Cardiology 1

Cardiac tamponade signs/symptoms?

*beck's triad* = elevated JVP, muffled heart sounds, hypotension symptoms: fatigue, confusion, agitation findings: cool extremities, tachycardia, JVP has blunted y-descent, ecg has low voltage and electrical alternans. *pulsus paradoxus*

What are the major causes of acute pericarditis?

*most cases of acute pericarditis are idiopathic* Virus - Coxsackie virus, echovirus (both of these also cause dilated cardiomyopathy), HBV, EBV, HIV Bacteria - staph aureus, strep pneumonia Tuberculous - M. Tuberculosis

What is a friction rub auscultation finding?

A friction rub is a physical exam finding associated with pericarditis. The inflamed pericardial layers are sliding across each other with each beat of the heart. The layers are normally slick and oily. During pericarditis the layers may have fibrin between them or may just be sticky and inflamed. High-friction sliding creates a squeaky sound as if you were rubbing a balloon.

What is acute cardiac tamponade?

Acute cardiac tamponade is a rapid onset fluid filling of the pericardium. This is a life-threatening condition and must be emergently treated by removing the blood (via a needle or drain) from the pericardial cavity. Acute cardiac tamponade can be caused by trauma, cardiac rupture (post MI), aortic rupture, or complications of a surgical procedure.

Acute pericarditis summary

Acute pericarditis is inflammation of the pericardium lining the heart. Causes: Post-MI, Dressler's Syndrome, Echovirus, Coxsackievirus, Strep pneumoniae, tuberculosis, idiopathic Types: Serous (early), fibrous (fibrin has been deposited in pericardial cavity), purulent (bacterial late-stage infection), tuberculous (tuberculosis late-stage infection) Symptoms: Retrosternal chest pain radiating to trapezius. Pleuritic pain made better by sitting up/leaning forward. Dyspnea. Findings: Friction rub, ECG diffuse ST-wave elevation (concave) & PR depression, elevated WBC, elevated ESR, elevated CRP. Treatment: NSAIDs, colchicine (if NSAIDs don't work), steroids (if patient has SLE/RA/uremic pericarditis)

What is acute pericarditis?

Acute pericarditis is rapid-onset inflammation of the pericardium. Pathophysiology: *most acute pericarditis cases are idiopathic*. Can be caused by coxsackievirus, neoplasia, SLE, RA, uremia, STEMI, Dressler's syndrome, post-radiation. Inflamed pericardium pushes against heart and pushes against chest wall. Symptoms: Sharp chest pain aggravated by inspiration and relieved by leaning forward while seated. Findings: Pericardial effusion. Friction rub. Widespread ST-segment elevation (concave elevation) and PR depression. Treatment: treat the cause. Give *NSAIDs* = ibuprofen

What is the pathophysiology of constrictive pericarditis?

Acute pericarditis led to irreversible damage and scarring of the pericardium. The pericardium becomes thick and non-compliant. The heart now has a limit to how much it can fill during diastole, because there's a large barrier surrounding the heart. Constrictive pericarditis leads to mid/late diastolic dysfunction.

What are causes of cardiac tamponade?

Acute: Trauma Cardiac rupture Aortic rupture Complication of surgery Subacute: Cancer Renal failure Idiopathic Viral

What are the major hormones involved in controlling blood pressure?

Angiotensin, antidiuretic hormone (vasopressin), norepinephrine, epinephrine

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Answer below: Acute pericarditis + pericardial effusion. Thickening/inflammation of the pericardium

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Answer below: Concave ST-elevation Inverted T wave Acute pericarditis

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Answer below: Do you see how yellow the visceral pericardium is? And there are pools of pustule fluid on either side of the heart. The yellow color indicates neutrophils were doing some damage. This is purulent pericarditis.

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Answer below: PR depression Concave ST-elevation in many non-contiguous leads Acute pericarditis

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Answer below: Parietal pericardium is clearly inflamed. See the clear/red fluid accumulating at the bottom of the pericardial cavity? This is not yellow, but it is fluid, so we must be at the serous pericarditis stage. Serous pericarditis

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Answer below: Pericardium is messed up. Is it thickened or is there a third layer? Here it looks like a third layer. The middle layer is fluid, blood probably, that's filled the pericardial cavity. Cardiac tamponade.

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Answer below: ST elevations (concave, diffuse) PR depression Acute pericarditis

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Answer below: ST elevations in most leads PR depression tachycardia consider MI, but the ST elevations are in a bunch of leads that aren't positioned together. *acute pericarditis*

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Answer below: See the fluid lining the anterior portion of the heart? Cardiac tamponade

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Answer below: See the thick sheath-like pericardium on the outside of the heart? Constrictive pericarditis

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Answer below: Thickened pericardium, you can see a dark sheath around the heart. some fluid (you can see the black around the heart between the layers of pericardium) Constrictive pericarditis

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Answer below: You can see the web-looking stuff between the layers of the pericardium? This is fibrous pericarditis

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Answer below: tachycardia pretty low voltage QRS voltage changes Cardiac tamponade

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Answer below: Cardiac tamponade You can see massive pools of blood anterior and posterior to this heart.

How do reflexes influence mean arterial pressure?

Baroreceptors and the juxtaglomerular apparatus recognize changes in blood pressure. Baroreceptors call for sympathetic nervous system activity when blood pressure is low and encourage parasympathetic nervous system activity when blood pressure is high. *increased blood pressure = increased baroreceptor firing rate* *decreased blood pressure = decreased baroreceptor firing rate*

What is the mechanism behind baroreceptor reflexive influence on arterial blood pressure?

Baroreceptors fire more during increased pressure, less during decreased pressure. Baroreceptor firing inhibits the sympathetic autonomic nervous system. If you're firing a bunch, you'll be decreasing sANS activity. Baroreceptor signals go to the nucleus of the solitary tract (in the medulla oblongata)

What factors influence rate of diffusion in capillary beds?

Blood flow Molecule concentrations in blood/interstitial space Capillary membrane permeability to molecule Capillary surface area

What is bulk flow?

Bulk flow is the transport of h2o, electrolytes, and small molecules in the capillaries, from the blood to tissues. Bulk flow refers to the flow of fluids and small solutes *between* capillary endothelial cells. Bulk flow occurs in continuous, fenestrated, and sinusoidal capillaries.

What disease is associated with pulsus paradoxus?

Cardiac tamponade Asthma Croup

What diseases are associated with pulsus paradoxus?

Cardiac tamponade Asthma Croup

Cardiac tamponade summary

Cardiac tamponade is filling of the pericardial cavity with fluid. Cardiac tamponade leads to heart failure, because fluid is applying a constant pressure on all of the chambers of the heart. Causes: Trauma, cardiac/aortic rupture, neoplasm, renal failure, post-viral, idiopathic. Pathophysiology: Pericardial cavity fills with fluid, which stops the heart from being able to fill normally. RV volume increases, LV volume decreases. Stroke volume & cardiac output decrease. This causes heart failure/ischemia throughout the body. Symptoms: Fatigue, confusion, agitation (sympathetic nervous system input) Findings: Beck's triad (elevated JVP, muffled heart sounds, hypotension). Pulsus paradoxus. Electrical alternans, low voltage QRS, cool extremities. *blunted y-descent in JVP describes impaired RV filling* Treatment: Stick a needle in the chest and get fluid out.

What is cardiac tamponade?

Cardiac tamponade is fluid filling the pericardial cavity and compressing the heart. Pathophysiology: Rupture, or infection, leads to effusion of the pericardial cavity. Fluid builds up and applies a pressure on all of the chambers of the heart. This decreases diastolic function, and can eventually mess with systolic function as well. *acute cardiac tamponade is one of the most serious cardiac conditions you can have*. As tamponade progresses, *diastolic pressures in all 4 chambers equillibrate* Symptoms: Dyspnea, chest pain, confusion, agitation, Findings: *beck triad* = hypotension, jugular venous distention, distant heart sounds. *pulsus paradoxus* = decreased blood pressure with inspiration. Low voltage QRS and *electrical alternans* in ECG. Treatment: Stick a needle in the pericardial cavity and remove the fluid.

What is the major conceptual difference between cardiac tamponade and constrictive pericarditis?

Cardiac tamponade leads to a pressure being constantly applied on all chambers of the heart, because the blood is always there. Constrictive pericarditis leads to decreased diastolic filling, but only impacts cardiac function once the heart has begun to expand and reaches its new boundary. Constrictive pericarditis only messes with the heart during late diastole.

What role does hormonal control play in regulation of blood flow?

Catecholamines (epinephrine and norepinephrine) are released from the adrenal medulla (which is directly linked up to the sympathetic nervous system). NE binds to alpha 1 receptors on vascular smooth muscle. Epinephrine binds to alpha 1 receptors, but only at *high concentrations*. Epinephrine will bind to beta 2 adrenergic receptors, opposing alpha1 vasoconstriction. beta 2 receptors are mostly in the skeletal and coronary smooth muscle capillary beds. Angiotensinogen (made by the liver) is converted to angiotensin 1 by renin and then to angiotensin II by ACE. Angiotensin causes vasoconstriction. Vasopressin (Anti-diuretic homrone) is a vasoconstrictor released from the pituitary gland. Vasopressin increases MAP. *all hormonal control of blood flow is initiated by sympathetic autonomic nervous system input*

What primary diseases are associated with acute pericarditis?

Connective tissue disorders: SLE, Rheumatoid Arthritis, systemic sclerosis

What is constrictive pericarditis?

Constrictive pericarditis is a chronic progression of acute pericarditis. An unresolved pericarditis leads to irreversible scarring and thickening of the pericardium. Most common cause in developing world is *TB*. Most common cause in USA is untreated viral illness (coxsackievirus, echovirus) Pathophysiology: Severe acute pericarditis leads to permanent tissue damage in the pericardium. Pericardium thickens and becomes fibrous. Symptoms: Right heart failure = peripheral edema, ascites, fatigue. Findings: Rapid y descent in JVP (RA empties really fast into RV before being stopped by the stiff pericardium). *kussmaul sign* = increased JVP on inspiration. Treatment: pericardiectomy (rip the pericardium off the heart. this has a lot of complications)

What are the major types of capillaries?

Continuous capillaries and fenestrated capillaries. Continuous capillaries have tight connections and allow only fluid/small solutes through into interstitial space. These are the most common Fenestrated capillaries have holes within each endothelial cell, which allows more flow of molecules between the bloodstream and tissues. There are also sinusoidal capillaries, which allow whole blood cells to leave the bloodstream. These are seen more in the spleen and near bone.

What are continuous capillaries?

Continuous capillaries are the most common type of capillary seen in our bodies. Continuous capillaries have tight endothelial cells lining the lumen which are connected by tight junctions. Continuous capillaries have small gaps between endothelial cells to let fluids and solutes pass into interstitial space. Continuous capillaries are most abundant in skin, muscles, the thymus, lungs, and CNS.

What is diastolic pressure?

Diastolic pressure is the peak pressure in the large arteries during diastole.

What is the mechanism of nutrient exchange in capillary beds?

Diffusion! Nutrients (high in blood, low in tissue) diffuse out of the lumen into tissue. Waste (high in tissue, low in blood) diffuse from tissue back into blood). Diffusion rate is based on concentration gradient of molecule, capillary permeability, capillary surface area, and total blood flow.

What is dressler's syndrome?

Dressler's syndrome is inflammation of the pericardium that occurs 1-4 weeks after a large MI. It's believed to be an autoimmune process. Symptoms: Chest pain, fever, pericarditis (pericardial friction rub), pericardial effusion (fluid in pericardium)

What causes pulsus paradoxus?

During inspiration, blood in the pericardial cavity pools around the pulmonary circulation. This increases pulmonary pressure and makes it hard for the RV to push fluid through. LV has less fluid to push out, so CO decreases. Pulsus paradoxus = blood pressure decreasing significantly during inspiration.

Acute pericarditis signs/symptoms?

Early symptoms = fever, malaise (general ill-feeling), myalgia (muscle pain) As pericarditis progresses, you'll have retrosternal chest pain, radiating out to the trapezius. Acute pericarditis chest pain usually *worsens with inspiration/cough*. Chest pain *gets better if you sit up and lean forward* Dyspnea is experienced throughout a bout with acute pericarditis.

What viruses are associated with acute pericarditis?

Echovirus and coxsackivirus are the major viral causes of acute pericarditis. Echovirus and coxsackievirus are also associated with causing dilated cardiomyopathy EBV, HBV, HIV

Cardiac tamponade ECG changes

Electrical alternans (QRS voltage peak changes beat-to-beat as heart swings through pooled, swishing blood) Low-voltage QRS (blood decreases signal throughput)

What causes electrical alternans?

Electrical alternans is seen in cardiac tamponade. Electrical alternans is caused by fluid in the pericardial cavity which is messing with transmission of electrical activity in the heart. Since the fluid is swishing around, and the heart is swishing around, this dampening is seen in different leads during different heart beats. The changing QRS voltage beat-to-beat = electrical alternans

What are laboratory findings associated with acute pericarditis?

Elevated C reactive protein Elevated erythrocyte sedimentation rate Elevated white blood cell count

Pathology of serous pericarditis

Epithelial pericardial cells respond to inflammation/infection by releasing serious fluid into the pericardial cavity.

What are common symptoms of acute pericarditis?

Fatigue, chest pain (radiating backwards to trapezius, feels better when you lean forward, worse when breathing), dyspnea.

What are fenestrated capillaries?

Fenestrated capillaries are capillaries where endothelial cells lining the lumen have small holes, almost gaps, which allow fluid to travel into neighboring tissue. The basement membrane of fenestrated capillaries is continuous (unlike sinusoidal capillaries) Fenestrated capillaries are seen in the small intestine, endocrine glands, and kidneys (areas in the body where a lot of filtration/absorption occurs)

What is fibrinous pericarditis?

Fibrinous pericarditis is a stage of acute pericarditis where inflammatory vasodilation causes leakage of plasma proteins into the pericardial space. Fibrinogen is converted to fibrin and deposited in the pericardial cavity. Fibrinous pericarditis is associated with echovirus, coxsackievirus, HIV/HBV/EBV, SLE/Uremia (renal failure), and post-MI.

What are symptoms/findings associated with constrictive pericarditis?

Findings: *kussmaul sign* = JVD during inspiration, JVP rapid y descent, thickened pericardium in CT. . Symptoms: peripheral edema, ascites, fatigue, dyspnea, elevated JVP, hepatomegaly, pleural effusion

How is arterial blood pressure influenced by hormones?

Hormones (EPI/NE/angiotensin/vasopressin) are activated/released after sANS activity in response to baroreflex. sANS stimulates release of EPI/NE from adrenal gland. sANS stimulates angiotensin by releasing renin from kidney sANS induces vasopressin All of these hormones are initiated by baroreflex input to sympathetic nervous system. It takes *10-15 minutes to get hormone levels up* *hormone response to baroreceptor input lasts for hours/days, compared to short but immediate sANS*

What is beck's triad of clinical findings?

Hypotension, muffled heart sounds, and jugural venous distention. Beck's triad of clinical findings indicate that someone has cardiac tamponade.

How do you treat cardiac tamponade?

If it's caused by hemorrhage you need to do surgical removal of fluid. If it's subacute or not a large hole in the heart wall you can use a needle to create a vacuum and pull the blood out. This doesn't work for an open hole in the heart because the vacuum would pull all of the blood out of your heart and not fix anything.

How do cardiac hemodynamics change in constrictive pericarditis?

In constrictive pericarditis there's now a huge barrier surrounding the heart and keeping it from expanding as much during diastole. Late diastolic filling is impeded. During inspiration you'll have impaired filling of the RV. Blood backs up into SVC and into the jugular veins. You'll see a giant jugular vein during inspiration *kussmaul's sign*

How does rate of blood flow influence capillary blood-tissue exchange?

Increased blood flow leads to increased molecule exchange. A high concentration of molecules in the blood is constantly being exposed to new capillary wall, rapidly diffusing.

Pathology of fibrinous pericarditis

Inflammation causes vasodilation. Vasodilation allows endothelial leakage. coagulation cascade proteins enter the pericardial cavity. Coagulation cascade is initiated and fibrinogen is converted to fibrin. Fibrin clumps up and deposits within the pericardial cavity.

How does JVP change in someone with cardiac tamponade?

JVP will have a blunted descent during diastole. The *y-descent* of JVP will be *blunted*

What changes in jugular venous pressure are seen in people with constrictive pericarditis?

Jugular venous pressure will drop really quickly during diastole as the RV rapidly fills. However, the RV will quickly expand up to its new limit (the fibrous pericardium doesn't stretch) and is suddenly stopped from filling more. Rapid y-descent in JVP graph represents rapid diastolic filling. You'll see a rapid increase in JVP afterwards, which represents impaired late diastolic filling.

What is kussmaul's sign?

Kussmaul's sign is when you have jugular venous distention during inspiration. In a healthy heart you have JV collapse during inspiration. In a heart with *constrictive pericarditis* you have impaired RV filling, and fluid backs up into the SVC and the jugular veins.

How is blood flow controlled in the microvasculature?

Local control: Myogenic (stretch-sensitive ca 2+ channels leads to increased contractile function under pressure) Metabolic (release of metabolic byproducts leads to vasodilation) Autacoid (endothelin, NO) Central control: Neural (NE from sANS) Hormonal (NE/Epi from adrenal gland, angiotensin, vasopressin)

What is mean arterial pressure?

MAP = 1/3*systolic pressure + 2/3*diastolic pressure

What is microcirculation?

Microcirculation describes the arterioles, metarterioles, precapillary sphincters, capillaries, and small venules embedded in organs responsible for actually getting blood into tissues.

What is electrical alterans?

Muffled electrical activity seen in cardiac tamponade. There's fluid sloshing around in the pericardial cavity and causing transient electrical conduction blocks back to each lead. This causes a variable QRS voltage.

What pathogen is associated with acute pericarditis in immunocompromised patients?

Mycobacter Tuberculosis

What do you use to treat acute pericarditis?

NSAIDs (usually ibuprofen) If NSAIDs don't work give colchicine If colchicine doesn't work, give steroids. Give steroids if there is SLE, RA, or uremic pericarditis.

What is neurogenic tone?

Neurogenic tone is the base level of sANS activity in your blood vessels.

How do you treat constrictive pericarditis?

Pericardiectomy = ripping the pericardium off of the heart so it can expand again. This is obviously super painful and leads to a lot of complications.

In what ways does pericarditis show up after an MI?

Pericarditis can show up as a quick-onset post-MI pericarditis or as Dressler's syndrome. The two conditions have very similar symptoms but different causes. Post-MI pericarditis occurs 1-7 days after an MI. It's caused by spreading inflammation from the site of infarct to epicardial tissue and the pericardium. Dressler's syndrome occurs 1-4 weeks after an MI. It's caused by an autoimmune reactivity against pericardial tissue. Both causes of pericarditis present as a friction rub, chest pain, and fever.

What is post-mi pericarditis?

Post-MI pericarditis is an inflammation of the pericardium that happens within a week of a large MI. Inflammation from the endocardial infarct has spread through the heart wall and is now irritating the epicardium/visceral pericardium/parietal pericardium.

What are precapillary sphincters?

Precapillary sphincters are regions of smooth muscle that create a layer of separation between arteriolar and capillary blood flow. Some sphincters are inherently closed, some are open (this is called vasomotion), allowing flow through 1/3 of capillaries at rest. Precapillary sphincters are influenced by sympathetic nervous system input.

What is the pulse pressure?

Pulse pressure = Systolic pressure - Diastolic pressure

What is pulsus paradoxus?

Pulsus paradoxus is a physical finding associated with cardiac tamponade. As you breath in, your blood pressure measurement drops more than 10 mmHg. This is abnormal. Pulsus paradoxus is caused by pooling of blood that puts pressure on pulmonary circulation during inspiration. This stops forward flow and decreases cardiac output significantly. The RV fills with fluid and expands, pushing the interventricular septum into the LV's chamber. The LV has decreased filling because of the temporary pulmonary circulation block.

What is purulent pericarditis?

Purulent pericarditis is late-stage acute pericarditis associated with bacterial pericarditis. Purulent pericarditis leads to yellowing of the visceral pericardium and fluid deposition in the pericardial cavity.

What makes you thirsty when you have low effective arterial blood volume?

RAAS Angiotensin II binds to receptors in the subfornical organ in the brain, which makes us thirsty and also gives us an appetite for salt.

What causes constrictive pericarditis?

Severe acute pericarditis that does not heal reversibly but scars will become constrictive pericarditis. Scarring leads to deposition of collagen and other connective tissue in replacement of the normally stretchy pericardium.

What regions of the body are fed by blood vessels that have serious sympathetic nervous system innervation?

Skin, splanchnic muscle, the kidneys, and skeletal muscle.

what bacterial pathogens are associated with acute pericarditis?

Strep pneumonia, staph aureus

What is subacute cardiac tamponade?

Subacute cardiac tamponade is a slow leaking of fluid into or accumulation of fluid in the pericardial cavity. Subacute cardiac tamponade can be caused by cancer, renal failure, viral infection, or can be idiopathic. Treat by removing fluid from pericardial cvity.

What are the primary extrinsic vasoregulatory mechanisms?

Sympathetic adrenergic alpha 1 receptors. Hormonal release of norepinpherine and epinephrine

What are the mechanisms though which the sympathetic nervous system causes vasoconstriction?

Sympathetic nervous activity leads to release of norepinephrine and binding of NE to alpha 1 adrenergic receptors on vascular smooth muscle cells. Alpha1 receptors are present in basically all capillary beds, arteries, arterioles, venules, and veins. Sympathetic nervous system innervation is most prevalent in the blood vessels feeding the skin, splanchnic muscles, skeletal muscles, and kidneys.

What is systolic pressure?

Systolic pressure is the peak pressure in the large arteries during systole

What are the main functions of the capillaries?

The capillaries are the primary site of gas, nutrient, and waste exchange in the body. This is where oxygen gets from the blood to tissues. Capillaries are small and impregnated in tissues, so they provide a great site for materials exchange.

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The heart almost looks like it is encased in a shell. This is an extremely thick layer of connective tissue. *constrictive pericarditis* you can see how constrictive pericarditis would limit expansion of the heart during diastole.

What is the pathogenesis of acute pericarditis?

The normally empty pericardial cavity begins to fill with serious fluid produced by epithelial cells of the pericardium in response to infection. Inflammatory vasodilation leads to leakage of plasma proteins into the pericardial cavity. Fibrinogen is cleaved into fibrin, and clots begin to form in the cavity. Inflammation attracts neutrophils, macrophages, and lymphocytes to the site of infection/irritation. In tuberculous pericarditis you'll see the formation of granulomas in the pericardium (macrophages + lymphocytes + collagen) Widespread acute pericarditis can turn into constrictive pericarditis if the pericardium scars.

What is the nucleus of the solitary tract?

The nucleus of the solitary tract is the arterial blood pressure control center of the brain stem. The nucleus of the solitary tract takes baroreceptor input and directs pANS or sANS activity based on perceived blood pressure.

What is the pathophysiology of cardiac tamponade?

The pericardial cavity fills with blood which increases pressure applied to each of the chambers. Diastolic and systolic dysfunction ensues as pressures in each chamber start to equilibrate. Cardiac tamponade can be made worse during inspiration: increased right sided venous return --> impaired RV filling/RV dilation --> impaired LV filling --> decreased cardiac output.

What are the functions of the pericardium?

The pericardium has three functions. 1. Keep the heart in place within the mediastinum 2. Keep the heart from getting infections passed along from other organs 3. Keep the heart from expanding too much (pericardium creates a boundary)

How does the sANS influence blood pressure?

The sANS innervates blood vessels (alpha1, beta2), activates RAAS, the adrenal medulla, and works on the heart. In the heart, sANS activity increases ventricular myocyte contractility, activates the SA node and the AV node

What baroreceptors are involved in arterial pressure regulation?

There are baroreceptors in the aortic arch and the carotid baroreceptors. The vagus nerve (CN x)innervates aortic arch baroreceptors. The glossopharyngeal nerve (CN xi) innervates the carotid sinus baroreceptors

What regions of the body are fed by blood vessels with limited sympathetic nervous system innervation?

Think "core" tissues: Cerebral, coronary, and pulmonary blood flow must always be preserved, so there's not going to be sympathetic innervation (remember that sympathetic activity is systemic, not tissue-specific. You wouldn't want blood flow to your brain to stop while you worked out)

What is the diastolic pump?

This is a passive characteristic of the compliant large arteries and the aorta. The aorta expands a little bit (distends) during systole, storing what would be a higher pressure fluid as potential energy (the walls will "spring back" into place). During diastole, the aorta/large artery walls begin to push on our blood and push it forward. *the diastolic pump is a passive mechanism of aortic compliance that decreases our systolic pressure and increases our diastolic pressure*

What is tuberculous pericarditis?

Tuberculous pericarditis is acute pericarditis caused by m. tuberculosis. You'll see granuloma formation in the pericardium. Otherwise tuberculous pericarditis has similar symptoms to any type of acute pericarditis: chest pain radiating to back that gets better when you lean forward, dyspnea.

How do vasodilators influence precapillary sphincter activity?

Vasodilators increase flow through the arterioles by decreasing pressure. Vasodilators also decrease precapillary sphincter muscle tone, allowing more blood to flow into the capillary beds.

What is vasomotion?

Vasomotion is random opening/closing of the precapillary sphincters at rest. Vasomotion typically results in 1/3 of capillaries being open to flow during rest. This can be influenced by increased activity, hormones, nervous system input, or medications.

What is the normal pericardial anatomy?

Visceral pericardium lines/interfaces with the epicardium of the heart. Parietal pericardium is a second, much thicker layer, that interfaces with other tissues in the mediastinum. The pericardial cavity is the potential space between the two pericardial layers. The pericardium has three functions: 1. keep the heart in place in the mediastinum 2. protect the heart from infection spreading from other organs 3. Protect the heart from expanding too much (provide a boundary to control volume changes)

How does the baroreflex respond when you stand up?

When you stand up, you have a rapid decrease in central venous pressure. You have a decreased preload, so you have decreased end diastolic volume and pressure. Decreased preload = decreased stroke volume. Decreased stroke volume = decreased cardiac output Decreased cardiac output = decreased afterload Decreased afterload = decreased pressure on baroreceptors = decreased baroreceptor firing. Baroreceptor activates sANS: increase heart rate & contractility, increase RAAS, increase arterial constriction = increase MAP back towards normal.

How does an ECG change when someone has pericarditis?

You will see different ECG changes depending on how long someone has had pericarditis. They'll usually have tachycardia and low-voltage QRS Immediately at onset of chest pain there are concave ST-elevations, PR depressions. Early into a bout with acute pericarditis you'll have ST-segment resolution but will still have PR depression. Late pericarditis will show T wave inversion. Eventually the ECG will return to normal.

Acute pericarditis ECG changes

in general: low voltage, tachycardia 4 different ECGs can be seen: At onset of chest pain: *Diffuse concave ST-segment elevation. PR depression* Early acute pericarditis: PR depression Late acute pericarditis: T-wave inversion Post-disease: T-waves return to normal upright orientation.

How does the pANS influence blood pressure?

pANS only innervates the SA and AV nodes in the heart. pANS will decrease conduction velocity and slow heart rate, but doesn't influence contractility or blood vessel constriction.