1. Pericardium- Fibrous sac that covers the heart
2. Myocardium- Muscle layer
3. Endocardium- Membrane that lines the heart

Tell me about the Myocardium

(Sarcomers)

(intercalted disc)

• Sarcomers- contracts heart interwoven in myocardium then called Synctium- all these fibers will wrk together so we have good even smooth contractions= good start top to bottom
• Intercalted disc- connect sarcomers provide easy conduction for action potential from one fiber to the next keep their from being a delay.

1. Small amount of extracellular calcium move in cell as action potential begins.
2. This opens up SR releases large amounts of intracellular CA+ into the cytosplasma.
3. Intracellular free ca+ attaches to troponin.
4. Troponin turns and becomes thick filament
5. Actin and myocin hook up causing cell shortening
6. ATP comes to start power stroke
7. After power stroke myocin lets go
8. filament turns away and muscle moves

Isololumetric contraction= vessels has been loaded full of fluid stretches- stretch creates contraction amount og stretch determins strenght of contraction

1. Ventricals fill with blood and contract
2. Pushes through tricuspid & mitral closing= closing is 1st heart sound
3. Semilunar valve open and allows blood to flow into aorta and pulm artery out of the heart

1. Ventricles relax pressure on pulm and aortic valve stop they close = 2nd heart sound
2. Blood enters atria and flows thru av valves into ventricals
3. Atrial kick forces blood into ventricals

1. Preload- Volume(what comes back to heart)/ Stretch of the heart.
2. Afterload- Pressure work of heart(BP)
3. Conctractility-( Orderly Progression of electrical single from top to bottom)

• HR- determins time in diastole and filling time of ventricle and perfusion of arteries
• Rythem-Orderly Progression of the electrical single from to bottom

• Arteries- thick muscle layers can control easier, Left ventrical is the pump
• Veins -can exspand more they depend on one way valves and skeletal muscle for movement

Nitric oxide causes constant smooth muscle relaxation making vessels bigger on the other side we have vasonconstrictors like endothelins, ang 2 and PG that are constricting and making vessel smaller.

(We have constant regulation by way ofr hormones)

1. High levels of lipid in the blood
2. Endothelial cell injury
3. Migration of inflammatory cells(macrophages engulf LDL)
4. lipid accumulation and smooth muscle proliferate-(macrophages engulf as much lipid as they can and turn into foam cells that are still secreting inplammatory mediators.
5. Platelets form a patch over the top muscle
6. Collegen comes and tries to heal fibrous cap.
7. Vessel occlude and eventually rupture and move down stream to clog vessel.

1. Large lipid core
2. thin fibrous cap- very easy to knock off
3. fissured cap- cap with a bruise/ grove wrosion
4. inflammation within  cap
5. superficial endotheial wrosion- plaate aggregation-

Women c/o pain in LLE

1. Foot cool pale
2. reports red/ warm sitting
3. pain with walking
4. skin LLE shinier then RLe

1. no b/f weak pedal pulse
2. b/f decreased
3. 0 prostiglandin
4. lose fat layer under skin can
5. t maintain tissues

1. Neural control- lower pons and medulla cardivascular center rapid short term regulation.
2. Peripheral control- Barorecepters in carotid and aortic arch respond to pressure changes SNS heart rate and vasoconstric

1. Decreased BP
2. renin release angiotensinogen activates
3. angiotensis 1 this hooks up to ace in the lungs
4. Angio 2 is released causes strong vasoconstriction
5. aldosteron is released to save sodium and water and excrete K+ causing a increase in blood volume/afterload

Released d/t over stretched atria

increase NA+/water excretion= vaso dil decreased preload & after load= decreased BP

Classification of BP

1. Normal
2. pre-hyp
3. stage1
4. stage2

1. 120/80
2. 120-139 0r 80-89
3. 140-159 or 90-99
4. >160 or >100

What is problem with pericardial effusion

& How can we fix this problem?

Fluid gets build up in pericardial sac causing Tampnade= heart can't move at all d/t decreased space d/t the increase in fluid.

Tube drain or window

1. Stable anginia-Pain when heart 02 demaind increases if this person stops activity the will go away
2. Variant angina-Pain when artery spasm, not associated with activity not due to arterosclerosis
3. Unsable anngina-Pain at rest or increase or in stable anginia, pain now does no stop when you stop activity.

• chest pain
• SOB- d/t blood settles in lungs- NOT 02 PROBLEM
• Diaphoreses d/t sympathetic ns release epi & norepi
• n/v d/t vasoncontriction of bv and decreased blood flow to gut and kidney

Look @ cardiac markers

CK-MG elevated

Troponin less then 4% GOLD STANDARD

1. Transmural Mi=stemy= st elevation complete occlution entire thickness of  muscle
2. Subendocardial mi= no stemy or st elevation= only part wall.

Morphine= vasodilation

oxygen= increase suplly

Nitrates= dialate coronary arteries and bring blood flow to the heart

aspirin= antiplatelet

• also want to start on heparin drip to stop clot from getting bigger does not break it

1. Thrombolysis= BEST break down clot, could avoid mi must catch right away to get this drug 2-3 hrs.
2. PCI(percutaneous coronary intervention) cath femoral artery, run it to coronary artery

• PTCA- heart cath ballon open up artery jam plaque back in wall
• PTCA w/ stent
• ( 6 months people will go back to their normal life)

1. CABG- Different vessel and bypass the clot

Inability of heart to pump enough blood to meet the demand on of the body.

• FIRST SYSTEM

1. Cardiac output is decreased heart fails
2. Hypothmus know this do it activates baroreceptors and SNS
3. nor and epi increase Heart rate & contractility
4. cardiac output increases

• SECOND SYSTEM

1. RAS activated and decrease GFR
2. Kidney holds on to fluid
3. Preload and after load are increased
4. cardiac output increases

Fluid back up in body

• hematomegly
• ascietes
• splenomegly
• anorexia
• sbq edema
• JVD

What happens to the lungs during LEFT and RIGht sided hrt failure

You can't get 02 blood to body

• fatique
• obliguria
• increased hrt
• restless
• confusion
• anxiety

Fluid builds up in the lungs

• dyspnea on excertion
• orthopena
• cough
• paroxymal noctura dyspnea
• cyanosis
• basilar crackles

Stenotic- can't open- hear a murmur of blood shooting through narrown opening when the valve should be opened

Regurgiant- can't close- hear a murmur of blood leaking through valve when shoould be closed

Mediators

it is how ever caused by

• Decreased c/o= decreased perfusion
• tissue hypoxia= anarobic metabolism and little energy
• lactic acid builds up= tissue damage
• inflammatory process= decreased cardiac output
• decreased circ volume= decreased cardiac output

Where it starts @.

Distribuative start when their is bad perfusion

Cardiac starts at the heart.

1. Posiitive inoptrop- increase cardiac putput increased force of contraction.(becare ful have to balance out ability of hrt)

• Dobutamin- drug that increases force of contraction

1. Fluid restriction- Diuretic decrease fluid decrease the prload which decreases force of contraction
2. Intra- aortic ballon pump- support heart take over wrk of hrt letting it to rest

1. Filtration- where blood enters bowmans capsule intial formation of urine( no plasma protien, RBC, WBC this stays in blood)
2. Reabsorption- You had gotten rid of everything but you pull fluid back in to try and create near perfect blood. (electrolytes, water, bicard, acid)
3. Secretion-final adjusments we have almost perfect blood put things back in urine we really don't need occurs in distal tubuls

Controls urine flow by controling BP & BV

1. Macula densa- checks NA
2. J-cells- chck BF

Controls GFR

What does ANP & BNP Do?

causes kidneys to stop reabsorbing Na+ & Water

(acts as a diuretic) sodium and water will be loss in urine decreasing blood volume, afterload, BP & stretch of the heart

ANP= overstretch atria

BNP= over stretched Ventricals

Anemia= d/t no erythropoetin

Weak bones d/t no vitamin d activation d/t kidney disease, which is used to reabsob calcium.

I don't know i want to know what it was yesterday.

• Serum creatinin norm is .8-1.2 - serum creatinin represents kidney function it is the end product of muscle metabolism. Gold standard

yesterday it was 3.4 so 2.4 is comming down

Progressive process

Chronic inflammation creates obstruction

prevents healing of tubes

promotes inflam process ( not normal tissue scar tissue)

HTN contribuites to risk and progression

can lead to kdney failure

What is Glomerulonphritis what causes the ITIS

IT is damage to glomerulus and happens in two ways- Both cause inflamation

1. membrane antibodies- these are antibodies that form against the glomerular protiens- type 2 hyper sensitivity
2. Complex decomposition- this is where cirulating immune complexes lodge in glomerulus and block formation of urine- type 3

What happens to Glomerulus during glomerulonephritis

1. edema- from fluid retention and protein loss
2. Hyperlipidemia- liver crank out cholesterol to try and replace plasma proteins
3. hypercoagibility- alters levels of clotting facter, exsess factors are loss in urine, but their is a decrease in urine their for incauses increase in factor consintration. 
4. Decreased immune competance- loss of globuline & complement protiens loss albumin which needs to be carried around.

1. prerenal- decreased blood supply to kidney(shock dehydration, vasoconstriction)
2. intrinsic or intrarenal- tubular function decrease(ishemia, toxins)
3. post renal- urine flow is blocked cause build up and leading to compartment syndrome(stones, tumors)

1. Onset- first decrease in urine
2. Maintance- Anything from olguira or anuria (decreased or 0 urine) bun creatine , K all rise
3. Recovery- repairs itsself and returns to normal function

Azotemia- accumulation of nitrogenous waste lab values

Uremia- clinical manifestation of renal failure

1. Neurilogical problems- seziures, MSC, coma death
2. Fluid and electrolyte imbalance- bun creating potassium all rise
3. Cardiovascular and resp problem- cirrculatory overload.

Renal osteodysttrophy-vit d not activated so can't absorb calcium , decreased Ca causes increased PTH, increase PTC caused increase bone ca loss, so increased phosporus causes decreased ca levels.... GET RID OF PHOSPHEROUS

Gastestinal disorders- metalic taste in mouth, gastrits ulcers d/t increase ammonia, increased pth increase gastric secretions

Uremic encephalophaty-muscle weakness, decrease mental, malaise coma death

What is hemodialysis

this is for patient that can't handle regular dialysis- main purpose to get fluid off d/t AT necrosis or fluid over load

....DO it slowly

Movement

breaking down

absorption

• keeps dangerous gut content out of blood

What is so bad about GERD

can we cure this?

and it leads to?

It causes Barrets Esophogus which is a velvet pink lining pressence of gobulet cells that normaly are musouc cells in small intestine.

• Can't cure just stop reflux
• monitor for dysplasia leads to esophageal CX

1. Franhemotenisi- bright red from esophagus about stomach
2. Coffee ground- in stomach with partial digetstion
3. Occult- intesting with blood mixing in stools can't see this
4. Malena- intestin large amount blood tary stool
5. Hemachezia- Rectum blood coats stool not in stool

H- pylorie- bacteria in gut secrets urease

NEDS TO BE TREATED WITH MULTIPLE DOSES OF ATB

1. Hemorrage- anemia
2. Perferation- peritonitis
3. decrease mucosal function- mealabsoption
4. decrease bacterial containment- sepsis

1. Ulcerative collitis- the problem is the mucousa lining
2. Chrons- goes all the way thru tissue(transmural) the gut more dangerous..more likely to die with infection

One we create surggial and the other is gynetic

1. Surgically produced treated with time- dumbing syndrome/short bowel
2. Genetically- Celiac intolerance to gluten, Tropical nothing to do with what you eat.

1. Carb metabolism- sugar stored as glycogen converted to glucose- to make fats
2. Protein metabolism- synthesied from amino acids
3. Fat metabolism- Synthesied and oxidied for energy packaged to lipoproteins
4. Process and stores vitaming and minerals
5. Synthesies clotting factors and stimulates Blood cell production- clotting facter made in liver
6. Drug and hormon metabolism- detox and inactivates
7. Immune system support- kuffer cells
8. Bile production- waste products dumbed in bile
9. Most important>>converts ammonia to urea

Structure of the liver

• Venous & arterial supply
• Along with all the rich resourses coming in liver we also have a nice supply of arterial blood loaded with 02
• Hepatic cels lie along vessels with good access to resourses from the blood
• Products come through back way thru sinus soid and out central vein
• many sinousids that come to gether empty into one vein= lobule
• back side of cells is bile duct

Liver Failure shows what disorders?

Skin

Renal

Hepatic encephalapathy

1. jaundic, cherry red palsm, spider nevi
2. Heporenal syndrome & decreased renal perfusion
3. increase ammonia and toxin leves in head will see ASTERIXIS( flapping hands)

1. Fatty liver(steatosis)- liver can't metabolize fat d/t getting rid of alcohole
2. Alocoholic hepatitis- Liver inflammed d/t build up of fatty spots(edema obstruction mediators hepatocyte failure.
3. Cirrhosis- fibrous scar tissue that blocks sinusoids and bile canal THIS CAN'T BE TURNED AROUND

• Fibrotic tissue that builds up from liver makes hard for blood to get into liver
• Blood backs up into stomach esophagus and intest
• venous systems tries compensate and finds aternate routes for blood
• Veins get stretch out varices forms.. bleeding occurs
• Will now have bleeding in stomach or esophagus

aspiration

affixiation

esophageal erosion

1. decreased in colloid osmotic pressure(lack of plasma proteins in blood)
2. increased in hydrostatic pressure( and mesentary)
3. aldosterone and adh remains in blood (retain NA & Water)

1. inflammation from a stone that is blocking common bile duct  backs up into pancreas activated digestive enzymes( HUGE INFLAM EVENT)
2. Alcohole
3. idopathic

1. increases pressure peri cap leads to ascites

2. Shunting of blood leads to blood going other places causes varices collateral chanells, caput medusae hemrroids.

3. Shunting of amonia leads to Hrpatic encephalopathy

4. This cause Splenomegaly which leads to anemia, leukopenia, thrbocypenia  along with ammune system problems