Cardioenzymes, pathologic changes in MI

Other pathologic myocardial changes with MI
Stunning - ischemic but not infracted cells may take time to recover even after reperfusion. Avoiding this stunned period might save their lives. Cooling people off to reduce inflammation and anti oxidants are being used.
Hibernating- some cells remain ischemic and nonfunctional. Cells that are getting a little bit of collateral flow. Their main blood supply is cut off, but they shut down. Learn to live without as much oxygen and sugar. Restore perfusion to these cells. Maybe by bypassing to a collateral vessels or gene therapies, lasers, etc…
Remodeling. Myocyte changes that lead to decreased contractility, mianly mediated by RAA but also role for SNS. Biggest strides are being made. This is about the heart itself. Some of the heart muscle itself tries to compensate in ways that aren’t good. Everybody who has an MI gets directly with the RAA, ace inhibitors and blocking the SNS, beta blockers. Very significantly reduce mortality after MI.

Non stemie can have st depression
Stemie has a characteristic big Q qave and big elevation in ST elevation.

Cardioisoenzymes, serieal every 4 hours
TROPONIN,
CPXMB
Arrythmia,
PVCs.
Vtac
Vfib
Acute congestive heart failure
Shock - 80% mortality.
Ventricular aneurism- clotting is a problem
Pericarditis
Everyone with chest pain should chew an aspirin.
In a pt with stemie: use emergency thrombolitic therapy and PCI (put a catheter in, open the vessel, and stent) all kinds of different ways to do it. Give ace inhibitors, beta blockers, and statins because of their anti-inflammatory effects.
Pt education/rehab. Allot of psychological issues. Pg. 150. Talking about MI.
Non stemie_
Unstable plaque rupture with prolonged obstruction by clot, some tissues infaction but clot solves before all of the at rik myocardium is ckilled
Infarction is confined to area just insie the endocardium.
Cardiac is enzymes ar elevated Troponin and CPK MB
Severe prolonged chest pain and heart failure.
ST elevation.
Manage with asprin, thrombolytics or PCI and later adde ACE inhibitors and Beta blockers.
More likey to be complicated by arrhythmias, CHF, shock, or rupture of valve or heart wall.

ECG with pain: st depression. When they stop having pain, return to normal. No increase in iso enzymes. So just ask when the pain came on?
Chest pain, nausia, st depression. Cardiac is enzymes



Prolonged severe, crackles, ECG shoes ST elevation. Interventions for all acute coronary syndromes try to rpevent clot formation. Antithrombootics and thrhombolytics. MI: add beta blockers and ace inhibitors. Stable angina. Immediately to thrombolytics and PCI. Stress stesting

Heart failure: pathological condition where the heart can’t generate adequate cardiac output. Second half: 40-60% have diastolic filling pressur eof the left ventrical thus that pulmonary capillilariy pressures are increased. If you can’t pump the blood out, you have more blood left in so the and is not the problem. It’s the or that’s the problem. Non-compliant. Even a n ormal amount of blood creates pressure. Systolic heart failure. Then diastolic failure. Refers to primary dysfunciton of the left ventrical. LV.
May be systolic, diastolic or both. Most common reason for elderly to be admitted to the hospital.

Cardio Myo Pathy: disease of the heart muscle.
Leucotropy; ability to relax normally.

Systolic Heart failure:
Decreased centrality
Increased after load: increased resistance to LV ejection. Usually due to increased peripheral vascular resistance (HTN) can olso occur with aortic outlet obstruction and aortic stenosis. Resulsts in myocardial hypertrophy. Increased LV muscle mass and increased oxygen demand.
Increased preload.

LDEDV: optimally, ejection fraction is optimized and volume is euvolemia .
Too much volume: decreases ejection fraction. Increaes in vlume can occur ecause you work t he heart too har or you have fluid overload because of renal falilure or too many iv fluids.
What did hypertension do to the ventricular muscle? Made it thick, and then remodeled it. This is scarring. Think of two balloons before this idea. When a ventrical is hypertrophied and scarred it’s the baloon that’s stiff and hard to blow up. So if a heart is supposed to be a little bit strenchy and you take one breathe to blow into it vs. the really stiff balloon . One breath won’t go so far. Not a problem of increasd LVEDV. Even a normal amount of problem clauses a presssure problem. Increased in LVEDP. Even a normal amount of volume put into a stiff ventrical means you have increased pressure.
After MI sometime the heart muscle gets so scarred this is a problem. The one we should remember is hypertension. The most common cause of diastolic heart failure. Another bullet with algorhythm.
Increases in HR makes this worse.

Very clinical test questions:
When you have a thick stiff ventrical forcing that last bit of blood into ti it made a knocking sound. Tennessee. Tennessee. Was the S4.
S3 is Kentucky. Kentucky.

Pt: dyspnea on exertion. Clear lung fields and an S4. That pt has diastolic heart failure. Doesn not get treated.
Another pt. Hist of HTN. Crackles in lungs. Evidence of lfuid overload. S3: pt has systolic heart faiure.
Exact question on exam.

JVD: bet that drawing done. Forward and backward. Heart fialure was in the Left ventrical. To the right of the most important organ in the body. Pressure backing up, it goes first to the left atrium in the lungs. Pulmonary edema. Pt will be tachypnic. And tachycardia . We’ve
Fetal edema. JVD ut this car is how we used to do coronary artery byb pass grafting. Beif aside: very particular we’re supposed to do it. Pt at 45 degrees measure from seconmd intercostal space. Ruler, etc… It’s one of those things were people sometimes try to quiantitate it so you make it up. You see big neck veins or you don’t.
One main take home: can aperson be in heart failure and have an MI? Yes. MI caused heart failure. So if they come in with heart failure, ask if they are having a life threatening MI. Are they in renal fialure? Are they having a HTN crises? Heart failure is a result form something else. If you are just reating heart fialure you might have them die.
Ace inhibitos and beta blockers. Ifyou look under treatment under acute CHF under 3a n the midle. It’s 4 that she wants to talk about.
VMP: Vatriuretic neuron? Peeing salt. In heart failure the ody tries as hear da s in can to be its own diuretic bu tit can’t do it is you’re nto perfusing ht ekidneys properly so the hear keeps tyring othe bmp is not causing heart failure. It’s trying ot respond and it can’t. We give people even more BMP to help them pee even more salt. So two points we ant to make. We measure BMP as a way to quantify the severity of heart fialure. And we give VMP IV to help the person pee more salt. If the perosn’s already got a BMP through the roof, then it won’t help. Same thing as giving more insulin to insulin resistanc DM. You can put in a balloon pump helping with after load. PCI of osme sort. Same things: use diuretics may use digoxin, ace inhiitors, and beta blockers as well. Instead of just using lasiks, you may put them on more than one diuretic. So summarizing, and then take questions. We’re going to almost certiantly get a pt who ahs had an ischemic heart. Maybe in the past or maybe right now, and then you’re also going to get a pt with bad hypertnesion. So I might get you ap t who is acutely having hcest pain. ST elevation and tropon tin gh the foof and stmeie so to be mangin gtha tyou are goig to be thining aobut aspirn oxygen thonobotiic or PCI and don the road we oook at ace inhibotrs and et a blcoker but hat the same time they ar complaining of severe hsortness of brehat lots of cracles and S 3 systolic hear falure os at the ame you’re reaitng hteir stmei you are also thinning about what kidn ofintervnetions> Oxygen. Idreetics. Ace inhitors. Beta lbockers. And baye dopamine. Or dpoutamie to try to support the hreat. Because that’s rthe real world.
She will give us a pt like that and we nneed the pathophyiologic of heart failure and ischemic heart dieseaes.
Then definitely a more chronic HTN pt starts out with diastolic disfunciotn and ending up with systolic disfunciton. We should explain it out loud. Think of what pt might complian of. You can reason it out.

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