop

Usual Rate of paper speed 5 big boxes = _______ msec "big box" = _____ msec 1 "small box" = _______ msec X-axis = Y-axis =

Paper speed: 25 mm/sec Divided into heavy lines every 5 mm 5 big boxes = 1 second (1000 msec) (each box = .2 seconds (200 msec) For Voltage (vertical measurement) one "small box" = 0.1 mV, therefore there are 0.5 mV in one "big box" and 1 mV in two "big boxes"Y axis X -axis = time Y- axis = millivolts

Valve structure ad heart sounds Papillary muscles First sound (S1): Second (S2) sound: Healthy heart valves silent when they open, sound comes from when they close

Papillary muscles help keep valves closed while pressure is building up (prevent prolapse) S1: Caused by closure of mitral and tricuspid valve (AV Valves) S2: Closure of aortic (A2: closes first) and pulmonic (P2: second) valves *Normally A2 Precedes P2 (left ventricular systole ends before right)

Fastest to slowest conduction velocity

Park (purkinje) At (atria) Venture (ventricles) Avenue (AV node)

S4 Heart Sound (low frequency sound) In rushing of blood into _________ from ________ contraction

Pathologic Not valvular origin Coincident with atrial contraction during last part of filling In rushing of blood into ventricles from atrial contraction Produced when atrium contracts against a stiff ventricle like in concentric hypertrophy. *Long term high BP or aortic stenosis Wall thikens,, walls less distensible/compliant

Peak coronary blood flow occurs during ___________________________,

Peak coronary blood flow occurs during early diastole, which begins as the aortic valve closes. Of the five answer options, line C represent the earliest part of diastole. Systolic pressure peak at B

Atrial Enlargment Peaked P wave = over _________ mm

Peaked P wave = over 2.5 mm

Bundle of His Conduction Velocity: Divides into:

Penetrates through fibrous skeleton of the heart •Conduction velocity ~2 meters/second Below membranous septum at crest of interventricular septum Divides into L and R bundle branches

Pharmacologic vs physiologic doses of epi

Physiologic levels of epinephrine act on b2-receptors and induce vasodilation (in skeletal muscle) Pharmacologic levels of epinephrine act on a-receptors and induce vasoconstriction Increased levels of epi overcome B2 dilation and cause constriction Low dose binds B2 (fits better) BASICALLY: Low dose = vasodilation, high/pharmacologic dose = vasoconstriction

Hemodynamic Response to Epinephrine and Phenylephrine Epinephrine is an agonist for: (2) Phenylephrine is an agonist for: (1)

Physiologic levels of epinephrine act on b2-receptors and induce vasodilation (in skeletal muscle) Pharmacologic levels of epinephrine act on a-receptors and induce vasoconstriction Increased levels of epi overcome B2 dilation and cause constrictionLow dose binds B2 (fits better) BASICALLY:Low dose = vasodilation, high/pharmacologic dose = vasoconstriction Epinephrine is an agonist for: •cardiac b1 receptors •vascular a1 and b2 receptors Phenylephrine is an agonist for: •vascular a1 receptors *Epi binds B1 -> increase HR and CO? BUT baroreflex = Increased BP< epi binds baroreceptors => activates PNS, decrease SNS = Decreased CO (Baroreceptor superceded hormonal effect)

Routes of Exchange Across Capillary Wall

Pinocytosis: large proteins Diffusion and bulk flow account for most capillary exchange Fenestrations = space b/n enodthelial cells

Platelet Plug: 1. vWF 2. Collagen and thrombin 3. Conformational change in GPIIb/IIIa glycoprotein complex: starts to bind fibrinogen 4. ADP release from dense granules 5. Release ____ 6. _ granule releases proteins, _-_________ localized to cell membrane 7. Factor __ Receptor Unmasked

Platelet Plug: 1. vWF 2. Collagen and thrombin 3. Conformational change in GPIIb/IIIa glycoprotein complex: starts to bind fibrinogen 4. ADP release from dense granules 5.Releases TXA2 that binds to TXA2 receptors of nearby dormant platelets and activate them (suppressed by NSAIDs) 6.The α-granule releases proteins (platelet factor IV, thrombospondin, fibrinogen, and factor V) contribute to hemostasis •P-selectin localized to membrane, interacts with leukocytes and endothelium 7. Factor Xa Receptor Unmasked

Hemostasis: Clot Stabilization

Polymerized fibrin + platelet aggregates undergo contraction -> form solid, permanent plug Counter regulatory mechanisms (tissue plasminogen activator, t-PA) limit clotting to injury site, eventually cause resoprtion/repair

Preload/Afterload

Preload affects the amount of blood going into ventricle. Afterload is the systemic resistance after leaving the heart. If you start out with less, then you have a smaller preload next round = decreased stroke volume

A 66-year-old female presents to the emergency department with altered consciousness and fever for the past 12-hours. She is found to be in septic shock, with a blood pressure of 62/40. She is administered phenylephrine. Following administration of this drug: Pressure at which aortic valve opens (dec or inc) Venous Return (Dec or inc)

Pressure at which aortic valve opens Increases Venous Return decreases (less blood returning to heart/ more blood trapped on arterial side b/c of increased TPR) Start w/ low BP: Give phenylephrine (alpha-adrenergic 1 receptor agonist) = increased total peripheral resistance and BP Increased BP means pressure required to open aortic valve would increase

Pulmonary vs Systemic Pressure

Pressure higher on the left (systemic) (100 mmHg vs 15 mmHg on right (pulmonary)) Takes more pressure to pump through something smaller, like an arteriole

Afterload MI results in _ radius, _ wall thickness, _ wall stress, _ afterload (Increase of decrease for each)

Pressure the heart works against to eject blood: Ventricular wall stress that occurs during systole Diastole (aortic valve shut) Ventricular pressure must exceed aortic pressure to move blood forward (systole) The law of Laplace states that wall stress, or tension (σ), is proportional to pressure (P) and radius (r) and inversely proportional to wall thickness (h).

Causes of Increased capillary pressure Starling forces

Pulmonary edema increased by Increased pulmonary capillary hydrostatic pressure Excessive kidney retention of salt and water -Acute or chronic kidney failure -Mineralocorticoid excess High venous pressure and venous constriction: Heart failure Venous obstruction Failure of venous pumps 2. Decreased plasma proteins Loss of proteins in urine (nephrotic syndrome: Protein peed out, levels go down)) Loss of protein from denuded skin areas Burns Wounds Failure to produce enough proteins Pregnancy- Synthesis of plasma proteins by the mother does not keep pace with the expanding plasma volume and fetal nutritional demands Liver disease (e.g., cirrhosis) Serious protein or caloric malnutrition

Pathologic split of S2 4 causes:

Pulmonic stenosis (narrowing of pulmonic valve) Right ventricular failure (delayed closure of pulmonic valve) Pulmonary hypertension (longer to move blood: Slowing of pulmonary valve = splitting) Right bundle branch block *Caused by anything that delays emptying = delays closure of valve

Poiseuille's Law (Q = blood flow)

Q = change in pressure X radius^4/ LXV Just know resistance to blood flow varies in to 4th power of radius (small change in diameter = big changes in relative flow) Smaller tube = less blood volume but faster speed VOLUME of blood flow is how MUCH blood flows past a point in a given period of time

Measuring Cardiac Activity QT: shouldn't be more than _____ for females, ____ for males PR Interval: QRS Complex:

QT: shouldn't be more than 460 for females, 420 for males PR Interval: 160 QRS Complex: Time it takes for the ventricle to depolarize: 80-100 (over 100 = block) *Atrial depolarization, AV node depolarization, His bundle depolarization *Each box = 200 msec (contains 5 boxes that each contain 40 msec)

QTc Calculation Methods Prolonged QT has what effect on membrane? (depolarize or repolarize) The R to R interval on an ECG is 1.5 seconds. What is the ventricular rate? A. 30 B. 35 C. 40 D. 45 E. 50

QTc = QT + 154(1- RR) [Framingham method] Upper normal Men: 450 msec Women: 460 msec (When the QT is more than half of the RR interval, it is usually prolonged!) Prolonged QT = calcium in -> depolarize membrane 60/ RR seconds = Ventricular rate

A 60-year-old woman had an ECG recorded at a local emergency department after an automobile accident. Her weight was 70 kg (154 lb), and her aortic blood pressure was 140/80 mm Hg. What is the mean electrical axis calculated from standard leads I, II, and III shown in the woman's ECG? A) −90 degrees B) −50 degrees C) −12 degrees D) +100 degrees E) +170 degrees What is the heart rate using lead I for the calculation? (estimated)

R axis deviation: QRS + in leads II, III and aVF and - in I L axis devation : QRS + in lead I, aVL, negative in II, III, and aVF B: -50 degrees is the only reading really in the L-axis deviation range Between 75-100

Cutaneous Circulation Range from: Primary Function: Apical vs non-apical skin *Blood vessels only reach dermis...epidermis does not have blood supply 2 Types of sympathetic nerves in non-apical skin

Range from 6mL/ min to 8 LITERS/min *At rest only 2% of CO, up to 60% during severe heat stress (huge vasodilatory capacity) Function: Maintain body temp Cold = Constrict Hot = dilate to lose heat Apical skin- present in nose, lips, ears, palms, soles Non-apical skin- everywhere else: no AV anastomosis, but has superficial capillaries 2 types of sympathetic nerves: -Norepinephrine -> vasoconstriction -Acetylcholine -> vasodilation ØTonic sympathetic tone at rest

Hyperventilation

Rapid exhale blos off more CO2 = cerebral blood flow drops Breathing into paper bag = inhale more CO2 back in = Cerebral dilation

A 36-year-old male is seen in the emergency department for extreme weakness and fatigue, shortness of breath, abdominal distension and rapid heart rate. The patient indicates that he felt completely normal just 36 hours ago. Physical exam reveals a blood pressure of 85/60 mmHg (normal: 120/80 mmHg). An echocardiogram reveals an ejection fraction of 35% (normal: 55-65%). A drug that decreases which of the following would improve this patient's symptoms? Blood pressure Contractility Intracellular Ca2+ Intracellular Na+ Na+-K+-ATPase activity

Rapid onset , low blood pressure and ejection fraction are indicative of acute heart failure. Blocking sodium-potassium ATPase activity with digoxin increases intracellular sodium levels in cardiac myocytes, which reduces the efflux of calcium via the sodium-calcium- exchanger, thereby leading to increased intracellular levels of calcium = increase contractility. *Increase blood pressure and ejection fraction. Wrong: D: Lowering intracellular sodium would increase sodium-calcium-exchanger activity and decrease intracellular calcium and further impair contractility.

Active Hyperemia and reactive hyperemia Increased afterload/ HR/ Contractility = __ myocardial metabolism = _ myocardial PO2 = Coronary ____________ (vasodilation or constriction)

Reactive hyperemia: If blood supply cut off then restored, flow increases above normal *comes from completely restricted blood flow

ECG Frontal vs Transverse Plane (axis of heart)

Records time dependent changes in electrical activity records the Direction of Cardiac Electrical Activity

The Axis of the Electrical Activity Changes as different areas of the Heart Depolarize

Red is right, purple is left (base) Waveforms are swinging around from septum down to apex then up to base , so looks backwards when its going up towards base Waveform usually down and to the left

Extrinsic Control: Cardiac Sympathetic Neural Control a1 receptors release _________ causing _________ (vasoconstriction or vasodilation) B1 Receptors release _________ causing _________ (vasoconstriction or vasodilation)

Release of nitric oxide (from B1?), induced by shear stress of increased coronary flow -opposes α1 adrenergic vasoconstriction limiting potential reduction in myocardial perfusion during augmented sympathetic drive Heart disease = decreased CO output = decreased BP so we increase peripheral resistance using symp activity = excess symp activity *Now BP maintained primarily by symp. activity (vasoconstriction)

Right Axis Deviation: QRS (+ or -) in II, III, AVF and (+ or -) in I Left Axis Deviation: QRS (+ or -) in I, AVL and (+ or -) in II, III, and AVF

Right Axis Deviation: QRS positive in II, III, AVF and negative in I Left Axis Deviation: QRS positive in I, AVL and negative in II, III, and AVF

Left and Right Bundle Branches Depolarizes in _ to _ direction Conduction velocity _______ (fast or slow) APs and __________ gap junctions (few or many)

Run along sides of Interventricular septum Depolarizes septum first (L to R direction)(bottom of heart = left ventricle)(compare to SA node which goes from R to L) Conduction velocity same as bundle of His (2m/s) Fast action potentials and lots of gap junctions From Bundle of His, to Purkinje fibers

After __ node initiates an action potential there is a specific sequence and timing for conduction to the rest of the heart What is the correct order AV node SA node atrium His-Purkinje system ventricles

SA node (top right)(spontaneous depolarization (from up to down, right to left ) - initiates AP) Atria and atrial internodal tracts (4 total, 1 left, 3 right) •AV node •Bundle of His •Purkinje system (Bundle branches) •Ventricles •SA nodal discharge drives ventricular response in 1:1 ratio (deviation = blockage) -All SA discharges elicit ventricular depolarization (rate of 60-100 beats/min)

Afterload PV Loop If arterial pressure or resistence is increased: Stroke volume: End systolic volume (Return of blood to heart will initially not change) End Diastolic volume Fibers length? Ensuing stroke volume

SV and afterload = inverse relationship High pressure but lower stroke volume Pressure/resistence increased = Stroke volume: decreased End systolic volume (volume of blood remaining in heart): Increased *Seen in aortic stenosis (Return of blood to heart will initially not change) End Diastolic volume: increased Fibers length? Stretched more Ensuing stroke volume ???

Serum

No blood cells, fibrinogen, lacks most clotting factors Can't clot = low platelets *plasma if serum before stuff clots out of it

Sympathetic neurons: ________________ stimulates __ receptors on myocytes Increased: Chronotropism Dromotropism Inotropism Lusitropism What does each mean? Parasympathetic Neurons: ______________ activates ________ receptors on myocytes One main effect What is one place where there is no PNS Input

Norepinephrine, stimulates B1 receptors on myocytes •Increased Chronotropism (Rate) (think chronological) •Increased Dromotropism (Conduction) •Increased Inotropism (Contractility) •Increased Lusitropism (Relaxation) PNS Neurons: Acetylcholine: Activates Muscarin M-2 receptors on myocyte Main effect = negative chronotropism (rate) NOTE: Parasympathetic input to SA node, atria, AV node(Not to Ventricles) Sympathetic input to all areas *PNS DOMINATES at rest *one has to decrease (vagal or SNS) for the other to increase •Sympathetic: Paravertebral Ganglia T1-T5: Atria, Ventricles, Conduction SystemParasympathetic: Vagus Nerves: SA and AV nodes (minimal effect on ventricles)

7. In a resting adult, the typical ventricular ejection fraction has what value? A) 20% B) 30% C) 40% D) 60% E) 80%

Normal: 55-65 Correct answer = D

Myocardial Oxygen Consumption, Work and Coronary Blood Flow

Olympic athletes = more workload ability b/c they have increased SV = don't have to increase other stuff as much (same amount of ATP, but they can do more with it)

On an ECG, a wave of (positive) Depolarization heading for a lead results in a ___________ (positive or negative) deflection A wave of (positive) Depolarization heading away from a lead gives a _____________ deflection In Repolarization, a wave (negative) heading towards the lead gives a ___________ deflection A wave of (negative) Repolarization heading away from the lead gives a ____________ deflection

On an ECG, a wave of (positive) Depolarization heading for a lead results in a positive deflection A wave of (positive) Depolarization heading away from a lead gives a negative deflection In Repolarization, a wave (negative) heading towards the lead gives a negative deflection A wave of (negative) Repolarization heading away from the lead gives a positive deflection

Heart Sounds: S3 In rushing of blood into ____________ in ________ part of __________

Origin not valvular Just after opening of AV valves during rapid filling of compliant (thin walls) ventricle In rushing of blood into ventricles in early to middle part of diastole •Low frequency vibration •Normal finding in children and young adults •In older adults, occurs with volume overload (ventricular walls become thinner) -> sign of cardiac disease

Impairment of Baroreflex and Orthostatic Hypotension Reflex response to standing:

Standing: Blood pools in legs = less coming back to heart = less stretch Blood pools in veins = less preload, less CO, less BP, then normally baroreflex mediates contraction thanks to ANS, but vascular changes/ poor diet decrease elasticity (scletoric aorta) No contraction = les cerebral perfusion -> "light headed) CVP decreases when standing becuase gravity pulls blood down to legs*decreases right ventricular filling pressure (preload) = decrease SVLeft ventricular SV also falls b/c of reduced pulmonary venous return/decreased left ventricular preload= Decreased CO and MAPWhen stand, barorecptor reflexs restore arterial pressure, needs increased systemic vascular resistance (sympathetic mediated), decreased venous compliance (due to sympathetic activation of veins), decreased stroke volume (due to decreased preload), and increased heart rate (baroreceptor-mediated tachycardia). Problems with this system = orthostatic hypotension = edema in legs Lying down: Increase preload, SV, CO (more even blood distribution to heart)

Valvular Disease Stenosis and Regurgitation (valvular insufficinecy) Stenosis increases __________load Regurgitation increases ________load *Each type of valve disease has its own distinct murmur

Stenosis: Narrowing: Harder for blood to get through, requires more force/pressure = more work makes it thicker over time *increases Afterload Regurgitation: Leaky valve *Increases preload * In aortic valve insufficiency blood regurgitates from the aorta into the left ventricle after ventricular ejection.

Isolated Systolic HTN with aging

Stiffer arteries BP increases from birth (After 50, systolic increases at greater rate) *A compliant vessel does not resist stretch

Renin-angiotensin-aldosterone system Dehydration leads to: __ Blood volume __ BP Reflex __ in symp nerve activity

Stimuli for Renin release: Decrease BP, Incresaed renal sympathetic nerve activity, decreased NaCl to macula densa Dehydration: •Decrease blood volume •Decrease blood pressure Reflex increase in symp nerve activity (Increase Na+ and H2O reabsorption)(vasoconstriction) Vasopressin tells kidney to reabsorb water Within afferent juxtoglomerular cells secrete renin (decreased BP stimulates renin release) Liver releases angiotensiogen Renin is a proteolytic enzyme that is released into the circulation by the kidneys. Its release is stimulated by: 1.sympathetic nerve activation (acting through β1-adrenoceptors) 2.renal artery hypotension (caused by systemic hypotension or renal artery stenosis) 3.decreased sodium delivery to the distal tubules of the kidney. Increase in blood osmolarity stimulates vasopressin release

Stroke volume and Ejection Fraction If volume in ventricle prior to contraction is 75 mL (diastole) and the volume after contraction is 50 ml (systole), what is SV and EF?

Stroke Volume: Volume of blood ejected during 1 cardiac contraction Ejection fraction: % of blood in ventricle at end of diastole that is ejected with each stroke (Stroke volume - end diastolic volume) SV = 25 ml Ejection fraction = Stroke Volume 25 ml/end diastolic volume 75 ml = 33% Normal Resting EF = 55-65%

A 48-year-old male is seen by his primary care physician with chief complaints of weakness, fatigue and shortness for breath, all of which have persisted for 3 days. On physical exam he is diaphoretic, blood pressure is 85/55 mmHg and heart rate is 110 bpm. Echocardiography detects left ventricular enlargement and ejection fraction is 37%. The physician immediately gives dobutamine, a B1-adrenergic agonist. Which of the following measures of cardiac function would increase when compared to immediately before administration of the drug? Right atrial pressure End-diastolic volume Stroke volume Ventricular filling time

Stroke volume

Summarizing Pressure-Volume Loops Stroke volume and afterload are __________ related Two ways to change stroke volume:

Stroke volume and afterload are inversely related Two ways to change stroke volume: •Preload •Contractility

Series vs Parallel Resistance *Distribution of CO changes b/n rest and strenuous exercise (more to muscle in exercise, less to visceral organs via vasoconstriction)

Series resistances: •E.g., artery -> arteriole-> capillary-> venule-> vein Parallel resistances: •E.g., brain, kidney, liver, lower limbs are all connected in parallel The total resistance of the system arranged in series is equal to the sum of the individual resistances Modifying vascular resistance in one organ or tissue redirects that blood flow to other organs or tissues

Sinus Tachycardia

Sinus Tachycardia with PAC's (Pre atrial contraction) (5th & 8th beats)

AV Nodal depolarization

Slow conduction velocity (allows ventricular filling from atrial contraction) •0.05 meters/sec (vs 0.5 meter/sec atrium -Limits frequency of impulses traveling to ventricles in case of too fast atrial rate Fewer gap junctions = fewer ions can go through = less rapid depolarization? Slow secondary to calcium based AP in AV nodal cells? Cell to cell conduction velocity reduced secondary to reduced slope of phase 0

Naming Waveforms: _ Wave: Atrial depolarization _ Wave: Ventricular depolarization _ Wave: Ventricular repolarization _ Wave: Etiology uncertain, present with hypokalemia?

P wave: Atrial depolarization QRS: Ventricular depolarization T wave: Ventricular repolarization U wave: Etiology uncertain (little bump after T wave) NOTE: atrial repolarization not seen on ECG (hidden by QRS)

Why ST elevation in Transmural ischemia?

PAY ATTENTION TO THE ELECTRODE Here, the current is going away from the lead, in subendocardial ischemia, the current was going towards the electrode Why ST elevation: Ischemic region generates current travelling away from lead, causing baseline voltage to be depressed.With all LV depolarized, the ST reads true zero (elevated), then with repolarization, the baseline is depressed from current going away from lead Dying tissue = depolarized Larger infarct = more leads showing problem

Sinus Rhythm Bradycardia

PR ~ 160 msec QRS ~ 80 msec HR ~ 46 QT ~ 460 msec

ECG Practice

PR ~ 280 msec QRS ~ 80 msec QT ~ 460 msec HR ~ 58 Possible U wave Sinus Rhythm with First Degree AV Block (PR> 200msec) = first degree heart block

PR: ________-______ msec QRS: ________-______ msec QT: ________-______ msec

PR: 100-200 msec QRS: 70-110 msec QT: 460 msec (upper limit for females)

Carotid Sinus Massage to treat Paroxysmal Supraventricular Tachycardia (PST)

PST: Decreases time for ventricle refill = increased HR *Less blood to pump = decreased BP Massage Stretches Baroreceptors: actually ends up increasing BP

Equation for total peripheral resistance (TPR) 63. A 60-year-old man has a mean arterial blood pressure of 130 mm Hg, a heart rate of 78 beats/min, a right atrial pressure of 0 mm Hg, and a cardiac output of 3.5 L/min. He also has a pulse pressure of 35 mm Hg and a hematocrit of 40. What is the approximate total peripheral vascular resistance in this man? A) 17 mm Hg/l/min B) 1.3 mm Hg/l/min C) 13 mm Hg/l/min D) 27 mm Hg/l/min E) 37 mm Hg/l/min 27. A 50-year-old woman has a renal plasma flow of 600 ml/min and hematocrit of 50. Her arterial pressure is 125 mm Hg and renal venous pressure is 5 mm Hg. What is the total renal vascular resistance?

TPR = (arterial pressure - right atrial pressure) / Cardiac output OR TPR = (mean arterial pressure - mean venous pressure) /CO CO = HR X SV BP = CO x TPR E) Total peripheral vascular resistance = (arterial pressure − right atrial pressure) ÷ cardiac output. In this example, total peripheral vascular resistance = 130 mm Hg ÷ 3.5 l/min, or approximately 37 mm Hg/l/min. Example 2: 27. B) Vascular resistance is equal to arterial pressure divided by blood flow. In this example, arterial pressure is 125 mm Hg, venous pressure is 5 mm Hg, and blood flow is 1200 ml/min ( plasma flow/hematocrit). Thus, vascular resistance is equal to 120 divided by (600/.50 or 1200), or 0.10 mm Hg/ml/min.

9. A 59-year-old male presents to the doctor's office with chief complaints of fatigue, general weakness and swelling in his feet and ankles over the past threemonths. Physical exam shows blood pressure 95/70 mmHg, 3+ edema in the lower extremities and jugular venous distension. Echocardiography shows wall thickening in both the right ventricle and atrium, while left ventricular size and function appear normal. What is the most likely cause of lower extremity edema in this patient? Impaired lymphatic drainage Increased capillary hydrostatic pressure Decreased capillary oncotic pressure Decreased cardiac output Decreased interstitial hydrostatic pressure Increased interstitial oncotic pressure

The hypertrophy of the right ventricle and atria would cause pressures on the venous side to be elevated. This is supported by the jugular venous distension. These higher central venous pressures oppose the flow of blood from the systemic capillaries and veins toward the heart, thereby causing the hydrostatic pressure in the systemic capillaries to rise. Increased capillary hydrostatic pressure increases filtration, and once the appearance of fluid in the interstitium exceeds the capabilities of the lymphatic system to remove it, edema follows. Indeed cardiac output would be decreased. It is this decrease that causes blood to backup and capillary hydrostatic pressure to rise.

The muscle and respiratory pump increase __________ return, which promotes cardiac filling (during the (shortened or lengthened) ____________(diatolic or systolic) time), and thereby helps to sustain an elevated _____________________.

The muscle pump and respiratory pump increase venous return, which promotes cardiac filling (during the shortened diastolic time), and thereby helps to sustain an elevated cardiac output.

The ____________ valve is heard in the 2nd intercostal space on the left High pitch sounds signify regurgitation or stenosis? The ______________ valve is heard in the 2nd intercostal space on the right

The pulmonic valve is heard in the 2nd intercostal space on the left *High pitch sounds = regurgitation The aortic valve is heard in the 2nd intercostal space on the right

11. A 5-year old male is brought to the pediatric clinic by his mother. She indicates that over the past month, her son has experienced fatigue, dizziness, shortness of breath and cyanosis upon exertion. Physical exam reveals a crescendo-decrescendo systolic murmur that is in harsh quality. There is noticeable splitting of S2. 2D-echocardiagram reveals thickening of the right ventricular free-wall and increased mass. How would the slope of the ventricular filling line on the right ventricular pressure-volume loop in this patient's heart change in comparison to a healthy heart? Cannot determine Decreased Increased Unchanged

The slope of the ventricular filling line represents compliance of the ventricle. Since there was thickening of the right ventricular free-wall and increased mass, one would expect a less compliant (stiffer) ventricle. Thus by definition, pressure would increase more for a given volume (i.e., increased slope).

Tendency for turbulent flow is greatest in:

The tendency for turbulent flow occurs at vascular sites where the velocity of blood flow is high. The aorta has the highest velocity of blood flow.

Blood Flow to Apical skin

Thick skin: nose, lips, ears, soles, palms ØVery high surface-to-volume ratio that favors heat loss ØDensely innervated with sympathetic vasoconstrictor nerves ØHigh sympathetic tone at rest ØGlomus bodies begin shunt blood away from skin when exposed to cooler temperatures No active vasodilation (only passive): no cholonergic sympathetic nerve ØUnique feature are A-V anastomosis, which is non-nutrient flow Lets us get lots of blood to surface to dissapate heat

Three steps of ecg changes in STEMI (ST Elevation Myocardial Infarction)

Three steps of ecg changes in STEMI 1. early repolarization (peaked T waves) 2. decreased action potential amplitude (depolarized baseline) 3. delayed initiation of upstroke (delayed depolarization)

Anything that delays emptying of one of the ventricles will delay closure of the respective valve Physiologic split Inspiration, which increases the return of blood to the right heart (and stroke volume of the right ventricle), delays P2, and ____________________(increase/widens or decreases/shrinks) the split. *S1 = mitral and tricuspid closure S2 = aortic and pulmonary

Thus, inspiration, which increases the return of blood to the right heart (and stroke volume of the right ventricle), delays P2, and increases or widens the split. *during inspiration: Increased output from right = delayed closure of pulmonic valve (splitting of S2 seen on inspiration but not expiration) *Vena cava pulled open when you breathe in

Holding blood flow constant, predict the effect of:_____________ on O2 Extraction Tissue cooling? Warming? Catecholamines ? Thyroxin (thyroid hormone)

Tissue cooling decreases metabolism/ oxygen extraction Warming increases metabolism/ oxygen extraction Catecholamines cause contraction, requires ATP/energy = increase metabolism/ oxygen extraction More thyroxin = more metabolism/ oxygen extraction

Secondary Hemostasis (fibrin deposition)

Tissue factor exposed -> activates factor VII (extrinsic clotting cascade) = formation of thrombin Thrombin cleaves fibrinogen into fibrin (insoluble, precipitates) = fibrin meshwork Furtjer activates/aggregates platelets

Venous return Must exactly equal: Venous pressure : Decrease compliance would ___________ walls = _______________ pressure Compliance is property of vessel wall, don't mix it up with resistence

Total flow of blood into right atrium from systemic circulation Must equal left ventricular cardiac output (CO = quantity of blood pumped into aorta each minute by heart) Decreased resistance opens up vessels Increased resistance traps blood on arterial side (increased resistence = increased pressure) Venous pressure : Decrease compliance would stiffen walls = increase pressure Can hold more volume at low pressure Increase pressure gradient b/n veins and right atrium drives blood back to heart

A 62-year-old male is seen by his primary care physician with chief complaints of general fatigue, nocturnal dyspnea, orthopnea and extreme exercise intolerance for the past four months. Cardiac auscultation reveals a crescendo-decrescendo murmur at the right sternal border. Echocardiogram reveals increased left ventricular wall thickness and mass, reduced chamber diameter and an ejection fraction that is within normal range. What hemodynamic parameter would increase progressively as cardiac function declines in this patient? Arterial blood pressure Cardiac output Total peripheral resistance Ventricular filling time

Total peripheral resistance Decreased cardiac output, low arterial blood pressure and elevated total peripheral resistance.

Overview of Hemostasis Contraction results from (3)

Trauma -> blood vessel smooth muscle contraction (reducing blood flow) Contraction results from Local myogenic spasm, local autacoid factors (platelets: Thromboxane A2), Endothelin), nervous reflex

Order of Heart valves

Tricuspid Pulmonic Mitral (Bicuspid) Aortic (TP My ass) BM = Bicuspid/Mitral

Abnormal Jugular Venous Waveforms and Pulse

Tricuspid Insufficiency: Valve not completely closed: R ventricle contracting, but some blood squirts back into R atrium -> jugular vein *Increase in right ventricular afterload Tricuspid stenosis: Hard to squeeze blood through small, stenotic valve

Turbulent vs Laminar Flow Reynolds Number

Turbulent = noisy *Reynolds Number = pdv/n blood density X Diameter X Mean velocity/ Blood viscosity *turbulence increases the loss of energy in the form of friction Laminar = smooth, quiet (not heard with stethescope), parabolic profile (V0 near vessel wall (lowest speed), V3 = center of vessel/ Vmax)

Transmural Ischemia ECG

Usually thrombotic occlusion of coronary artery affecting entire thickness of Myocardial wall: Seen in ST elevated MI (STEMI) 1 mm elevation of ST segment at J point in 2 adjacent leads

Placement of Chest Leads Septum depolarizes L -> R

V1 (right)-V2 (left) = 4th interspace parasternal ( R and L) V4: 5th interspace (midclavicular line) V3: B/N V2 and V4 (anterior wall of left ventricle) V5- 5th interspace ant. Ax. line V6- 5th interspace mid Ax. line Septum depolarizes L -> R -Forwards to backwards Postrerior wall = recipricol/opposite

Precordial Leads

V1-V6 Looks like an accordian

Velocity vs Flow

Velocity: distance an object moves with respect to time (i.e., the distance traveled per unit of time) (cm/sec) Flow= volume of liquid moving per unit of time. (ml/min) (cm3/min; 1 ml = 1cm3). Velocity at constant flow is inversely related to radius squared. For example, if radius (or diameter) is doubled, the velocity decreases to one-fourth its normal value *big openings = slow velocity velocity = flow rate / area *Increased CO or decreased blood viscosity or higher velocities enhance turbulence, murmurs intensify as flow increases Turbulent flow occurs at vascular sites where the velocity of blood flow is high. The aorta has the highest velocity of blood flow.

Summary: Factors That Impact Central Venous Pressure

Venous pressure influenced by: cardiac output, respiratory activity, contraction of skeletal muscles (particularly legs and abdomen), sympathetic vasoconstrictor tone, and hydrostatic forces (i.e., gravity). Venodilator drugs, ( for acute heart failure and angina) relax venous vessels (increase compliance) = lower central venous pressure. •A decrease in cardiac output either due to decreased heart rate or stroke volume (e.g., in ventricular failure) results in blood backing up into the venous circulation (increased venous volume) as less blood is pumped into the arterial circulation -> increase in thoracic blood volume increases CVP. •An increase in total blood volume as occurs in renal failure or fluid retention through activation of the renin-angiotensin-aldosterone system increases venous pressure. •Venous constriction caused by sympathetic activation of veins, or by circulating vasoconstrictor substances (e.g., catecholamines, angiotensin II) decreases venous compliance, which increases CVP. •A shift in blood volume into the thoracic venous compartment that occurs when a person changes from standing to supine position increases CVP. •Arterial dilation as occurs during withdrawal of sympathetic tone or with arterial vasodilator drugs causes increased blood flow from the arterial into the venous compartments. This increases venous blood volume and CVP. This is what occurs when the heart is functioning normally. It is important to note, however, that arterial dilation in ventricular failure leads to a decrease in CVP instead of an increase. This occurs because the arterial dilation decreases afterload on the ventricle leading to an increase in stroke volume. Ventricular stroke volume is more strongly influenced by afterload when the ventricular is in failure than when it has normal function. •Increase blood back to heart = increase CVP -> also increased during a force expiration, particularly against a high resistance (as occurs with a Valsalva maneuver) •Muscle contraction, particularly of the limbs and abdomen, compresses the veins (i.e., decreases compliance) and forces blood into the thoracic compartment, thereby increasing thoracic blood volume and CVP.

Atrial Flutter

Ventricular Rate of ~ 75 and Atrial Flutter rate ~ 210 (Sawtooth wave pattern)

QRS Wave

Ventricular depolarization QRS: If time it takes for ventricle to depolarize is greater than 120 = block PR Interval: up to 200 m/s If QT is over half your RR interval = abnormal

T-Wave Proceeds from _____cardium to ______cardium

Ventricular repolarization (Outside -> in )(compare to depolarization, which happens from inside out) Epicardium repolarizes first (faster/ repolarizes faster) , then endocardium

Vascular Cross Sectional Area & Velocity of Blood Flow Which segment of circulatory system has lowest velocity<

Vessel diameter decrease from artery to capillary, but total cross sectional area increases CO distributed, so Velocity of blood actually slows ever though diameter is smaller This is good for diffusion Capillaries = lowest velovity because blood flow inversely proportional to total cross sectional area

Subendocardial Ischemia

Subendocardial Ischemia: Seen with increased metabolic demand (Exercise induced). Can be transient or result in NON-STEMI *Demand Ischemia (depressed P value) Why ST depression? Ischemic area slightly depolarized, elevating baseline at rest With all LV depolarized, lead reads true zero (even though its higher), then with repolarization baseline elevates False impression of base line: Shifted up Okay so first, only the ischemic part is depolarized, so its elevated. Then, when everything gets depolarized it brings it back to where everyone else is. Then, in repolarization, the ischemic part is still depolarized so its elevated again When ventricle is at rest ( repolarized ), the depolarized ischemic subendocardium generates electrical currents that are recorded. If the depolarizing currents are traveling toward a positive recording electrode, the baseline voltage prior to the QRS complex (which is normally isoelectric / zero mV) will be elevated. In contrast, when the ventricle becomes depolarized, all the muscle is depolarized so that zero voltage is recorded by the electrode as usual. After repolarization, the voltage following the T wave remains positive as in the resting state. Net effect of the elevated baseline voltage is that the ST segment appears to be depressed relative to the baseline.

Extravascular Compression and Left Ventricular Myocardial Blood Flow Epicardial vs subendocardial vessels _______________________ regions more susceptible to ischemic injury when coronary heart disease or reduced aortic pressure is present

Subendocardial regions are more susceptible to ischemic injury when coronary heart disease or reduced aortic pressure is present During diastole: Epicardial coronary vesels (run along outer surface of heart) and subendocardial vessels (run along internal surface of <3) remain patent During SYSTOLE, subendocardial coronary vessels compressed due to high intraventricular pressures → blood flow in subendocardium nearly stops.

ECG P wave

Summation of R and L atrial depolarization Low voltage b/c not much muscle tissue

ECG Practice II

Supraventricular Tachycardia with HR of 210

Systole vs Diastole 7 Phases of cardiac cycle

Systole: Contracting -> blood ejected Diastole: Relaxation: Chamber filling 7 Phases of cardiac cycle: 1.Atrial systole (contracting) 2.Isovolumic ventricular contraction (same volume, pressure change) 3.Rapid ventricular ejection 4.Reduced ventricular ejection 5.Isovolumic ventricular relaxation (valves closed) 6.Rapid ventricular filling 7.Reduced ventricular filling (diastasis)

Ventricular Systole: QRS Wave of ECG At what point does the mitral (bicuspid) valve close

Systole: Pressure in ventricles rises As soon as pressure in LV exceeds LA, mitral valve closes (2) Rapid increase in ventricular pressure, no change in ventricular volume (aortic and mitral valves closed) Ventricular volume / end diastolic volume is maximum (3) = isovolumic contraction Rapid increase in ventricular pressure causes mitral valve to bulge into atrium = transitory pressure increase (c wave) When ventricular pressure exceeds aortic pressure, aortic valve open (4): End of isovolumic contraction , beginning of ejection Opening of aortic valve = mitral valves returns to normal, pressure in atrium falls (x descent)

What do blood pressure values mean What happend at the dicrotic notch *Since atmospheric pressure is 760 mmHg, mean arterial blood pressure is actually 853 mmHg (i.e., 760 + 93). Zero reference point!

Systolic blood pressure (SBP): peak pressure during contraction of heart (systole) Diastolic blood pressure (DBP): minimum arterial pressure during relaxation of heart (diastole) Pulse pressure = SBP - DBP Mean arterial blood pressure = DBP + 1/3 (SBP - DBP) Dicrotic notch = end of systole/ beginning of diastole

Calcium storage and release (review)

T tubules and terminal cisternae of SR Ca2+ enters during plateau, calcium induced calcium release from SR •Ca++ binds to troponin C •Actin/Myosin cross-bridging •Contraction of muscle •Ca++ reaccumulated in SR by sarco-endoplasmic reticulum calcium ATPase pump •Relaxation •Ca++ pumped out of cell

When Depolarization travels towards a lead, the deflection is ____________ When depolarization is traveling away: deflection is ___________ If it travels at 90 degrees, the complex is ___________

When Depolarization travels towards a lead, the deflection is positive. When depolarization is traveling away: deflection is negative. If it travels at 90 degrees, the complex is isoelectric

Does figure A or B represent decreased vascular compliance? Why did the change in compliance cause pulse pressure (amplitude of wave) to change? Increase in compliance will __________ pulse pressure

Young arteries = more compliant, slower pulse than old Pulse pressure is the difference between systolic and diastolic blood pressure. Increasing the compliance of an artery will decrease pulse pressure. *Pulse pressure can be increased by increase in systolic pressure or stroke volume More compliant = more constant flow of blood (diastolic recoil drives blood forward)

Tissue hydrostatic pressure (Pt) is determined by: (3)

a)filtration and reabsorption at the capillary level, b) tissue compliance c) lymph drainage

Augmented Limb Leads aVR aVL aVF *

aVR: Right arm (make right arm positive, connect left arm and right leg and make them negative)(augmented lead to the right) aVL: Left arm (make left arm positive, connect right arm and left leg and make them negative) aVF: Left leg (make left and right arm negative, left leg positive -> goes towards left leg) Left to right

Systolic vs. diastolic blood pressure

ventricle contraction vs. ventricular relaxation

Mean Arterial Pressure (MAP)

cardiac output x systemic peripheral resistance *ANS/Neural Mechanism: Fast, short term (moment to moment changes) -SNS: Short preganglionic, long postganglionic fibers *Humoral mechanism: Slow, long term (takes up to 2 days to be fully en gaged in response to change in BP: Renin-angiotensin Aldosterone system)

Inotropy

contractility Intrinsic vigor of cardiac muscle contraction independent of preload or afterload Caused by cellular mechanisms that regulate actin/myosin interaction Indices of contractility •dP/dt •End-systolic pressure-volume relationship

A 19-year-old male college student, with no history of cardiac problems, is required to take a public speaking course. However, the mere thought of public speaking causes the student to have tremors and heart palpitations. His physician prescribes a β-blocker that should be taken 60-min prior to public speaking. The mechanism of relief of this patient's heart palpitations is an increased blood pressure. a decreased effective refractory period. activation of the funny channel. delayed opening of L-type calcium channels. enhanced ventricular repolarization.

delayed opening of L-type calcium channels. Blockade of beta-1-adrenergic receptors on SA nodal cells leads to a reduction in cAMP and PKA formation, and delayed opening of L-type-calcium channels. This will decreased heart rate.

A 67-year-old male is seen in the clinic with chief complaint of fatigue during light exercise over the past 2-months. The patient has a 15-year history of diabetes mellitus, hypertension and coronary artery disease. Coronary blood flow during exercise in this patient may be expected to be low in comparison to a healthy subject because of a decreased coronary adenosine release flow-mediated dilation oxygen extraction vascular resistance

flow-mediated dilation During exercise, the coronary microvasculature release nitric oxide and additional metabolites that dilate the coronary arterioles and lead to subsequent increased in blood flow termed flow-mediated vasodilation (FMD). People with coronary artery disease (CAD) have impaired FMD.Option A: Reductions in coronary blood flow cause ischemia and subsequent release of adenosine. Thus, adenosine levels would be expected to be increased in this subject. Option C: In healthy individuals coronary oxygen extraction is high, and it would be expected to be even higher in individuals with CAD.Option D: The impaired release of metabolites and FMD in this subject would be accompanied by an increased coronary vascular resistance.

Renin

hormone secreted by the kidney; it raises blood pressure by influencing vasoconstriction (narrowing of blood vessels)

Active Hyperemia

increased blood flow through a tissue associated with increased metabolic activity (Increased O2 demand or decreased supply = increased vasodilator metabolites) More metabolism more metabolites (like adenosine, PO4-, lactate, CO2, K+. H+) = decreased arteriolar resistance = increased blood flow/ vasodilation

Angiotensin II

increases blood pressure by stimulating kidneys to reabsorb more water and by releasing aldosterone

Obstructive Sleep Apnea

Ørepeated collapse of the upper airway during the night causing intermittent reductions in blood oxygen levels (Decreased arterial PO2) Need CPAP mask/ positive pressure

Alpha Granules: Fibrinogen vWF

α-granules: von Willebrand factor, platelet fibrinogen, and clotting factor V •Fibrinogen: Secreted by liver in blood -> endocytosed by platelets vWF: Glue b/n GPIb (platelets) and collagen

Peripheral Sensors: •Skeletal muscle afferent sensors (Exercise-pressor reflex) Class III Class IV

‒Class III- Thinly myelinated nerve endings that are mechano-sensitive Class IV- Unmyelinated nerve endings that are chemo-sensitive.

Heart block: Progressive dysfunction of AV nodal transmission 1st degree 2nd degree (Type 1 vs Type II) 3rd degree

•1st degree: PR interval over 200 msec •2nd degree Type I: Lengthening PR interval until p wave without conducted beat (Mobitz type I or Wenckebach) from prolonging AV nodal conduction •2nd degree Type II: Normal PR interval but then a non-conducted beat (usually from a block below the AV node in His-Purkinje system) *random drops *Picture shown •3rd degree (Complete heart block): Complete AV dissociation. (Signals from the atria to ventricle are completely blocked, ventricle beats at its own intrinsic rhythm)

Partial Thromboplastin Time (PTT) or Activated Partial Thromboplastin Time (aPTT): Measure of integrity of _________ pathway Increased PTT:

•Blood isolated from a patient is immediately oxalated, mixed, and centrifuged •Excess Ca2+ added Add silica, celite, kaolin, or ellagic acid Time takes to clot (PTT) = 20-35 seconds Measures integrity of intrinsic and common pathway (Factors XII, XI, VIII, IX) •Increased PTT indicates lack of or missing clotting factors

Composition of blood vessel walls:

•Endothelial cells: Located in all vascular segments. •Elastic fibers: Rubber-like material -> accounts for stretch •Smooth muscle: Located in all vascular segments except capillaries. •Collagen fibers: Give tensile strength to vessel walls./ fibrous connective tissue (like a pool float, compliant at low pressure but not stretchy

•In contrast to most vascular beds, ________ control >>> local metabolic or thermal control in overall regulation of skin blood flow

•In contrast to most vascular beds, sympathetic control most important in overall regulation of skin blood flow

P wave : •PR segment : (not measured) •PR interval : •QRS interval : QT Interval QTc

•P wave : Atrial Depolarization 80-100 msec •PR segment : AV node and His depolarization (not measured) •PR interval : Atrial Depol. + AV node delay 120-200 msec •QRS interval : Ventricular Depolarization 60-100 msec QT interval :Depol. And Repol. Duration of ventricles200-400 msec QTc :QT interval corrected for heart rate Upper limit: 460 msec (females), 420 (males)

Blood-brain-barrier and cerebral capillaries

•Rarely form pinocytotic vesicles •No fenestrations •Adjacent endothelial cells are fused •O2 and CO2 (lipid soluble) readily cross •Many transporters for glucose, fatty acids, etc.

•ST segment (not measured) •T wave (not measured) •ST interval: (not measured) QT interval : QTc : Upper limit:

•ST segment Isoelectric period of depolarized ventricle (not measured) •T wave: Ventricular Repolarization (not measured) •ST interval: End of ventricular depolarization to end of ventricular repolarization (not measured) *this is where we look for ischemia (ischemia = lowered, infarct = raised) QT interval : Depol. And Repol. Duration of ventricles 200-400 msec QTc : QT interval corrected for heart rate Upper limit: 460 msec (females), 420 (males)

Cardiac Innervation: Sympathetic Parasympathetic What predominates at rest?

•Sympathetic: Paravertebral Ganglia T1-T5: Atria, Ventricles, Conduction System Parasympathetic: Vagus Nerves: SA and AV nodes (minimal effect on ventricles) *predominates at rest

Diseases that impact primary hemostasis •Von Willebrand Disease: • • •Bernard-Soulier Syndrome: • • •Glanzmann thrombasthenia:

•Von Willebrand Disease: Deficiency in vWF: defective interaction b/n platelets and walls •Bernard-Soulier Syndrome: -Giant blood platelets/low platelet counts -GpIb-V-IX complex deficiency •Glanzmann thrombasthenia:

Prothrombin Time (PT) and International Normalized Ratio (INR): Measure of integrity of ____________ pathway Low INR = chance of:

•indication of the prothrombin concentration in the blood •Blood isolated from a patient is immediately oxalated (to remove Ca2+) so that prothrombin is not converted into thrombin •Excess Ca2+ and tissue factor are added to the blood: •Ca2+ will nullify oxalate and allow prothrombin to be converted into thrombin •Tissue factor will cause activation of extrinsic coagulation cascade •The time it takes to clot is referred to as PT or prothrombin time: •Usually about 12-14 seconds Higher prothrombin = shorter the PT Low INR = chance of clotting

Cerebral Circulation The brain comprises about 2.5% of the total body weight and receives ___% of CO

High oxygen extraction At rest, 20% of O2 consumption Supplied by 4 main arteries 2 mechanisms of blood flow to circle of willis Highly oxidative and intolerant to ischemia (even 25% decrease in blood = lightheaded) ØRegional cerebral blood flow changes as neurons become more or less active Rigid cranium wont let volume expand Increased cerebral blood flow matched by oppsoing changes in less active brain areas •Rarely form pinocytotic vesicles •No fenestrations •Adjacent endothelial cells are fused •O2 and CO2 (lipid soluble) readily cross •Many transporters for glucose, fatty acids, etc

The P wave occurs just before __________ _____________ The QRS complex takes place just before __________ ___________ T wave occurs just before __________ _____________

The P wave occurs just before Atrial contraction Then after the atria contact, the AV valve closes The QRS complex takes place just before ventricular contraction T wave occurs just before ventricular relaxation

Stroke Volume Increase in Preload has what effect of SV and End distolic volume Increase in afterload has what effect of SV and End systolic volume Increase in intropy has what effect of SV and End systolic volume

The amount of blood ejected from the heart in one contraction. End diastolic - end systolic Increase in Preload = Increase in SV and End distolic volume Increase in afterload = decrease SV and increase end systolic volume Increase in intropy increases SV and decreases end systolic volume