Term
|
Definition
|
|
Term
| Name the two priciple mechanisms for vascular abnormalities |
|
Definition
1. narrowing or obstruction of lumens
2. weakening of walls resulting in dilation and rupture |
|
|
Term
| What are the 5 categories of disease that account for nearly all cardiac mortality? |
|
Definition
1. congenital heart disease
2. ischemic heart disease
3. hypertensive heart disease (systemic & pulmonary)
4. valvular heart disease
5. nonischemic, primary myocardial disease |
|
|
Term
| Describe Fetal Circulation |
|
Definition
| Fetal circulation: Oxygenated blood from the placenta is carried to the fetus by the umbilical vein. Half of the blood enters into the ductus venosus and is carried to the inferior vena cava. From the vena cava, it empties into the right atrium. The other half of the blood goes to supply the developing liver, entering portal circulation, and eventually ending up in the RA as well. The foramen ovale allows blood to go from the RA -> LA, thereby bypassing pulmonary circulation. Blood is pumped by the LV into systemic circulatoin. The ductus arteriosus connects the aorta and the pulmonary artery to prevent any blood to enter the lungs. |
|
|
Term
| List the two major functions of circulation |
|
Definition
1. Transport nutritents, hormones, and oxygen to cells of tissues and organs
2. remove waste products from the body |
|
|
Term
| Why is oxygen required by cells? |
|
Definition
| to produce ATP fror energy |
|
|
Term
| What is the distribution of blood in the different parts of the circulatory system? |
|
Definition
64% in venous circulation ( veins, venules, and venous sinuses)
13% - Arteries
7% - Arterioloes & capillaries
9% - pulmonary circulation |
|
|
Term
| Identify the components of the vascular system and their function |
|
Definition
Arteries: transport blood under high pressure from the heart to the capillary beds of tissues (thick muscular walls)
Arterioles: small branches of arteries that act as conduits between arteries and capillary beds of tissues (muscular walls & sphincters control how much blood is delivered to cap. bed)
Capillaries: extensive lattice of vessles that supply blood to the cells; substrate exchange (thin walls; permeable)
Venules: collect blood from the capillaries and coalesce to form veins
Veins: transport blood from venules back to heart and act as a reservoir (low pressure system, thin walls) |
|
|
Term
| Name the layers of a muscular artery from most superficial to most deep |
|
Definition
Intima (endothelium & internal elastic lamina)
Media (smooth muscle, connective tissue)
Adventitia (external elastic lamina, connective tissue) |
|
|
Term
| Describe the vascular differences between arteries and veins |
|
Definition
Arteries: thick wall that maintains an open, round lumen even in the absence of blood. Elastin is more organized
Vein: larger and collapsed lumen. Elastin is diffusely distributed |
|
|
Term
| What is systole? Diastole? |
|
Definition
Systole: contraction phase of the heart
Diastole: relaxation and refilling of the heart |
|
|
Term
| List the components of circulation from areas of highest pressure to areas of lowest presssure |
|
Definition
| Aorta & Systemic Arteries > LV > PA > RV > systemic capillaries > pulmonary capillaries > RA |
|
|
Term
|
Definition
| Volume of blood returning to the heart from the systemic circulation. This is equal to RA pressure or central venous pressure |
|
|
Term
|
Definition
| Systemic pressure - pressure against which the LV has to pump in order to circulate blood throughout the body. Equal to mean arterial pressure |
|
|
Term
| What four variables determine flow through a blood vessel? |
|
Definition
1. Pressure difference or gradient (Delta P)
2. Resistance (R = 1/r4)
3. Viscosity
4. Length |
|
|
Term
| What two variables are often manipulated in cardiac patients? |
|
Definition
1. pressure difference/gradient
2. resistence (size of lumen) |
|
|
Term
| How does vascular resistence differ between a narrow vessel and a wide vessel? |
|
Definition
| higher resistence in more narrow vessels and lower resistence in wider vessels. More force is necessary to move blood through a narrow vessel and less in a wide vessel. |
|
|
Term
| Describe the difference between laminar and turbulent flow |
|
Definition
| Turbulent flow is caused by narrowing of a vessel |
|
|
Term
| How is vascular resistence measured? |
|
Definition
wood units
Systemic vascular resistence (SVR) from greatest to lowest: child/adolescent > 1-2 yo > infant
Pulmonary vascular resistence (PVR) drops at 8wks old |
|
|
Term
| What is arterial vascular resistence and what is it controlled by? |
|
Definition
constriction /relaxation of the smooth muscle of arteries and arterioles (pre-capillary sphincters)
Controlled by: local tissue metabolism, sympatethic nervous system, hormonal responses |
|
|
Term
| Describe vascular compliance |
|
Definition
| Compliance is a measure of blood vessue dispensability/flexibility |
|
|
Term
| What is the difference in compliance between veins and arteries? |
|
Definition
| Veins are 8x as compliant as arteries |
|
|
Term
| Describe venous resistance |
|
Definition
| There is almost no resistence in distended veins. Physiologically, veins are compressed by surrounding structures so resistence does exist |
|
|
Term
| What is the fuction of venous valves? |
|
Definition
| keeps blood from backflowing and assists venous return to the heart |
|
|
Term
| What four factors help facilitate venous return? |
|
Definition
1. movement of body parts
2. contrxn of surrounding skeletal muscle
3. pulsations of adjacent arteries
4. compressoin of tissues from objects outside the body |
|
|
Term
| What is venous stasis and why is it dangerous clinically? |
|
Definition
| Stasis is the pooling of venous blood in the absence of contraction of surrounding musculature. Statis increases predisposition to thrombosis |
|
|
Term
| What is venous thromboembolism (VTE)? |
|
Definition
| Venous status, vasuclar damamge, and activation of coagulatoin cascade leads to DVT and PE. |
|
|
Term
| What are three clinical signs associated with a large saddle pulmonary embolus? |
|
Definition
1. obstructed pulmonary blood flow
2. hypoxemia
3. decreased cardiac output |
|
|
Term
| Describe the pathophysiology of a large saddle pulmonary embolus. |
|
Definition
| Cause: a VTE that has travelled to the lung, obstructing blood flow to the lungs. This results in hypoxemia. Cardiac output is also affected (decreased) because there is less blood circulating to the LA/LV. |
|
|
Term
| Describe the Phsyiology of clot formation |
|
Definition
Virchow's Triad:
1. Circulatory stasis (e.g. immobility)
2. Endothelial injury (e.g.secondary to a central catheter)
3. Abnormal blood composition - hypercoagulable state (e.g. patient who is on Estrogen or pregnant, or with increased risk for thrombsis) |
|
|
Term
| Describe the increased risk for clot formation in patients under anesthesia. |
|
Definition
1. Circulatory stasis: immobility and decreased/lack of contraction of surrounding skeletal muscle
2. Endothelial injury: inflammation and vasodilation by anesthetics |
|
|
Term
| What protective mechanisms do prepubescent children have against clot formation? |
|
Definition
1. healthier blood vessels
2. decreased plasma concentrations of coagulation factors
3. thrombin inhibition by alpha-2-macroglobulin*** |
|
|
Term
| Are neonates at risk for clot formation? |
|
Definition
| Yes. Neonates are deficient in inherent anticoagulant proteins made by the liver --> increased clotting. |
|
|
Term
| What is the most common prophylaxis for VTE in pediatrics? |
|
Definition
| Sequential compression stockings |
|
|
Term
| Identify the three major epicardial coronary arteries |
|
Definition
1. left anterior descending (LAD)
2. left circumflex (LCX)
3. right coronary artery (RCA)
*LCA bifurcates to form LAD and LCX |
|
|
Term
| When does coronary arterial blood flow to the myocardium occur? |
|
Definition
| During ventricular diastole when microcirculation is not compressed by cardiac contraction |
|
|
Term
| Identify the coronary veins |
|
Definition
1. Coronary sinus
2. great cardiac vein
3. posterior vein of the left ventricle |
|
|
Term
| Identify the four major determinants of myocardial oxygen consumption |
|
Definition
1. heart rate (chronotrophy)
2. contractility (inotrophy)
3. systolic wall tension and shortening against a load (afterload)
4. direct metabolic effects of catecholamines (Epi and Nepi) |
|
|
Term
| Describe the relationship between oxygen and myocyte survival |
|
Definition
| Decreased oxygen and substrate delivery to the myocytes results in unmet metabolic demands and anaerobic metabolism --> cell injury and death |
|
|
Term
| What is the most common cause of death in adults? |
|
Definition
| obstruction by atherosclerosis and thrombus |
|
|
Term
| Differentiate between myocardial ischemia and athlersclerotic ischemia |
|
Definition
atheroschlerosis results in discreet areas of ischemia
unmet metabolic demands result in tachycardia and diastolic dysfunction leads to global ischemia |
|
|
Term
| What is collateral circulation |
|
Definition
| small anastomoses that form in areas of ischemia - protective factor |
|
|
Term
| Why do diabetic patients also often have coronry heart disease? |
|
Definition
| Diabetes impedes collateral formation by increasing the production of antiangiogenic factors (endostatin & angiostatin). High blood glucose also increases fatty deposits in vessels increasing risk of develop atheroschlerosis |
|
|
Term
| Which is more dangerous: hypoxemia or ischemic heart disease? Why? |
|
Definition
Ischemic heart disease.
Hypoxic patients (induced by cyanotic congenital heart disease, severe anemia, or respiratory failure) will still be perfusing. |
|
|
Term
| Describe how reperfusion can prevent necrosis |
|
Definition
| ischemia does not cause immediate cell death. Reperfusion within 15-20 minutes may prevent necrosis |
|
|
Term
| What condition is associated with reperfusion? |
|
Definition
Reperfusion injury.
Reperfusion injury is mediated by free radicals. Tissues are deprived of oxygen and nutrients during ischemia. Restoring circulation can cause inflammation and result in oxydative stress. Damaged cell membranes also release free radicals that go on to create more free radicals. Xanthine oxidase also plays a role in creating free radicals |
|
|
Term
| Descrube the potential loss of function related to myocardial cell death |
|
Definition
1. tissue thinning, aneurysm and rupture
2. decreased contractile strength
3. dysrhythmia
4. papillary muscle dysfunction --> incompetent valves |
|
|
Term
| What are the clinical signs and symptoms of myocardial Ischemia? |
|
Definition
1. pain (chest, arm, jaw)
2. ECG (ST segment) & dysrhythmia
3. decreased CO
4. dying myocytes leak myoglobins, creatine kinase, lactate dehydrogenase, and troponins |
|
|
Term
| What are a clinical marker used to indicate myocardial ischemia? |
|
Definition
1. elevated serum cardiac troponins (Troponin-I and Troponin-T)
2. Creatine kinase with isoenzymes M & B (CK-MB) *less sensitive |
|
|
Term
| Describe the relationship between myocardial infarction and Acute Coronary Syndrome |
|
Definition
|
|
Term
| Identify the most common compilcations of myocardial infarction |
|
Definition
1. anterior myocardial rupture
2. rupture of the ventricular septum
3. complete rupture of papillary muscle
4. fibrinous pericarditis
5. wall thinning and mural thrombosis
6. ventricular aneurysm |
|
|
Term
| Describe the vascular structure of arterioles |
|
Definition
| extension of arteries that contain bands of smooth muscle that create pre-capillary sphincters |
|
|
Term
| Describe the vascular structure of true capillaries |
|
Definition
| made of endothelium surrounded by smooth muscle an elastic connective tissue |
|
|
Term
|
Definition
|
|
Term
| Name the two priciple mechanisms for vascular abnormalities |
|
Definition
1. narrowing or obstruction of lumens
2. weakening of walls resulting in dilation and rupture |
|
|
Term
| What are the 5 categories of disease that account for nearly all cardiac mortality? |
|
Definition
1. congenital heart disease
2. ischemic heart disease
3. hypertensive heart disease (systemic & pulmonary)
4. valvular heart disease
5. nonischemic, primary myocardial disease |
|
|
Term
| Describe Fetal Circulation |
|
Definition
| Fetal circulation: Oxygenated blood from the placenta is carried to the fetus by the umbilical vein. Half of the blood enters into the ductus venosus and is carried to the inferior vena cava. From the vena cava, it empties into the right atrium. The other half of the blood goes to supply the developing liver, entering portal circulation, and eventually ending up in the RA as well. The foramen ovale allows blood to go from the RA -> LA, thereby bypassing pulmonary circulation. Blood is pumped by the LV into systemic circulatoin. The ductus arteriosus connects the aorta and the pulmonary artery to prevent any blood to enter the lungs. |
|
|
Term
| List the two major functions of circulation |
|
Definition
1. Transport nutritents, hormones, and oxygen to cells of tissues and organs
2. remove waste products from the body |
|
|
Term
| Why is oxygen required by cells? |
|
Definition
| to produce ATP fror energy |
|
|
Term
| What is the distribution of blood in the different parts of the circulatory system? |
|
Definition
64% in venous circulation ( veins, venules, and venous sinuses)
13% - Arteries
7% - Arterioloes & capillaries
9% - pulmonary circulation |
|
|
Term
| Identify the components of the vascular system and their function |
|
Definition
Arteries: transport blood under high pressure from the heart to the capillary beds of tissues (thick muscular walls)
Arterioles: small branches of arteries that act as conduits between arteries and capillary beds of tissues (muscular walls & sphincters control how much blood is delivered to cap. bed)
Capillaries: extensive lattice of vessles that supply blood to the cells; substrate exchange (thin walls; permeable)
Venules: collect blood from the capillaries and coalesce to form veins
Veins: transport blood from venules back to heart and act as a reservoir (low pressure system, thin walls) |
|
|
Term
| Name the layers of a muscular artery from most superficial to most deep |
|
Definition
Intima (endothelium & internal elastic lamina)
Media (smooth muscle, connective tissue)
Adventitia (external elastic lamina, connective tissue) |
|
|
Term
| Describe the vascular differences between arteries and veins |
|
Definition
Arteries: thick wall that maintains an open, round lumen even in the absence of blood. Elastin is more organized
Vein: larger and collapsed lumen. Elastin is diffusely distributed |
|
|
Term
| What is systole? Diastole? |
|
Definition
Systole: contraction phase of the heart
Diastole: relaxation and refilling of the heart |
|
|
Term
| List the components of circulation from areas of highest pressure to areas of lowest presssure |
|
Definition
| Aorta & Systemic Arteries > LV > PA > RV > systemic capillaries > pulmonary capillaries > RA |
|
|
Term
|
Definition
| Volume of blood returning to the heart from the systemic circulation. This is equal to RA pressure or central venous pressure |
|
|
Term
|
Definition
| Systemic pressure - pressure against which the LV has to pump in order to circulate blood throughout the body. Equal to mean arterial pressure |
|
|
Term
| What four variables determine flow through a blood vessel? |
|
Definition
1. Pressure difference or gradient (Delta P)
2. Resistance (R = 1/r4)
3. Viscosity
4. Length |
|
|
Term
| What two variables are often manipulated in cardiac patients? |
|
Definition
1. pressure difference/gradient
2. resistence (size of lumen) |
|
|
Term
| How does vascular resistence differ between a narrow vessel and a wide vessel? |
|
Definition
| higher resistence in more narrow vessels and lower resistence in wider vessels. More force is necessary to move blood through a narrow vessel and less in a wide vessel. |
|
|
Term
| Describe the difference between laminar and turbulent flow |
|
Definition
| Turbulent flow is caused by narrowing of a vessel |
|
|
Term
| How is vascular resistence measured? |
|
Definition
wood units
Systemic vascular resistence (SVR) from greatest to lowest: child/adolescent > 1-2 yo > infant
Pulmonary vascular resistence (PVR) drops at 8wks old |
|
|
Term
| What is arterial vascular resistence and what is it controlled by? |
|
Definition
constriction /relaxation of the smooth muscle of arteries and arterioles (pre-capillary sphincters)
Controlled by: local tissue metabolism, sympatethic nervous system, hormonal responses |
|
|
Term
| Describe vascular compliance |
|
Definition
| Compliance is a measure of blood vessue dispensability/flexibility |
|
|
Term
| What is the difference in compliance between veins and arteries? |
|
Definition
| Veins are 8x as compliant as arteries |
|
|
Term
| Describe venous resistance |
|
Definition
| There is almost no resistence in distended veins. Physiologically, veins are compressed by surrounding structures so resistence does exist |
|
|
Term
| What is the fuction of venous valves? |
|
Definition
| keeps blood from backflowing and assists venous return to the heart |
|
|
Term
| What four factors help facilitate venous return? |
|
Definition
1. movement of body parts
2. contrxn of surrounding skeletal muscle
3. pulsations of adjacent arteries
4. compressoin of tissues from objects outside the body |
|
|
Term
| What is venous stasis and why is it dangerous clinically? |
|
Definition
| Stasis is the pooling of venous blood in the absence of contraction of surrounding musculature. Statis increases predisposition to thrombosis |
|
|
Term
| What is venous thromboembolism (VTE)? |
|
Definition
| Venous status, vasuclar damamge, and activation of coagulatoin cascade leads to DVT and PE. |
|
|
Term
| What are three clinical signs associated with a large saddle pulmonary embolus? |
|
Definition
1. obstructed pulmonary blood flow
2. hypoxemia
3. decreased cardiac output |
|
|
Term
| Describe the pathophysiology of a large saddle pulmonary embolus. |
|
Definition
| Cause: a VTE that has travelled to the lung, obstructing blood flow to the lungs. This results in hypoxemia. Cardiac output is also affected (decreased) because there is less blood circulating to the LA/LV. |
|
|
Term
| Describe the Phsyiology of clot formation |
|
Definition
Virchow's Triad:
1. Circulatory stasis (e.g. immobility)
2. Endothelial injury (e.g.secondary to a central catheter)
3. Abnormal blood composition - hypercoagulable state (e.g. patient who is on Estrogen or pregnant, or with increased risk for thrombsis) |
|
|
Term
| Describe the increased risk for clot formation in patients under anesthesia. |
|
Definition
1. Circulatory stasis: immobility and decreased/lack of contraction of surrounding skeletal muscle
2. Endothelial injury: inflammation and vasodilation by anesthetics |
|
|
Term
| What protective mechanisms do prepubescent children have against clot formation? |
|
Definition
1. healthier blood vessels
2. decreased plasma concentrations of coagulation factors
3. thrombin inhibition by alpha-2-macroglobulin*** |
|
|
Term
| Are neonates at risk for clot formation? |
|
Definition
| Yes. Neonates are deficient in inherent anticoagulant proteins made by the liver --> increased clotting. |
|
|
Term
| What is the most common prophylaxis for VTE in pediatrics? |
|
Definition
| Sequential compression stockings |
|
|
Term
| Identify the three major epicardial coronary arteries |
|
Definition
1. left anterior descending (LAD)
2. left circumflex (LCX)
3. right coronary artery (RCA)
*LCA bifurcates to form LAD and LCX |
|
|
Term
| When does coronary arterial blood flow to the myocardium occur? |
|
Definition
| During ventricular diastole when microcirculation is not compressed by cardiac contraction |
|
|
Term
| Identify the coronary veins |
|
Definition
1. Coronary sinus
2. great cardiac vein
3. posterior vein of the left ventricle |
|
|
Term
| Identify the four major determinants of myocardial oxygen consumption |
|
Definition
1. heart rate (chronotrophy)
2. contractility (inotrophy)
3. systolic wall tension and shortening against a load (afterload)
4. direct metabolic effects of catecholamines (Epi and Nepi) |
|
|
Term
| Describe the relationship between oxygen and myocyte survival |
|
Definition
| Decreased oxygen and substrate delivery to the myocytes results in unmet metabolic demands and anaerobic metabolism --> cell injury and death |
|
|
Term
| What is the most common cause of death in adults? |
|
Definition
| obstruction by atherosclerosis and thrombus |
|
|
Term
| Differentiate between myocardial ischemia and athlersclerotic ischemia |
|
Definition
atheroschlerosis results in discreet areas of ischemia
unmet metabolic demands result in tachycardia and diastolic dysfunction leads to global ischemia |
|
|
Term
| What is collateral circulation |
|
Definition
| small anastomoses that form in areas of ischemia - protective factor |
|
|
Term
| Why do diabetic patients also often have coronry heart disease? |
|
Definition
| Diabetes impedes collateral formation by increasing the production of antiangiogenic factors (endostatin & angiostatin). High blood glucose also increases fatty deposits in vessels increasing risk of develop atheroschlerosis |
|
|
Term
| Which is more dangerous: hypoxemia or ischemic heart disease? Why? |
|
Definition
Ischemic heart disease.
Hypoxic patients (induced by cyanotic congenital heart disease, severe anemia, or respiratory failure) will still be perfusing. |
|
|
Term
| Describe how reperfusion can prevent necrosis |
|
Definition
| ischemia does not cause immediate cell death. Reperfusion within 15-20 minutes may prevent necrosis |
|
|
Term
| What condition is associated with reperfusion? |
|
Definition
Reperfusion injury.
Reperfusion injury is mediated by free radicals. Tissues are deprived of oxygen and nutrients during ischemia. Restoring circulation can cause inflammation and result in oxydative stress. Damaged cell membranes also release free radicals that go on to create more free radicals. Xanthine oxidase also plays a role in creating free radicals |
|
|
Term
| Descrube the potential loss of function related to myocardial cell death |
|
Definition
1. tissue thinning, aneurysm and rupture
2. decreased contractile strength
3. dysrhythmia
4. papillary muscle dysfunction --> incompetent valves |
|
|
Term
| What are the clinical signs and symptoms of myocardial Ischemia? |
|
Definition
1. pain (chest, arm, jaw)
2. ECG (ST segment) & dysrhythmia
3. decreased CO
4. dying myocytes leak myoglobins, creatine kinase, lactate dehydrogenase, and troponins |
|
|
Term
| What are a clinical marker used to indicate myocardial ischemia? |
|
Definition
1. elevated serum cardiac troponins (Troponin-I and Troponin-T)
2. Creatine kinase with isoenzymes M & B (CK-MB) *less sensitive |
|
|
Term
| Describe the relationship between myocardial infarction and Acute Coronary Syndrome |
|
Definition
|
|
Term
| Identify the most common compilcations of myocardial infarction |
|
Definition
1. anterior myocardial rupture
2. rupture of the ventricular septum
3. complete rupture of papillary muscle
4. fibrinous pericarditis
5. wall thinning and mural thrombosis
6. ventricular aneurysm |
|
|
Term
| Describe the vascular structure of arterioles |
|
Definition
| extension of arteries that contain bands of smooth muscle that create pre-capillary sphincters |
|
|
Term
| Describe the vascular structure of true capillaries |
|
Definition
| made of endothelium surrounded by smooth muscle an elastic connective tissue |
|
|
Term
| From deep to superficial, name the 5 layers of arterial vasculature in order |
|
Definition
1. Endothelium
2. Basal Lamina
3. Elastic lamina
4. Smooth muscle
5. Adventitia |
|
|
Term
| What is the media portion of the arterial wall made up of? |
|
Definition
| Smooth muscle and connective tissue |
|
|
Term
| Describe the vascular structure of capillaries |
|
Definition
| unicellular (no smooth muscle). Endothelial cells surrounded by basement membrane of connective tissue |
|
|
Term
| What is the significance of the size of intercelluar clefts in capillaries? |
|
Definition
| Pores between adjacent cells are ~7nm - just smaller than albumin. This creates permeability for RBCs, WBCs, and other water soluble components while maintaining impermeabilitiy towards albumin to prevent third spacing. |
|
|
Term
| What are plasmalemmal vesicals? |
|
Definition
| Vesicles that caeey plasma or extracellular fluid though endothelium? SIGNIFICANCE????? |
|
|
Term
|
Definition
| single cell thick layer that create a continuous lining of the entire cardiovascular system |
|
|
Term
| What is the function of the endothelium? |
|
Definition
1. maintain connective tissue and smooth muscle homeostasis by
2. participate in blood-tissue interactions - inflammatory responses and coagulation
3. create semi-permeatble membrate that controls the transfer of fluid and molecules |
|
|
Term
| What phsyiological processes are modulated by endothelial cells? |
|
Definition
1. modulation of vascular resistance
2. maintainence of a normaly non-thrombogenic blood-tissue inteface and induction of thrombosis when neede
3. regulation of immune and inflammatory reactions
4. metabolism of hormones
5. growth regulation of other cells |
|
|
Term
| A person with systemic hypotension may be suffering from a dysfunction in what? |
|
Definition
| Impaired vasoreactivity of endothelial cells. Resulting mainly in vasodilation. There are exceptions when imapired vasoreactivity will cause constriction and decreased perfusion |
|
|
Term
| How does endothelial dysfunction relate to the inflammatory response? |
|
Definition
| Injury induces a surface that is thrombogenic and abnormally adnesive to inflammatory cells. |
|
|
Term
| What is the key mediator of the inflammatory response? |
|
Definition
|
|
Term
| Describe the physiology of a capillary "leak" |
|
Definition
| fluid moves outside of the capillaries into adjacent tissue --> third spacing |
|
|
Term
| What are precapillary sphincters made of? |
|
Definition
|
|
Term
| Describe how pre-caillary sphincters affect vaso-motor tone |
|
Definition
Contraction --> constriction --> increased vascular resistence --> decreased blood flow to tissue
Relaxation --> dilation --> decreased vascular resistence --> increased blood flow to tissue. |
|
|
Term
| What factors affect the constriction/relaxation of pre-capillary sphincter smooth muscle? |
|
Definition
| Constriction/relaxation is stimulated by nerves, hormones, and/or changes in chemical environment. |
|
|
Term
| Describe the process of smooth muscle contraction |
|
Definition
1. action potential triggers calcim ions to bond with calmodulin
2. Ca2+/calmodulin complex joins with and activates myosin kinase
3. myosin kinase phosphorylates the myosin head.
4. ATP is converted ADP generating enery for the formation of myosin-actin crossbridges ---> CONTRACTION
5. when Ca2+ levels drop, myosin phosphatase cleaves phosphate from the myosin head to end contraction |
|
|
Term
| Which vascular receptors are involved in vasoconstriction? |
|
Definition
| alpha adrenergic receptors & vasopressin receptors |
|
|
Term
| Describe the action of beta adrenergic receptors in heart muscle |
|
Definition
|
|
Term
| Describe the action of beta adrenergic receptors peripheral and pulmonary vascular receptors |
|
Definition
|
|
Term
| Name the major vasoconstrictors |
|
Definition
Norepinephrine
Epinephrine
Angiotensin
Vasopressin
Endothelin |
|
|
Term
| Name the major vasodilators |
|
Definition
Bradykinin
Histamine
Nitric Oxidase (NO)
Prostacyclins |
|
|
Term
| What is the most important factor in auto-regulation of vascular tone. |
|
Definition
| local oxygen concentration of the tissue supplied by the capillary bed |
|
|
Term
| What role does oxygen play in contraction? |
|
Definition
oxygen is needed to provide ATP for contractiion
organs with high metabolic rate get more blood flow because they consume more available oxygen = less atp = sphincter relaxation |
|
|
Term
| Chronic ATP and oxygen deficiency cause the release of what substances? |
|
Definition
| Adenosine, CO2, H ions (i.e. from lactate), Histamine, nitric oxide, |
|
|
Term
| What acts to negate the effects of chronic ATP and oxygen deficiency? |
|
Definition
| release adenosine, CO2, H ions, histamine, nitric oxide causes further vasodilation to increase flow |
|
|
Term
| What causes the need for the development of collateral circulation? |
|
Definition
| consistently high metabolic rate and/or oxygen debt of tissue. Increased vascularity is needed to increase blood flow to the tissue in need of more oxygen |
|
|
Term
| What are vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and angiogenin? |
|
Definition
| angiogenic factors involved in collateral circulation formation |
|
|
Term
| Describe the auto-regulation of vascular tone involved in preventing high MAP |
|
Definition
increased BV or strong myocardial contractility --> increased MAP --> increased blood flow through the vasculature --> vessel stretch stimulating a nervous response & streth of endothelium triggers release of NO --> smooth muscle relaxation -->induces vasodilation --> prevents high MAP
dilation of capillary beds |
|
|
Term
| Describe the endothelium mediated release of vasoactive sustances in terms of NO |
|
Definition
1. Endothelium releases NO and other vasoactive substances
2. Vasoactive substances diffuse through the basement membrane and elastin layer
3. Vasoactive substance acts on adjacent smooth muscle causing contraction/relaxation |
|
|
Term
| How does NO induce smooth muscle contraction? |
|
Definition
1. Mechanical injury, toxin exposure, mediator of inflammation
2. Nitric oxide synthase (NOS) in the endothelium is activiated
3. L-arginine is converted to nitric oxide
4. Nitric oxide diffuses out of the endothelium and acts on adjacent cells
5. NO increases c-GMP which induces smooth muscle relaxation |
|
|
Term
| Describe the progression of inflammatory response to "distributive shock" and "septic shock" |
|
Definition
| Vasoactive substances (e.g. NO) act on adjacent smooth muscle of precapillary sphincters to induce vasodiation. Vasodilation --> decreased SVR --> hypotension --> dsitributive shock/septic shock. At the same time gap junctions widen allowing fluid to shift into interstial tissue. |
|
|
Term
| What are the three shock states? |
|
Definition
vasodilation: decreased venous return --> hypotension
capillary leak: tissue edema (anasarca) --> increased volume depletion which contributes to hypotension
coagulation: DIC. thrombosis induced --> coagulation factors quickly depleted --> hypocoagulation state with bleeding --> |
|
|
Term
| Describe the relationship between lung expansion and pulmonary vascular resistance |
|
Definition
| physical expansion of the lungs increases total cross-sectional area of pulmonary capillary bed and lowers PVR |
|
|
Term
| What is oxygen's unique effect on pulmonary arteries (compared to other arteriroles)? |
|
Definition
| Oxygen is a potent pulmonary vasodilator. This may be counter-intuitive because arterioles of other organ systems dilate in response to oxygen deprivation |
|
|
Term
| What effect does increased blood flow have on the pulmonary capillary bed? |
|
Definition
| Blood flow shears the endothelium leading to the release of bradykinin, prstacyclins, and nitric oxide (NO) to result in vasular dilation. |
|
|
Term
| Name the common causes of pulmonary vasuclar resistance |
|
Definition
1. atalectasis - lung collapse
2. chronic high pulmonary blood flow - will cause fixed hypertrophy and vasoconstriction of the pulmonary capillaries
3. decreased oxygen tension from decreased blood folow/hypoxia/hypoventilation |
|
|
Term
| What is the hypoxic pulmonary vasoconstrictor response? |
|
Definition
| compensatory mechanism to shunt blood flow to areas of better oxygenation = oxygenation-ventilation matching |
|
|
Term
| Name two common pulmonary vasodilators |
|
Definition
| inhaled nitric oxide and prostacyclins |
|
|
Term
| Describe the difference between lipid soluble substances and water soluble substances in fluid exchange. |
|
Definition
lipid soluble substances diffuse through cell membranes and endothelium of blood vessels
water soluble substances diffuse through the pores of the endothelium and or protein channels/carriers (depending on molecular size |
|
|
Term
| Name the four primary forces that determine fluid movement |
|
Definition
1. capillary pressure - det. By blood volume and vessel diameter
2. interstitial fluid pressure - det. By fluid volume and tissue encasement
3. plasma colloid (oncotic) pressure - det. By solute concentration of the blood
4. interstitial fluid colloid (oncotic pressure - det. by solute concentration of the interstitial fluid |
|
|
Term
| What causes tissue edema? |
|
Definition
1. loss of capillary membrane integrity: "capillary leak" due to an inflammatory reponse of the endothelium
2. low blood oncotic pressure: protein malnutrition, protein loss, hyponatremia
3. high intravascular hydrostsatic pressure: hypervolemia/vascular congestion from heart failure |
|
|
Term
|
Definition
| abnormal communication between arteries and veins. Often a result of developmental defects but can also be due to rupture of an arterial aneurysm from penetrating injuries or inflammatory necrosis. |
|
|
Term
| Why are AV fistulas potentially dangerous |
|
Definition
| short-circuit blood flow from A-V circulation causes the heart pump additional volume --> high cardiac output failure. In the brain: may rupture and cause hemorrhage. |
|
|
Term
| Compare true and false aneurysms. |
|
Definition
Aneurysm: is localized, abnormal dilation of a BV/wall of the heart
True aneurysm: bound by arterial wall components
False aneurysm/pseudoaneurysm: breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space - "pulsating hematoma" |
|
|
Term
| What is arterial dissection? |
|
Definition
| when blood enters the wall of the artery, as a hematoma, causing dissection between the layers |
|
|
Term
|
Definition
| inflammation of the inner walls of blood vessels |
|
|
Term
| What are the most common mechanisms of vasculitis? |
|
Definition
1. direct invasion of vascular walls by infectious pathogens
2. immune-mediated mechansims - autoimmune
3. physical and chemical injury - radiation, mechanical trauma, toxins |
|
|
Term
| What are the common non-infectious immune mediated vasculitis? |
|
Definition
| Allergy, drug reaction, toxin induced, SLE, Wegners, Kawasaki and other autoimmune diseases |
|
|
Term
| What is Wegener Granulomatosis triad? |
|
Definition
1. necrotizing, granulomatosus vasculitis affecting small to medium sized vessles (capillaries, venules, arterioles, and arteries), most prominent in lungs/upper airways
2. acute necrotizing granulomas of the respiratory tract (ear, nose, sinuses, throat, lungs)
3. renal disease = focal necrotizing glomerulitis.
clinically similar to PAN with addition of respiratory involvement |
|
|
Term
| What are the common findings of inflammatory vasculitis? |
|
Definition
1. anti-endothelial cell antibodies
2. antinetrophil cytoplasmic antibodies - ANCAs
3. immune complex deposition into vessel wall |
|
|
Term
| What is Takayasu arteritis? |
|
Definition
| Autuimmune vasculitis and subsequent fibrous thickening of the aorta, particularly the aortic arch and its branches. Predominantly found in females <40yrs old. |
|
|
Term
| What is polyarteritis nodosa (PAN)? |
|
Definition
-systemic vasculitis of small/medium sized muscular arteries typically renal and visceral vessels. NOT arterioles, capillaries, venules or pulmonary circulation
-disease of young adults but may occur in children and older individuals
-30% of PAN pts have hep B antigens in their serum
-no association with ANCAs |
|
|
Term
| What is Henoch- Schonlein Pupura? |
|
Definition
| depositions of circulating immune complexes in the walls of blood vessels. |
|
|
Term
| What are the clinical s/s of Henoch Schonlein Purpura? |
|
Definition
| -purpuric rash, abdominal pain, polyarthralgia, acute glomerulonephritis |
|
|
Term
| What is Raynaud Phenomenon. |
|
Definition
paroxysmal pallor or cyanosis of the fingers/toes and occasionally the tips of the nose/ears
*exaggeration of normal vasomotor response to cold/emotion causing vasoconstriction of the digital arteries and precapillary arterioles with cutaneous A-V shunts.
**can be secondary symptom of SLE or other autoimmune diseases |
|
|
Term
| Who does Raynaud's Phenomenon affect? |
|
Definition
| 3-5% of the population/ median age of 14 years. |
|
|
Term
| What are the clinical symptoms of Raynaud's Phenomenon? |
|
Definition
| usually benign. May cause atrophy of the skin, subcutaneous tissues and muscles, ulceration and ischemic gangrene. |
|
|
Term
| What is Kawasaki Disease? |
|
Definition
arteritis that involves coronary arteries. Usually affects young children. 80% of cases in children <4years old
**leading cause of pediatric acquired heart disease. 20% of pts develop cardiovascular sequelae. |
|
|
Term
| What are the clinical symptoms of Kawasaki's Disease? |
|
Definition
fever
enlargement of cervical lymph nodes
conjunctival and oral erythema and erosion
edema of the hands/feet
erythema of the palms/soles
skin rash often with desquamation |
|
|
Term
| What are the potential life threatening events related to Kawasaki Disease? |
|
Definition
| coronary aneurysm formation --> predisposition to rupture/thrombosis --> myocardial infarction and sudden death |
|
|
Term
| Describe the changes in vasculature associated with Aging. |
|
Definition
-crosslinking of collagen
-increased collagen
-changes in elastine --> narrowing of vessel lumens -->predisposition to ischemic disease (MI, VTE, stroke) |
|
|
Term
| What is the lymph system? |
|
Definition
accessory route through which fluid can drain from interstitial spaces into the vascular space/blood
-drains proteins and large particles that cannot diffuse through capillaries bc of size of is not lipid soluble |
|
|
Term
| What fluid drains into the thoracic duct? |
|
Definition
| lower body, left head/neck/chest/arm. |
|
|
Term
| What fluid drains into the right lymph duct? |
|
Definition
| right head, neck, chest, arm |
|
|
Term
| Where does the thoracic duct empty? |
|
Definition
|
|
Term
| Where does the right lymph duct empty? |
|
Definition
| juncture of the right subclavian and the internal jugular vein |
|
|
Term
| What facilitates lymph return? |
|
Definition
*compression of lymph vessels
-movement of body part
-contraction of surrounding skeletal muscle
-pulsations of adjacent arteries
-compression of tissues from objects outside the body |
|
|
Term
| What is the most common cause of infectious lymphangitis? |
|
Definition
| Group A beta-hemolytic streptococci |
|
|
Term
| What is infectious lymphangitis? |
|
Definition
infections spread into the lymphatics and create acute inflammation
-lymph system becomes dilated and filled with an exudate that may infect perilymphatic tissues and produce cellulitis or focal abscesses |
|
|
Term
| What are the clinical findings of infectious lymphangitis? |
|
Definition
| subcutaneous red streaks that extend along the lymphatic system with painful enlargement of the regional lymph nodes. Bacteremia may ensue if lymph nodes fail to stop the spread of bacteria |
|
|
Term
| What can cause the occulsion of lymphatic drainage? |
|
Definition
1. tumors
2. removal or ligation of lymph channels/nodes
3. postirridiation fibrosis
4. filariasis - elephantitis
5. post-inflammatory scarring |
|
|
Term
| What are the risks associated with obstructive lymphadema? |
|
Definition
| chylous ascites, chylothorax, chylpericardium can be caused by the rupture of obstructed lymphatics into the peritoneum, pleural cavity, or pericardium |
|
|
Term
| Name the three types of cardiac muscle |
|
Definition
1. atrial/ventricular - highly contractile
2. excitatory muscle
3. conductive muscle |
|
|
Term
| What causes the striations on cardiac muscle? |
|
Definition
| actine-myosin latticework |
|
|
Term
| What structural factors contribute to the rapid conduction of electrical impulses? |
|
Definition
-intercalated discs (low resistance)
-longitudinal gap junctions that allow: free diffusion of ions and negligible hindrance of electrical impulses
-AV bundle (conductive fibers that can cross the fibrous septum between the atria/ventricles |
|
|
Term
| Name the components of myocarial anatomy |
|
Definition
-sarcolemma - specialized cell membrane
-myofibrils: actin (light bands, thin protein filament, I band) and myosin (thick protein filament, dark bands, A bands, crossbridges)
-Z-discs: site of actin attachments
-scarcomere: myofibril that lies between two z-discs
-scarcoplasma: intracellular matrix in which teh microfibrils are suspended
- scarcoplasmic reticulum - ER throughout sarcoplasma |
|
|
Term
| What is unique about the sarcoplasma? |
|
Definition
-high concentration of mitochondria to generate ATP for muscle contraction
-high quantity of K+, Mg++, and Phos |
|
|
Term
| What are the components of Actin Filaments? |
|
Definition
1. Actin
2. Tropomyosin - wrapped around F-actin to block active sites
3. Troponin- 3 subunits: I, T, C; attached to tropomyosin |
|
|
Term
| Describe the affiinities of the different troponin subunits |
|
Definition
Troponin I: affinity for actin
Troponin T: affinity for tropomyosin
Troponin C: affinity for calcium |
|
|
Term
| What are the components of Myosin filaments? |
|
Definition
Tail: 2 polypeptide chains spiraled in a double helix (heavy chains)
Head: globular polypeptide (light chains)
myosin filaments: myosin molecules bundled together
cross-bridge: flexible hinge and arm connected to myosin heads
ATPase: enzyme in head for energy |
|
|
Term
| What is the contractile unit of a cardiac muscle? |
|
Definition
|
|
Term
| Describe the process of cross-bridge formation between actin and myosin |
|
Definition
1. @ rest: active sites on actin filaments are blocked by overlying troponin-tropomyosin complexes
2. During an AP: troponin C binds with Ca2+ to change the configuration of the troponin-tropomyosin complex and moves the complex off the actin active sites
3. actin-myosin interact forming a cross-bridge |
|
|
Term
| What is the mechanism for muscle contraction? |
|
Definition
|
|
Term
| Describe the Walk-along theory |
|
Definition
-myosin heads attach to actin filaments at active sites.
-POWER STROKE: Intra-molecular forces cause the myosin head to tilt the arm forward and draw the actin filament along
-Myosin head breaks away and interacts with next active site
-Z discs pull filaments together at the sarcomeres => muscle contraction |
|
|
Term
| What is the energy source for muscle contraction? |
|
Definition
|
|
Term
| What is the formula for CO? |
|
Definition
|
|
Term
| What is end diastolic volume? |
|
Definition
| volume of blood in a heart chamber after filling/before systole |
|
|
Term
|
Definition
| volume of blood ejected with each contraction of the heart |
|
|
Term
| The olume of blood that remains in a heart chamger after systole is called what? |
|
Definition
|
|
Term
| What is ejection fraction? |
|
Definition
| Percent of blood in hcamber that is ejected with each systole |
|
|
Term
|
Definition
| volume of blood pumped into the aorta each minute |
|
|
Term
| Dilated Cardiomyopathy is associated with what mechanism of heart failure? |
|
Definition
| impairment of contractility - systolic dysfunction |
|
|
Term
| What cardiomyopathy results from impairment of compaliance? |
|
Definition
| Hypertrophic & restrictive cardiomyopathy (diastolic dysfunction) |
|
|
Term
| Histology stains of a a heart with dilated cardimyopathy will have what components? |
|
Definition
| myocyte hypertrophy and increased collagen from interstitial fibrosis |
|
|
Term
| Patients with dilated cardiomyopathy are at risk for what potentially life threatening process? |
|
Definition
| clot formation due to stasis of blood from ineffective contraction of ventricles |
|
|
Term
| Describe the difference between Dilated and Hypertrophic cardiomyopathy |
|
Definition
| -chest radiograph shows severe cardiomegaly for HCM |
|
|
Term
| What is the pathophysiology behind hypertrophic cardiomyopathy? |
|
Definition
| Mutations of proteins related to contraction result in defective contraction, hypertrophy, and myocyte disarray. - most common mutation is B-myosin heavy chain |
|
|
Term
|
Definition
| inflammation of the myocytes |
|
|
Term
| What are the common causes of myocarditis? |
|
Definition
1. viral infections - particularly Coxackieviruses A & B and other enteroviruses
2. Lyme disease - spirochete Borrelia burgdorferi (5%)
3. Autoimmune diseases - JRA & SLE |
|
|
Term
| What are the potential cardiac sequlae of untreated Lyme disease? |
|
Definition
| AV block (30%) and myocarditis |
|
|
Term
| What electrolytes are important in action potential propagation? |
|
Definition
|
|
Term
| Compare and contract the electrical environment of a cell at rest and during an action potential |
|
Definition
At rest: Na conc low inside cell, high outside; K conc high inside membrane, low outside
Auring AP: Na diffuses into cell to increase intracellular charge; K diffuses outside - more negative intracellular charge |
|
|
Term
| What are the two ways that faciliate Na/K movement in/out of the cell? |
|
Definition
| Na+/K+ pump (against conc. Gradient) and K+/Na+ leak channels (follows conc. Gradient) |
|
|
Term
| How is a myocardial action potential generated? |
|
Definition
there is a negative intracellular charge at rest
During depolarization: Na+ leaks into the cell decreasing the negative charge and opening up voltage gated ion channels to allow more Na+ and Ca2+ to enter RAPIDLY. When the cell interior becomes very positive, an action potential is generated/propagated. K+ then rapidly diffuses out of the cell during repolarization to reduce the positive intracellular charge until resting membrane potential is attained. |
|
|
Term
| How long does cardiac muscle remain depoliarized after the initial spike? |
|
Definition
|
|
Term
| What accounts for the plateau of a ventricular action potential? |
|
Definition
| Calcium entry into the interior of myocytes & the decreased permeability to K+ after the onset of the action potential |
|
|
Term
| What is the voltage difference across the membrane of a myocyte during an action potential? |
|
Definition
| 105mV - charge difference between -85mV (resting) to +20mV (depolarization |
|
|
Term
| What is a refractory period? |
|
Definition
| Period of time when cardiac muscle will not respond to stimulation (unless it is a very strong excitatory signal) |
|
|
Term
| Describe the process of excitation-contraction coupling |
|
Definition
1. AP spreads to the interior of the cardiac muscle along the T-tubules of the sarcoplasmic reticulum.
2. sarcoplasmic reticulum releases calcium ions into the muscle
3. T-tubules open allowing calcium from extracellular fluid to enter cell and initiate contraction
4. Calcium ions are actively pumped out of the cells back into the T-tubules and sarcoplasmic reticulum. Ca2+ is also removed from troponin-tropoyosin compelxes by ATP to end cross-bridges. |
|
|
Term
| How do T-tubules store calcium? |
|
Definition
| Calsequestrin - a negatively charged molecule stores Ca2+ |
|
|
Term
| What allows the SA node to maintain a rhythmicity of 60-100bpm? |
|
Definition
| Slow leak Na+ ions that works to increase intracellular charge until an AP is fired |
|
|
Term
| Briefly describe the path of excitation-contraction coupling in the heart. |
|
Definition
| SA node => AV node => Bundle of His => Right/Left Bundle branch => Purkinje fibers |
|
|
Term
| What is the major difference between a sinus nodal and ventricular muscle fiber action potential? |
|
Definition
| greater charge difference needed by ventricular muscle to generate AP ==> slower inherent rate |
|
|
Term
| What is the function of the AV node? |
|
Definition
| Creates a pause between atrial and ventricular contraction to faciliated additional blood emptying from the atria into the ventricle - the atrial kick |
|
|
Term
| Describe the steps of the cardiac conduction pathway |
|
Definition
1. SA node initiates an electrical impulse that travels to the R/L atria
2. Atrial contraction
3. impulse reaches the AV node, experiences delay
4. Impulse travels down to the bundle of his then right/left bundle branches
5. Impulse spreads to ventricles via purkinje fibers.
6. Ventricular contraction |
|
|
Term
| During which phase of the cardiac cycle does perfusion of coronary arteries take place? |
|
Definition
|
|
Term
| Describe the cardiac cycle |
|
Definition
Initiation = generation of AP by SA node
1. AP spreads down atria to stimulate contraction of r/l atria
2. Atria empties blod into relaxed ventricles via mitrial/tricuspid
3. AP reaches AV node and pauses to allow for further ventricular filling
4. Signal travels through bundle of His to the R/L bundle branches and to the purkinje fibers
5. Purkinje fibers cause ventricular contraction. Tricuspid & mitrial valves close at this point
6. RV ejects blood through pulmonic valve into pulmonary artiers
7. LV ejects blood through aortic valve into aorta
8. Pulmonc and aortic valves close when PA and Aorta are completely filled.
9. Blood flows into the relaxed atria |
|
|
Term
| Why is diastole an active phase? |
|
Definition
| Calcium ions have to actively be pumped back into the sarcoplasmic reticulum and t-tubules for relaxation to occur |
|
|
Term
| What is the reason for a split S2 heard during auscultation? |
|
Definition
| BRIEF delayed closing of the pulmonary valve compared to the aortic valve |
|
|
Term
| Relate ECG wave froms and the cardiac cycle. |
|
Definition
P wave: depolarization of the atria
P-R interval: pause in conduction at the AV node
QRS complex: ventricular depolarization & contraction
T wave: ventricular repolarization |
|
|
Term
| How do beta-blockers work? |
|
Definition
| 1. decrease Na+ conduction to decrease HR |
|
|
Term
| What is the function of beta-1 receptors? |
|
Definition
| increase HR and contractility |
|
|
Term
| What will the heart rate of a person with SA conduction block be? |
|
Definition
| 40-60 (inherent rate of bundle of his), or 20-40 (inherent rate of ventricular contraction |
|
|
Term
| What are the common causes of AV block? |
|
Definition
| Ischemia, scar tissue, inflammation (myocarditis), extreme vagal stimulation |
|
|
Term
| What condition results in a ventricular escape rhythm? |
|
Definition
| ventricular escape rhythm |
|
|
Term
| What are premature contractions? Examples? |
|
Definition
| impulses from ectopic foci that fire before the next impulse from the SA node and overcome the refractory period. Examples: PACS, PVCs, supraventricular (AV node) |
|
|
Term
| Define paroxysmal tachycardia |
|
Definition
| raid rhythmic firing of impulses from atria, ventricles, or AV node that over-take the pace set by the SA node. |
|
|
Term
| What is a risk to monitor with paroxysmal tachycardia? vfib? |
|
Definition
| decreased cardiac ouput. There is minimal to almost no cardiac output in vfib. |
|
|
Term
| What is ventricular fibrillation and why does defibrillation work as a teatment method? |
|
Definition
Vfib: rapid erratic firiing from multiple ectopic foci
Defibrilllation may cause all firing cells to go into refraction and allow SA node to set the rate again |
|
|
Term
| Compare and contrast atrial flutter and fibrillation |
|
Definition
Atrial flutter: rhythmic firing from multiple loci
atrial fibrillation: rapid, erratic firing from multiple loci |
|
|
Term
| What happens to cardiac output in atrial arrhythmias? |
|
Definition
| cardiac output may not be affected severely because passive blood flow to the ventricles along with ventricular contractsions maintains cardiac output. |
|
|
Term
| Why is it important to anticoagulate a person who lives with aflutter or afib? |
|
Definition
| stasis of blood in the atria may occur and thrombi may form |
|
|
Term
| What is one major diference between AV valves and the aortic/pulmonary valves? |
|
Definition
| AV valves are connected to chordae tendonae and then papillary muscle and aortic/pulmonic valves aren't |
|
|
Term
| What are cardiac valves made of? |
|
Definition
| made of collagen (connective tissue) and lined with endothelium |
|
|
Term
| Compare and contrast stenotic valves and incompetent valves |
|
Definition
Stenotic valves osbstruc cardiac output. Increases end diastolic volume + congestion
incompetent valves allow regugitation: decreases CP, increases end diastolic volume and congestion |
|
|
Term
| What is the treatment options for incompetent valves? |
|
Definition
-decreasing afterload with systemic and/or pulmoncary vasodilators.
-repair the valve |
|
|
Term
| What are the treatment options for stenotic valves? |
|
Definition
-increased preload to help force blood flow across stenotic valve
-increased myocadial contractility (inotropy) to help pump blood through valve
-repair the valve |
|
|
Term
| What is the pro/con of bioprosthesis valve? |
|
Definition
Pro: no need for continued anticoagulation
Con: limited lifespan - 5 to 10 years because of wear and calcification |
|
|
Term
| Why do mechanical valves require anticoagulation therapy? |
|
Definition
| clots form easily on non-biologic surfaces |
|
|
Term
| What is the major advantage of mechanical valve prosthesis? |
|
Definition
|
|
Term
|
Definition
| acute, immulogical, multi-system inflammatory disease that occurs following group A streptococcal infections (pharyngitis). Antibody response to acute infection |
|
|
Term
| What is the impact of rheumatic fever? |
|
Definition
| It can cause deforming fibrotic valvular disease (e.g. mitrial stenosis) and pancarditis (inflammation of any of three heart layers) |
|
|
Term
| How is Rheumatic fever diagnosed? |
|
Definition
| Aschoff bodies (swollen eosinophili collagen surrounded by lymphocytes) |
|
|
Term
| What are some common examples of rheumatic heart disease? |
|
Definition
1. mitrial valvulitis (vegetations)
2. mitrial stenosis
3. neovascularization
4. aortic stenosis |
|
|
Term
| What is the diagnostic criteria of Rheumatic Fever? |
|
Definition
1. Jones critera: migratory polyarthritis of the large joints, carditis, subcutaneous nodules in arms/legs, erythema marginatum of skin, and sydenham chorea
any 2 of these or 1 + fever, rash, sore throat |
|
|
Term
| What elements would be found in a blood culture of someone with rheumatic fever? |
|
Definition
| cultures for streptococci will be negative by antibodies such as streptolysin O and DNAse B are present and can be detected. |
|
|
Term
|
Definition
| inflammation/infection of the valves and endocardium --> formation of vegetations and tissue destruction |
|
|
Term
| What bacteria most commonly cause endocarditis? |
|
Definition
| Staphylococcus aureus & Streptococcus viridans. |
|
|
Term
| What assessment data from the physical exam might indicate infective endocarditis? |
|
Definition
|
|
Term
| Describe Libman-Sacks endocarditis |
|
Definition
-associated with SLE
-is mitral and tricupsid valvulitis with small, sterile vegetations
-rarely cause problems because not large vegetations and rarely embolize |
|
|
Term
| Describe the structure of the pericardium |
|
Definition
-double layer of CT
-pericardial sac in between CT layers
-pericardial fluid in pericardial sac - 30-40mL thin, straw-colored fluid |
|
|
Term
| Why is a cardiac tamponade life-threatening? |
|
Definition
| severely decreased CO can result in circulatory failure |
|
|
Term
| Compare/contrast fibrinous, pururulent, and hemorrhaggic pericarditis. |
|
Definition
Fibrinous: fibrinous exudate extends from epicardial surface to pericardial sac
Purulent: yellowish exudate that pools in lower pericardial sac
Hemorrhagic: pericarditis with fibrin and hemorrahge. (This would be hemopericardium if no inflammation present) |
|
|
Term
| Where is the vasomotor center of the brain stem? |
|
Definition
| medulla and lower thrid of the pons |
|
|
Term
| How does the vasomotor center communicate to the rest of the body? |
|
Definition
| parasympathetic signals via the vagus, glossopharyngeal, and hering's nerves; direct innervation of the heart via the spinal nerves |
|
|
Term
| What condition does the Cushing's triad indicate? |
|
Definition
| elevated intracranial pressure |
|
|
Term
| What are the three components of Cushing's Triad? |
|
Definition
1. bradycardia
2. Hypertension (wide pulse pressure) - to increase cerebral perfusion as blood flow is blocked
3. irregular respirations/apnea |
|
|
Term
| What cardiovascular functions does the sympathetic nervous system control? |
|
Definition
1. direct innervation of heart from brain stem
2. sympathetic nerves from the thoracic & lumbar spine innervate the periopheral blood vessels, heart, viscera
3. increases heart rate
4. vasoconstriction (sympathetic vasoconstrictor tone/vasomotor tone mediated by Norepinephrine |
|
|
Term
| What conditions are the chemoreceptors in the carotid arteris and the aorta sensitive to? |
|
Definition
-hypoxemia
-hypercarbia
-acidosis |
|
|
Term
| Explain the effect of Norepinephrine on the heart and blood vessels |
|
Definition
-stimulates alpha receptors of blood vessels to cause vasoconstriction
-stimulates beta1 receptors to increase chronotropy and inotropy (increasing na/ca2+ permeability) |
|
|
Term
| Compare and contrast norepinephrine and epinephrine |
|
Definition
Norepinephrine: secreted by nerves directly acting on heart/BV
Epinephrine: produced by adrenal glands; beta > alpha activity |
|
|
Term
| What is the effect of parasympathetic control on the heart & BV? |
|
Definition
-decreases heart rate via indirect innervation of the heart and release of Ach
-vasodilates via innervation of BV |
|
|
Term
| How does acetycholine lower heart rate? |
|
Definition
| Ach causes hyperpolarization by increasing K+ permeability. The more K+, the more negative the cell becomes making it harder to generate an action potential |
|
|
Term
| From where do parasympathetic fibers originate? |
|
Definition
| cardio-inhibitor sections of medulla & pons |
|
|
Term
| Which nerves participate in parasympathetic innervation? |
|
Definition
| vagus, glossopharyngeal, & Hering's nerve |
|
|
Term
|
Definition
| nerve endings embedded in vessel walls |
|
|
Term
| What is the effect of baroreceptor firing? |
|
Definition
| decreases sympathetic activity and increases parasympathetic activity |
|
|
Term
| Which baroreceptors are associated with Hering's nerve? Vagus nerve? |
|
Definition
Carotid sinus baroreceptors ==> Hering's nerve ==> medulla
aortic baroreceptors ==> vagus nerve ==> medulla |
|
|
Term
| What causes baroreceptors to fire? |
|
Definition
| increased pressure in arteries |
|
|
Term
| Describe the Frank-Starling Mechanism |
|
Definition
| Increased sarcomere stretch from adequate filling of the atria with blood results in increased contractile force. BUT there is a critical stretch point at which there is no increase incontractility and MAY decrease contractility. At this point there is no overlap between actin and myosin so fibers cannot contract. |
|
|
Term
| Decribe the Renin-Angiotensin system |
|
Definition
| Decreased arterial pressure --> hypoperfusion of kidneys --> renin is released by kidneys --> rennin converts renin substrate to angiotensin I --> ACE from lungs converts angiotensin I to angiotensin II ==> renal retention of salt and water, vasoconstriction ==>increased arterial pressure |
|
|
Term
| What role does aldosterone play in the RAAS system? |
|
Definition
| Aldosterone increases rental retention of salt (water follows) |
|
|
Term
| What are the physiological effects of angiotensin II? |
|
Definition
-vasoconstriction
-stimulates adrenal cortex to produce aldosterone
-stimulates brain to induce thirst and increase ADH to increase H2O absorption. |
|
|
Term
| Describe the effects of vasopressin |
|
Definition
1. reabsorption of water by renal collecting duct - aquaporins
2. increases sensation of thrist
3. vasoconstriction (binds to v-receptors on BV) |
|
|
Term
| What is the function of atrial naturietic peptide? |
|
Definition
increases sodium excretion by kidneys (water follows) ==> decreasing MAP
*released by stretched atria |
|
|
Term
| Define the limits for prehypertension/hypertension |
|
Definition
prehypertension: intermittent of sustained BPs of 120-139/80-90
hypertension: sustained elevation of BP of >/=140/90 |
|
|
Term
| What is primary hypertension? |
|
Definition
-essential or idiopathic hypertension
-genetic/environmental factors
-afftects 90-95% of individuals with hypertension. |
|
|
Term
| Name the risk factors for hypertension |
|
Definition
-family history
-advancing age
-gender: females <55; male >74
-black race
-high sodium levels
-glucose intolerance
-heavy alcohol use
-obesity
-cigarettes
-low K, Mg, Ca |
|
|
Term
| What is secondary hypertension? |
|
Definition
| secondary to systemic disease that raises peripheral vascular resistance/CO |
|
|
Term
| What is isolated systolic hypertension? |
|
Definition
| elevations of systolic pressure caused by increases in CO, total PVR, or both |
|
|
Term
| Define Complicated hypertension |
|
Definition
-chronic hypertensive damage of systemic BV
-hypertrophy/hyperplasia with fibrosis of BV walls |
|
|
Term
| What is malignant hypertension? |
|
Definition
-diastolic pressure >140mmHg
-rapid progression |
|
|
Term
| What is the pharmacologic treatment for Stage 1/Stage 2 HTN? |
|
Definition
-Stage 1: SBP >140-159 OR DBP >90-99. Thiazide diuretics, ACEi, ARB, beta blockers, CCB, combo
-Stage 2: SBP >160 or DBP>100. Two drug combo - usually a thiazide diuretic + ACEi/ARB/BB/CCB |
|
|
Term
| What is the pharmacologic treatment for HTN with compelling indications? |
|
Definition
-drug for compelling indication
-diuretics, ACEi, BB, CCB, as needed |
|
|
Term
| What is the treatment therapy for HTN prior to or in conjunction with medications? |
|
Definition
|
|
Term
|
Definition
| <140/90mmHg OR <130/80mmHg for those with diabetes and chronic kidney disease |
|
|
Term
|
Definition
-end-systolic volume
-venous return |
|
|
Term
| Afterload is determined by what two major factors? |
|
Definition
-aortic pressure
-aortic valvular function |
|
|
Term
| What major components determine contractility? |
|
Definition
-end diastolic volume
-sympathetic stimulation
-myocardial oxygen supply |
|
|
Term
| What are the major causes of cardiac failure and explain how they can lead to HF. |
|
Definition
1. failure to pump: ventricles cannot empty fully and coronary artery perfusion is decreased due to diastolic dysfunction
2. obstruction to flow: high pressurse in ventricles that then are overworked
3. regugitant flow: additional volume = additional workload
4. disorders of cardiac conduction: uncoordination of cardiac cycle leads to ineffective/inefficient contractions
5. disruption of the continuity fo the circulatory system: blood escapes the cardiovascular system or no oxygenation of systemic circulation |
|
|
Term
| Why do kids increase HR in response to decreased CO? |
|
Definition
| immature myocytes are not able to stretch as much to increase contractility to increase CO…so increase HR |
|
|
Term
| What are two ways that the heart can fail to pump properly? |
|
Definition
1. cardiac muscle contracts weakly or inadequately?
2. muscle cannot relax sufficiently - diastolic dysfunction |
|
|
Term
| What are two mechanisms of obstruction to flow? |
|
Definition
1. lesion prevents valve opening
2. high vascular resistance |
|
|
Term
| What is the most common cause of heart failure? |
|
Definition
deterioration of myocardial contraction related to systolic dysfuction from
-ischemic injury
-presure/volume overload
-cardiomyopathy |
|
|
Term
| What is diastolic dysfunction? |
|
Definition
-inability of the heart chamber to relax and fill completley
- inhibition of coronary artery perfusion |
|
|
Term
| What are some common causes of diastolic dysfunction? |
|
Definition
1. massive left ventricular hypertrophy
2. myocardial fibrosis
3. deposition of amyloid
4. constrictive pericarditis |
|
|
Term
| What are the compensatory mechanisms for Heart Failure? |
|
Definition
1. Activation of neurohumoral systems
2. Frank-Starling mechanism
3. Myocardial structural cahnges (hypertrophy) |
|
|
Term
| What neurohumoral systems are activated during heart failure? |
|
Definition
1.Norepinephrine/Epinephrine increase HR, and preload
2. Activation of RAAS - increase vascular tone/intravascular volume
3. Atrial naturietic peptide might be released from volume congestion to increase salt loss for diuresis |
|
|
Term
| How does the Frank-Starling mechanism compensate for HF? |
|
Definition
| increased preload stretches chambers causeing sarcomeres to stretch resulting in increased contractile force |
|
|
Term
| What causes left heart failure? |
|
Definition
1. poor ejection of blood from LV into systemic circulation?
2. high LV end diastolic pressure and obsturcted pulmomary venous blood return from lungs/body
3. secondary enlargement of the left atrium with resultant atrial dysrhythmias |
|
|
Term
| What are some of the pathologic changes associated with HF? |
|
Definition
| Remodeling occurs as a result of apoptosis, cytoskeletal alterations and ECM protein synthesis -> hypertrophy or dilation |
|
|
Term
| Describe the physiological effects of left heart failure |
|
Definition
1. poor ejection of blood from LV into systemic circulation
2. high LV end diastolic pressure and obstructed pulmonary venous blood return
3. pulmonary edema from increased hydrostatic pressure in pulm veins from congestion
4. impaired systemic venous return d/t right heart congestions
5. enlargement of the left atrium with resultant atrial dysrhythmias --> risk of clot formation
6. hypertrophied and dilated LV |
|
|
Term
| What is the effect of decreased renal perfusion in left heart failure? |
|
Definition
| Decreased perfusion activates the RAAS system but this compensatory reaction is counteracted by the release of ANP |
|
|
Term
| What is prerenal azotemia? |
|
Definition
| Severe hypoperfusion during LHF leads to an accumulation of toxic levels of nitrogen waste |
|
|
Term
| What is the result of severe hypoperfusion to the brain? |
|
Definition
|
|
Term
|
Definition
| Isolated RHF that occurs with chronic or severe pulmonary hypertension. |
|
|
Term
| What are the physiological effects of RHF? |
|
Definition
1. increased portal vein pressure --> hepatomegaly, splenomegaly, and ascites
2. decreased systemic venous return and systemic vascular congestion --> anasarca |
|
|
Term
| What are the anatomical effects of cor pulmonarlae? |
|
Definition
| marked dilated and hypertrophied right ventricle, hypertrophied trabeculae |
|
|
Term
| What are the basic principles of treating HF and what are some examples of those treatments? |
|
Definition
1. Improve cardiac output: increase inotrophy, decrease afterload
2. Prevent volume overload: balance diuresis
3. Prevent additional ischemic injury to the heart: decrease myocardial demand (prevent tachy) |
|
|
Term
| What are the three major catetgories of CHD? |
|
Definition
1. left-right shunt
2. right to left shunt or cyanotic heart disease
3. obstruction |
|
|
Term
|
Definition
| An abnormal communication between chambers or BV that permits blood flow from left to right or reverse depending on the pressure gradient |
|
|
Term
| Which CHD are left-right shunts? |
|
Definition
| ASD, VSD, PDA, and truncus arteriosus |
|
|
Term
| Explain the effects of left-right shunts |
|
Definition
-increases pulmonary blood flow
1. pulmonary edema
2. right ventricular hypertrophy and failure
3. induced pulmonary hypertension |
|
|
Term
| What is the Eisenmenger Syndrome? Describe the pathophysiology |
|
Definition
Eisenmenger Syndrome: a result of chronic increased pulmonary pressure
-PA respond to increased pressure by hypertrophy and vasoconstriction. Irreversible obstructive lesions form on vessels. Left-right shunting
-EVENTUALLY: PVR is equal to or greater than SVR and a right-left shunt is created. LV pumps deoxygenated blood into systemic circulation ==> late cyanotic congenital heart disease |
|
|
Term
| What are the common examples of cyanotic congeital heart disease? |
|
Definition
| Tetrology of fallot, tricuspid atresia, transposition fo the great arteries, total anomalous pulmonary venous connection, tructus arteriosus |
|
|
Term
| Name the CHD that are classified as obstructive |
|
Definition
| Coarcataion of the aorta, aortic valvular stenosis, pulmonary valvular stenosis |
|
|
Term
|
Definition
| opening in the atrial septum that allows left to right shunting across the atria. Commonly due to PFO. |
|
|
Term
| Why is there a risk for pulmonary edema with ASD? |
|
Definition
| pulmonary blood flow may be 2-4x normal |
|
|
Term
| What are the long term complications of ASD? |
|
Definition
| hypertrophy of the right atria and right ventricle. May develop cor pulmonale |
|
|
Term
|
Definition
-Usually associated with TOF
-located at and resulting from a deficient/fenestrated oval fossa --> MID LEVEL ASD
-occurs when ostium secundum becomes too large or from too little growth of septum secundum
- any size; single, multiple, fenestrated |
|
|
Term
|
Definition
-adjacent to the AV valves and w/ a cleft anterior mitral leaflet - LOW ASD
==> partial AV septal defect
-retention of foramen primum due to inadequate growth of septum primum or malformation of endocardial cushions |
|
|
Term
| What is sinus venous ASD? |
|
Definition
-located near the entrance of the superior vena cava - HIGH ASD
-sinus venosus not incorporated into right atrium and interatrial septum
-commonly associated with anamalous connections of the RPV to the superior vena cava or right atrium |
|
|
Term
|
Definition
| -incomplete closure of the ventricular septum with left to right shunting across the septum |
|
|
Term
| What are the effects of a large VSD? |
|
Definition
-pulmonary edema, right ventricular hypertrophy, pulmonary hypertension, and cor pulmonale
-usually at birth with signs of cardiac failure and a murmur |
|
|
Term
| Compare and contrast membranous VSD vs. infundibular VSD |
|
Definition
Membranous VSD (90%)
-involves region of the membranous septum
-abnormal contribution of endocardial cushion tissue; lack of connective tissue from muscular interventricular septum, lack of aorticopulmonary tissue
Infundibular VSD (10%)
-lies below pulmonary valve or muscular septum
-swiss cheese septum: multiple VSDs in muscular septum
-remanants of canals that are normally obliterated with the formation of teh muscular interventricular septum |
|
|
Term
| What CHD is PDA commonly associated with? |
|
Definition
| VSD, coarctation of the aorta, pulmonary stenosis, aortic stenosis |
|
|
Term
| How do you maintain PDA pharmacologically? Why is this imporant? |
|
Definition
| Prostaglandin E to preserve ductal patency. It is important to maintain PDA in children born with CHD that obstruct pulmonary or systemic blood flow |
|
|
Term
| What is CAVC and what are its embryologic origins? |
|
Definition
-superior and inferior endocardial cushions fail to fuse adquately
-RESULTS in:
-incomplete closure of the AV septum
-inadequate formation of the tricuspid and mitrial valves |
|
|
Term
| What is a partial AVSD compared to a complete AVSD? |
|
Definition
Partial
-primum ASD + anterior mitral leaflet cleft creating a VSD
Complete
-large septal defect + large common AV valve
-free communication between all chamers of the heart
-commonly with Trisomy 21 |
|
|
Term
| What are the four classic defects in TOF? |
|
Definition
1. VSD
2. Obstructed right ventricular outflow tract
3. Aorta that overrides the VSD
4. Right ventricular hypertrophy
classic xray: boot-shaped heart due to marked RV hypertrophy |
|
|
Term
| What is the embryological origin of TOF? |
|
Definition
| anterosuperior displacement of the infundibular septum ---> unequal partitioning of the aorta and the pulmonary artery so the RV outflow lumen is too small |
|
|
Term
| Compare and contrast classic TOF and pink TOF |
|
Definition
Classic:
-severe subpulmonic obstruct with great resistance to RV flow
-Eisenmenger syndrom --> cyanosis
-when babies cry - vasoconstriction increases PVR and causes right to left shunting --> turns blue
Pink Tet:
-subpulmonic stenosis is mild
-similar to isolated VSD
-shunt is left to right w/o cyanosis |
|
|
Term
| What is transposition of the great arteries (TGA)? |
|
Definition
| -ventriculoarterial discordance: aorta from RV and pulmonary artery from LV |
|
|
Term
| What is the embryologic origin of TGA? |
|
Definition
| abnormal formation of the truncal and aortopulmonary septa/improper spiraling |
|
|
Term
|
Definition
| when accompanied by a VSD |
|
|
Term
| What are the pathphys effects of TGA? |
|
Definition
-right ventricular hypertrophy ensues bc RV functions as the systemic ventricle
-LV becomes thin walled (atrophic) bc it supp pulmonary circulation |
|
|
Term
| What is truncus arteriosus? |
|
Definition
| developmental failure of separation of the embryologic truncus arteriosus into the aorta and pulmonary artery |
|
|
Term
| What are the pathophys effects of truncus arteriosus? |
|
Definition
-single great artery that receives blood from RV + LV
-underlying VSD
-systemic cyanosis
-decreased PVR increases pulmonary blood flow --> risk of pulm hypertension |
|
|
Term
| What is the embryological classification of Truncus Arteriosus? |
|
Definition
|
|
Term
|
Definition
Total anomalous pulmonary venous connection:
-no pulmonary veins directly join the left atrium
-drains into left innominate vein, coronary sinus, or vena cava
-usually accompanied by a PFO or an ASD |
|
|
Term
| What is the embryologic origin of TAPVC/TAPVR |
|
Definition
| common pulmonary vein fails to develop or become atretic causing primitive systemic venous channels from lungs to remain patent |
|
|
Term
| What are the pathophys effects of TAPVC? |
|
Definition
-hypertrophy of RV and RA
-LA becomes hypoplastic
-cyanosis (maybe) bc of mixing at anomoalous return and also ecause of r-l shunt at ASD |
|
|
Term
| What is tricuspid atresia and what is its embryoloical origin? |
|
Definition
-complete occulsion of the tricuspid valve orifice?
-ASD or PFO present to maintain circulation via right to left shunt
-VSD is present and allows blood to flow from LV to great artery that arises from hypoplastic right ventricle
-commonly associated with hypoplastic right heart syndrome
-Embryo: unequal division of the AV canal, mitrial valve is larger than usual |
|
|
Term
| What is pulmonary stenosis or atresia? |
|
Definition
| obstruction of pulmonary valve which may be mild/severe |
|
|
Term
| What are the pathyphys effects of Pulm stenosis/atresia |
|
Definition
stenosis:
- right ventricular hypertrophy
- post-stenotic dilation of pulmonary artery from jetstream wall injury
-mild stenosis may be asymptomatic
-if subpulm stenosis also exists then pulm trunk not dilated - may be hypoplastic
atresia:
-flow enters lungs through PDA and RV is hypoplastic with ASD |
|
|
Term
| What is coarctation of the Aorta? |
|
Definition
narrowing or constriction of the aorta
-can occur with bicuspid aortic valve, congenital aortic stenosis, ASD, VSD, mitral regugitation, and berry aneurysms of the circle of willis |
|
|
Term
| Compare the two types of Aortic Corarctations |
|
Definition
AC with PDA - infantile aortic coarctation
-tubular hypoplasia of the aortic artch proximal to PDA that is often symptomatic early in life
AC w/p PDA - Adult aortic coarctation
-discrete ridge-like infolding of the aorta just opposite the closed ductus arteriosus distal to the arch vessels
-less severe |
|
|
Term
| What are the different types of aortic stenosis/atresia? |
|
Definition
1. valvular
2. subvalvular
3. supravalvular |
|
|
Term
| Define subarotic stenosis |
|
Definition
| thickened ring or collar of dense endcardial fibrous tissue below the level fo the aortic valve cusps |
|
|
Term
| What affect does aortic stenosis/atresia have on the LV? |
|
Definition
| -pressure hypertrophy bc of obsturction to flow |
|
|
Term
| What advice would you give a pt with aortic stenosis/atresia? |
|
Definition
-avoid strenuous activity - exertion can cause sudden death.
-also antiobiotic prophylaxis is recommended |
|
|
Term
| What is hypoplastic left heart syndrom? |
|
Definition
| severe hypoplasia of the LV, mitral valve, and ascending aorta because of severe congenital aortic stenosis/atresia |
|
|
Term
| What rudimentry fetal structure is present with HLHS? |
|
Definition
| PDA. Necessary for blood flow to the aorta and coronary arteris |
|
|
Term
| Why are HLHS patients at risk for right heart failure? |
|
Definition
| RV has to supply blood fro pulm and systemic circulation, increased work load --> hypertrophy --> heart failure |
|
|
