CAD, MI, CHF Past Paper PDF

CARDIOVASCULAR (CAD, MI) NSG 306 C ARDIAC EFFECTS OF MENTAL STRESS CORONARY ARTERY DISEASE  ATHEROSCLEROSIS Modifiable: Non-modifiable: High levels of LDL, triglyceride Age (due to chronic build-up Hypertension...

CARDIOVASCULAR (CAD, MI) NSG 306 C ARDIAC EFFECTS OF MENTAL STRESS CORONARY ARTERY DISEASE  ATHEROSCLEROSIS Modifiable: Non-modifiable: High levels of LDL, triglyceride Age (due to chronic build-up Hypertension of plaque) Smoking Family history (1st degree relative) Diabetes Ethnicity Autoimmune disease or excess inflammation Exercise can make an impact on modifiable risk factors!  LIPIDS Total cholesterol should be < 200 LDL should be< 100 treatment recommended at 130 Triglycerides- 60, treatment < 40 Treatment for hyperlipidemia: Exercise, weight loss, fish oil, niacin, fibrates, statins Initiation of medication treatment depends on presence of CAD, lipid levels, success of diet interventions  ATHEROSCLEROSIS Main contributor to CAD Causes build up of fatty cholesterol- filled plaques Obstructs blood flow in the coronary arteries  Irritant in blood predisposes atherosclerosis Damage to endothelium Cholesterol collects under damaged endothelium (fatty streak) Cholesterol oxidizes, sends signal to immune system to attract STEPS OF monocytes ATHEROSCLEROSIS Monocytes enter fatty streak, becomes macrophage and eats LDL cholesterol in endothelium Macrophage is gorged with cholesterol and dies (foam cells) Foam cells (dead white blood cells) release cytokines stimulating inflammatory process and more endothelial cells are damaged  STEPS OF ATHEROSCLEROSIS CONTINUED… LDL continues to collect in vessel wall Mountain of foam cells continues to build and bulge out into blood vessel Smooth muscle cells migrate out of smooth muscle layer and into fatty plaque, covering plaque with elastin and collagen (fibrous cap) to reduce exposure of blood to thrombogenic factors in plaque Dead white blood cells also cause smooth muscle to deposit calcium into the plaque Blood flow is restricted and deposited calcium makes arteries hard.  STEPS OF ATHEROSCLEROSIS CONTINUED… Complete blockage of the artery can occur Fatty plaque ruptures, releases thrombogenic plaque material in blood and forms clot in the artery at the site of the plaque No blood then gets through, no oxygen gets through Irreversible damage to the part of the heart supplied by that blood vessel occurs within about 20 minutes (myocardial infarct)  MYOC ARDIAL ISCHEMIA Local, temporary deprivation of the coronary blood supply Stable angina- progressive narrowing-pain with exercise that resolves with rest. Treatment: long-acting nitrates Printzmetal's angina- vasospasm of coronary artery which doesn’t allow enough blood nutrients. Can progress to MI if spasm doesn’t stop. Treatment: Calcium Channel Blockers Silent ischemia- more common in women, don’t have traditional symptoms of ischemia, fatigue, back pain. Can be brought on by mental stress.  UNSTABLE ANGINA Does not STOP with rest Treatment for angina – MONA ---OLD WAY of DOING THINGS… Morphine Oxygen Nitrates Aspirin “MORPHINE, OXYGEN, NITROGLYCERIN USED TO BE OUR ABCS TO DO FOR AN ACUTE HEART ATTACK,” DR. GUGLIN SAYS. “BUT NOW THE WHOLE FOCUS IS ON GETTING TO THE CATH LAB TO REMOVE THE BLOCKAGE AND PRESERVE AS MUCH MUSCLE AS POSSIBLE.” THROMBINS2 For Heart Attack Treatment Since healthcare providers stopped being taught MONA, no new catchy acronym has emerged to fill its place that encapsulates the broad range of emergency heart attack interventions that are commonly deployed today. In a 2015 paper, Dr. Winchester proposed a mnemonic, THROMBINS2, that could be used to replace MONA. But he is the first to acknowledge that it hasn’t widely caught on. However, it’s still a useful summary of all the available treatments (though not necessarily all given to a heart attack patient) today. The list retains some aspects of MONA, since they are still used on some heart attack patients—just not across the board. Here’s what it stands for: Thienopyridines: Drugs in this family of anti-platelet therapies, or blood-thinners, include prasugrel and clopidogrel. Similar to aspirin, they’re used to help restore blood flow and prevent clotting after a heart attack. Heparin: This drug may be administered by IV or injection after a heart attack to help prevent clotting. Renin-angiotensin system blockers: This includes drugs known as angiotensin-converting enzyme (ACE) inhibitors and drugs called angiotensin II receptor blockers (ARBs) that are used to lower blood pressure. Oxygen therapy: Even though this is no longer standard care for all heart attack patients, it’s still used for some patients who have what’s known as hypoxia, or dangerously low levels of oxygen levels in tissues throughout the body. Morphine: Because this pain reliever can also slow the heart rate and depress respiration, it’s only used as a last resort in heart attacks. Beta-blockers: These drugs are often prescribed after a heart attack to help reduce heart rate and lower blood pressure. Invasive surgery: This can actually be done without open-heart surgery. It involves procedures like PCI that can minimize tissue damage and lower mortality rates after a heart attack. Nitrates: These drugs are still sometimes used to reduce pain and restore blood flow. Statins and salicylate (aspirin): Statins reduce fatty deposits in blood vessels that can form clots and cause heart attacks, while aspirin acts as a blood thinner, reducing clots and restoring blood flow. MYOC ARDIAL INFARCTION Blood rushing through arteries can rupture plaque, clot develops Cardiomyocytes surround coronary vessels, clot decreases blood flow and oxygen to cardiomyocytes Decreased oxygen to myocytes causes pain signals to be sent to brain Normal coordinated way the heart beats is compromised when some myocytes not working well, (slowing contractions) Signals to brain cause surge of adrenaline to be released and the undamaged portions of the heart try to compensate by beating faster  MYOC ARDIAL INFARCTION Cell membranes of affected cardiomyocytes starts to break down and rupture Ruptured cardiomyocytes leak proteins into the bloodstream (troponins) Heart is becoming weaker, allows buildup of blood in heart that backs up in the lungs. Blood supply to brain can become compromised Permanent damage occurs after around 20 minutes; begin losing heart muscle cells at a rate of 500/second MYOC ARDIAL INFARCTION  TYPES OF MI Partial thickness infarct, N-STEMI Full thickness infarct, STEMI  MI INTERVENTIONS AND TREATMENT Coronary angiogram: dye injected and vessels visualized Percutaneous Coronary Intervention (PCI): catheter threaded into femoral artery, thread up to coronary vessels, depending on findings either perform angioplasty or stent placement Coronary artery bypass graft (CABG): open heart surgery, done for severe CAD. Blood vessels from elsewhere in body and use them to re-route the blood past the atherosclerotic plaques.  DIAGNOSIS OF MI Medical history – what happened? Symptoms, how long did they last EKG – measures electrical activity of the heart Compare pattern of patient with normal pattern Helps identify location of heart damage – elevated ST segment indicates full thickness infarct; depressed ST segment indicates partial thickness infarct Lab work – cardiac markers (troponins, myoglobin, and creatine kinase MB) If 2 of the above 3 are present, probable MI, if all 3 present, definite MI  MI MEDIC ATIONS - STEMI Admit to ICU bed with continuous monitoring, lie down in bed to decrease workload, supplemental oxygen Morphine: reduces pain, anxiety, and hopefully decreases heart rate Aspirin: reduces further development of clot Goal is reperfusion: if presented to hospital within 2 hours of onset, will be given medication to break down clot (thrombolysis)  MEDIC ATIONS FOR MI (STEMI) Beta blockers: heart beats slower and with reduced force (decrease in O2 demand Nitrates: vasodilators (opens blood vessels) Anticoagulants: reduce the development of clots Statins: Lower blood cholesterol ACE inhibitors: reduce blood pressure and reduce negative structural changes that occur after MI  HEALING AFTER MI 0-4 hours: decreased O2, cells using up energy stores, cells breaking down 4-12 hours: cardiomyocytes die but structure preserved, coagulative necrosis occurs (“gel” of denatured proteins), may have bleeding in area 12-24 hours: neutrophils enter area of infarction and start cleaning area and signal for more neutrophils 1-3 days: lots of neutrophils present, further lysing of debris 4-7 days: neutrophils die, macrophages ingest debris 7-10 days: macrophage activity continues; ingrowth of thin blood vessels into area, providing oxygen for working cells. Fibroblasts lay down scaffold of type 3 collagen (granulation tissue) 1-1.5 months: Type 3 collagen replaced by Type 1 collagen (scar tissue). Psychological effects of MI: shock to go from maybe no meds to multiple meds daily, increased risk of depression, and effects on loved ones.  Most occur within the first few weeks Decreased contractility Hypotension Development of COMPLIC ATIONS AFTER thrombi/emboli MI Electrical instability Causes arrhythmias If the infarct is in the right atrium where SA and AV nodes live, almost certainly will develop  Tissue necrosis: death of heart muscle cells Immune cells involved in the inflammatory process Septum can necrose causing oxygenated and deoxygenated C O M P L I C AT I O N S AFTER MI blood to mix Can cause rupture of the ventricle, trapping blood in the pericardium and causing cardiac tampanode Papillary muscles/chordae tendineae can rupture, causing regurgitation of valves  NITRATES Nitroglycerin-can be given SL, IV, or patch Promotes vasodilation of vascular smooth muscles. Primarily on veins, small affect on arterioles Rapid metabolism by liver: ½ life 5-7 minutes ADR-headache, orthostatic hypotension, reflex tachycardia. Severe hypotension if given with PDE5 inhibitors (Sildinofil) SL given every 5 minutes X 3 for chest pain. Onset 1-3 minutes Transdermal: need patch free period of 10-12 hours. Put on in AM and remove at bedtime. IV titrate to effect-pain free or drop in B/P  DRUG THERAPY FOR HYPERLIPIDEMIAS Drug class: HMG-CoA Reductase Inhibitors (Statins) Atorvastatin Actions Inhibit enzyme responsible for converting HMG-CoA to mevalonate, ultimately reduce liver cholesterol Uses In conjunction with dietary therapy to reduce LDL and total cholesterol levels Common adverse effects Headaches; nausea, abdominal bloating, gas Serious adverse effects Liver dysfunction; myopathy, rhabdomyolysis; myoglobinuria  DRUG THERAPY FOR HYPERLIPIDEMIA Drug class: Fibric Acids Drugs: gemfibrozil (Lopid), fenofibrate (Tricor) Actions Lower triglyceride levels; mechanism of action unknown Uses In conjunction with dietary therapy to treat hypertriglyceridemia Common adverse effects Nausea, diarrhea, flatulence, bloating, malaise Serious adverse effects Jaundice, early symptoms of gallbladder disease and hepatotoxicity  DRUG THERAPY FOR HYPERLIPIDEMIA Bile Acid Binding Resins: Colesevelam Actions: Bind to bile acids, promote increased metabolism of cholesterol Uses: In conjunction with dietary therapy to decrease elevated cholesterol Common adverse effects: Constipation, bloating, fullness, nausea, flatulence Serious adverse effects:Vitamin K deficiency (rare) See special mixing instructions  MISCELLANEOUS ANTILIPEMIC DRUGS Drug: ezetimibe (Zetia) Actions Block absorption of cholesterol from small intestine Uses In conjunction with dietary therapy to decrease elevated cholesterol Common adverse effects Abdominal pain, diarrhea Should not be used with fibric acid  Heparin: Used to prevent clot from getting bigger. Most facilities have an order set that A N T IC OAG U L A N T S describes parameters for drip infusion and goal aPTT ADR-bleeding, thrombocytopenia Antidote: protamine sulfate  Warfarin: Action: inhibit activity of vitamin K, which activates certain clotting factors Uses: treatment/prophylaxis of DVT, embolization from atrial fibrillation or heart valve replacement, A N T IC OAG U L A N T S pulmonary embolism Target: INR of 2-3 for patients with atrial fibrillation, stroke, MI, and DVT INR of 2.5-3.5 for patients with mechanical heart valve device  Low molecular weight heparin (LMWH) Uses Prevent deep vein thrombosis after hip replacements or abdominal surgery; prevent MIs, combined with aspirin A N T IC OAG U L A N T S Common adverse effects Hematoma formation, bleeding at injection site Serious adverse effects Bleeding, thrombocytopenia  ASPIRIN Actions Inhibit platelet aggregation Uses Primary prevention of MIs and stroke; PLATELET prevent blood clots from forming INHIBITORS Common adverse effects Abdominal distress, hypotension Serious adverse effects Neutropenia, agranulocytosis, bleeding  Drugs: abciximab (ReoPro), eptifibatide (Integrilin), tirofiban (Aggrastat) Actions Block receptors on platelets, preventing aggregation and clot formation GLYCOPROTEIN IIB/IIIA Uses INHIBITORS Prevent clots forming from the debris often released during percutaneous coronary intervention (PCI) procedures Serious adverse effects Bleeding, thrombocytopenia  Drugs: streptokinase, alteplase (tPA)(Activase), reteplase (Retavase), tenecteplase Actions Stimulate the body’s own clot-dissolving mechanism, converting plasminogen to plasmin, FIB R IN O LY T IC AG E N T S which digests fibrin Uses Dissolve fibrin clots secondary to coronary artery occlusion (MI), pulmonary emboli, cerebral emboli, deep venous thrombosis  FILL IN THE BLANKS ON THE TABLE… Classification Medication MOA Indication Adverse Effects 1 atorvastatin 4 Hyperlipidemia, CHD, 11 CVA prevention , CV event in pts with DM 2 ezetimibe 5 8 12 Bile-acid sequestrants 4 Binds to bile acids in the 9 13 intestine and prevents them from being reabsorbed into the blood, decreased LDL. 3 gemfibrozil 6 10 GI upset, ABD pain, N/V/D, and gallstones (RUQ pain) Niacin 7 hyperlipidemia 14 HEART FAILURE AND SHOCK NSG 306  HEART FAILURE Complex syndrome resulting from functional or structural impairment of ventricular filling or ejection of blood into the circulation Can result from: disorders of the pericardium, myocardium, endocardium, cardiac valves, or great vessels metabolic abnormalities  HEART FAILURE Pathophysiologic condition in which the heart is unable to generate adequate cardiac output, resulting in an inadequate perfusion of tissues or an increased diastolic filling pressure of the left ventricle, or both Inability of the heart to supply the metabolism with adequate circulatory volume and pressure HF can result from pump failure or resistance to filling Most common causes: CAD, hypertension, dilated cardiomyopathy, valvular heart disease  HEART FAILURE Left or Right Systolic or Diastolic Ejection Fraction (reduced or normal) Preload and Afterload  PRELOAD AND AFTERLOAD Preload: Volume of blood stretching the ventricles at the end of diastole Determined by venous return to the heart Also known as the end-diastolic volume, increases length of heart muscle fibers Afterload: Force that contracting heart muscle generates to eject blood from the filled ventricles Determined by systemic vascular resistance and ventricular wall tension  C ARDIAC RESERVE Maintained through compensatory mechanisms: Frank-Starling mechanism Activation of sympathetic nervous system reflexes RAAS Natriuretic peptides Locally produced vasoactive substances Myocardial hypertrophy Remodeling  REDUCED EJECTION FRACTION HFrEF: EF < 40% Results from conditions that: impair contractile performance of the heart produce volume overload Generate pressure overload on the heart Increase in preload Leads to excess blood in atrium and pulmonary venous system Symptoms: dyspnea, fatigue, peripheral edema, orthopnea, paroxysmal nocturnal dyspnea, jugular venous distension, cardiac enlargement  PRESERVED EJECTION FRACTION HFpEF: Systolic function is preserved (EF > 50%) Left ventricle unable to fill sufficiently during diastole Hypertension is leading cause Other causes: anything that impedes filling of the ventricles, increased ventricular wall thickness, reduced chamber size, or delayed diastolic relaxation With diastolic dysfunction, there is an increase in intraventricular pressure Transmitted backward from LV into LA and pulmonary venous system Diastolic function is influenced by heart rate PPT - BNP ＆ Heart failure PowerPoint Presentation, free download - ID:3263819 (slideserve.com) Clinical manifestations of Left and right ventricles heart failure depend on function as two pumps which side is dysfunctional connected in series LEFT- VS RIGHT- SIDED HEART Initial event that leads to FAILURE To function effectively, left heart failure may be of primarily left or right and right must maintain equal outputs ventricular origin, heart failure progresses over time to involve both ventricles Result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation Include dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema LEFT-SIDED HEART FAILURE Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, an S3 gallop, and evidence of underlying CAD or hypertension May lead to Right-sided heart failure Is the inability of the right ventricle to provide adequate blood flow into the pulmonary circulation Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation RIGHT-SIDED HEART FAILURE Most common cause: diffuse hypoxic pulmonary disease Jugular venous distension, Clinical manifestations peripheral edema, hepatosplenomegaly LEFT VS RIGHT HEART FAILURE  MANIFESTATIONS OF HEART FAILURE Depend on the extent and type of cardiac dysfunction and how rapidly it developed Can be precipitated by conditions such as infection, emotional stress, uncontrolled hypertension, or fluid overload Signs and symptoms reflect the physiologic effects of impaired pumping, decreased renal blood flow, and activation of sympathetic compensatory mechanisms  HIGH OUTPUT HEART FAILURE Thiamine deficiency – “wet” beriberi – affects CVS  PHARMACOLOGIC TREATMENT 1st LINE Beta blockers ACE/ARB Diuretics NEXT STEPS Aldosterone antagonists Digoxin Vasodilators  CIRCULATORY FAILURE (SHOCK) Acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply, resulting in cellular hypoxia Usually hypotension and hypoperfusion present, but vital signs can be normal Not a specific disease, but a syndrome Can occur with many conditions or disease states Can be classified by the cause, primary pathophysiology, or clinical presentation All types reflect an imbalance between oxygen supply and demand “SHOCK WAVE” – Cellular Response to SHOCK TYPES OF SHOCK  Usually result of severe ventricular dysfunction associated with MI CARDIOGENIC Diagnostic features: SHOCK Elevated left ventricular end- Narrow pulse Decreased CO S3 heart sounds Pulmonary edema diastolic pressure pressure (preload) Therapy aimed at improving CO and myocardial oxygen delivery, decreasing workload Inotropic, preload reducing, and afterload reducing agents Intraaortic balloon counterpulsation, ventricular assist devices, heart transplantation  HYPOVOLEMIC SHOCK Results from inadequate circulation blood volume precipitated by hemorrhage, burns, dehydration, or leakage of fluid into interstitial spaces External hemorrhage: most common cause Low CO and intracardiac pressures (low preload) lead to SNS activation = elevated HR, vasoconstriction, increased contractility  OBSTRUCTIVE SHOCK Results from mechanical obstructions that prevent effective cardiac filling and stroke volume Common causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax Manifests as right-sided heart failure Rapid management of underlying obstruction is required to prevent cardiovascular collapse  DISTRIBUTIVE SHOCK Characterized by excessive vasodilation and peripheral pooling of blood CO inadequate due to reduced preload Types include: Anaphylactic shock Neurogenic shock Septic shock  ANAPHYLACTIC SHOCK Clinical symptoms include: Urticaria Bronchoconstriction Stridor Angioedema Wheezing Itching Treatment includes maintenance of airway patency, use of epinephrine, bronchodilators, antihistamines, vasopressors, and IV fluids NEUROGENIC SHOCK Results from loss of sympathetic activation of arteriolar smooth muscle Causes include medullary depression (brain injury, drug overdose) or lesions of sympathetic nerve fibers (spinal cord injury) Treatment includes vasopressors, fluids, elevation of the legs, slow position changes, and the use of pressure stockings on the legs  SEPTIC SHOCK Results from severe systemic inflammatory response to infection Body’s response to infection or other insults results in systemic signs and symptoms of widespread inflammation: systemic inflammatory response syndrome (SIRS) Common causes: Gram-negative and gram-positive bacteria, fungal infections Gram-negative shock: endotoxins in bacterial cell walls stimulate massive immune system activation  SEPTIC SHOCK Characterized by release of immune mediators resulting in widespread inflammation Widespread inflammation leads to profound peripheral vasodilation with hypotension, maldistribution of blood flow with cellular hypoxia, and increased capillary permeability with edema formation Initially characterized by high CO due to sympathetic activation of the heart and warm extremities Even though CO is high, cellular hypoxia is present Reduced cellular oxygen utilization is manifested as high SvO2 Can deteriorate to a hypodynamic phase Decreased CO and organ ischemia Therapy aimed at improving the distribution of blood flow and managing infection with antibiotics Administration of fluids and drugs to improve cardiac and vascular performance to improve distribution of blood flow  C ASE STUDY HPI: You are called to the emergency room to assess F.T., a 62-year-old man with long- standing congestive heart failure. He was brought into the ER by ambulance after collapsing at home. His wife reported that 3 days ago, he developed cold symptoms and a fever. While his cold symptoms have not progressed, he became increasingly tired over the past 24 hours and had increased swelling of his ankles. PMI: FT was diagnosed 4 years ago with CHF secondary to long-standing hypertension. His medications include ACE-Inhibitor, digoxin, and furosemide. P/E: FT is unconscious but rousable to painful stimuli. Vitals: HR 122; BP85/50; RR 24; Temp 38.3°C (101°F). Carotid pulses are faint. A third heart sound is present as is a systolic ejection murmur in the apex region. Crackles (rales) are heard throughout the lung fields. Peripheral pulses are barely palpable and a pulse deficit exists. FT’s extremities are cool to touch and his capillary refill exceeds 4 seconds. Investigation: During your resuscitation of FT, you get a chest X-ray (see Figure 1).  CXR RESULTS http://www.radiologyassistant.nl/en/p42023a885587e/welcome-to-the-radiology-assistant.html WHAT IS THE MOST LIKELY DIAGNOSIS AND WHY? WHAT ARE THE TYPES OF THIS CONDITION? HOW DOES THIS RELATE TO HIS PAST MEDICAL HISTORY? HTTPS://B ARABUS.TRU.C A/HLTH2501/C ARDIOVASCULAR /C AD/C ASE.HTML HTTPS://BARABUS.TRU.CA/HLTH2501/C ARDIOVASCULAR/SHOCK/CASE.HTML