Heart: RAA,

Implications of short stay on 4E. Short.
Endothelial lining of heart.
Critical role for nursing.
Valves
1. Tricuspid
2. Plutonic
3. Aortic
4.
Superior inferior vena cava out plutonic to pulmonary artery to lungs.
Left corroded/ left subclavians. Which get more blood flow? Subclavians do the arms and are pretty active, also the brain which is the most needy organ in the body. So if you have a problem in your heart.
Brachiocephalic.
Coronary circulation. First branches off the aorta. Right off the aortic valve. Two main arteries: L branches into l anterior descending and L circumflex. LAD= left antioer decending, Left Cirq, RCA= right circulating artery,
Athroschlerosis: coronary arteries of particular concern. Starts at SA node.

WILL NOT HAVE TO LEARN ABOUT ACTION POTENTIALS. Automoticity= will beat on its own. Major two influences on heart rate with relation to the nervous system. Driven by the autonomic nervous system. Three major hormnes of the autonomic : epinephrine, norephinephrine, and Ach. Speed up will epi/norepi. AcH will slow the heart down.
Marjor cause of death in heart disease: dysrhythmias. May have end state heart disease, valvular disease, but that last even that happens one day is usually a dysrythmia. ECG is relied on. Won’t show us picture on exam, but we should be able to recognize the verbal description.
S1: blood ejected through pumonic and ventricular ejection: systole.
When 2/3 ejected mitral and tricuscpid open and that’s S2, dubb.
Then blood flows from atria into ventriacals called diastole, and when the ventrals are full again, that’s SI again.
Early diastolic filiing: high volume, high rate
Gallop: S3, a gallopy knocking noise. Early in diastoly and indicated ventricular dialation. Heart failure. Kentrucky.
Atrium contracts to get last bit of blood out of antriam an dinto ventrical. IF walls are stiff then atrial ejectio will make a very succato sound called an S4. Hypertrophy. Bigger cells, thicker muscle. S4. Tennesee.

Other thing that’s key is murmers.
Bruie: peripheral artery swishing noise, turbulent blood flow.
Murmer: turbulent bloof flow in the heart. Adults: muermers almost always caused by valvular heart disease.
Systole: ventricular ejection. Ventrical is contracting.
Stenosis: valve is too small. Which valve being steno tic is going to giv eyou a systolic murmer. Ventricular ejection Pushing blood through aortic valve. Systeolic ejection murmer due to stenosis is ogiong to be aortic stenosis
Mitral stenosis: blood mvoes through during diastole.
Regurgitation.
Systolic murmer due to narrowing of aortic valve.
Loud systolic murmer to second intercostal space radiating to neck you would thin aortic stenosis.
Slow rumibing during diastole heard beat at base: mitrl stenosis.
Think about where blood is moving.
Pge 28. Cardiac output. Extremely important.
Heart rate times stroke volume Number of berats per minute times the amount of blood per beat. So you come out with liters per minute.
Contractility: how good is the muscle.
Myocardial infartion: #1 way to mess with contractiiity.
What is peripheral resistance swhcih increaes our blood pressure. If vessels are really clamped down pushing it into a smaller container that’s called after load. Third component has todo with how much blood it has to work with when it starts contracting.
Preload: determines how hard it can pump. Not enough blood with which to work before contraction, like if the blood is not in the cardiovascular system but on the floor
Too mch fluid: heart stretched tooo big. Give them too much volume or kidneys don’t work.
Vaso dialators: beta blockers, calcium channel inhibitors
EF: ejection fraction
LVEDV: preload;
Veins dialate and accept volume.
Arteries are much stiffer; low compliance and low capacitance much higher pressure system. Can constrict.
Pressure in whole system related to how much volume.
Increase blood volume to increase BP or resistance.
Diuretics and vasodialtors: manage high BP
Sympathetic nervus system/ renin-angiotensin.
Pulse pressure: difference between systolic and diastolic. Higher in elderly people. Indicate stif fvessels.
Peripheral resistance:
Ace inhibitors:
Kidney: decided its in charge of BP. Sense renal blood flow t hrough JGA Juxa glomerular apparatus. Tells CVS to increae blood pressure. Renin: interacts with angiotensinin to make angiogenesis 1 Goes to lungs, where there is an enzyme called ACE: Angiotensin converting enzyme from 1 to 2, which is a powerful vasco constrtictoer of arteriorles. Stimulates adrenal cortext to make aldosterone which tell sthe kidney to hang ont o salt and water. So ace inhibitor is vasodialtor and a diuretic becase it prevents salt and water retention Improves ability to get rid of it if youdind’t have mechanism having you hang onto it.
RAA:
-bock ace
-block angiotensin receptors
-block aldosterone
This is more or less the endocrine system: effects all over the body, acting like hormones. Paracrine system in our tissues. The cardiovascular tissues themselves make angiotensin II. Endothelial and myocardial cells can do this. A growth factor and vascoconstirctor.
Remodeling.
-scarring. Not just from fibroblasts but growth of certain tissues. Disruption of norma tisssue sctrcuture. Angiotensin II constributes ot myocardial and vascular remodeling. Funcional problems of basco cnstriction and long term s structural problems that actually damage bood vesses.
Statins, Ace inhibitors: nmot ony prevenitn g but reversing. Ischemic heart disease and heart fialure. Must use ace inhibitors for people With DM, etc… more expensive.
Popurri of pt evaluations:

Pg. 130. Chest pain of heart diesease tends to be substernal and tends to be dull vs. sharp . Innervation that tells you that your heart hurts runs through the vagus nerve and the sympathetic as well. Also runs through arm and jaw. Classic symptom of heart diesase: dyspnea and dethrone (when laying down). PND


Pt; sense of impending doom. Tachycardia, tachypnea, BP elevated, murmers, gallops, Ralls, edema
Pg. 145:
ST depression or elevation: myocardial ischema.

This will become my friend:
Physiologic drawing:
L ventrical not enough blood getting out. Increase in LEVDV? Which will stretch the heart

Ischemic syndromes

Wednesday, November 19, 2008
Ischemic syndromes
Stable angina vs. unstable
Stemi vs. nonstemi
A stemi, plaque rupture rapid thrombus formation through the whole wall. A much bigger infarcton. This is something you have on page 146.
They all relate to atherosclerotic plaque
If it’s stable, it sticks way out into the vessel
Unstable plaques tho, might be completely flat. Pts may have no symptoms at all until they rupture. We go to acute coronary syndromes. If it’s sustained it leads to MI which is stemi and nonstemi. Page 143. We are only looking at part of this picture. Left main divides into the LAD and left cirq.
Right coronary comes off the aortic valves and perfuses the right ventrical and the nodes and wraps around in the inferior part of the heart. SA nodes. Responsible as the pacemaker of the heart and controlling conduction in the heart. IF you had an infarction that damaged your nodes you might not generate an adequate heart rate. Right coronary disease can cause bradycardia. And if conduction can’t go from the av node you call it heart block. Obstruction to right coronary artery affects the inferior heart and is associated with bradycardia and heart block.
The left coronary artery perfuses the major heart muscle which is required for normal ventricular function. When you have an infarction involving the distributino of the LAD you worry about tachyrhythmias. Morelikely to result in heart fialure.
In men of middle age, the symptoms of ischemic heart disease are extremely predictable. Nausia diaphorses, anxiety, substantial pain chest pain radiating to arm and neck, dypnea.
Women often present with atypical symptoms most commonly the sudden onset of extreme fatigue. Elderly pts and pts with diabetes frequently have silent ischemia. Just know they feel bad. The absence of classis symptoms does not rule out someone having a heart attack.
Stable plaque partially obstructs flow. Increase demand by some form of exercise. Pain is predictable and relieved with rest. Measuring something called cardiac iso enzymes. Troponin. CPKMB. Not elevated during stable angina. ST depression which returns to normal with cessation of pain. Treat with antithrombitcs like aspirin and treating risk factors like statins and PCI or CABBG.
Changes on the ECG.
Lactic acidoses stimulates the autonomic nervous system and the sympathetic nerves enter thes pine in the same place as the arm and the jaw. Arm is getting enough flow, its just a cross stimulation of nerves.
Krebs cycle requires oxygen and sugar to make ATP and if you don’t have nough it releases lactate which is an acid and an acidic environment is bad for tissue function and it hurts.
Coronary stenting. You probably don’t have just one problem. You must deal with it systemically. Get nitrates to deal with vasospasms. May be beta blockers and calcium channel blockers. And Every one with atherosclerotic heart disease will get STATINS. They help to stabalize plaques.
Coronary Artery bipass graph: used to be more common than anything. Pypass the obstruction.
Acute Coronary Syndromes: all characterized by the rupture of an unstable plaque. How long did that clot stick there? If they have ST elevaation, we know what they have. ST depression of ischemia with exercise. Lesion may not obstruct the vessel very much. Thin cap and vulnerable to rupture. IF that clot is big enough and stays a long time, we see ST elevation and stemie. So we just did stable plaque and stable angina. Alteration of rupture. Sustained ischemia infarction. Fabulus artists rendition.
The plaque ruptures. Stress and Cold weather, so it may have to do with SNS. Also more in moring when theres a busrt of cortical. Unstable angina often occurs at rest. So the thing just ruptures and once it rupture it exposes all this damaged tissue and we see them stick until they obstruct the vessel. If we have spontaneous dissolution of this clot, which does happen, then less than 20 mins perfusion is restored and we have unstable angina. If it was to stay there more than 20 minutes then we would see noontime or stemie depending on whow long it stuck there./
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Next step. Understnaidng anatomy of coronary perfusion. Whqat we have is across section of the ventricle. Clot forms an area of ischemia. If clot dissolves in more than 20 minutes then is this unstable angina a prescursor to ? No heart damage to eleveation fo cardiac is enzymes. If a clot stays longer, you get infarction. Yellow part is infarction. Because of anatomy of coronary vessels. Infarction stays near the . Sub endocardial MI = non stemie.
Watching desperate housewives and gets tremendous chest pain. Rushes to Er and gets there in 20 minutes. ST deprssion and no elevation of cardiac is enzymes: Unstable angina
ST depression and cardiac enzymes elevated. If didn’t get there till 40 minutes…
Later…transmural
And when that occurs we see .
Chest pain at rest, ECG shoes transient changes relieved with rest: unstable angina.
Review thse stemie things.