WEEK+6+Alterations+in+Cardio

Cardiovascular Objectives Page 2

abnormalities to various disease processes. __** (MS p. 752, ppt p16-18, 25) The table 32-7 in medsurg is quite extensive and should be reviewed. The specifics from class were: EKG ** - Can detect rhythm of heart, activity of pacemaker, conduction abnormalities, position of heart, size of atria and ventricles, presence of acute injury, and history of MI. Assess for serial changes ~assess serials to assess changes ~assess line and tube placement Cardiac Biomarkers(Serial blood draws for these to assess changes)- ** Initial rise in 4-6 hours, peaks in 18-24 hours normal after 2-3 days Initial rise in 4-6 hours Peaks in 18-24 hours Normal in 7-10 days Initial rise in 1-2 hours Peaks in 4-10 hours Norrmal in <24 hours
 * __ 4. Examine the diagnostics utilized to evaluate the cardiovascular system and relate
 * Chest X-ray- ~ ** assess silhouette and position of heart and lungs,
 * ~**assess patho-cardiomegaly,pulmonary edema
 * Troponin- ** contractile proteins released during an MI.
 * CK-MB-** Immunochemical process using monoclonal antibodies that measures this cardiospecific enzyme. Concentrations >5% of total creatine kinase (CK) are highly indicative of MI.
 * Myoglobin**- Low-molecular-weight protein that is 99%-100% sensitive for myocardial injury. Serum concentrations rise 30-60 min after MI. Cleared from the circulation rapidly and most diagnostic if measured within first 12 hr of onset of chest pain.  // Normal //// : // <92 ng/ml (men)  <76 ng/ml (women)

Cholesterol<200 LDL<100 HDL>60 Triglyc <150 Cholesterol/HDL ratio <5 ~high HDL neg correl with CAD ~**high** chol, triglyc,LDL and **low** HDL=CAD 5. Identify the risk factors for atherosclerosis. __** (MS p787, ppt p9-10) ~Geographic(increased in US,Europe ,Aus) ~Smoking ~Hypertension ~Sedentary with central obesity ~High Cholest. (low HDL in men) greater chance ~hyperfibrinogon ~yo-yo dieting women ~Diabetes Mellitis
 * Serum Lipids(ppt p10)** Cholesterol is a blood lipid. Elevated cholesterol is considered a risk factor for atherosclerotic heart disease. Level can be measured at any time of the day in a nonfasting state.
 * Angiogram- ** Study involves injection of radiopaque contrast medium directly into coronary arteries by same procedure as for cardiac catheterization. It is used to evaluate patency of coronary arteries and collateral circulation.
 * __
 * __ Modifiable __**

~**Heredity** ~**age** >45 for men >55 for women ~**Gende**r #1 killer of women postmenopause 2-3X Estrogen is cardio- protective- softens plaque
 * __Nonmodifiable__**

~**cultura**l White men Afro-amer Native-Amer < in Hispanics

The process of atherosclerotic plaque progression can be gradual. However, when there is sudden coronary obstruction caused by thrombus formation over a ruptured or ulcerated atherosclerotic plaque, the acute coronary syndromes result. **Unstable angina** is the result of reversible myocardial ischemia and is a harbinger of impending infarction. **Myocardial infarction (MI)** results when there is prolonged ischemia causing irreversible damage to the heart muscle. MI can be further subdivided into **non-ST elevation MI (non-STEMI)** and **ST elevation MI (STEMI).** Sudden cardiac death can occur as a result of any of the acute coronary syndromes. The American Heart Association Committee on Vascular Lesions provided criteria for subdividing coronary atherosclerotic plaque progression into five phases with different lesion types corresponding to each phase. The main point of this system is that some atherosclerotic lesions are “stable” and progress by gradually occluding the vessel lumen, whereas other lesions are “unstable” or complicated lesions and (even before there is any significant coronary occlusion) are prone to sudden plaque rupture and thrombus formation resulting in the acute coronary syndromes of unstable angina, myocardial infarction, and even sudden death. **__ Figure 23-20 __** provides an overview of the steps in the development of the acute coronary syndromes. Plaque disruption (erosions, fissuring, or rupture) occurs because of shear forces, inflammation with release of multiple inflammatory mediators, secretion of macrophage-derived degradative enzymes, immune cell activation, and apoptosis of cells at the edges of the lesions. Exposure of the plaque substrate activates the clotting cascade.__ 49 __ The resulting thrombus can form quickly. The thrombus may break up before permanent myocyte damage has occurred (unstable angina), or it may cause prolonged ischemia with infarction of the heart muscle (myocardial infarction)
 * __6. Explain the concept of acute coronary syndromes and its progression. (__**MS p802,patho 629, ppt p14-15)

When the plaque is **unstable** the threatens the entire myocardial thickness(**transmural**). Seen in clients with AMI, abrupt reocclusion, or transient episodes in clients with unstable angina.
 * __Remember__** when the plaque is **stable** it only threatens the subendocardial layer(**non-transmural)**, typical in clients with stable angina.

Coronary Artery Disease, AKA Ischemic Heart Disease, AKA Coronary Heart Disease, AKA Atherosclerotic Heart Disease is a chronic process that begins during adolescence and slowly progresses throughout life. Modifiable and nonmodifiable (see question 8) risk factors can accelerate or modify this chronic inflammatory process that ultimately manifests as fibrous atherosclerotic plaque in the coronary vessels.The process represents an attempt at healing in response to endothelial injury. The first step in the process is the development of fatty streaks, which contain atherogenic lipoproteins and macrophage foam cells. These streaks form between the endothelium and intima & form toxic oxygen radicals. Over time, a lesion made up of a lipid core formed w/Ca+ deposits develops and thickens. The deposits are what initiate the inflammatory response. Layers of fibrous tissue (collagen) eventually form a fibrous cap. Platelets stick and aggregate to the cap. Some plaques are considered stable, while others are unstable and more likely to rupture. The edge of the fibrous cap, sometimes called the “shoulder region”, is the site where most plaques lose their integrity or rupture. Plaque rupture exposes the underlying thrombogenic core (grunge) of lipid and necrotic material to circulating blood. This causes further obstruction to already narrowing vessel walls, resulting in more platelet adherence, aggregation, and progressive luminal narrowing, which prevents adequate blood flow to the myocardium. The heart doesn’t receive enough O2 & nutrients, resulting in various degrees of tissue damage due to ischemia. Complete blockage results in ischemia, death, and necrosis of the heart tissue (heart attack/MI).  Modifiable risks are the factors you can change to help prevent CAD, like: DIET! Diet is the biggest factor. Others include: excessively fatty diet, weight yo-yo, smoking, obesity (central obesity- apple shape), sedentary lifestyle, stress level, diabetes, HTN, medication compliance, knowledge level, high cholesterol level, dyslipidemia & hyperfibrinogen. South Asians (Indian, Pakistani, Sri Lankans) have the highest incidence of CAD. Nonmodifiable risks you can’t change, like: age, race, gender, & genetics/family history. Risk is greater in men older than 45 & women older than 55, but women catch up with men w/incidence of CAD after menopause. CAD is the #1 killer of women after age of menopause. **9. Discuss the progression of coronary artery disease from ischemia to infarction, including clinical symptoms, diagnostic evaluation of myocardial infarction, and critical timing for intervention. **  CAD is the end result of the accumulation of plaques within the walls of the coronary arteries that supply the myocardium (heart muscle) with oxygen and nutrients. Limitation of blood flow to the heart causes ischemia (cell starvation due to lack of oxygen) of the myocardial cells. Tissue damage might be the only result from ischemia, but when myocardial cells die from lack of oxygen, a myocardial infarction results. MIs usually result from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system, it fills the artery w/”grunge” to the point of sudden closure. It leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth. Since the heart is the pump that supplies oxygenated blood to our vital organs, any problem there immediately affects the supply of oxygen to the brain, kidneys etc. This leads to the death of tissue within these organs and their eventual failure or death. Clinical Symptoms of Ischemia and MI: ** No symptoms. ** Or “silent ischemia.” Blood supply to your heart may be restricted due to coronary artery disease, but you don't feel any adverse effects. 10. Describe angina pectoris and its related classifications: a) stable angina, b) unstable angina, c) prinzmetal’s angina (variant), and d) postinfarction angina. Patho page 626 and Lewis page 796, 802 a) Stable angina,= chest pain caused by myocardial ischemia. Discomfort is transient lasting 3-5 minutes and if blood flow is restored there is no permanent change or damage. Pain is presumably caused by a build up of lactic acid or abnormal stretching of ischemic myocardium. Caused by the gradual luminal narrowing and hardening of the arterial walls so that affected vessels cannot dilate in response to increased myocardial demand associated with physical or emotional stress. b) Unstable angina, = the result of reversible myocardial ischemia and is the harbinger of impending infarction. It is chest pain that is new in onset, occurs at rest or has a worsening pattern. It is unpredictable and represents an emergency. c) Prinzmetal’s angina (variant) = attributable to transient ischemia of myocardium. Occurs unpredictably and often at rest. Caused by vasospasm of one or more major coronary arteries with or without associated atherosclerosis. Often occurs at night during rapid-eye-motion (REM) sleep and may have cyclic pattern of occurrence. Angina may result from hyperactivity of sympathetic nervous system, increased Ca+ flux in arterial smooth muscle.
 * 7. Examine the pathophysiology of coronary artery disease. **
 * 8. Differentiate between modifiable versus nonmodifiable risk factors of the client with impaired health associated with coronary artery disease. **
 * Stable angina. ** If your coronary arteries can't supply enough blood to meet the oxygen demands of your heart, the result may be chest pain called angina. It's often described as a pressure or tightness in the chest — as if someone were standing on your chest. Angina is usually brought on by physical or emotional stress. The pain typically goes away within minutes after stopping the stressful activity- no permanent change or damage is done.
 * Unstable angina. ** Chest pain caused by transient ischemia of the myocardium that occurs unpredictably & often when at rest. Pain often occurs at night during REM sleep.
 * Shortness of breath. ** Or dyspnea. Some people may not be aware they have coronary artery disease until they develop symptoms of heart failure — extreme fatigue with exertion, shortness of breath and swelling in their feet and ankles. Heart failure occurs when your heart becomes so weakened from insufficient blood supply or from a heart attack that it can't pump enough blood to meet your body's needs. ** Classic symptoms of an MI also include: **** sudden chest pain- typically radiating to the left side of neck or down left arm, discomfort in 1 or both arms, dyspnea, nausea, vomiting, palpitations, sweating, cold sweating, weakness, feeling of indigestion, abdominal pain, aching, tightness, pressure, fullness, tingling & anxiety. **
 * Diagnostic evaluation for suspected MI include: **
 * electrocardiogram (ECG, EKG) ****, (12 lead) Imaging techniques- **** Angiogram, **** a **** chest X-ray(CXR) **** and **** blood tests **** (serum cardiac dx) to detect elevations in cardiac biomarkers (blood tests to detect heart muscle damage). Most often used markers are **** creatine kinase-MB (CK-MB) **** fraction and the **** troponin ** ** I (TnI) or troponin T (TnT) levels **** . **** Also MYoglobin. **** On the basis of the ECG, a distinction is made between **** ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI) **** . Most cases of STEMI are treated with thrombolysis or if possible with percutaneous coronary intervention (PCI, angioplasty and stent insertion). NSTEMI is managed with medication. **
 * *Cardiac cells can withstand ischemic conditions for about 20 minutes before cell death.* **** Acute MI requires hospitalization with continuous monitoring of cardiac rhythms and enzyme changes, because the 1st 24hrs after onset is the time of highest risk for sudden death. **

11. Examine the concept of oxygen supply and demand to the myocardium. Patho page 579 Oxygen supply to the myocardium is delivered exclusively by the coronary arteries. 70-75% of oxygen is used immediately. Any increase in demand can only be meet by increasing coronary blood flow. Adenosine is one of the local metabolic factors that will increase in concentration to dilate coronary arterioles to increase coronary blood flow. Myocardial oxygen consumption (MVO2) is closely correlated with total cardiac energy requirements. It is determined by three major factors.1) the amount of wall stress during systole, which can be measured by systolic blood pressure. 2) Duration of systolic wall tension, which is measured indirectly by heart rate. And 3) contractile state of the myocardium for which there is no clinical measurement.

__//**12. Examine the various locations of a myocardial infarction with the corresponding coronary artery of a client with impaired health.(Lewis, 803)**//__


 * Inferior wall** infarctions - occlusion in the **right coronary artery**
 * Anterior wall** infarctions- occlusion in the **left anterior descending artery**
 * lateral and/or posterior wall** infarctions- occlusion in the **left circumflex artery**


 * //__13. Describe the potential complications and related pathophysiology related to a myocardial infarction.(Heuther 631-632)(Lewis, 803-805)__//**

Associated with deterioration of a once stable atherosclerotic plaque that ruptures stimulating platelet aggregation and thrombus formation. Cardiac cells can withstand ischemia for 20 min before cell death occurs. Within 8 seconds o2 reserves are used up, glycogen stores are gone and anerobic metabolism starts to produce lactic acid. Myocardial cells don't handle changes in PH well which furthers damage. heart cells lose contractility, diminishing pumping ability. Catacholomines are released because of significant occlution, leading to sypathetic/parasympathetic imbalances, dysrythmias, and heart failure. //**Dysrhythmias-**// most common complication and cause of death. Dysrhmias that occur with anterior wall infarction, HF, or shock are life-threatening. V-fib is lethal and occurs 4 hours after onset of pain //**heart failure**// -Pumping power is diminished s/s are subtle with mild dyspnea, restlessness, agitation, tachy. Pulmonary congestion in x-ray, s3or s4 sound, crackles, JVD from rt sided HF //**cadiogenic shock-**// inadequate o2 and nutrients are supplied to tissue because of LFT vetricular failure, high mortality rate(Renal failure)is a complication //**papillary muscle dysfuntion-**// happens if MI mitral valve regurgitation, which increases blood volume in the left atrium. Aggrevates left ventricle and reduces CO. Rapid deterioration. ventricular aneurysm: Results when the infracted myocardial wall becomes thinned and bulges during contraction, can cause thrombi or rupture (which is fatal) //**dressler syndrome**//: pericarditis with effusion and feer developing 4-6 week after MI Caused by and antigen-antibody reaction to the nevrotic myocardium.
 * Patho**
 * Potential complications**
 * //percarditis//:** inflammation of the visceral and /or parietal pericardium, resulting in cardiac compression, decresed ventricular filling and emptying and HF. Causes chest pain aggravated by inspiration, caoughing, different from MI pain. Friction rub sound over the pericardium at the mid to lower sternal border


 * //__14. Examine the phases of the cardiac cycle: ventricular systole and ventricular diastole.(743 lewis) (571 heuther)__//**
 * Diastole:** during relaxation blood fills the ventricles rapidly, the residual pressure of the arterial system during ventricular relaxation (filling)
 * Systole:** The ventricular contraction after filling, contraction in left ventricle(systemic) is slightly earlier than the right (pulmonic). Peak pressure exerted against the arteries when the heart contracts

Expulsion of blood from the ventricles marks the end of one cardiac cycle.

15. Examine the pathophysiology and the compensatory mechanisms associated with congestive heart failure.

16. Correlate the clinical manifestations with the classifications of heart failure.

17. Illustrate the potential complications associated with heart failure and their related Pathophysiology, clinical manifestations, and collaborative management.

18. Examine the pathophysiology of congestive heart failure of the pregnant client and contrast to the non-pregnant client with congestive heart failure. Pillitteri 354 This is stupid, I don’t know what she wants here so I am going to ask her in class next week and fill it in then. Sorry guys. 19. Examine the pathophysiology of the cardiac defect, tetrology of fallot, that results in decreased pulmonary bloodflow, related clinical manifestations and collaborative management. Pillitteri 1304 Complex cardiac condition, congenital heart defect present at birth, abnormal fetal development in the 1st 8 weeks. Minimal to severe obstruction varies. (Tetra=4) Tetralogy has 4 anomalies present: Pulmonary stenosis (varying degree of stenosis, puts increased workload on R ventricle, RV has to work harder to overcome the resistance, decreased bf to lungs), VSD(causing unoxygenated blood mixing w/oxygenated blood, shunt can also occur L to R), RV Hypertrophy (muscle enlarges & thickens, overtime may lead to decreased compliance & failure), Overriding Aorta (Aorta shifted slightly to R, above the VSD, receiving blood from both R & L V’s, mixing of O2 poor blood w/O2 rich blood). Clinical manifestations: children w/Tetralogy of Fallot exhibit bluish skin during episodes of crying/feeding (known as “Tet spell”), SOB, tires easily, decreased appetite, decreased weight gain, fainting- Syncope, cyanosis, polycythemia, systolic murmur. Collaborative Management: Final management of TF is surgery to correct heart defects, done @ 1-2yrs of age. Instruct parents to try to keep hypoxic episodes to a minimum during this waiting time. If baby begins to have hypoxic episode, administering O2, placing him or her in knee-chest position (to trap blood in the lower extremities & keep heart from being overwhelmed), and administering morphine sulfate generally reduces symptoms. If not, propranolol (Inderal, a beta-blocker) may be given orally to aid pulmonary artery dilation. A temporary or palliative surgical repair, called the Blalock-Taussig procedure, can create a shunt between the aorta and the pulmonary artery (thereby creating a ductus arteriosus). This will allow blood to leave the aorta and enter the pulmonary artery, oxygenate in the lungs, and return to the left side of the heart, the aorta, and the body. B/c the subclavian artery is used in Blalock-Taussig procedure, a child will not have a palpable pulse in the R arm after this procedure. For this reason, blood pressure and venipunctures should be avoided in the affected arm. A full repair that relieves the pulmonary stenosis, VSD, and overriding aorta can be accomplished (a Brock procedure). Postop, observe for arrhythmias, which may result from any ventricular septal repair, edema, and conduction interference.